|Page #||Chapter||Included in Published Errata||Section||Fact Name||Needs Illustration Team Review||Supporting Reference(s)||Main Comment||Submission type||Illustration Author Comment||Submission type triaged by staff||First author comment||Second author comment||Editor comment||Editor determination based on Prelim feedback||First Expert Reviewer||1st Expert Reviewer Feedback||2nd Expert Reviewer||2nd Expert Reviewer Feedback||Editor determination based on Expert feedback||Final wording on Errata||Added to Annotate||GC amount||GC paid||Date Submitted||First Name||Last Name||Null|
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|1||34||Biochemistry||Molecular||Chromatin structure||N/A||Heterochromatin --> column 2 --> Barr bodies (INACTIVATED X chromosomes) - Not inactivate X chromosomes||Spelling/formatting||Reject, test states "Barr bodies (inactive X chromosomes) may be visible..." spelling is correct. - Victor Martinez||Verified||Agree with rejection.-Anup||Reject.|
|Agree with authors.||Reject by 2 authors + 1 editor||01/01/19 12:34 PM||Behnam||Nabavizadehfirstname.lastname@example.org|
|2||34||Biochemistry||Molecular||Chromatin structure||Not needed, mnemonic||Histone Deacetylation Deactivates DNA||Mnemonic||Verified||06/10/19 8:10 PM||Estefanía||Henríquez Luthjeemail@example.com|
|3||35||Biochemistry||Molecular||Nucleotides||FA 2019 Page 35||Why (-1 ring ) is colored in red?||Spelling/formatting||Agree. It is a minor formatting issue. It should be in black font color. - Victor Martinez||Verified||We can correct in 2020. -Anup||Agree with both Anup and Victor. We can fix it in 2020.|
|Agree - JA||01/06/19 6:33 AM||Moatasem||Al-Janabifirstname.lastname@example.org|
|4||35||Biochemistry||Molecular||Nucleotides||aaa||Purines (A, G); 2 rings -- PURe As Gold; Exchange 2 gold Rings in a wedding||Mnemonic||Verified||Reject.|
Not a fan of this one.
|Would be easy to think of one ring, agree this is not helpful.|
|03/01/19 6:26 AM||Elana||Molchoemail@example.com|
|5||35||Biochemistry||Molecular||Nucleotides||Self-created.||I have created a helping mneumonic for the major deamination reactions. C U At Home Get Xtra 5 Toppings. It allows one to remember the order of the deamination reactions and which reactions are paired.||Mnemonic||Verified||LY imo. Not an easy mnemonic to remember or understand either.|
|Agree with rejection. -Anup||05/21/19 9:09 AM||Brianna||Olamijufirstname.lastname@example.org|
|6||36||Biochemistry||Molecular||De novo pyrimidine and purine synthesis||http://tmedweb.tulane.edu/pharmwiki/doku.php/proguanil https://www.uptodate.com/contents/antimalarial-drugs-an-overview#H14||Add proguanil (anti-malarial) to list list of medications that inhibit dihydrofolate reductase.||High-yield addition to next year||Agree we should consider adding proguanil to the next edition, the prodrug that produces an active metabolite, cycloguanil that inhibits DHFR. - Victor Martinez||Verified||Agree with addition. -Anup||Reject|
I don't think this is a HY drug to know for the USMLE Step1. We only mention it as a prophylaxis in several other places of the text but we don't discuss its pharmacology in any detail anywhere else.
|02/18/19 1:52 AM||Basim||Aliemail@example.com|
|7||36||Biochemistry||Molecular||De novo pyrimidine and purine synthesis||FA 2019 page 416 Orotic aciduria||In main pyrimidine base production diagram i think it would be better if you add (UMP synthase) enzyme on arrow from Orotic acid to UMP as it's clinically high yield.||Clarification to current text||I agree with the student and Vasily. It would reduce cognitive load - Victor M||Makes sense. Let's migrate to Annotate and discuss with the illustration team.|
|Reasonable to consider this for 2020.|
|Prelim accept but NOT publishable errata||04/18/19 3:43 AM||Muhanad||Shaibfirstname.lastname@example.org|
|8||37||Biochemistry||Molecular||Genetic code features||https://www.ugg.com/men-footwear/||Add mnemonic "when you wear your UGG, you Tryp (trip; for Tryptophan)" to remember that UGG codes for tryptophan and that it is an exception to the Degenerate/Redundant feature of the genetic code||Mnemonic||It is good. We should consider this mnemonic for the next edition. -Victor Martinez||Verified||Could be considered for addition, but not sure if this is HY. -Anup||I don't think this is HY. Vote to reject.|
|02/08/19 11:45 AM||Ralph||Zeitounemail@example.com|
|9||37||Biochemistry||Molecular||Genetic code features||Personal Mnemonic||The 4 genetic code features are: Unambiguous, Degenerate, Commaless, and Universal. Take the first letters of these 4 features and you can spell "CUUD." The mnemonic would be: Genetic "CUUD" features.||Mnemonic||Verified||LY, IMO.|
|Agree, unnecessary. - Huzaifa||04/28/19 12:58 PM||Milan||Terzicfirstname.lastname@example.org|
|10||37||Biochemistry||Molecular||Purine salvage deficiencies||https://reference.medscape.com/drug/elitek-rasburicase-342255#90||Rasburicase is colored as an enzyme with green. Please color it like a drug so as we don't get confused.||Clarification to current text||It should be changed to keep consistency - Victor M||Agree, a change is needed here. Suggest adding an arrow from uric acid to a new item "allantoin". This conversion is stimulated (arrow with a plus sign) by rasburicase (drug). One more arrow should be added from allantoin to urine.|
|Agree with editing this info. -Anup||Minor but not unreasonable to edit this so it is not as confusing, agree with consideration of change as per Vasily.|
|Prelim accept but NOT publishable errata||04/27/19 2:33 PM||Charilaos||Chourpiliadisemail@example.com|
|11||37||Biochemistry||Molecular||Purine salvage deficiencies||https://reference.medscape.com/drug/elitek-rasburicase-342255#10 link2: https://www.researchgate.net/figure/Mechanism-of-action-rasburicase-and-allopurinol-Depicted-is-the-pathway-of-purine_fig1_11995629||uric acid is the normal end of metabolism in human body. If rasburicase(urate oxidase) is taken as MEDICATION then it transform uric acid to allantoin||Major erratum||I believe it is the same comment about the color of rasburicase, which should be black (drug) instead of green (enzyme). - Victor M.||Agree with user. Humans do not have much activity of uricase and ASA and probencid do not have any effect on uricase or conversion of uric acid to allantoin. ASA and probencid affect the secretion of uric acid. The illustration needs to be changed to reflect this.|
|Agree. We have already proposed a suggestion in annotate. -AC||Proposal already in place to remove both aspirin and probenecid from this diagram. This is therefore a duplicate.|
|Reject by 2 authors + 1 editor||05/13/19 11:33 AM||Elaf||Mohamed||Elafmohamed38@gmail.com|
|12||38||Biochemistry||Molecular||DNA replication||Mnemonic||"2 'sides' to every 1 coin ['can']" hint for Etoposide/teniposide inhibit TOP II and irinotecan/topotecan inhibit TOP I. This can also be placed on page 434||Mnemonic||Reject. I agree with Anup. It is a complicated mnemonic to remember. -Victor Martinez||Verified||Complicated mnemonic for an already busy page. -Anup||Reject.|
Agree with Anup and Victor.
|Reject, I agree with Anup & Victor - JA||01/09/19 7:30 AM||Nathaniel||Borochovfirstname.lastname@example.org|
|13||38||Biochemistry||Molecular||DNA replication||Mnemonic||FlUORoquinolones inhibit TOP IV(4).||Mnemonic||The mnemonic is not bad. However, I feel that it is incomplete since TOP II is not included. - Victor Martinez||Verified||Agree with Victor. I think this page is already too busy as is. -Anup||Reject.|
Agree with other authors.
|01/12/19 8:15 AM||Moatasem||Al-Janabiemail@example.com|
|14||38||Biochemistry||Molecular||DNA replication||Mnemonic||To remember that DNA Polymerase reads DNA 3’ to 5’ and DNA is synthesized 5’ to 3’ write out the words “reads” and “synthesized” but replace every letter “E” with the number “3” and every “S” with the number “5”. This works both for prokaryotic and eukaryotic DNA replication and synthesis. Clarifying image attached.||Mnemonic||I don't like this suggestion. This mnemonic is not easy to remember. -Victor Martinez.||Verified||Defer to 2020. A suggestion, not errata. -Anup||Reject.|
Not very good.
|02/06/19 9:28 PM||Matthew J.||Christensenfirstname.lastname@example.org|
|15||38||Biochemistry||Molecular||DNA replication||Mneumonic||DNA polymerase III (III, red color) proofreads with 3' (3, red color) --> 5' exonuclease. DNA I (I, red color) degrades RNA primer (prime, red color)||Mnemonic||I don't feel that these numbers on red font will add extra value to the current information. -Victor Martinez.||Verified||Reject.|
Agree with Victor.
|Not in favor of addition. -AC||02/19/19 1:51 AM||Heewon||Choiemail@example.com|
|16||38||Biochemistry||Molecular||DNA replication||https://www.ncbi.nlm.nih.gov/pubmed/15137905||Regarding Bloom Syndrome it would be better if add more information about it like it's autosomal recessive. clinical manifestations include : growth retardation, facial anomalies, photosensitive skin rash, and immunodeficiency.||High-yield addition to next year||Not sure if this is HY for the Step exam. -Anup||Bloom is LY. Majed||04/18/19 4:46 AM||Muhanad||Shaibfirstname.lastname@example.org|
|17||39||Biochemistry||Molecular||Mutations in DNA||N/A||In the image provided for "Mutations in DNA", the silent mutation coding DNA (GAA) is the same as the mRNA codon (GAA). This would be a correct translation... not a silent mutation.||Minor erratum||Reject. A silent mutation happens when there is a substitution of a single nucleotide. But, it codes for the same or original amino acid. GAG is the original sequence coding for Glu, GAA is the mutated sequence (G substituted for A) which also codes for Glu. So, the mutation is silent since the protein will have the same amino acid at the same position as if the nucleotide substitution never happened. - Victor Martinez||Verified||Text is correct as is. No changes recommended. -VV||Reject by 2 authors + 1 editor||02/16/19 3:53 PM||Douglas||Mossemail@example.com|
|18||40||Biochemistry||Molecular||DNA repair||https://www.ncbi.nlm.nih.gov/pubmed/16238440||Fanconi Anemia is given as example under "homologous recombination", it is actually an example of "Non-Homologous End Joining" repair mechanism.||Minor erratum||Verified||This was changed per faculty recommendation last year. Also, A quick pubmed search returns many results linking FA mostly to HR.|
Example this recent review: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5904331/
|Agree, no changes to the text, as we have changed per faculty recs. -VV||Reject by 2 authors + 1 editor||01/16/19 10:09 AM||Sara||Khanfirstname.lastname@example.org|
|19||40||Biochemistry||Molecular||DNA repair||https://en.wikipedia.org/wiki/Non-homologous_end_joining||NHEJ is also defective in many forms of SCID.||High-yield addition to next year||Agree. We could consider adding SCID as an example of NHEJ. "NHEJ deficiency confers (severe) combined immunodeficiency - (S)CID - due to a failure to carry out V(D)J recombination efficiently" https://www.ncbi.nlm.nih.gov/pubmed/24629483 -Victor Martinez||Verified||Not sure if this is HY. May need X-ref. -Anup||Reject.|
There are more "classical" and more testable mechanisms of SCID that we cover elsewhere in the book.
|01/20/19 7:06 PM||Charles||de Leeuwemail@example.com|
|20||41||Biochemistry||Molecular||DNA replication||https://www.genscript.com/molecular-biology-glossary/12074/ATG-or-AUG||This submission is referring to a video associated with page 41 -- not an errata in the text. The title of the video / section is "Functional organization of a eukaryotic gene." I believe the error is spoken starting at time 1:09 -- "Also recall, the start codon is AUG when referring to DNA, and ATG when referring to RNA."||Minor erratum||Will be forwarded to Rx videos team.|
|05/29/19 9:53 PM||Jessica||Lifirstname.lastname@example.org|
|21||41||Biochemistry||Molecular||Functional organization of a eukaryotic gene||Uworld Question #2033||Poly-A tail is NOT AAAAAA its AAUAAA||Minor erratum||May need faculty input. And would be HY info replacing current text. -AC||The tail depends on the type of signal. For DNA, it is AATAAA. For pre-mRNA, it is AAUAAA. For mature mRNA, it is AAAAAA as we show.|
In short, we could add AAUAAA to the pre-mRNA line, but this is not critical. Moreover, there is already work in progress to modify this section that that the poly-A tail is not shown being the entire 3' end (as opposed to what our diagram shows now). All in all, based on this submission, no change is needed.
|Reject by 2 authors + 1 editor||07/25/19 9:46 PMemail@example.com|
|22||41||Biochemistry||Molecular||Functional organization of a eukaryotic gene||https://easylifescienceworld.com/addition-of-3′-poly-a-tail-mrna-processing-in-eukaryotes/||The graphic is inaccurate and highly confusing with its depiction of the addition of a poly-A tail. The way it is currently drawn makes it seem as if the polyadenylation signal – drawn as AATAAA on the coding strand – is itself transcribed into the poly-A tail, drawn on the mature mRNA as “AAAAAA.” Again, this is highly misleading and confusing. 1) On the graphic, clarify that pre-mRNA is the same as hnRNA, which is the term that you use everywhere else. 2) Draw the polyadenylation signal on the pre-mRNA strand as ‘AAUAAA’. The polyadenylation signal is specifically designed as being the 5’-AAUAAA-3’ sequence in the 3’UTR of the pre-mRNA which signals specific proteins to come and add the poly-A tail. The way it is currently drawn as being on the DNA is misleading, because the signal’s function is on the pre-mRNA. 3) The ‘mature RNA’ should show AAUAAA – since the signal is not excised – followed by a stretch of ~200 A’s. This is the biggest inaccuracy here – it really makes it seem like the poly A tail is just 7 adenine residues that were somehow directly transcribed from ‘AAUAAA’. Additionally, I think the graphic could be improved by drawing the 5’ cap as being more than just a blue terminal piece of the transcript. It would be much better to show it visually as a “7Me-G” linked by 3 “P”s to the 5’ end. Also, I think you should label “start codon” and “stop codon” on RNA, not the DNA. I’ve attached a really bad picture I drew to show how you could make the graphic better (with an artist more talented than me I hope).||Major erratum||11/24/19 9:28 PM||Rob||Shvartsfirstname.lastname@example.org|
|23||41||Biochemistry||Molecular||Protein synthesis||Mnemonic||The directionality of protein synthesis proceeds from the amino (N) terminus to the carboxy (C) terminus. This can be remembered by “proteiNs are Created N → C terminus"||Mnemonic||Verified||This seems familiar, maybe because it is mentioned in Kaplan videos? -Anup||Not a fan to be honest. I don't think that this is important enough to have its own mnemonic.|
|03/01/19 8:43 AM||Matthew J.||Christensenemail@example.com|
|24||41||Biochemistry||Molecular||RNA polymerases||https://www.ncbi.nlm.nih.gov/books/NBK22085/||RNA polymerase 2 synthesizes 5' to 3'; it does not read 5' to 3'||Major erratum||Reject. As I understand, this submission refers to "Functional organization of eukaryotic gene" fact. Confusion arises from the fact that we provide image of the coding strand, while it is the template strand that is actually transcribed.|
|Agree with Vasily. There is no erratum here. Just a slight misinterpretation on the part of the student in terms of what is being shown/actually influenced by the enzyme.|
|Reject by 2 authors + 1 editor||05/12/19 2:50 PM||Kinza||Sultanfirstname.lastname@example.org|
|25||42||Biochemistry||Molecular||RNA polymerases||It's Mnemonic||Actinomycin *D* (also known as *D*actinomycin) inhibits RNA polymerase in *D*ual (both) prokaryotes and eukaryotes.||Mnemonic||I agree with Anup. It may be considered for the next edition. -Victor Martinez||Verified||Could be considered for 2020. -Anup||Reject.|
What is the significance of knowing that it inhibits both enzymes?
|01/12/19 9:13 AM||Moatasem||Al-Janabiemail@example.com|
|26||42||Biochemistry||Genetics||Splicing of pre-mRNA||mnemonic for existing material in book||GULAG - A mnemonic for the sequences at either end of an intron: FU at 3' end and AG at 5' end. The L stands for Lariat/Loop.||Mnemonic||I am not inclined to agree or reject. However, according to google GULAG means "A system of labor camps maintained in the Soviet Union from 1930 to 1955 in which many people died". -Victor Martinez.||Verified||I would reject. Too many mnemonics. -Anup||Reject.|
Agree with Anup.
|02/07/19 9:25 AM||Joshua||Moranfirstname.lastname@example.org|
|27||44||Biochemistry||Molecular||tRNA||https://www.ncbi.nlm.nih.gov/books/NBK6236/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848691/ ;and also UWorld||In the diagram explaining the structure of a tRNA, the acceptor stem is incorrectly labeled; it should include the whole length of the vertical 3' end attached to the T arm (so basically the CCA end is only part of the acceptor stem)||Minor erratum||There are many diagrams and illustrations about this topic showing the stem in different ways. We need faculty input. - Victor M.||Verified||Could ask illustration team to look into it. -Anup||Agree with Anup, reasonable to consider this year.|
|Prelim accept but NOT publishable errata||03/08/19 6:45 PM||Hasan||Alarouriemail@example.com|
|28||44||Biochemistry||Molecular||tRNA||https://en.wikipedia.org/wiki/D_arm#cite_note-hardt1993-1||The D-arm is a portion of the tRNA molecule that acts as a recognition site for aminoacyl-tRNA synthetase; wording is unclear "D-arm detects the tRNA by aminoacyl-tRNA synthetase."||Clarification to current text||We could change the text to read: "D-arm allows detection of the tRNA by aminoacyl-tRNA synthase."|
|OK to migrate over clarification for consideration in 2020.|
|Prelim accept but NOT publishable errata||03/29/19 6:49 AM||Elana||Molchofirstname.lastname@example.org|
|29||45||Biochemistry||Molecular||tRNA||Typing error||Page37says wobble codons differ in 3rd position.But in page44,in the figure below wobble is indicated in 1st position as tRNA is read from 5 to 3||Minor erratum||11/26/19 1:42 AM||Javohir||Nazarovemail@example.com|
|30||46||Biochemistry||Cellular||Cell cycle phases||https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1365-2443.1996.d01-234.x||EPO is Non-receptor tyrosine kinase, while insulin, PDGF, EGF are receptor tyrosine kinase of the family tyrosine kinases.||Minor erratum||Many types of research and literature show EPO as a Janus Tyrosine kinase receptor (JAK). However, I agree with Anup, I think we need faculty input to be sure about this fact. -Victor Martinez.||Verified||This article tends to suggest otherwise: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC49475/ . Needs expert review to determine if the user is correct or not. I found a bit of controversial info in these articles, so please kindly review. -Anup||Reject. The article mentions Tec, a non-receptor tyrosine kinase. However, there is no mention of EPO in the student's cited article. As pointed out by Anup, there are several articles that clearly establish that EPO is a receptor tyrosine kinase. No changes to the text. -VV||Reject by 2 authors + 1 editor||02/06/19 7:26 AM||ahamd||Obeidatfirstname.lastname@example.org|
|31||46||Biochemistry||Cellular||Cell cycle phases||mnemonic, FA 19 p. 46||*P*hosphorylated Rb allows cell cycle to *P*roceed||Mnemonic||Verified||05/07/19 6:00 PM||Elan||Baskiremail@example.com|
|32||46||Biochemistry||Cellular||Cell cycle phases||https://www.ncbi.nlm.nih.gov/pmc/articles/PMC23451/||hypophosphorylation (activation) of Rb should be hyperphosphorylation (activation) of Rb||Minor erratum||Reject. Hypophosphorylation induces the activation of Rb. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC137861/ - Victor M||Reject suggestion per Victor. -AC||Reject, Victor is correct, HYPOphosphorylation is the activating signal here. Text is correct as is, no change needed.|
|Reject by 2 authors + 1 editor||05/30/19 10:17 PM||Mohammed Sakil Ahmed||Shahfirstname.lastname@example.org|
|33||46||Biochemistry||Cellular||Cell cycle phases||not needed||Cyclin-dependent kinases is Constitutive and inactive (in absence of cyclin)||High-yield addition to next year||08/06/19 2:02 PM||Ra'ed||Ababnehemail@example.com|
|34||46||Biochemistry||Cellular||Cell cycle phases||Self-written||CDK's phosphorylate proteins like RB. When RB is phosphorylated is means it takes a phosphate, so it becomes heavy and can't do its normal function of stopping G1->S as it's now lazy and lets G1->S occur instead of stopping it.||Mnemonic||10/30/19 10:03 AM||Khalid||Alattarfirstname.lastname@example.org|
|35||46||Biochemistry||Cellular||Rough endoplasmic reticulum||aaa||N-glycosylation occurs in the eNdoplasmic reticulum; O-glycosylation occurs in the gOlgi apparatus||Mnemonic||Verified||I like this mnemonic. I think we should add it.|
|03/02/19 3:34 AM||Elana||Molchoemail@example.com|
|36||46||Biochemistry||Cellular||Smooth endoplasmic reticulum||Self-written||Smooth Endoplasmic Reticulum (SER) - want's body to run SMOOTH so removes poisons and drugs. Makes Steroids for us to run smooth + has SMOOTH surfaces without ribosomes on it.||Mnemonic||10/30/19 10:06 AM||Khalid||Alattarfirstname.lastname@example.org|
|37||47||Biochemistry||Cellular||Cell trafficking||https://www.uniprot.org/locations/SL-0075||COPI transports from Golgi -> Endoplasmic Reticulum (currently says from Golgi -> Golgi)||Minor erratum||Agree with Vivek and Vasily. The text states Golgi to Golgi since it is the retrograde type of transport. - Victor Martinez||Verified||Reject. Agree with Vivek.|
"The coat protein I (COPI) complex manages traffic from the Golgi back to the ER (retrograde transport), or between different compartments of the Golgi (intra-Golgi transport)."
|I feel current text is correct as is as quoted below:|
"vesicles with a COP I coat mainly transport proteins in the retrograde direction BETWEEN Golgi cisternae and from the cis-Golgi BACK to the rough ER."
|Text correct as is. No change needed. -VV||Reject by 2 authors + 1 editor||01/11/19 12:19 PM||Lauren||Allenemail@example.com|
|38||47||Biochemistry||Cellular||Cell trafficking||N/A||I-cell disease: “I” is a part of the alphabet, so we start there. Ignoring A through E, we start with F to recall the clinical features of I-cell disease: Facial features coarse/ Gingival hyperplasia/ Hand deformity “claw”/ “I’s” (eyes) corneal clouding/ Joints/ Kyphoscoliosis/ Lysosomal enzymes ↑↑||Mnemonic||Verified||08/15/19 3:38 PM||Andrei||Allicockfirstname.lastname@example.org|
|39||47||Biochemistry||Cellular||Peroxisome||not needed||Zellweger syndrome: Renee Zellweger has WEAK PEX (hypotonia; PEX gene mutation) and SEIZES (seizures) big livers (hepatomegaly); Refsum disease: ALPHA (alpha-oxidation disorder) males are PHYTAN A LOT (buildup of phytanic acid) because the REF's SON (Refsum) made the team but is CLUMSY (ataxia) and CAN'T SEE (cataracts/night blindness); Adrenoleukodystrophy: ß-A-L-D for ß-oxidation||Mnemonic||I find this mnemonic a bit long. But, if the rest feels is useful, then it would be perfect for me. -Victor Martinez.||Verified||Could be considered for 2020. -Anup||Not very good IMHO.|
|01/02/19 2:06 PM||Nicholas||Yeisleyemail@example.com|
|40||47||Biochemistry||Cellular||Peroxisome||https://www.uptodate.com/contents/peroxisomal-disorders ,,,https://www.ncbi.nlm.nih.gov/books/NBK22240/||we can use VLCFAS as mnemonic for zellweger syndrome , V--> vision problem , L --> liver enlargement, C --> copper high , F --> fe high , A --> abnormal muscle tone, S--> seizure,,,,,, we can also use PEX in PEroXisome for PEX gene||Mnemonic||Verified||08/31/19 8:23 AM||Mohamed||Menofyfirstname.lastname@example.org|
|41||47||Biochemistry||Cellular||Peroxisome||-||ABCD gene ---> (A)drenoluekodystrophy, (B)-oxidation, (C)o long/so long chain fatty acid, Defect||Mnemonic||Verified||09/06/19 2:01 PM||Ahmad Y.||Obeidatemail@example.com|
|42||47||Biochemistry||Cellular||Peroxisome||Mnemonic||The “βALD BOYS” are wearing VERY LONG CHAINS. With *A*DDED [Adrenals] *B*RAINS [Brain] and *B*RAWN [Testicles], [*C*omma/Coma] they’re *D*EADLIER [Death] than *1* I think this is a very good mnemonic because it’s short but written out it contains every single detail from the fact. It produces a good mental image, and it rhymes (sort of). I capitalized and put astericks around the parts that represent facts. “βALD” reminds us of the name of the disease and the deficient process (Adrenaleukodystrophy, β-oxidation). I took this part from another submission. “BOYS” reminds us that this is an X-linked disease. The bald boys wearing “VERY LONG CHAINS” reminds us that there’s a buildup of very long chain fatty acids (VLCFAs). “ADDED BRAINS and BRAWN” represents the adrenals, the brain, and the testicles – the affected organs. “,” is a COMMA and reminds us that COMA is a complication “DEADLIER” reminds us that death is a complication Finally, you’ll notice that I placed the astericks around the first letter of some of the clues to help remember the affected gene: ABCD1||Mnemonic||12/04/19 11:46 PM||Rob||Shvartsfirstname.lastname@example.org|
|43||48||Biochemistry||Cellular||Cytoskeletal elements||https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2064177/||In 2006 a new systematic nomenclature for mammalian keratins was created, and the proteins previously called "cytokeratins" are simply called keratins||Minor erratum||08/07/19 8:17 AM||Ra'ed||Ababnehemail@example.com|
|44||48||Biochemistry||Cellular||Microtubule||nature.com/subjects/dynein||Tie-Dye is retro: Tie-Dye (dynein) in Retro(grade)||Mnemonic||Verified||I am personally not a big fan of this mnemonic, but I think we can migrate it, and see if the crowd likes it.|
|I like it better than what we have currently. Agree to migrate|
|02/24/19 4:41 PM||Myanna||Olsenfirstname.lastname@example.org|
|45||48||Biochemistry||Cellular||Microtubule inhibitors||https://www.ncbi.nlm.nih.gov/pubmed/17986648||"(Vin)cristine gets her tubes tied"||Mnemonic||11/24/19 3:49 PM||Kevin||Rivera||Kevin.Rivera@tcu.edu|
|46||49||Biochemistry||Cellular||Sodium-potassium pump||https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2949520/||The cardiac glycosides activate the Na+/Ca2+ exchanger which results in the exit of 3 Na+ ions and the entry of 1 Ca2+ ion||Minor erratum||Verified||Digoxin MoA from UTD:|
"Heart failure: Inhibition of the sodium/potassium ATPase pump in myocardial cells results in a transient increase of intracellular sodium, which in turn promotes calcium influx via the sodium-calcium exchange pump leading to increased contractility."
The wording really depends on the function of the Na/Ca exchanger.
If it can only move Ca outside of the cell and Na inside, then it is inhibited by high Na in the cell.
If it can move Ca inside the cell and Na outside of the cell, then it is activated by high Na in the cell.
I am pretty sure I saw it expained either way in a variety of qbanks. Whatever the exact function of the Na/Ca exchanger is, the end result is increased Ca inside the cell.
IMHO, UTD is a reliable enough resource, so it is worth migrating this suggestion to Annotate to continue the discussion.
The cited article is discussing the mitochondrial Na-Ca exchanger. The Na-Ca exchanger present on the plasma membrane is inhibited by the increased intracellullar sodium. Our currect text is correct and accurate.
|Seems controversial. Given the disagreement and nuance of this submission, will propose a migration with a high probability of expert review to ensure that we get things 100% right before making any changes to the text.|
|Disagreement/need expert||03/09/19 6:26 PM||Jeffrey||Sackeyemail@example.com|
|47||49||Biochemistry||Cellular||Sodium-potassium pump||https://www.medscape.com/viewarticle/785818||3 Na out(3 letters) , 2 K in (2 letters)||Mnemonic||Verified||08/31/19 8:29 AM||Mohamed||Menofyfirstname.lastname@example.org|
|48||50||Biochemistry||Cellular||Collagen||https://www.ncbi.nlm.nih.gov/pubmed/360747||As Type 1 collagen is important for late wound repair, Type 3 collagen is also important for EARLY WOUND HEALING||Clarification to current text||Agree - Victor M.||I think it is HY to contrast the roles of type III and type I collagen in wound repair.|
It might be a good idea to change "granulation tissue" to "early wound repair".
We could also use bold font for words "early" and "late".
|OK to migrate over to consider this for further debate.|
|Prelim accept but NOT publishable errata||04/20/19 1:58 PM||Muhanad||Shaibemail@example.com|
|49||50||Biochemistry||Cellular||Collagen synthesis and structure||none needed||Hosts Give Partygoers Champagne at their SOIREE. Each of the four first words corresponds with the step in collagen synthesis that has an associated deficiency/syndrome. SOIREE corresponds with the first letter in the associated problem. Hosts (hydroxylation) Give (glycosylation) Partygoers (proteolytic processing) Champagne (cross-linking) at their SOIREE (scurvy, osteogenesis imperfecta, SKIP step 4 (R), Ehlers-Danlos, Ehlers-Danlos and Menkes)||Mnemonic||It is difficult to remember. - Victor M.||Verified||I personally do not like this suggestion. -Anup||I don't get this at all. Agree it is not helpful|
|03/10/19 6:23 PM||Natalie||Jansenfirstname.lastname@example.org|
|50||50||Biochemistry||Cellular||Collagen synthesis and structure||https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3093059/||Clarify on the sentence: Glycine content best reflects collagen synthesis. For example, If i have two tissue samples, one of which is primarily made up of collagen (i.e, Bone or cartilage) and another one is devoid of collagen or containg negligible amount of collagen (i.e, synovial fluid). In this case, using glycine content reflects the amount of collagen present in these tissues. However, if i have two tissue samples, both made up of more or less collagen (let's say skin and ligaments). In this case, I can not use glycine to reflect the collagen amount present in these tissues as glycine though not abundant as much as in collagen, is still present in various other protiens such as elastin. Therefore, measuring glycine content could give me false results. In these cases, measuring hydroxylated proline (i.e, hydroxyproline) would be the best choice since it is very specific for collagen only.||Clarification to current text||I think this might be a valid clarification.|
Currently we use the following wording: "Glycine content best reflects collagen synthesis (collagen is 1/3 glycine)".
It would be probably more accurate to say that "glycine's content in collagen (1/3) is less variable than that of lysine and proline".
And indeed, it seems that hydroxyproline, not glycine, is used by labs for collagen quantification, and we can mention this as well if deemed HY by the crowd.
|Seems like a reasonable clarification, appreciate the detailed submission and critique. We can migrate over for 2020 consideration.|
|Prelim accept but NOT publishable errata||03/17/19 8:21 AM||Ketan||Daymaemail@example.com|
|51||50||Biochemistry||Cellular||Collagen synthesis and structure||NA||Vitamin C deficiency leads to a problem with Hydrox"C"lation.||Mnemonic||Verified||Not a big fan of this mnemonic, but let's discuss with the crowd.|
|Not a fan either. Wouldn't be helpful IMO. -AC||03/17/19 4:52 PM||Mazal||Haglerfirstname.lastname@example.org|
|52||50||Biochemistry||Cellular||Collagen synthesis and structure||self-made||I have created a helpful mnemonic for memorizing that lysine is involved in the collagen cross-linking process. "Do not lie or you will be cross-examined."||Mnemonic||Verified||05/21/19 9:13 AM||Brianna||Olamijuemail@example.com|
|53||50||Biochemistry||Cellular||Collagen synthesis and structure||not needed||"formation of procollagen to hydrogen and disulfide bonds " is better to be mentioned as independent step||Clarification to current text||08/07/19 2:34 PM||Raed||Ababehfirstname.lastname@example.org|
|54||50||Biochemistry||Cellular||Collagen synthesis and structure||https://www.ncbi.nlm.nih.gov/books/NBK21582/||I think the steps describing collagen synthesis are a little bit oversimplified, and it would actually be more clear to elaborate a bit. Firstly, it should be clear that "preprocollagen" refers to the alpha chains while they are undergoing translation in the cytosol but before they are translocated to the RER. Once in the RER, they are called "pro alpha chains." Second, "glycosylation of proline residues" should be its own step, and should not include the addition of disulfide bonds to form the triple helix. You should add a new step between step 3 and 4 that clarifies the stabilization of the triple helix with disulfide bridges. Each helical pro alpha chain is flanked at both ends (termini) by a globular “propeptide” – the disulfide bonds between the propeptides of 3 chains is what forms the triple helix. It would be a helpful addition to the graphic to draw these propeptides as circles at the termini of the chains and procollagen. In Step 5, it would be helpful to clarify that the “disulfide-rich terminal regions” are the same propeptides that were added in step 3. Now in the extracellular space, removing the propeptides causes the tropocollagen to be far less soluble, allowing the molecules to self assemble into fibrils for cross linking by lysyl oxidase in step 6. In step 5 for the graphic, add little circles representing the propeptides to the cleaved C- and N- terminals. Lastly, in step 6 of the graphic it is more accurate to call the final product a “fibril” than a “fiber.” A fiber is the collection of thousands of fibrils, each 50nm in diameter.||High-yield addition to next year||11/24/19 8:32 PM||Rob||Shvartsemail@example.com|
|55||51||Biochemistry||Cellular||Ehlers-Danlos syndrome||https://www.ncbi.nlm.nih.gov/books/NBK21582/||In describing the various types of Ehlers-Danlos Syndrome, the current text reads: "Hypermobility type (joint instability): most common type." It then starts a new line (as if introducing a completely distinct fact) and says "Classical type (joint and skin symptoms)". The next new line IS a distinct fact, describing a distinct type. The way that it's currently written really makes it seem like "Hypermobility type" and "Classical type" are different, but I believe they are exactly the same.||Clarification to current text||11/24/19 8:35 PM||Rob||Shvartsfirstname.lastname@example.org|
|56||51||Biochemistry||Cellular||Menkes disease||It's Mnemonic||Menkes protein (ATP7A ,vs ATP7B in Wilson) --->M precedes W and A precedes B alphabetically ,so " Menkes =ATP7A ,,Wilson =ATP7B".||Mnemonic||The mnemonic should reduce the cognitive load and this particular one is a bit difficult to remember. -Victor Martinez||Verified||Too complex for a mnemonic. Would be wasting time learning the mnemonic. -Anup||Agree this is not helpful|
|01/12/19 9:36 AM||Moatasem||Al-Janabiemail@example.com|
|57||51||Biochemistry||Cellular||Menkes disease||not required||Please see attachment: W=copper goes up, M=copper goes down||Mnemonic||Agree, I think it is a good mnemonic. We should add it to the next edition. -Victor Martinez.||Verified||Let's consider for 2020. I think the mnemonic is quite good.|
|Agree with addition. -Anup||02/04/19 10:06 PM||Joshua||Ladellafirstname.lastname@example.org|
|58||51||Biochemistry||Cellular||Menkes disease||Doesn't need one (just a mnemonic)||Tip for remembering ATP7A (Menkes Disease) v. ATP7B (Wilson's Disease): The B stands for Bronze, whose main ingredient is Copper||Mnemonic||Verified||07/10/19 4:08 PM||John||Mitchellemail@example.com|
|59||51||Biochemistry||Cellular||Menkes disease||N/A||ATP7A --> A for absorption. Contrast with Wilson disease, ATP7B --> B for bile.||Mnemonic||Verified||09/06/19 9:13 PM||Christopher||Yangfirstname.lastname@example.org|
|60||51||Biochemistry||Cellular||Menkes disease||Self-produced||ATP7A & ATP7B are both defects in copper processing with Menkes Disease and Wilsons Disease. 'M' in 'Menkes' comes before 'W' of 'Wilsons' in alphabet, therefore ATP7'A' Defect is due to Menkes, later 'B' is for Wilsons. Also, Menkes is due to defective copper 'A'bsorption and Wilsons due to defect excretion into 'B'ile.||Mnemonic||10/27/19 5:20 AM||Khalid||Alattaremail@example.com|
|61||52||Biochemistry||Cellular||Elastin||Mneuomnic||People with Marfans are so tall you have to look up to see them. Thus the subluxation of the lens is upward (and temporal)||Mnemonic||Verified||05/10/19 5:07 PM||Sofia||Chinchillafirstname.lastname@example.org|
|62||52||Biochemistry||Cellular||Elastin||mnemonic||Marfan syndrome lens subluxation is upward: look up to see Mars vs homocysteinuria lens subluxation which is downward: look down to see urine||Mnemonic||Verified||07/23/19 6:30 AM||Mohammed||Kamareddine||Mohammed.email@example.com|
|63||55||Biochemistry||Laboratory Techniques||Fluorescence in situ hybridization||N/A||Second to last line states "(two blue arrows...)" but the arrows are not blue. Irrelevant wording.||Spelling/formatting||Reject. There are two blue arrows on top of chromosome 8 showing duplication of the stated chromosome in the image. Therefore, the wording is correct. -Victor Martinez||Verified||Reject. Agree with Victor.|
|Agree with rejection. -Anup||01/22/19 9:22 PM||Audrey||Huntfirstname.lastname@example.org|
|64||55||Biochemistry||Genetics||Molecular cloning||Webster-Miriam Dictionary||Step two should say Add "reverse" transcriptase, not Add "reserve" transcriptase||Spelling/formatting||Reject, the current wording is appropriate " Add REVERSE transcriptase..." There is not "reserve" on step 2 (molecular cloning). - Victor Martinez||Verified||Agree with rejection. -Anup||Agree with rejection.|
|02/14/19 3:06 AM||Zev||Allisonemail@example.com|
|65||56||Biochemistry||Genetics||Genetic terms||https://www.uptodate.com/contents/li-fraumeni-syndrome?search=li%20fraumeni&source=search_result&selectedTitle=1~40&usage_type=default&display_rank=1||Li-Fraumenia syndrome is listed as an example of loss of heterozygosity but more often functions as a dominant negative mutation as having one mutant allele creates 1/16th functional proteins in the final tetramer.||Minor erratum||Reject. Li Fraumeni syndrome is linked to loss of heterozygosity and dominant negative mutations of p53. Therefore, current entry is accurate. -Victor Martinez||Verified||Reject.|
Cancer development in LFS can be due to both functional (dominant-negative mutations) or strcutural (loss of heterozygosity) loss of wild-type p53. Even the linked UTD article supports this.
|Agree, the text is fine as is per MA. Additionally LFS is just listed as an example. -VV||Reject by 2 authors + 1 editor||01/08/19 10:02 AM||Brian||Blankenshipfirstname.lastname@example.org|
|66||57||Biochemistry||Genetics||Genetic terms||www.Uworld.com||Heteroplasmy definition: It says ".....resulting in variable expression in mitochondrially inherited disease"............. UWorld says "Variable Expression is not a feature of Mitochondrial diseases" in QID: 596 Choice D, last line.||Major erratum||Reject. I agree with Vasily, the concentration of mutated mitochondrial DNA in the cell determines the variability of expression of clinical manifestation or the phenotype. "...Most mtDNA mutations are found in heteroplasmy, in which the proportion of mutant vs. wild-type species is believed to explain some of the observed high phenotypic heterogeneity..." https://www.ncbi.nlm.nih.gov/pubmed/17999439 If it is a matter of confusion we could add a small illustration of 3 cells showing different mutated Mt-DNA concentrations with variable phenotypes similar to the one provided in the following link. https://www.nature.com/articles/nrdp201680 - Victor Martinez||Verified||Thank you for your comment and supporting image. I am inclined to reject.|
Unfortunately, at present I have no access to UW to check the reference and better understand the context of the quote from UW. However, after some Internet search I have found the following.
1. "The expression of mitochondrial diseases is variable; a single cell may receive a uniform collection of mtDNA (homoplasmy) or a mixture of mutant and wild-type mtDNA (heteroplasmy). The proportion of mutant mtDNA molecules determines the penetrance and severity of expression."
2. "For individuals born with partial mitochondrial dysfunction, the accumulation of mtDNA mutations and mitochondrial damage could account for the delayed onset and progressive course of their diseases. The stochastic nature of this process could also explain variable expressivity and/or penetrance of disease."
3. While the nuclear genome is diploid, harboring only two homologous copies of each chromosome (one from the father and one from the mother), the mitochondrial genome is polyploid, containing 1 to 10 identical molecules of mitochondrial DNA within its matrix. This variable copy number, combined with the variable number of mitochondria in each cell, has important implications for the phenotypic expression of a mutation. (See 'Heteroplasmy' below.)"
Three different sources suggest that variable expression (expressivity) is a feature of mitochondrial diseases. Therefore, I am strongly inclined to reject.
Here is my take on why UW says that variable expressivity is not characteristic of mitochondrial diseases. According to the image attached by the reader, variable expressivity is all about the same disease having different clinical manifestations in different people (i.e. different organ systems involved). However, other sources (UTD, see link below) define variable expressivity as variable disease severity. It is probably this difference in defining variable expression that might cause the confusion.
|I suggest changing "variable expression" to "variation in disease severity". This applies to pages 57 (heteroplasmy) and 59 (mitochondiral inheritance).|
|I would really appreciate faculty input as to whether our current wording is correct. As far as I understand based on my reading, mitochondrial disease is associated with variable expressivity and penetrance depending upon the percentage of affected mitochondria. -VV||Disagreement/need expert||Jeff Hofmann||The authors and editors are correct and the student is wrong. No change is needed. UWorld is not a real source.||Howard Steinman||I'm not clear about what's being debated. I've not seen the terms "incomplete penetrance" and "variable expressivity" used in reference to inheritance of mitochondrial-encoded genes. Yes, they are used routinely in reference to autosomal dominant inheritance of nuclear-encoded genes. The relevant terms for mitochondrial-encoded genes are: "heteroplasmy", "polyplasmy" and "threshold effect". "Variable expression" where, e.g. environmental factors influence the degree of expression of a gene, isn't applied to mitochondrial-encoded genes. You get different levels of expression in different cells because (as noted above) you have -1- different numbers of mitochondrial genomes in each cell and -2- different percentages of wild type and mutant genome in each cell. My bottom line is: don't use variable expression when referring to genes encoded by mitochondrial DNA.||Reject||01/12/19 9:06 PM||Sara||Khanemail@example.com|
|67||57||Biochemistry||Genetics||Mutations in DNA||N/A||McCune-Albright Syndrome =3 "P"s: "P" recocious puberty, "P"igmentation, "P"olyostotic fibrous dysplasia||Mnemonic||This mnemonic is great. McCune-Albright syndrome is commonly tested, we should consider it for the next edition. -Victor Martinez.||Verified||Defer to 2020. -Anup||This is great if you can remember the letter P. We need to tie that in to the eponym somehow?|
|01/28/19 4:50 PM||Yoseli||Venturafirstname.lastname@example.org|
|68||58||Biochemistry||Genetics||Disorders of imprinting||Mneumonic||AngelMan has no Mama. The M in AngelMan helps think of deletion in the allele of the Mother V||Mnemonic||It is a good idea because since the mnemonic is similar to the one use for Prader-Willi syndrome, "Prader has no Papa (Paternal deletion)." -Victor Martinez.||Verified||Defer to 2020. -Anup||I always remembered it as angleMAN because only the MANs DNA is present. I prefer my way|
|01/24/19 12:13 PM||Hana||Aslamemail@example.com|
|69||58||Biochemistry||Genetics||Types of errors in morphogenesis||FA2019||Mnemonic for AngelMan syndrome: "Mom’s little Angel (Maternal deletion)". The M's are red/bold||Mnemonic||Verified||05/22/19 8:53 AM||Eirik||Kragerfirstname.lastname@example.org|
|70||59||Biochemistry||Genetics||Fragile X syndrome||Fact Sheet 54| FRAGILE X SYNDROME This fact sheet ... PDFwww.genetics.edu.au › fact-sheet-54-frag...||According to Harrison'' Principles of Internal Medicine -20th edition page 3363, Fragile X syndrome is classified as X linked Recessive, Robbins Pathology latest edition also says it as X linked Recessive. Wikipedia says XD but both these books says XR. I am not sure about the error||Minor erratum||Verified||I think we had a discussion on this matter. There are 2 links to support First Aid: https://ghr.nlm.nih.gov/condition/fragile-x-syndrome#inheritance https://rarediseases.info.nih.gov/diseases/6464/fragile-x-syndrome -Anup||Per OMIM, Fragile X is x-linked dominant. OMIM is a very reputable site where most geneticists reference. No recommendations to change the text. -VV https://www.omim.org/entry/300624?search=fragile%20x-associated&highlight=x%20fragile%20associated%20xassociated||Reject by 2 authors + 1 editor||02/07/19 7:15 AM||Ankur||Bhootemail@example.com|
|71||59||Biochemistry||Genetics||Modes of inheritance||https://www.uptodate.com/contents/mitochondrial-myopathies-clinical-features-and-diagnosis?search=gomori&source=search_result&selectedTitle=2~20&usage_type=default&display_rank=2||Better classification of Mitocondrial diseases: add Kearns-Sayre syndrome (KSS) and Leigh syndrome, and also the stain often used for diagnosis : GOMORI THRICOME STAIN||High-yield addition to next year||I wouldn't add Kearns-Sayre syndrome and Leigh syndrome to the next edition. I don't believe these are HY. -Victor Martinez.||Verified||Can have X-ref opinion for HY/LY. -Anup||I think these are HY but we don't have much room to include them. Also agree that Gomori is HY but again we don't have much room. I guess we could add the stain to the middle column of the table and just add the syndromes under the list for mitochondrial myopathies.|
|02/18/19 10:50 PM||Lissette||Orozcofirstname.lastname@example.org|
|72||59||Biochemistry||Genetics||Modes of inheritance||https://www.uptodate.com/contents/inheritance-patterns-of-monogenic-disorders-mendelian-and-non-mendelian?search=autosomal%20recessive&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1||Both autosomal recessive and x-linked recessive inheritance skips generations: ''RECEssive (autosomal and x-linked) inheritance takes a RECEss from family (no past family history of the disease)''.||Mnemonic||Verified||07/29/19 4:05 PM||Francisco||Duenasemail@example.com|
|73||59||Biochemistry||Genetics||Modes of inheritance||https://emedicine.medscape.com/article/922305-overview||X-Linked Dominant diseases: A-mericas F-unniest X V-ideos (A: Alport , F: Fragile X , V: Vitamin D resistant rickets)||Mnemonic||Verified||09/01/19 8:37 PM||Angelo||Piazzafirstname.lastname@example.org|
|74||60||Biochemistry||Genetics||Cystic fibrosis||https://www.drugbank.ca/drugs/DB08820||Indication for Ivacaftor - not approved for patients with a Phe508 deletion UNLESS it's given in combination with lumacaftor. Indicated as monotherapy for other CF mutations, most notably, G551D, where the number of CFTRs is fine, but they just don't open enough.||Clarification to current text||Reject, the text states that it must be used in combination with lumacaftor. Current edition " In patients with Phe508 deletion: a combination of lumacaftor (corrects misfolded proteins and improves their transport to the surface) and ivacaftor..." - Victor Martinez||Verified||Not clear from the student's comment, but as far I understand we had correctly and clearly stated that in patients with Phe508 deletions ivacaftor is given in combination with lumacaftor. We are nowhere metioning that ivacaftor should be used as a monotherapy with Phe508 deletions.|
|Agree with Vivek and Victor. Reject.|
|Agree with authors. No change to the text. -VV||Reject by 2 authors + 1 editor||12/27/18 7:39 PM||Elizabeth||Tsuiemail@example.com|
|75||60||Biochemistry||Genetics||Cystic fibrosis||Found on update here: https://www.uptodate.com/contents/cystic-fibrosis-assessment-and-management-of-pancreatic-insufficiency?search=cystic%20fibrosis%20treatment&source=search_result&selectedTitle=6~150&usage_type=default&display_rank=6#H9 and tested on in multiple UWorld questions||Treatment for Cystic Fibrosis includes pancreatic enzyme replacement therapy (PERT) to correct for pancreatic insufficiency.||High-yield addition to next year||Agree, we should review this fact so we can include it in the next edition. It is highly tested on step 1 and step 2 CK. -Victor Martinez.||Verified||Agree that this is a HY topic. Can be added in 2020. Needs faculty/expert opinion and x-ref team review. -Anup||Agree.|
|01/30/19 6:14 AM||Nathaniel||Borochovfirstname.lastname@example.org|
|76||60||Biochemistry||Genetics||Cystic fibrosis||simple illustration attached||"defect in CFTR gene on chromosome 7"; Write CFTR as "C7TF" (where 7 is a laterally inverted image of F)||Mnemonic||Verified||Too confusing. Would opt to reject. -Anup||Too difficult to explain in limited space. Reject.|
|03/02/19 6:07 PM||M Marwan||Dabbaghemail@example.com|
|77||60||Biochemistry||Genetics||Cystic fibrosis||https://www.fda.gov/news-events/press-announcements/fda-approves-new-breakthrough-therapy-cystic-fibrosis||There is a new breakthrough treatment for cystic fibrosis which was approved by the FDA. It is called Trikafta (elexacaftor/ivacaftor/tezacaftor) and its mechanism of action is by enhancing the function of the CFTR protein. It is approved for use in CF patients with a F508del mutation, which is present in 90% of CF patients. The previous iteration (presently in First Aid) named lumacaftor requires that the patient be homozygous for this mutation, while the current FDA guidelines say that the patient only needs some of their transport proteins to have this mutation.||High-yield addition to next year||10/21/19 8:01 PM||James||Blumlinefirstname.lastname@example.org|
|78||61||Biochemistry||Genetics||Muscular dystrophies||https://www.ncbi.nlm.nih.gov/pubmed/25348330||book says that duchenne muscular dystrophy has truncated protein when in fact it should be beckers||Major erratum||The wording is correct. Duchenne displays truncated dystrophin. https://df6sxcketz7bb.cloudfront.net/manuscripts/95000/95918/jci.insight.95918.v1.pdf - Victor M.||Both disorders can do this. We show the most common patterns. The student's link is for variants that produce truncated proteins. Long story short, no erratum, no change needed, because what we show is what we consider to be the most common/most high-yield.|
|Reject by 2 authors + 1 editor||05/16/19 10:08 AM||Manjil||Basnetemail@example.com|
|79||62||Biochemistry||Genetics||Fragile X syndrome||Self-written||Fragile X Syndrome - patient/child with FRAGILE brain (intellectual disability), fragile large testes (macroorchidism), fragile large face, ears (long face, large ears)||Mnemonic||10/30/19 10:13 AM||Khalid||Alattarfirstname.lastname@example.org|
|80||62||Biochemistry||Genetics||Rett syndrome||mnemonic from my brain||Stereotyped hand-wringing (Rett-ers cramp)||Mnemonic||This mnemonic does not help to decrease cognitive load. I wouldn't consider it for the next edition. -Victor Martinez.||Verified||Not sure if I would refer to this one. -Anup||Ignores other key features of Rett syndrome. Reject.|
|01/19/19 10:06 AM||Sabrina||Swogeremail@example.com|
|81||62||Biochemistry||Genetics||Trinucleotide repeat expansion diseases||https://emedicine.medscape.com/article/943776-overview#a1||Fragile X is an X-linked recessive disorder according to Harrisons for Internal Medicine. In the 2019 version of first aid it states it is x linked dominant. If it was dominant you would not see carriers but there are carriers present.||Major erratum||Reject.|
The link provided by the reader says: "The pattern of inheritance most closely resembles X-linked dominance with variable penetrance". Other sources also say that Fragile X is X-linked dominant, eg:
|Agree with Vasily. This is an X-linked dominant disorder. The variable penetrance is accurate and may explain the "carrier" state. No change needed.|
|Reject by 2 authors + 1 editor||06/18/19 9:22 AM||Farina||Khanfirstname.lastname@example.org|
|82||63||Biochemistry||Genetics||Autosomal trisomies||Genetics: Glossary of terms - UpToDate||Nondisjunction in meiosis illustration: Replacing the words "Trisomy" with "Heterodisomy" and "Isodisomy" as specified in the attachment.||Minor erratum||Despite heterodisomy and isodisomy are correct terms. We don't mention them in the text and I don't think these are HY enough to be clarified on current illustration. Reject. -Victor Martinez.||Verified||Reject.|
Current illustration is correct. They are All trisomies and the terms/distinction suggested by the user are LY for step1 and we don't discuss them in the text.
|I agree with Victor and Majed.|
|Agree, not in favor of adding heterodisomy or isodisomy, as they are pretty LY for purposes of Step 1. No changes. -VV||Reject by 2 authors + 1 editor||01/02/19 12:41 PM||Bahaa' eddine||Succar||Bahaasuccar@gmail.com|
|83||63||Biochemistry||Genetics||Autosomal trisomies||https://www.ncbi.nlm.nih.gov/pubmed/25412855||<2% of cases of Down Syndrome are due to mosaicism.||High-yield addition to next year||I think we need faculty input regarding this comment since there are many available studies and sources showing different percentages of cases due to mosaicism. However, technically not an error. -Victor Martinez.||Verified||I think this is quite LY for Step 1, especially the percentages. However, this is not an errata and can be considered for 2020.. -Anup||01/25/19 6:24 PM||Ariya||Mobarakiemail@example.com|
|84||63||Biochemistry||Genetics||Autosomal trisomies||https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1684265/. Also UWorld question 8328||please add that the majority of cases of Down syndrome result from nondisjunction in Meiosis I specifically||High-yield addition to next year||I agree we should add this. - Victor M.||Agree. This fact is also emphasized in UW.|
|03/16/19 6:40 PM||Anna||Priddyfirstname.lastname@example.org|
|85||63||Biochemistry||Genetics||Autosomal trisomies||Usmle World question ID 1824 , (choices C and E) explanations||Myelomeningocele is also associated with Edward Syndrome (Trisomy 18)||Clarification to current text||Reject. I don't think this association is HY enough. -Victor M.||Inclined to reject.|
There is often a long list of conditions associated with inborn syndromes. How many symptoms should we list before we decide it is enough? I think in such cases it is better not to overload the text with detail and list only the most HY manifestations (especially those that are known to be tested and fit well into a mnemonic).
"In trisomy 18 the features may include agenesis of the corpus callosum, meningomyelocele, ventriculomegaly, chorioid plexus cysts, posterior fossa anomalies, cleft lip and palate, micrognathia, low-set ears, microphtalmia, hypertelorism, short radial ray, clenched hands with overriding index fingers, club or rocker bottom feet, omphalocele, diaphragmatic hernia, renal anomalies, cardiac defects, SUA, polyhydramnios, nuchal thickening or hygroma and cryptorchidism".
|Can migrate over for consideration of addition to the Edward syndrome entry.|
|Prelim accept but NOT publishable errata||04/23/19 8:43 AM||Muhanad||Shaibemail@example.com|
|86||63||Biochemistry||Genetics||Autosomal trisomies||https://emedicine.medscape.com/article/943463-clinical#b4||In Trisomy 18, the image is not accurate since the patients have "clenched hands with the index finger overriding the middle finger and the fifth finger overriding the fourth finger "||Minor erratum||"Many infants with trisomy 18 syndrome also have characteristic malformations of the hands and feet. The hands are typically clenched, with overlapping of the index finger (second finger) over the third finger and the “pinky” (fifth finger) over the fourth." https://rarediseases.org/rare-diseases/trisomy-18-syndrome/ We should review this image - Victor M.||I agree. Most questions I remember describe the clenched fists as suggested by the student.|
|Agree with authors. And thank you, Victor, for migrating. I will accept for credit. Due to time constraints and review with Jordan, it looks like this will be deferred to 2021.|
I would not call this critical and in need of inclusion in the official errata, as knowing that the fists are clenched is likely most of what you need to know at the Step 1 level.
|Prelim accept but NOT publishable errata||07/20/19 5:04 AM||Ra'ed||Ababnehfirstname.lastname@example.org|
|87||63||Biochemistry||Genetics||Autosomal trisomies||https://www.mayoclinic.org/tests-procedures/quad-screen/about/pac-20394911||mnemonic for quad screen test in down (see file attachment)||Mnemonic||Verified||08/31/19 8:47 AM||Mohamed||Menofyemail@example.com|
|88||63||Biochemistry||Genetics||Autosomal trisomies||Self-written||1st & 2nd Trimester Screening - PRINCE Edward (trisomy 18) makes everyone KNEEL DOWN before him! (All screening levels are LOW/DOWN)||Mnemonic||10/30/19 10:18 AM||Khalid||Alattarfirstname.lastname@example.org|
|89||63||Biochemistry||Pathology||Genetic terms||Uworld||"DITCH" down syndrome for all the GI abnormalities listed in Uworld for trisomy 21 (D)Deuodenal atresia (most common) (I)Imperforate anus, (T)Transeophageal fistula ,(C)Celiacs Disease, (H)Hischsprungs disease||Mnemonic||I like this mnemonic. Unfortunately, it does not list all the clinical manifestations or diseases related to Down syndrome. But, we could consider it for the next edition. -Victor Martinez.||Verified||Defer to 2020. A suggestion, not errata. -Anup||We don't discuss all of these and we discuss others. I don't think it is helpful since it does not include the cardiac and phenotypic signs.|
|02/06/19 4:23 PM||Ashton||Jacksonemail@example.com|
|90||64||Biochemistry||Genetics||Cri-du-chat syndrome||It's Mnemonic||*Cri du* - CHat =*5 letters * - CHromosome 5||Mnemonic||I don't understand the mnemonic. CHat = 4 letters, not 5 letters. Therefore it does not correlate with chromosome 5 where the genetic disorder is present. -Victor Martinez.||Verified||Agree with Victor. Would reject suggestion. -Anup||Agree to reject|
|01/11/19 11:58 AM||Moatasem||Al-Janabifirstname.lastname@example.org|
|91||64||Biochemistry||Genetics||Cri-du-chat syndrome||mnemonic||Cats are born with closed eyes (think epicanthal folds), have so cute paws like 5 fingers (think chromosome 5), your heart melts (VSD)||Mnemonic||Verified||This mnemonic would not serve its purpose, and would just make the reader even more confused. Would prefer to reject suggestion. -Anup||This is "sketchy" style mnemonic that does not fit our style. Agree with anup to reject.|
|03/02/19 6:17 PM||M Marwan||Dabbaghemail@example.com|
|92||64||Biochemistry||Genetics||Genetic disorders by chromosome||Mnemonic||Chromosome 3: Von-Hippel-Lindau Gene, associated with Renal Cell Carcinoma -Both VHL and RCC have 3 letters Chromosome 5: Familial Adenomatous Polyposis (FAP) -APC gene mutation Read as: "Five-APC" or "FAPC" Chromosome 6: Hemochromatosis - associated w/ HLA A3 Read as: "HA3mochromatoSIX" Chromosome 11: Wilms tumor -Read as "W11ms tumor" Chromosome 13: Wilson Disease -Wilson Disease has 13 letters in total (same with Patau Syndrome, chromosome 13)||Mnemonic||Verified||VHL and RCC mnemonics are already mentioned in Neuro and Renal chapters.|
FAPC is not bad, but pretty difficult explain concisely in writing.
Personally I am not a big fan of the HA3mochromatoSIX mnemonic, but we can ask GI team if they would like to use it.
Wilms tumor, Wilson disease and Patau - not a big fan.
|03/15/19 4:53 PM||Chia||Hsufirstname.lastname@example.org|
|93||64||Biochemistry||Genetics||Williams syndrome||It’s just a movie quote mnemonic but helpful to remember the chromosome.||Current mnemonic says “think Will Ferrell in Elf”. You can add the chromosome to the mnemonic by adding his famous line “First, I went through the 7 levels of the candy cane forrest.” For chromosome 7.||Mnemonic||Verified||This mnemonic would not work for me, but I am okay with migrating to Annotate for further discussion if other authors feel like it.|
|05/02/19 11:51 AM||Gregory||Motzkusemail@example.com|
|94||65||Biochemistry||Nutrition||Vitamins: water soluble||My brain||Proposed mnemonic for sorting B vitamins in order. TRN-PPB-FC "The RN - Placed Patient Bobs - Foley Catheter" Where there is a dash, the number skips. This covered B1-12 in order. I made this and have found it useful to keep the numbers straight with the names of the B vitamins.||Mnemonic||I don't find this mnemonic easy to memorize. However, if other authors think it is useful we could consider it for the next edition. -Victor Martinez||Verified||Agree with Victor. Would reject suggestion. -Anup||I like this for a biochem course but I don't think Step 1 commonly tests converting from a vitamins B# to its name so I agree to reject.|
|01/05/19 12:56 PM||Christopher||Tiptonfirstname.lastname@example.org|
|95||65||Biochemistry||Nutrition||Vitamins: water soluble||https://reference.medscape.com/drugs/vitamins-water-soluble||Thierry (Thiamin) Robben (Riboflavin) aNd (Niacin) Petr (Pentothenic) Played (Pyridoxine) Ball (Biotin) For (Folate) Chelsea (Cobalamin)||Mnemonic||Verified||05/15/19 4:37 AM||Charilaos||Chourpiliadisemail@example.com|
|96||66||Biochemistry||Nutrition||Vitamin A||Mnemonic||Chronic toxicity from PHAAD diets: pseudotumor cerebri, hepatoxicity/megaly, alopecia, arthralgias, dry skin||Mnemonic||Verified||I think this mnemonic is worth migrating to discuss it with the crowd.|
|03/15/19 5:37 PM||Jason||Tegethoff||Tegethoffjason@gmail.com|
|97||66||Biochemistry||Nutrition||Vitamin B1||N/A||"ATP BReakdown" for the four enzymes. Combination of 2018 and 2019 since Be APT is awkward. A=Alpha-ketoglutarate, T=Transketolase, P=Pyruvate, BR=BRanched-chain ketoacid (also reminds you of glucose BReakdown). All together reminds you that it is a loss of ATP due to impaired glucose breakdown.||Mnemonic||I do like the mnemonic. I think we can take it into consideration for the next edition. -Victor Martinez||Verified||Can be put up for discussion in 1st pass. -Anup||Agree. Easier to remember than what we have.|
|01/23/19 5:36 PM||Audrey||Huntfirstname.lastname@example.org|
|98||66||Biochemistry||Nutrition||Vitamin B1||https://www.uptodate.com/contents/wernicke-encephalopathy||if malnourishment is predispose, give thiamine before glucose||Mnemonic||12/04/19 1:25 PM||Obaida||Safiemail@example.com|
|99||67||Biochemistry||Nutrition||Vitamin B3||https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-gout?search=podagra&source=search_result&selectedTitle=2~150&usage_type=default&display_rank=2||Podagra is not an excess of vitamin B3. Podagra is a manifestation of gout, literally meaning "painful toe." The book implies that an excess of B3 is called podagra, in parallel to how a deficiency of B3 causes pellagra. Rather, an excess of B3 can increase the risk of podagra (gout).||Clarification to current text||Reject, we use arrows throughout the test to imply the consequence of a process or pathology. It does not mean synonym. Besides, the entry states that hyperuricemia is one of the clinical manifestations of vitamin B3 excess. Therefore, patients with this toxicity can display podagra. - Victor Martinez.||Verified||Agree with Victor's comment.|
|Reject. Agree with Victor and MA.|
|No changes to the text. -VV||Reject by 2 authors + 1 editor||12/24/18 1:41 PM||David||Nwachukwufirstname.lastname@example.org|
|100||67||Biochemistry||Nutrition||Vitamin B3||https://www-uptodate-com.library.iau.edu.sa/contents/overview-of-water-soluble-vitamins?search=vitamin%20b3%20b6%20and%20b2&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1||Vitamin B3 synthesis requires B6 and B2. 6 divided by 2 gives you 3||Mnemonic||Verified||Duplicated mnemonic. -AC||05/08/19 6:02 PM||Abdulrahman||Alghamdi||Abdulrahmanalghamdi707@gmail.com|
|101||67||Biochemistry||Nutrition||Vitamin B3||n/a||Requires Vitamin B6 and Vitamin B2 [B6/B2 = B3]||Mnemonic||Verified||I think this was proposed a year or so ago and rejected. -AC||07/10/19 9:44 PM||A||Pandeyemail@example.com|
|102||67||Biochemistry||Nutrition||Vitamin B5||none||I remember that Vitamin B5 is pantothenic acid because it sounds like "pento-thenic acid" and pento means 5||Mnemonic||Verified||Seems like a legitimate mnemonic. I am up for addition. -Anup||Sure. We have room to incorporate it. I think B5 in general is LY but if were keeping the vitamin we might as well keep this|
|03/04/19 1:24 PM||Jessica||Zimofirstname.lastname@example.org|
|103||68||Biochemistry||Nutrition||Vitamin B7||n/a||"Please Always Put Biofuel in Car" First P is for Pyruvate, A is for Acetyl-CoA, second P is for Propionyl CoA, Bio=Biotin, Car=Carboxylase||Mnemonic||Verified||05/28/19 9:12 AM||Cameron||Hansonemail@example.com|
|104||68||Biochemistry||Nutrition||Vitamin B9||https://www.ncbi.nlm.nih.gov/pubmed/23957651||Small intestinal bacterial overgrowth is characterized by overproduction of *K9* (vitamins K, B9)... K9 to be highlighted in red||Mnemonic||Verified||From UTD: "folate and vitamin K levels are elevated in SIBO due to bacterial synthesis. Increased intestinal permeability also contributes to increased vitamin K levels".|
I am not sure if this kind of info would fit in well in Biochem chapter, but it might fit in GI chaper. Bacterial overgrowth is mentioned a couple of times there, so why not consider creating a separate fact?
|04/24/19 3:51 PM||Elan||Baskirfirstname.lastname@example.org|
|105||69||Biochemistry||Nutrition||Vitamin C||n/a||Bold the 'C' in 'Vitamin C', and also bold/capitalize the 'C' in sCurvy.||Mnemonic||It is good. We should add it to the next edition. -Victor Martinez.||Verified||Can be considered for 2020. -Anup||We already have this.|
|01/28/19 4:56 AM||Adam||Kurnickemail@example.com|
|106||69||Biochemistry||Nutrition||Vitamin C||Mnemonic||To remember which charged state of iron (Fe2+ or Fe3+) can and cannot be readily absorbed, use your fingers to represent each charge. Fe2+ = two fingers = peace sign = good; Fe2+ is readily absorbed. Fe3+ = three fingers = “read between the lines” = bad; Fe3+ cannot be absorbed.||Mnemonic||I am not inclined to favor or reject. I think this mnemonic is quite large. If we consider to add it to the next edition, we should simplify it. -Victor Martinez.||Verified||Can be used as story mnemonic for 2020. -Anup||This takes a lot of space to explain for something not very HY. I am not a fan.|
|02/06/19 11:29 PM||Matthew J.||Christensenfirstname.lastname@example.org|
|107||69||Biochemistry||Nutrition||Vitamin C||Mnemonic||Fe3+ can be reduced by Vitamin C, the 3rd letter in the alphabet. Color coded image attached.||Mnemonic||I would not include it in the next edition. It is not easy to remember. -Victor Martinez.||Verified||Seems a lot of things to remember for a small info. Would consider rejecting. -Anup||This takes more space to explain than it is worth.|
|02/06/19 11:34 PM||Matthew J.||Christensenemail@example.com|
|108||70||Biochemistry||Nutrition||Vitamin E||It's Mnemonic||*E*xcess of Vitamin *E* increases risk of *E*nterocolitis in *E*nfants (infants).\ Highlight in red letter "E".||Mnemonic||Agree. I like the mnemonic since it correlates vitamin E excess with enterocolitis. - Victor Martinez||Verified||Can be considered for 2020. -Anup||Agree to incorporate. We could also use blEEding for the anticoagulant effect.|
|01/11/19 8:50 AM||Moatasem||Al-Janabifirstname.lastname@example.org|
|109||70||Biochemistry||Nutrition||Vitamin E||It's Mnemonic||vitamin *E* ---> High-dose supplementation may alter metabolism of vitamin K : *E*nhanced anticoagulant effects of warfarin.||Mnemonic||If we use the mnemonics in the upper row, we could use this one too since is the same principle of using "E" as "E"ncreased or "E"nhanced. - Victor M.||Verified||Can be added for 2020. -Anup||I prefer blEEding as I mentioned in line 38 above.|
|01/11/19 8:58 AM||Moatasem||Al-Janabiemail@example.com|
|110||70||Biochemistry||Nutrition||Vitamin E||n/a||Excess Vit E = Enterocolitis = Enfants “High dose Vit E goes into WAR with Vit K” = Enhances anticoagulant effect of WARfarin by altering the metabolism of Vit K.||Mnemonic||Verified||07/10/19 9:49 PM||A||Pandeyfirstname.lastname@example.org|
|111||72||Biochemistry||Metabolism||Ethanol metabolism||https://step1.medbullets.com/biochemistry/102041/ethanol-metabolism||In ethanol metabolism under point number 2 it reads - “ 2) Fasting hypoglycaemia - decreases gluconeogenesis due to increased OAA—> malate. The correction is a decrease in OAA.Alcohol inhibits gluconeogenesis by depleting the pool of cytoplasmic NAD+. Depletion of cytoplasmic NAD+ by alcohol metabolism affects the re-oxidation of cytoplasmic malate to oxaloacetate by the cytoplasmic malate dehydrogenase, inhibiting gluconeogenesis. The inhibition of gluconeogenesis in response to alcohol ingestion results in alcohol-induced hypoglycemia||Spelling/formatting||Reject, ethanol metabolism increases NADH: NAD ratio (same info as per the student's link), this favors the reaction of OAA to Malate. The current text says decreased (downward arrow) gluconeogenesis due to increase (upward arrow) OAA to (horizontal arrow) malate. Therefore, the wording is appropriate. -Victor Martinez||Staff accepts||Agree with Victor. Text is fine as is. No changes to the text recommended. -VV||Reject by 2 authors + 1 editor||02/07/19 11:39 PM||Vyshnavy||Balendraemail@example.com|
|112||72||Biochemistry||Metabolism||Ethanol metabolism||On the same page, next to the diagram, it says " Fasting hypoglycemia - decreased gluconeogenesis due to INCREASED OAA --> malate', which is correct||The DIAGRAM doesn't match with the caption. The diagram shows "decreased" OAA but it should be shown as "increased" OAA||Minor erratum||Verified||I remember running across this errata in Flash Facts, and I think both the diagram and the text are correct. -Anup||We could make the caption clearer.|
"Fasting hypoglycemia—↓ gluconeogenesis due to↓ OAA → malate"
"Fasting hypoglycemia—↓ gluconeogenesis due to ↑ conversion of OAA → malate"
|We can consider making the caption clearer, I agree. Otherwise, suspect no erratum here needing addressing.|
|Prelim accept but NOT publishable errata||03/03/19 4:05 PM||Heewon||Choifirstname.lastname@example.org|
|113||72||Biochemistry||Metabolism||Ethanol metabolism||https://www.khanacademy.org/science/biology/cellular-respiration-and-fermentation/glycolysis/a/glycolysis||In the glycolysis pathway, it shows DHAP -> Glycerol-3-P using an NAD+ to make NADH. The pathway rather uses up an NAD+ to make NADH. There fore someone with lactic dehydrogenase deficiency will use up all NAD+ inhibiting glycolysis. In the current printing, these patients will stimulate glycolysis.||Minor erratum||10/25/19 1:05 PM||Paul||Karroum||Paul.email@example.com|
|114||73||Biochemistry||Metabolism||Enzyme terminology||Marks' Basic Medical Biochemistry: A Clinical Approach Fifth, North American Edition||Synthase does not use ATP while synthetase requires ATP.||Minor erratum||I agree with the student we should change current wording. According to Lippincot's illustrated review: biochemistry, fifth edition, page 55. Synthase (does not require ATP). - Victor M.||So we used to state this (synthetase uses ATP, synthase does not use ATP), but on further review, it turned out to be somewhat controversial. Moreover, both required sources of energy that could vary. Thus, we "generalized" it to what we have now, showing that both enzymes facilitate a reaction using some form of energy such as ATP of nucleotide sugar.|
Not to use Wikipedia as a primary reference, but it actually does summarize well why the synthase/synthetase ATP/no ATP nomenclature is out of date:
I would say not to go back and revert as it will just introduce the same controversy next year. I propose leaving as is, for in the current form it is not at all inaccurate.
|Reject by 2 authors + 1 editor||06/11/19 3:43 PM||Minji||Baefirstname.lastname@example.org|
|115||73||Biochemistry||Metabolism||Rate-determining enzymes of metabolic processes||Lippinicott Illustrated Reviews Biochemistry 6th ed, page 121 "Regulation by intracellular energy levels".||Fructose-1,6-bisphosphatase is also stimulated by high ATP levels. It should say "+Citrate +ATP".||Minor erratum||Agree, this makes sense. I think we can add "ATP (+)".|
This is the citation from the supporting reference: "Fructose 1,6-bisphosphatase is inhibited by elevated levels of adenosine monophosphate (AMP), which signal an "energy poor" state in the cell. Conversely, high levels of ATP and low concentrations of AMP stimulate gluconeogenesis, an energy requiring pathway."
Although it does not bluntly say that "ATP stimulates fructose-1,6-bisphosphatase", I think this is exactly what is implied. Especially considering that it is written under "Dephosphorylation of fructose 1,6-bisphosphate" heading.
|Agree with Vasily. Would migrate this over to allow for consideration in the 2020 edition since it appears that it is likely accurate.|
|Prelim accept but NOT publishable errata||03/21/19 3:04 AM||Nicolas||Curi Gawlinskiemail@example.com|
|116||74||Biochemistry||Metabolism||Summary of pathways||https://www.uptodate.com/contents/overview-of-maple-syrup-urine-disease#H3||Metabolism of "Odd-chain Fatty acids, branched-chain amino acids, methionine, and threonine" to Propionyl-CoA is incorrect. NOT all branched-chain amino acids can be catabolized to propionyl-CoA;||Major erratum||Maybe LY for Step 1, as it may not specifically test which BCAA aren't catabolized to propionyl-CoA. -AC||Did some digging and have to agree with Anup, there are obviously some exceptions, but in the vast majority of cases and at the level of the Step 1, knowing that most odd chain fatty acids yield propionyl-CoA when metabolized is fine. We do not say "all" or "only" to avoid any absolute statements that open us up for errata.|
For these reasons, I propose no change.
Some good reading on the subject: https://www.ncbi.nlm.nih.gov/books/NBK22387/#_A3064_
|Reject by 2 authors + 1 editor||07/02/19 2:37 PM||Will||Pikefirstname.lastname@example.org|
|117||74||Biochemistry||Metabolism||Summary of pathways||First Aid Page 77||To complete the list of all enzyme deficients, pyruvate dehydrogenase deficiency should be added in the parentheses next to the PDH enzyme name (#10 in the list), similar to how other enzyme deficiencies/conditions are listed. This can also be repeated for OTC deficiency.||Minor erratum||I don't understand this suggestion. PDH is number 14 on the list. -VM||Reject. The idea is to add "(PDH deficiency)" after "14 Pyruvate dehydrogenase", and to do the same for all other enzyme names in the list. IMO, this would clutter the page. There is no erratum. No change needed here.|
|Agree with authors. We state the enzyme clearly and adding extra text to discuss a deficiency would be too much text. And we would need to do it for other deficiencies to be consistent.|
|Reject by 2 authors + 1 editor||07/11/19 7:49 PM||Abhishek||Gamiemail@example.com|
|118||74||Biochemistry||Metabolism||Summary of pathways||https://www.ncbi.nlm.nih.gov/pubmed/25037503||Enzyme No. 6 Transketolase should have a bidirectional arrow as it is also possible to to yield Ribulose-5-Phosphate from Fructose-6-Phosphate.||Minor erratum||08/11/19 5:35 AM||Noam||Degnerfirstname.lastname@example.org|
|119||74||Biochemistry||Metabolism||Summary of pathways||https://en.wikipedia.org/wiki/3-hydroxy-3-methylglutaryl-CoA_lyase||I suggest to add 24th enzyme "HMG-CoA lyase" , which is needed for ketogenesis, to the list and to the scheme.||Clarification to current text||09/04/19 12:50 PM||Alsu||Zagorulkoemail@example.com|
|120||75||Biochemistry||Metabolism||Hexokinase vs glucokinase||N/A||In the chart, when it is reported the Km of the enzymes, while the arrows are correctly directionated, it is written the opposite: lower with upward arrow for hexokinase and higher with downward arrow for glucokinase.||Minor erratum||09/11/19 11:12 AM||Valentina||Milanifirstname.lastname@example.org|
|121||76||Biochemistry||Metabolism||Pyruvate dehydrogenase complex||You know this||I have a better way for remembering the 5 cofactors (please see the attached picture). “The FAmous Nerds Like CoenzymeA” goes in order (B1 thiamine pyrophosphate, B2 FAD riboflavin, B3 NAD niacin, Lipoic acid (and the L can be seen in part of the strokes for the number “4”), B5 CoA pantothenic acid||Mnemonic||I am in favor of keeping the current text mnemonic since it is not adding extra value. - Victor Martinez||Verified||Agree that the current mnemonic is well recognized and used more often than the proposed one. But we can have a crowd debate on this! -Anup||I prefer our current mnemonic.|
|01/12/19 2:27 PM||Julia||Gao||Jgao@gwu.edu|
|122||76||Biochemistry||Metabolism||Pyruvate dehydrogenase complex||N/A||Recommend red-bolding of "Ar"senic and G"ar"lic breath. This clinical finding is often mentioned in question stems and could help us quickly differentiate from Cyanide poisoning with Almond breath.||Mnemonic||Verified||I do not think this is a good one.|
|03/15/19 2:23 PM||Jason||Tegethoffemail@example.com|
|123||76||Biochemistry||Metabolism||Pyruvate dehydrogenase complex||Up to Date: Arsenic exposure and poisoning Author:Rose H Goldman, MD, MPH Section Editor:Michele M Burns, MD, MPH Deputy Editor:Lisa Kunins, MD Contributor Disclosures All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Apr 2019. | This topic last updated: Jan 07, 2019.||Please consider adding "peripheral neuropathy" to the list of symptoms of arsenic poisoning. It is a symptom NBME expects students to recognize in identifying arsenic poisoning and is mentioned in UWorld and Amboss.||High-yield addition to next year||Can be considered for addition. -AC||05/20/19 1:05 PM||Wenzheng||Yufirstname.lastname@example.org|
|124||76||Biochemistry||Metabolism||Pyruvate dehydrogenase complex||n/a||Another way to remember the cofactors: There are 5 things, in order B1, B2, B3, Lipoic Acid, B5. In addition to the current mnemonic||Mnemonic||09/25/19 1:06 PM||Tricia||Scalesemail@example.com|
|125||76||Biochemistry||Metabolism||Regulation by fructose-2,6-bisphosphate||UW QID 1031||FBPase 2 it's same as fructose 2,6-bisphosphatase and it's written on the text fructose bisphosphotase 2 without 6 number on it. and FBPase 1 it's same thing as fructose 1,6-bisphosphatase , So it would be better for good understanding..||Clarification to current text||I agree with Vasily. It will be simplified by using a bold font. -Victor||This is a good point! But it might be challenging to demonstrate what the reader is refering to without being too wordy. We can try using bold font for "2" and "1" both for enzyme and substance names in the figure.|
|Can migrate over and see what others, such as the crowd, think.|
|Prelim accept but NOT publishable errata||04/26/19 12:38 PM||Muhanad||Shaib||mohanad,firstname.lastname@example.org|
|126||76||Biochemistry||Metabolism||Regulation by fructose-2,6-bisphosphate||n/a||uctose bisPHOSPHATASE-2 removes phosphate when FASTING GLUCONEOGENESIS. PhosphofructoKINASE-2 adds phosphate while FED GLYCOLYSIS.||Mnemonic||Verified||07/10/19 9:50 PM||A||Pandeyemail@example.com|
|127||77||Biochemistry||Metabolism||Amino acids||I dont have one||This is mnemonic for differentiation between keto a gluco essential amino acid : I saw (isoleucine) phen (phenylalanine) fixing three(threonine) tires(tyrosine) with kit glue ( ketogenic and glucogenic||Mnemonic||Verified||05/13/19 11:10 AM||Elaf||Mohamed||Elafmohamed38@gmail.com|
|128||77||Biochemistry||Metabolism||TCA cycle||https://www.sciencedirect.com/topics/medicine-and-dentistry/citric-acid-cycle||On page 77 of the 2019 edition, it is noted that "[T]he TCA cycle produces 3 NADH, 1 FADH2, 2 CO2, 1 GTP per acetyl-CoA = 10 ATP/acetyl-CoA (2x everything per glucose)." This is, in fact, incorrect. The TCA cycle amounts to 12* ATP/acetyl-CoA. The "10" should be changed to "12."||Clarification to current text||We used to say 12, however, after adjusting for rounding, we edited this down to 10. I would not edit this as the original value of 12 was associated with several errata submissions!|
|Reject by 2 authors + 1 editor||06/03/19 4:33 PM||Marco||Lawandyfirstname.lastname@example.org|
|129||78||Biochemistry||Metabolism||ATP production||not indicated or refer to wiki||There is disaggrement in the net ATP production in page 74 and page 78, on Page 78, NADH produces 2.5ATP and FADH2 produces 1.5 ATP, but the calculation here is based on the newer estimates that NADH produces 3 ATP and FADH2 produces 2ATP. So in order to avoid confusion, I suggest either page 74 or page 78 be corrected. If we correct page 74, then it should be 27 net ATP via malate aspartate shuttle or 25 ATP via glycerol -3 P shuttle||Major erratum||May need faculty input. -Anup||According to my calculations, there is no diagreement.|
Per 1 glucose molecule, glycolysis produces 2+2*1.5 = 5 or 2+2*2.5 = 7 ATP molecules.
Per 1 glucose molecule, pyruvate dehydrogenase complex produces 2*2.5 = 5 ATP molecules.
Per 1 glucose molecule, TCA cycle produces 6*2.5 + 2*1.5 + 2 = 20 ATP molecules.
This adds up to 30 or 32 ATP molecules per 1 glucose molecule, depending on the shuttle by which NADH electrons reach mitochondria.
Recommend no changes to current text.
|Disagreement/need expert||04/09/19 5:17 AM||Hang||Songemail@example.com|
|130||78||Biochemistry||Metabolism||ATP production||https://www.sciencedirect.com/topics/neuroscience/atp-synthase||ATP synthase inhibitors decrease proton gradient||Major erratum||Reject. Oligomycin inhibits ATP synthase leading to accumulation of protons and increasing the gradient (difference). - Victor M.||Agree with Victor. Text is correct that these inhibitors increase the gradient, not decrease it.|
|Reject by 2 authors + 1 editor||05/10/19 10:27 AM||Abdulrahman||Alghamdi||Abdulrahmanalghamdi707@gmail.com|
|131||78||Biochemistry||Metabolism||Electron transport chain and oxidative phosphorylation||It's Mnemonic||thermogenin in b*r*own fat (has mo*r*e mitochondria than white fat).||Mnemonic||The mnemonic is not bad. However, I don't know if HY enough to be added. -Victor Martinez.||Verified||The suggested mnemonic seems to be built around the fact that words "brown" and "more" both contain letter "r". IMO, this does not seem like a strong enough basis for a good mnemonic.|
|Agree with Vasily, this is not easy to remember because the relevant letter is in the middle of the word. A student could think it is brOwn fat and nO mitochondria just as easily. Reject.|
|01/11/19 9:09 AM||Moatasem||Al-Janabifirstname.lastname@example.org|
|132||78||Biochemistry||Metabolism||Electron transport chain and oxidative phosphorylation||It's Mnemonic||N*O* ATP is produced because electron transport st*O*ps ----> *O*ligomycin||Mnemonic||Reject. I think students could find this mnemonic misleading. The use of the arrow implies that the consequence of the inhibition is oligomycin when it is actually the cause. I prefer the DRACCO mnemonic since it shows the order of inhibition and the first letter of the inhibitor. -Victor Martinez.||Verified||Agree with rejection. -Anup||01/11/19 9:15 AM||Moatasem||Al-Janabiemail@example.com|
|133||78||Biochemistry||Metabolism||Electron transport chain and oxidative phosphorylation||https://www.ncbi.nlm.nih.gov/pubmed/16676004||Cytochrome c is found in the intermembrane space. But on page 78, cytochromc c is illutrated as overlaping with the inner mitochondrial membrane which causes confusion. Please consider moving cytochome c to the intermembrane space in the next edition of FA.||Minor erratum||Agree. Cyt C should be placed in the intermembrane space. -Victor M||We already show it by the intermembrane space! It is on the membrane surface. Yes, it "overlaps" but that's more of a diagram nuance than a reflection of where it is found and what it does. Almost every diagram I can find has placement similar to what we currently depict.|
I suppose in many cases, the membranes are flipped vertically, which may explain the confusion.
|Reject by 2 authors + 1 editor||06/12/19 9:41 PM||I-Chun||Hungfirstname.lastname@example.org|
|134||78||Biochemistry||Metabolism||Urea cycle||It is a mneomonic||Ornithine went by the car (carbomyl phosphate) to the city (citrulin) she met aspartae (added aspartate )they spended money (added ATP) they argued successively (arginine succinate)fume went out (fumerate product) the arguing (arginine) ended by drinking water (added water)and passing urine (urea product) and ornithine went back home (cycle completion)||Mnemonic||Verified||05/13/19 11:04 AM||Elaf||Mohamed||Elafmohamed38@gmail.com|
|135||80||Biochemistry||Metabolism||Disorders of galactose metabolism||http://www.jbc.org/content/280/7/5510.full||The metabolic pathway for galactose has an incorrect abbreviation for UDP-Glu when referencing glucose bound to UDP. The abbreviation for glucose is Glc, not Glu (glutamate), so the correct term to use is UDP-Glc.||Minor erratum||Verified||I do not think we have a mistake here. Btw, the cited reference uses Glu-6-P (not Glc-6-P) for glucose-6-phosphate.|
The article below uses "UDP-glu".
Recommend no change.
|Agree with Vasily. Appears to be no erratum here, no change.|
|Reject by 2 authors + 1 editor||03/03/19 10:15 AM||Max||Yudovichemail@example.com|
|136||81||Biochemistry||Metabolism||Amino acids||https://en.wikipedia.org/wiki/Ketogenic_amino_acid||There are 5 Glucogenic/ketogenic amino acid: Isoleucine, Phenylalanine, Tyrosine, Tryptophan, Threonine (some don't recognize it as ketogenic)||Major erratum||I agree we should include tyrosine as part of the Glucogenic/ketogenic group in the next edition. However, not as part of the errata. "Tyrosine upon metabolism produces one molecule of fumarate and one molecule of acetoacetate. Fumarate is a glucogenic component because it is a TCA intermediate and gets converted to oxaloacetate which is channeled toward the path of gluconeogenesis. Acetoacetate is cleaved to form Acetyl CoA a precursor of ketone bodies. Hence, tyrosine is both glucogenic as well as ketogenic" http://usmle.biochemistryformedics.com/which-amino-acid-is-both-glucogenic-as-well-as-ketogenic/ - Victor Martinez||Verified||Reject. This change was made last year based on well-sourced resources. Would not recommend any changes -VV||Reject by 2 authors + 1 editor||02/14/19 2:49 AM||SHICHENG||SONGfirstname.lastname@example.org|
|137||81||Biochemistry||Metabolism||Amino acids||https://en.wikipedia.org/wiki/Tyrosine, https://en.wikipedia.org/wiki/Tryptophan||Essential Amino acids PVT TIM HaLL Phenylalanine Valine Tyrosine Threonine Isoleucine Methionine Histidine Leucine Lysine.Tyrosine is not an essential amino acid, it has to be replaced with Tryptophan||Major erratum||Tyrosine was not mentioned in this fact in FA19.|
Currently no change is needed.
|Must be from a pre-2019 version. Current text is correct and shows tryptophan. No change needed.|
|Reject by 2 authors + 1 editor||03/28/19 2:22 PM||Chris||Robertemail@example.com|
|138||81||Biochemistry||Metabolism||Amino acids||https://en.wikipedia.org/wiki/Glucogenic_amino_acid||Tyrosine is also both glucogenic and ketogenic; change mnemonic to "PITTT"||High-yield addition to next year||I faced this errata in Flash Facts as well, and I think I may have already added it to the FA page. -Anup||04/01/19 2:07 AM||Elana||Molchofirstname.lastname@example.org|
|139||81||Biochemistry||Metabolism||Amino acids||https://medlineplus.gov/ency/article/002222.htm||An addition to PV TIM HaLL: Van Halen says MILK FTW. Glucogenic AAs are V, H and M. Ketogenic AAs are L and K. I was thinking the letters could be highlighted in a different color. I have provided an image for student's enjoyment.||Mnemonic||Verified||Ha! Thank you for sharing this. It looks like a creative take on essential amino acid mnemonic. However, there are a couple of issues preventing me from accepting this suggestion.|
1. As I see it, there two main ways in which our current mnemonic (PVT TIM HaLL) can be imroved. Firstly, it would be nice to arrange the mnemonic in such a way that the essential amino acids be split accordingly into ketogenic, glucogenic and glucogenic/ketogenic. Secondly, it would be nice to get rid of extra letters ("a" in "HaLL"). Unfortunately, the suggested mnemonic does not address these two issues.
2. The suggested mnemonic uses one-letter abbreviations for amino acids which are conventional, but which are not obligatory to know for Step 1 and are not used anywhere in the book.
3. I am not sure if we will be able to get the copyright holder's permission to use the picture.
Thanks for the creativity. Please keep it up.
|04/30/19 4:07 PM||Armando||Gallegos, Jr.||email@example.com|
|140||81||Biochemistry||Metabolism||Amino acids||https://www.diapedia.org/metabolism-and-hormones/5105758814/amino-acid-metabolism||TRY (tryptophan) ISOLating (isoleucine) KGs (ketogenic/glucogenic) THRough (threonin) funnels (phenylalenin)..||Mnemonic||Verified||07/19/19 7:20 PM||Mohammed||Kamareddinefirstname.lastname@example.org|
|141||81||Biochemistry||Metabolism||Amino acids||https://www.ncbi.nlm.nih.gov/books/NBK11035/||Maybe add the following as they are often tested and referred to in question stems: 1) Excitatory AAs/Neurotransmitters - GLUTAMATE. 2) Biogenic AA's (3 catecholamines/tyrosine derivates + others) - Dopamine, Norepinephrine, Epinephrine, Histamine, Serotonin.||High-yield addition to next year||10/30/19 10:31 AM||Khalid||Alattaremail@example.com|
|142||81||Biochemistry||Metabolism||Sorbitol||Mnemonic||Update mnemonic to "Sorbitol LuRKS around" --> adding "around" makes mnemonic make more sense/be more applicable/easy to remember. "Sorbitol LuRKS around" means sorbitol stays around/accumulates since LuRKS lack Sorbitol Dehydrogenase and/or have low levels of Sorbitol Dehydrogenase (Lens).||Mnemonic||Verified||05/03/19 6:50 PM||Shadia||Salehfirstname.lastname@example.org|
|143||82||Biochemistry||Metabolism||Urea cycle||https://en.wikipedia.org/wiki/Allosteric_regulation#Essential_activators||N-acetylglutamate is an OBLIGATE/ ESSENTIAL allosteric activator of carbamoyl phosphate synthetase I. Unlike allosteric activators, which induce enzymatic activity, obligate activators are required for enzymatic activity.||Clarification to current text||Reject. Current fact is correct - Victor M.||Verified||From the supporting reference, it seems that obligate activators are a subset of allosteric activators. There is no mistake in current text. Recommend no change here.|
|Agree with Vasily, no change.|
|Reject by 2 authors + 1 editor||03/11/19 3:51 AM||Elana||Molchoemail@example.com|
|144||82||Biochemistry||Metabolism||Urea cycle||https://www.ncbi.nlm.nih.gov/books/NBK513323/||N-acetylglutamate is an OBLIGATE allosteric activator. Currently, it is written that it is an allosteric activator which implies that the enzyme can still work without N-acetylglutamate (just works better in the presence of it), however this is not the case. The enzyme cannot work without N-acetylglutamate, which makes it an obligate activator.||Major erratum||This is a duplicate submission.|
IMO, this level of detail seems LY, unless there is evidence that it is tested in qbanks or nbmes.
|Duplicate, and still agree that it is low yield and not reflective of an erratum. Vasily's reasoning from prior submission still applies. No change here.|
|Reject by 2 authors + 1 editor||04/29/19 7:36 AM||Opal||Seklerfirstname.lastname@example.org|
|145||82||Biochemistry||Metabolism||Urea cycle||Mnemonic FA2019 (p. 82)||"NAG ("nag" as in bother/pester) CPS-1 to start the urea cycle." (N-acetylglutamate is the allosteric activator of CPS-I, which is the rate-limiting enzyme in urea cycle.)||Mnemonic||Verified||05/03/19 6:55 PM||Shadia||Salehemail@example.com|
|146||82||Biochemistry||Metabolism||Urea cycle||N/A||Urea cycle, Carbamoyl phosphate synthetase ONE, think "I have to use number 1(pee)"||Mnemonic||Verified||05/28/19 5:16 PM||Danny||Ibrahimfirstname.lastname@example.org|
|147||83||Biochemistry||Metabolism||Amino acid derivatives||https://www.ncbi.nlm.nih.gov/pubmed/9326301||a small bidirectional arrow next to tyrosine hydroxylase would be really nice, especially because this reaction is what let's us use certain dopaminergic drugs||Spelling/formatting||Maybe I am missing something, but it seems that the article says something along the following lines: "Tyrosine hydroxylase posesses DOPA oxidase activity. The products of DOPA oxidase activity are thioether derivatives of DOPA" (not tyrosine).|
In other words, I do not see it explicitly written that tyrosine hydroxylase can turn DOPA into tyrosine. Even if it was the case, this is likely LY for Step 1.
Inclined to reject.
|03/30/19 8:17 PM||Trevaughn||Baptisteemail@example.com|
|148||83||Biochemistry||Metabolism||Catecholamine synthesis/tyrosine catabolism||N/A||A mnemonic for remembering the order of catecholamine synthesis I use is "tldr". Tyrosine --> L-dopa --> Dopamine --> noRepinephrine. You can also expand it if you want: "Please TLDR Ever" = Phenylalanine --> Tyrosine --> L-dopa --> Dopamine --> noRepinephrine --> Epinephrine||Mnemonic||Verified||Thank you for the suggestion. Inclined to reject, as "d" can be misinterepreted as "dopa" and because "r" does not fit in the mnemonic that nicely.|
|03/04/19 1:58 PM||Justin||Winklerfirstname.lastname@example.org|
|149||84||Biochemistry||Metabolism||Alkaptonuria||https://emedicine.medscape.com/article/941530-overview#a5||first aid says: "Congenital deficiency of homogentisate oxidase in the degradative pathway of tyrosine to fumarate".||Major erratum||Reject. Tyrosine deviates from catecholamine synthesis to produce a final product, fumarate which is part of the TCA cycle. Homogentisate and homogentisate oxidase belong to one of the steps of this process. Consequently, the wording is appropriate "Congenital deficiency of homogentisate oxidase in the degradative pathway of tyrosine pathway to fumarate..." -Victor Martinez||Verified||Reject. Do not see any mistake here. There are several consecutive reactions that degrade tyrosine to fumarate. One of these reactions is catalyzed by homogentisate oxidase. If this enzyme is broken, alkaptonuria occurs.|
|Reject. -VV||Reject by 2 authors + 1 editor||01/25/19 7:02 AM||Mohammad ALWahadneh||ALWahadnehemail@example.com|
|150||84||Biochemistry||Metabolism||Alkaptonuria||Not needed||Use "All Caps" (Alkaptonuria) when Typing (tyrosine) Furiously (fumarate) -- to remember that problem converting tyrosine to fumarate in alkaptonuria||Mnemonic||Verified||05/17/19 1:05 PM||Opal||Seklerfirstname.lastname@example.org|
|151||84||Biochemistry||Metabolism||Homocystinuria||Page 84 of First Aid 2019 - In homocystinuria, lens sublexes "down and in."||You look "down and in" (lens sublexes) when you PEE (homocystinURIA); vs MarFAN Syndrome ("FANS up and out").||Mnemonic||Great mnemonic!||Verified||Nice mnemonic. Up for addition from my side. -Anup||04/16/19 12:05 PM||Orr||Shaulyemail@example.com|
|152||84||Biochemistry||Metabolism||Maple syrup urine disease||I just thought of this on my own||"MSUD patients can't LIVe with these amino acids" (Leuicine, Isoleucine, Valine)||Mnemonic||10/25/19 9:32 PMfirstname.lastname@example.org|
|153||85||Biochemistry||Metabolism||Glycogen regulation by insulin and glucagon/epinephrine||https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5195864/, https://en.wikipedia.org/wiki/Phosphorylase_kinase||Glycogen phosphorylase kinase has calmodulin as one of its subunits. Therefore calcium binds directly to the enzyme and activates it. Furthermore, calcium is released from the endoplasmic reticulum in both muscle contraction and a1 receptor stimulation. This relationship can be summarized with the following arrows: Muscle contraction or a1 receptor stimulation -> Ca2+ (from endoplasmic reticulum) -> glycogen phosphorylase kinase (has calmodulin subunit). In the current graph in the book, the following sequence of arrows “calcium released from the endoplasmic reticulum -> Ca2+-calmodulin complex -> glycogen phosphorylase kinase” is conceptually wrong and unnecessary, as it is already shown with an arrow that calcium directly activates glycogen phosphorylase kinase.||Major erratum||Agree. The student is correct, calmodulin is the delta subunit of glycogen phosphorylase kinase (GPK). The illustration shows "Calcium-calmodulin in muscle during contraction" activates the GPK. However, We don't show that calmodulin is the subunit of this enzyme. It seems that Ca-Calmodulin complex activates GPK when it is only by Calcium. - Victor Martinez.||Verified||Text is correct as is. When epinephrine bines the a-receptor, the PIP2-Ca2+ signal transduction system is activated, and calcium binds calmodulin. Would be beyond the scope of Step 1 to know that calmodulin is a binding receptor of glycogen phosphorylase kinase. Would recommend leaving text as is. -VV 1. Mark's Biochemistry||Reject by 2 authors + 1 editor||01/07/19 2:45 AM||Panagiotis||Kaparaliotisemail@example.com|
|154||86||Biochemistry||Metabolism||Glycogen||https://www.uptodate.com/contents/glycogen-debrancher-deficiency-glycogen-storage-disease-iii||Glycogen debrancher is an enzyme with two catalytic activities (as already stated in the text). Cori disease is caused by congenital deficiency of glycogen debrancher, therefore none of these catalytic activities would occur. Thus, both steps 5 & 6 are inhibited (not only step 6).||Major erratum||Agree with the student. The enzyme has two catalytic sites and Glycogen storage disease has many subtypes including deficiency of both catalytic sites. We only mention n the table alpha-1,6-glycosidase. We need faculty input in this case. -Victor Martinez https://www.sciencedirect.com/topics/medicine-and-dentistry/glycogen-storage-disease-type-iii||Verified||This information is factually correct. Might need some expert review as well. Seems like a major errata to me. -Anup||Not technically an error, so let's defer this to the main cycle. I'm reading that deficiency in glycogen debranching enzyme, amylo-1,6-glucosidase,4-α-glucanotransferase (AGL gene) is the cause of Cori disease. Please add a red box"III" to step 5 of Glycogen Storage Disease illustration. -VV https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2678930/ https://emedicine.medscape.com/article/119597-overview https://en.wikipedia.org/wiki/Glycogen_storage_disease_type_III||Prelim accept but NOT publishable errata||01/07/19 2:51 AM||Panagiotis||Kaparaliotisfirstname.lastname@example.org|
|155||86||Biochemistry||Metabolism||Glycogen||1. https://en.wikipedia.org/wiki/Dextrin. "Depolymerization of glycogen by phosphorylase halts when glycogen branches have been reduced to two to four linked glucose molecules (limit dextrins). Glycogen debrancher enzyme has two catalytic activities. One is the cleavage of a dextrin branch from the remaining glycogen molecule (amylo-1,6-glucosidase activity). The other is the transfer of the dextrin to the free end of a dextran polymer (oligo-1,4-1,4-glucanotransferase activity). The transferred dextrin may then be further depolymerized by phosphorylase." 2. https://www.uptodate.com/contents/glycogen-debrancher-deficiency-glycogen-storage-disease-iii||Limit dextrin refers to 2-4 residues, not 1-4. The smallest form of a dextrin is a disaccharide.||Major erratum||The 4-alpha glucanotransferase enzyme is in charge of cleaving the outer branch of glycogen until it reaches the last glycosidic link which is 1,6. The last one is cleaved by alpha-1,6-glucosidase. Therefore, dextrins should have at least one residue in the branch. This student's comment sounds a bit nitpicky to me. But, it would help to have input from faculty for this one. "The 1,4-α-D-glucan 4-α-D-glycosyl transferase component transfers the terminal three glucose molecules to the parent chain and the amylo-1,6-glucosidase component cleaves the alpha 1,6 bond to release free glucose." https://www.ncbi.nlm.nih.gov/books/NBK26372/ -Victor Martinez.||Verified||Most of the sources I referenced define limit dextrin as "short" without specification of the number of sugars. There were no reference to the number of residues in the wiki article provided. However, UTD does define as two to four residues. Would appreciate faculty input for clarification. -VV https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/dextrin https://www.uptodate.com/contents/glycogen-debrancher-deficiency-glycogen-storage-disease-iii||Disagreement/need expert||Howard Steinman||Is the debate about the number of sugar residues in the "limit dextrin". I agree that the smallest number of residues should NOT be 1. If you have 1, then the glycosidase acts to release free glucose. Our textbook says that the limit dextrin has 4 residues. If you want to say 2-4, I'd go for it. Main point: limit dextrin isn't 1 residue because that's not aceted on by the transferase activity of the debrancher enzyme. When it's just 1 residue, it's the glycosidase activity of the debrancher enzyme that acts. The figure shows it right. Bottom line: say that limit dextrin is 2-4 residues (or 4 residues)||Accept||01/07/19 2:55 AM||Panagiotis||Kaparaliotisemail@example.com|
|156||87||Biochemistry||Metabolism||Glycogen storage diseases||1. Already mentioned in the book on page 86, 2. https://www.uptodate.com/contents/glycogen-debrancher-deficiency-glycogen-storage-disease-iii||Cori disease is caused by glycogen debrancher deficiency, which has two catalytic activites (not only a-1,6-glucosidase).||Minor erratum||Agree with the student. The enzyme has two catalytic sites and Glycogen storage disease has many subtypes including deficiency of both catalytic sites. We only mention n the table alpha-1,6-glycosidase. We need faculty input in this case. -Victor Martinez https://www.sciencedirect.com/topics/medicine-and-dentistry/glycogen-storage-disease-type-iii||Verified||Agree with the user. Please see the comment in the previous post for further workup. -Anup||Not technically an error, so let's defer to main cycle. If faculty approves above, can replace "(a-1,6-glucosidase)" with "(1,6-glucosidase, 4-α-D-glucanotransferase)"||Prelim accept but NOT publishable errata||01/07/19 2:59 AM||Panagiotis||Kaparaliotisfirstname.lastname@example.org|
|157||87||Biochemistry||Metabolism||Glycogen storage diseases||1. https://rarediseases.info.nih.gov/diseases/7864/glycogen-storage-disease-type-1a, 2. https://www.uptodate.com/contents/glucose-6-phosphatase-deficiency-glycogen-storage-disease-i-von-gierke-disease, 3. https://www.uptodate.com/contents/image?imageKey=PEDS%2F54417||Von Gierke disease refers to the most common subtype of glycogen storage disease type 1, termed 1A, that is caused by glucose-6-phoshatase deficiency. Type 1B is caused by G6P transporter deficiency and is NOT termed Von Gierke disease.||Minor erratum||Reject. It is correct that the disease has 2 types, type Ia, caused by the deficiency of glucose-6-phosphatase (G6Pase) catalytic activity, and GSD type Ib, caused by a defect in glucose-6-phosphate exchanger SLC37A4 (transporter). In spite of this, The two subtypes (GSDIa and GSDIb) are clinically indistinguishable. Historically, GSDI is also referred to as von Gierke disease after Dr. Edgar von Gierke, who first described the disease in 1929. https://www.ncbi.nlm.nih.gov/books/NBK1312/ https://myriadwomenshealth.com/diseases/glycogen-storage-disease-type-ib/ - Victor Martinez||Verified||Agree with Victor. No changes to the text. -VV||Reject by 2 authors + 1 editor||01/07/19 3:01 AM||Panagiotis||Kaparaliotisemail@example.com|
|158||87||Biochemistry||Metabolism||Glycogen storage diseases||https://www.uptodate.com/contents/glycogen-branching-enzyme-deficiency-glycogen-storage-disease-iv-andersen-disease||Differentiate Cori disease (GSD 3) from Andersen disease (GSD 4). A-B/C-D. Andersen- Branching enzyme/ Cori- Debranching enzyme||Mnemonic||Verified||Although I like the mnemonic (it would be helpful for a Biochem class), I think Andersen disease is LY for the exam. Hence, reject.|
|03/02/19 9:14 AM||Grecia Haymee||Alvarez Fernandezfirstname.lastname@example.org|
|159||87||Biochemistry||Metabolism||Glycogen storage diseases||Made up.||Mcardle disease: Myo/Muscle Pains, Pees and Palpitations (Pains=Muscle cramps, Pees=Myoglobinuria, Palpitations=Arrhythmia)||Mnemonic||Verified||I am borderline about addition. Waiting suggestions from other authors. -Anup||I think it is an okay mnemonic. Suggest migrating to Annotate for further discussion.|
|03/29/19 11:57 PM||Alec||Hastyemail@example.com|
|160||87||Biochemistry||Metabolism||Glycogen storage diseases||My mind||'There are 2 glycogen storage diseases that are always difficult to remember and often we use to forget it, so a easy way to remember (type III and IV glycogen storage disease) is with the next mnemonic: DCBA, (D) for debranching enzyme and the name of the disease is Cori/type III (C) and Branching enzyme with the name Andersen/type IV, so Debranching-Cori/Branching-Andersen so you only have to remember the leters DCBA.||Mnemonic||Verified||09/22/19 8:41 PM||Jorge Andres||Rios Duartefirstname.lastname@example.org|
|161||87||Biochemistry||Metabolism||Glycogen storage diseases||https://www.history.com/topics/ancient-history/pompeii||POMPE Disease - Like POMPEII Volcano, heart is huge and pumping out may be affected (cardiomegaly, hypertrophic cardiomyopathy)||Mnemonic||10/30/19 10:38 AM||Khalid||Alattaremail@example.com|
|162||87||Biochemistry||Metabolism||Glycogen storage diseases||Andersen Disease: https://rarediseases.org/rare-diseases/andersen-disease-gsd-iv/ Hers Disease: https://emedicine.medscape.com/article/119690-overview Tarui Disease: https://emedicine.medscape.com/article/949388-overview||The main pneumonic I would like to contribute is: “ABCD” Andersen->Branching enzyme ; Cori ->Debranching enzyme. I noticed a similar one in the Errata table, but with letters switched around. I believe ABCD is a little easier to remember. In order for the pneumonic to make sense in the text, I added a section for Anderson's disease. I also added sections for Hers disease and Tarui disease because there is a lot of blank space on that page, and it helps complete knowledge about glycogen storage diseases. (see attached pdf, I also have .ai formats). Please feel free to send me an email with any additional questions! Thank you!||Mnemonic||11/21/19 7:21 PM||Forrest||Yehfirstname.lastname@example.org|
|163||88||Biochemistry||Miscellaneous||Lysosomal storage diseases||N/A||Tay-Sachs and Niemann-Pick both have 2 parts in their names just like Cherry-Red which is present in both of them||Mnemonic||I don't find this correlation easy to remember. But, if others think it is useful, I wouldn't be opposed. - Victor Martinez.||Verified||Reject suggestion. Too confusing. -Anup||Ha! This is actually the mnemonic I use. I think of the hyphen in the name of the diseases as of the cherry-red spot. It is challenging, however, to explain the mnemonic in writing.|
I suggested this mnemonic previously but it did not make it into the book.
I still like this mnemonic. We could use a bold red dot in the name of the diseases (instead of the hyphen) and highlight with red the term "cherry-red spot" in the text.
|01/04/19 4:26 AM||Feras||Al-Moussallyemail@example.com|
|164||88||Biochemistry||Metabolism||Lysosomal storage diseases||First Aid 2019||What is deficient and accumulated in Gaucher Disease? Gaucher = Groucher and needs sugar (glucose/glucocerebrosidase and glucocerebroside) What is deficient and accumulated in Krabbe disease? The krab is part of astrology/celestial galaxy signs, thus (galactocerebrosidae and galactocerebroside)||Mnemonic||Verified||The table is already too crowded. Not sure if I would vote for or against this addition. -Anup||I agree with Anup the page is really crowded with text already.|
As for the mnemonic itself, it is not bad, but I am not a big fan of it either.
|03/12/19 1:37 PM||Weston||Klosterfirstname.lastname@example.org|
|165||88||Biochemistry||Metabolism||Lysosomal storage diseases||N/A||FABry disease (F-fingers [episodic peripheral neuropathy]; A-angiokeratomas; you always look FABulous since you barely sweat)||Mnemonic||Verified||05/07/19 5:16 AM||Adam||Kurnickemail@example.com|
|166||88||Biochemistry||Metabolism||Lysosomal storage diseases||Alana Ghanim||How to remember the deficient enzyme in Hunter syndrome vs. Hurler syndrome. Hunter= iduronate which sounds like "I'd rather date" so think "I'd rather date a Hunter than a Hurler"||Mnemonic||Verified||06/27/19 11:05 PM||Alana||Ghanimfirstname.lastname@example.org|
|167||88||Biochemistry||Metabolism||Lysosomal storage diseases||n/a||A blind (destruction of oligodendrocytes - optic neuropathy) KRAB with regression is lost in the GALAXY (Galacto-).||Mnemonic||Verified||07/10/19 9:55 PM||A||Pandeyemail@example.com|
|168||88||Biochemistry||Metabolism||Lysosomal storage diseases||not applicable||hun(two)er deficient enzyme: iduronate 2;sulfatase, Hur(L)er: a-L-iduronidase||Mnemonic||Verified||07/13/19 8:35 AM||Awab||Elnaeemfirstname.lastname@example.org|
|169||88||Biochemistry||Miscellaneous||Lysosomal storage diseases||https://www.uptodate.com/contents/fabry-disease-clinical-features-and-diagnosis||FABRYS - F: Foam Cells in kidney, A: Alpha-galactosidase or Angiokeratoma, B: Burning pain in extremities (peripheral neuropathy or Boys of moms (X-linked recessive), R: renal failure, Y: Y is fine (because again its XLinked), S: Sphingolipidosis or S:Sweatless (hypohydrosis)||Mnemonic||10/03/19 4:16 PM||Mesude||Rahmetiemail@example.com|
|170||88||Biochemistry||Metabolism||Lysosomal storage diseases||Self-written||Tay-Sachs Disease - The general manager (GM) chose the wrong SAXophone GANG to play because their music but a HEX on the audience. (GM2 GANGlioside, HEXosamindase) /// Niemann-Pick Disease - Hey-MAN please PICK (NIEMAN-PICK) me to SING (SPHING). I think I sound great because i'm very drunk on FOAMY Beer (FOAMY LIPID-laden macrophages) with my big LIVER and SPLEEN. (Extreme alcohol use may lead to hepatosplenomegaly, these drunk people believe they/re great singers/SPHINGERS). /// Gaucher Disease - You go to the GAUCHER restaurant with your BRO's to eat GLUCOSE-containing food (GLUCO-cereBROside) where you use your TISSUE PAPER handkerchiefs and CRUMBLE it up when finished eating (Gaucher cells resemble crumpled paper).||Mnemonic||10/30/19 8:14 AM||Khalid||Alattarfirstname.lastname@example.org|
|171||89||Biochemistry||Metabolism||Fatty acid metabolism||First Aid 2019 pg 73.||The rate determining enzyme for Fatty acid synthesis is Acetyl-CoA Carboxylase (which is listed on pg 73). However it is not listed in the diagrams on page 89 and 74 despite its cofactor Biotin being listed.||High-yield addition to next year||Agree. In spite of not being an error, I do think we should include acetyl carboxylase which is the limiting step of the fatty acid synthesis. That would include the integration of pathways on page 74 and the FA metabolism entry on page 89. This way we keep the same line of action by mentioning all the different rate determining enzymes. -Victor Martinez||Verified||HY addition for 2020. Suggest deferring for further workup. -Anup||01/25/19 4:15 PM||Joseph||Cannizzoemail@example.com|
|172||89||Biochemistry||Metabolism||Fatty acid metabolism||https://ghr.nlm.nih.gov/condition/primary-carnitine-deficiency#genes||Systemic carnitine deficiency is a defect in the transport of carnitine (not LCFA) into the mitochondria||Major erratum||We do not have a major erratum here, but a clarification to the text might be considered: "Systemic primary carnitine deficiency -> no cellular uptake of carnitine -> no transport of LCFAs into mitochondria -> toxic accumulation of LCFAs in the cytosol -> weakness, hypotonia, hypoketotic hypoglycemia".|
|Agree that this is not an erratum. But I am not at all opposed to Vasily's proposed clarification which I do agree makes the text read much more clearly. We can consider this change for 2020 or 2021 depending on time.|
|Prelim accept but NOT publishable errata||03/25/19 1:08 PM||Tammy||Huafirstname.lastname@example.org|
|173||89||Biochemistry||Metabolism||Fatty acid metabolism||https://ghr.nlm.nih.gov/condition/medium-chain-acyl-coa-dehydrogenase-deficiency#inheritance||MCAD deficiency has an autosomal recessive inheritance pattern||High-yield addition to next year||I don't think this is HY either. - Victor M.||Provided reference supports the suggestion. I am not 100% sure that the suggestion is really HY.|
|03/30/19 6:14 PM||Lisa-Qiao||MacDonaldemail@example.com|
|174||91||Biochemistry||Metabolism||Metabolic fuel use||pneumonic, link n/a||carb/whey have 4 kcal (which is already there).... new submission: alcohol (how many letters in ALCOHOL=7; 7/kcal... fats how many kcal, 9/kcal (the FAT CAT has 9 lives)||Mnemonic||Verified||Reject. Suggested mnemonic almost completely repeats our current mnemonic on page 91.|
|06/25/19 10:17 PM||Stanley||Abrahamfirstname.lastname@example.org|
|175||92||Biochemistry||Metabolism||Familial dyslipidemias||http://nlaresourcecenter.lipidjournal.com/Content/PDFs/Tables/1.pdf||In type III-- dysbetalipoproteinemia, if Apo E is defective, there should be increased chylomicrons and IDL, not VLDL||Minor erratum||May need faculty input. -Anup||OK to migrate over, but agree expert input would be helpful to ensure we address this accurately.|
|Disagreement/need expert||04/01/19 10:43 AM||Elana||Molchoemail@example.com|
|176||93||Biochemistry||Metabolism||Key enzymes in lipid transport||per figure in page 92||Hepatic lipase; degrades TGs remaining in IDL and "Chylomicron remnants"||High-yield addition to next year||I don't think this is HY enough to be mentioned. Current text and illustration are consistent. Reject. -Victor M.||Verified||On the one hand, I do not think that the provided reference supports the suggested change. As I see it, page 92 figure shows that chylomicron remnants are taken up via ApoE receptor - ApoE interaction. I do not see how the figure shows hepatic lipase's role in chylomicron degradation.|
On the other hand, there are papers stating that hepatic lipase plays a role in chylomicron remnant metabolism. E.g.:
"HL, present in the basolateral surface of hepatocytes and the luminal and subluminal surfaces of endothelial cells or freely circulating in the bloodstream, hydrolyzes triglycerides and phospholipids present in circulating plasma lipoproteins, including IDL, chylomicron remnants..."
I do not think that this level of detail is HY for Step 1. I would leave the text as is unless other authors feel strongly otherwise. I do not think there is conflict between the figure and the text in terms of the role hepatic lipase.
I also do not remember seeing questions regarding the role of this enzyme in chylomicron metabolism in qbanks or nbme.
|03/01/19 7:36 PM||Ala||Jamalfirstname.lastname@example.org|
|177||93||Biochemistry||Metabolism||Key enzymes in lipid transport||https://www.uptodate.com/contents/pcsk9-inhibitors-pharmacology-adverse-effects-and-use?search=pcsk9&source=search_result&selectedTitle=1~33&usage_type=default&display_rank=1#H3046621671 LINK 1 - First paragraph of Mechanism of Action section. LINK 2 - Genetic Considerations < Mutations in the PCSK9 Gene https://www.uptodate.com/contents/familial-hypercholesterolemia-in-adults-overview?search=ldl%20receptor&source=search_result&selectedTitle=1~47&usage_type=default&display_rank=1||It is listed that the end result of PCSK9 is the decrease of serum LDL. This should say increase of serum LDL. The pathway in First Aid lists that the increase in LDL Receptor recycling is what leads to a decrease in serum LDL. In fact, when PCSK9 exerts its actions, the LDL Receptor is not recycled to the cell surface, but rather sent to lysosomes to be degraded. This would lead to less LDL uptake, and higher serum LDL levels. Therefore. PCSK9 does NOT lead to decreased serum LDL. I believe this may have been a mix up with the PCSK9 Inhibitor section, which would lead to decreased serum LDL. I've attached two different Uptodate links that state the MOA & effects. Thanks!||Major erratum||09/07/19 2:43 PM||Michael||Garmoemail@example.com|
|178||93||Immunology||Lymphoid Structures||Lymphatic drainage associations||First Aid 2017 Material||Para-Aortic Lymph Nodes - "you have a PAIR OF(para) testes, ovaries, kidneys"||Mnemonic||I don't find this mnemonic useful since it neglects the uterus. - Victor Martinez.||Verified||Reject.|
This is cute, but I agree with Victor, it leaves out the uterus which is important.
|Agree with authors, reject. -VV||Reject by 2 authors + 1 editor||02/07/19 4:49 PM||Haley||Basingerfirstname.lastname@example.org|
|179||93||Biochemistry||Metabolism||Major apolipoproteins||https://www-uptodate-com.ezproxy.rosalindfranklin.edu/contents/image?imageKey=PC%2F112742&topicKey=PC%2F4560&search=hdl&source=outline_link&selectedTitle=1~150||Currently, it is listed that the B-100 apolipoprotein is only on particles originating from the liver. However, HDL is synthesized in the liver and doesn’t contain B-100 which would contradict this statement.||Clarification to current text||Reject. The table on page 93 "Major apolipoproteins" has a check sign only in VLDL, IDL and LDL columns in the B-100 row. HDL has not a check. The only apoliproteins checked are those produced in the liver with B-100 (LDL, IDL, and LDL.) - Victor Martinez||Verified||Likely a misunderstanding of the text. Would not recommend changes. -VV||Reject by 2 authors + 1 editor||01/16/19 5:27 PM||Nakib||Mansuriemail@example.com|
|180||94||Biochemistry||Metabolism||Familial dyslipidemias||n/a||Type thrEE has defective ApoE||Mnemonic||Verified||08/21/19 4:37 PM||Jordan||O'Steenfirstname.lastname@example.org|
|181||94||Biochemistry||Metabolism||Lipid-lowering agents||https://www.uptodate.com/contents/effects-of-exercise-on-lipoproteins-and-hemostatic-factors?search=HDL%20exercise&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H472188367||Effects of exercise on lipoproteins and hemostatic factors: Exercise training programs produce favorable changes in the lipoprotein profile in patients who already have CHD. Most studies have shown a significant increase in serum HDL-cholesterol and a decrease in serum triglycerides. Exercise training also may have a modest lowering effect on serum LDL-cholesterol. The mechanism of benefit may derive from positive changes in the proteins, and in particular the enzymes that regulate lipid metabolism. Exercise training may influence the functionality of lipoproteins as well as the levels of lipoproteins. Exercise may alter hemostatic risk factor by reducing the risk of acute thrombus formation, improving blood viscosity, and positively influencing rate of progression of atherosclerotic lesions.||High-yield addition to next year||This is overly specific and not HY for step 1in my opinion. I can't think of a question that could be written from this information that a student couldn't correctly guess the answer to. It may be worthwhile to devote a new fact/page to the benefits of exercise but this would be a huge undertaking to determine what is the more HY for step 1. We could consider for next year.|
|07/31/19 9:24 PM||Pavel||Aksionavemail@example.com|
|182||96||Immunology||Lymphoid Structures||Lymph node||Not needed||Replace the term "Postcapillary venule" with "High endothelial venule" in the lymph node schematic. High endothelial venules are mentioned in the text but not in the schematic. This can lead to confusion.||Clarification to current text||Verified||Reject.|
HEVs are specialized post-capillary venous endothelial cells.This diagram is not at a high enough magnification to be able to visualize that. Also, the labeled item in our diagram is a post-capillary venule which is correct.
|Agree with Connie. No change to the text. -VV||Reject by 2 authors + 1 editor||01/07/19 3:08 AM||Panagiotis||Kaparaliotisfirstname.lastname@example.org|
|183||96||Immunology||Lymphoid Structures||Lymph node||https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1892634/||Medulla consists of medullary cords (closely packed lymphocytes and plasma cells) must be changed to (closely packed B lymphocytes and plasma cells)||Minor erratum||Verified||Reject.|
Looked at source, there is nothing that specifies "B" lymphocytes. Attaching another source from a higher impact journal (Cell) that says medullary cords "contains strings of lymphocytes." https://www.cell.com/immunity/image-resource-lymphnode
|No changes to the text. -VV||Reject by 2 authors + 1 editor||01/07/19 2:56 PM||Najat||Fadlallahemail@example.com|
|184||96||Immunology||Lymphoid Structures||Lymph node||https://www.uptodate.com/contents/evaluation-of-peripheral-lymphadenopathy-in-adults?csi=fe144795-2d9e-4501-a120-17fd294659e2&source=contentShare||Lymphadenopathy (LAD) : Painful LAD is seen with acute inflammation (e.g., Strep). Painless LAD is seen with chronic inflammation (e.g. autoimmune disease), metastatic carcinoma, or lymphoma . Abnormal lymph nodes if - firm/hard -immobile - >2cm -systemic symptoms (fever, night sweats, weight loss)||High-yield addition to next year||05/16/19 1:05 PM||Rayan||El Hajjarfirstname.lastname@example.org|
|185||97||Immunology||Lymphoid Structures||Lymphatic drainage associations||UpToDate, USMLE World.||In the lymphatic drainage table, under "Area of body drained" column for Superficial Inguinal nodes, skin of "Glans Penis" (which drains into the deep inguinal nodes along with the popliteal nodes) can be added as another exception along with popliteal area.||High-yield addition to next year||08/14/19 9:12 AM||Ahmed Ali||Khanemail@example.com|
|186||98||Immunology||Lymphoid Structures||Spleen||Myself||9 10 11, keep the spleen livin||Mnemonic||Verified||Reject.|
The rhyme is just slightly too much off for me. And it's not super intuitive that it's referring to the rib numbers.
|Agree with Connie, reject. -VV||Reject by 2 authors + 1 editor||02/22/19 8:36 AM||Zaid||R Najdawifirstname.lastname@example.org|
|187||98||Immunology||Lymphoid Structures||Thymus||https://www.ncbi.nlm.nih.gov/pubmed/16121185||text says; Medulla is pale with Mature T cells and Hassall corpuscles. I recommend adding "Hassall Corpuscles have lymphopoietin important for maturing T cells". And to add mnemonic "Thymus Medulla goes through the hassle (Hassall) to "Mature T cells utilizing lymphopoietin"||High-yield addition to next year||Verified||Reject.|
The detail here is way beyond the scope of T cell maturation details needed for step 1.
Also, lymphopoietin is pretty upstream in the story of T cell maturation. Thymic stromal lymphopoietin expressed by Hassall's corpuscles actually activates CD11c+ DCs residing in the thymus, causing them to upregulate surface costimulatory molecules CD80/86, which enables them to induce the proliferation/differentiation of CD4+ T cells into Treg cells (CD25+FOXP3+). Treg induction by DCs can also be achieved by other pathways.
|Agree with Connie, lymphopoietin is a concept beyond the scope of Step 1 and is not the only pathway for T cell maturation. Would not recommend addition to the text. -VV||Reject by 2 authors + 1 editor||03/01/19 8:11 PM||Ala||Jamalemail@example.com|
|188||98||Immunology||Lymphoid Structures||Thymus||N/A||Under "Thymoma", it says "Good syndrome" where it is likely mean "Goodpasture syndrome"||Minor erratum||No, Good syndrome is correct. -VV||Reject by 2 authors + 1 editor||07/05/19 10:38 PM||Jenna||Nickasfirstname.lastname@example.org|
|189||98||Immunology||Lymphoid Structures||Thymus||https://www.ncbi.nlm.nih.gov//articles/PMC4012878/R||Thymoma is associated with many autoimmune diseases including SLE||Clarification to current text||11/19/19 8:41 PM||Elizabeth||Ancion||Eancion@hotmail.com|
|190||100||Immunology||Cellular||HLA subtypes associated with diseases||It's Mnemonic||Psoriasis (there is a s*C*ale lession) --->HLA subtype *C* .||Mnemonic||Currently, we don't have mnemonic for psoriasis. The mnemonic is not bad since it correlates psoriatic lesion which is a scale with the HLA subtype (C). -Victor Martinez||Verified||Reject -Scott||Oo I think we should consider this.|
Maybe rephrase in a way that incorporates the "c" sound in psoriasis with the buzzwords "silver scale" in addition to HLA C.
Maybe pSoriasis presents with Silver Scale, HLA-C? This definitely needs some improving haha but just a thought?
|Agree, please add to annotate. -VV||Prelim accept by 2 authors + 1 editor||01/05/19 3:53 PM||Moatasem||Al-Janabiemail@example.com|
|191||100||Immunology||Cellular||HLA subtypes associated with diseases||https://www.ncbi.nlm.nih.gov/pubmed/29072309||In psoriasis, add the specific HLA-C allele that is strongly associated with the disease. All people have HLA-C in their genome. The specific allele that is associated with psoriasis is HLA-Cw6.||High-yield addition to next year||Reject, already specified on current edition. -Victor Martinez||Verified||We already have this in the table titled HLA subtypes associated with diseases -Scott||I think what the reader is suggesting is that we add that the specific allele associated with psoriasis is HLA-Cw6. The reader is technically correct, HLA-C is one of the three MHC class I genes we all have. Interestingly, I remember this being tested as just HLA-C, without going into detail about the specific allele. Interestingly, everything else on the list refers to a specific allele.|
Maybe we can crosscheck to see if psoriasis is still being tested as just associated with a mutation in HLA-C, and that students don't have to know the specific allele?
Regardless, I'm on the fence, because this is the only tested disease related to HLA-C and I don't think step 1 will make student differentiate between different HLA-C alleles, so students should recognize HLA-C or HLA-Cw6. I feel like including it for completeness is not a bad thing, but this is already a confusing section so I don't want to include superfluous information if it's not needed.
|Reject. For the purposes of Step 1, it is more important to know that HLA-C can be associated with psoriasis rather than the specific allele. I recall having to memorize the association with the specific subtypes rather than the alleles associated with the subtypes. Honestly, HLA-B*5701 is one of the only mutations that are really needed to be memorized, and this is associated with hypersensitivity with abacavir than with a specific disease. Would not recommend addition. -VV||Reject by 2 authors + 1 editor||01/07/19 3:13 AM||Panagiotis||Kaparaliotisfirstname.lastname@example.org|
|192||100||Immunology||Cellular||HLA subtypes associated with diseases||It's Mnemonic||Psoriasis(Psoriati*C*) --->HLA subtype *C* .||Mnemonic||I think that the mnemonic n first-row "Psoriasis (there is a sCale lesion) - HLA subtype C" is easier to remember and has a clinical correlation. -Victor Martinez||Verified||Reject. -Scott||Reject, using letters at the end of a words is generally less intuitive for mnemonics.|
|Agree, reject. -VV||Reject by 2 authors + 1 editor||01/13/19 2:18 PM||Moatasem||Al-Janabiemail@example.com|
|193||100||Immunology||Immune Responses||HLA subtypes associated with diseases||Toxicity of NRTIs - First Aid 2019 Pg-203; Its good to have this fact together with the other HLA associated disorders.||HLA-B*5701 - Increased risk of Hypersensitivity with Abacavir (Anti RetroViral)||High-yield addition to next year||Reject. This fact is present in the HIV therapy entry, page 203. I don't think we should repeat it in the HLA subtypes table, page 100. -Victor Martinez||Verified||Reject. This doesn't fit under neither the HLA Subtypes heading nor the MHC I and II headings. It fits best when we're discussing antiviral drugs though. -Scott||Well this actually fits fine under the HLA subtypes. HLA-B*5701 is just a genetic variation of HLA-B, one of the 3 MHC class 1 genes (others are HLA-A, HLA-B). All this means is that people who have the 5701 variation of HLA-B are more susceptible to abacavir sensitivity.|
We discuss this on page 203, I think that is the appropriate location. However, I would defer to the editor on whether it's worth a mention here. It is nice to have this grouped together with the other HLA allele-associated conditions, even though this is technically not a disease, but if I had to pick one location for this fact, I still think it fits better with the abacavir entry.
|Agree, this entry is more appropritae on page 203 related to abacavir. This is not technically an association with a disease, which is what the immunology table really focuses on. Therefore, would recommend leaving the text as is. -VV||Reject by 2 authors + 1 editor||01/26/19 10:52 PM||Arpit||Jainfirstname.lastname@example.org|
|194||100||Immunology||Cellular||HLA subtypes associated with diseases||https://www.nejm.org/doi/full/10.1056/NEJMra0808284?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub%3Dpubmed||T1DM also has a strong association with HLA DQ2 and DQ8. This is the reason patient with T1DM are at high risk for developing celiac disease (which is also associated with HLA DQ2 and 8) and the ADA recommends screening all patients T1DM for celiac disease once.||High-yield addition to next year||Verified||Agree, but would want to verify how HY this is first.|
American Diabetes Association currently says that the pts with the highest risk for TD1 are pts with DR3 or DR4+DQ8. UTD also mentions that TD1 is a risk factor for celiac, but doesn't mention the specific alleles.
We cover TD1 on page 346 and mention DR3 and DR4, but it might be worth adding in DQ8.
We cover celiac disease on page 375 and mention several associations, but not TD1. If we decide this is HY, may be worth adding TD1 to the list of associations.
|Celiac disease is more associated with DQ2/DQ8 for purposes of Step 1. Not convinced how HY association of Type 1 diabetes with DQ8 would be. Would not recommend any change to the text. -VV||Reject by 2 authors + 1 editor||02/14/19 11:33 PM||Basim||Aliemail@example.com|
|195||100||Immunology||Immune Responses||HLA subtypes associated with diseases||n/a||A better Mnemonic for DR2 associated disease is "DRive 2 multiple hay pastures."||Mnemonic||Verified||Yes!|
This is definitely an improvement on the current mnemonic, which doesn't specify the DR number. Also this one flows a little better than the current one (multiple hay pastures are dirty).
|Love it! Please replace: "Multiple hay pastures are dirty" WITH "DRive 2 multiple hay pastures" with appropriate red mnemonic font. -VV||Prelim accept by 2 authors + 1 editor||03/01/19 8:45 AM||Chima||Amadifirstname.lastname@example.org|
|196||100||Immunology||Cellular||HLA subtypes associated with diseases||Mnemonic||HLA-C for Psoriasis hint: Pronounce "C-riasis"||Mnemonic||Verified||There are several mnemonics proposed this year for psoriasis and HLA-C, this one is medium. We can compile and pick the best one once we migrate to annotate? Maybe we can compile the related smartsheet comments into one annotation so it's easy to see the options.|
|Agree, please add to annotate and we can pick the best one -VV||Prelim accept by 2 authors + 1 editor||03/24/19 1:17 PM||Nathaniel||Borochovemail@example.com|
|197||100||Immunology||Cellular||HLA subtypes associated with diseases||Made up||"C"oriasis||Mnemonic||Verified||05/13/19 3:24 PM||Mohamad Othman||El Heloufirstname.lastname@example.org|
|198||100||Immunology||Lymphocytes||HLA subtypes associated with diseases||https://www.uptodate.com/contents/human-leukocyte-antigens-hla-a-roadmap||mnemonic for DR2 ---> DRs get GOOD scores in 2nd year studying Histo MULTIPLE time SYSTEMatically( good--> good pasture, Histo-->Hay fever, MULTIPLE--> MULTIPLE sclerosis, SYSTEMatically--> SLE)||Mnemonic||Verified||08/31/19 9:05 AM||Mohamed||Menofyemail@example.com|
|199||100||Immunology||Cellular||HLA subtypes associated with diseases||n/a||DR5 is "pent"icious anemia.||Mnemonic||09/27/19 5:15 PM||Jordan||O'Steenfirstname.lastname@example.org|
|200||100||Immunology||Cellular||HLA subtypes associated with diseases||https://www.uptodate.com/contents/prediction-of-type-1-diabetes-mellitus?search=type%20i%20diabetes%20dr3%2Fdr4&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1||DR3/DR4 hurts beta cells to the core. (DM type I)||Mnemonic||09/27/19 6:36 PM||Jordan||O'Steenemail@example.com|
|201||100||Immunology||Cellular||HLA subtypes associated with diseases||https://www.uptodate.com/contents/prediction-of-type-1-diabetes-mellitus?search=type%20i%20d||DR3/DR4, Sugar no more (for DM1)||Mnemonic||10/14/19 10:47 AM||Daniel||Zhu||Dzhu5@pride.hofstra.edu|
|202||100||Immunology||Cellular||HLA subtypes associated with diseases||N/A||PAIR of B-27 Bombers (fly undetected - seronegative arthropathies)||Mnemonic||10/17/19 5:56 PM||Abhijit||Battarfirstname.lastname@example.org|
|203||100||Immunology||Lymphocytes||Major histocompatibility complex I and II||https://www.uptodate.com/contents/major-histocompatibility-complex-mhc-structure-and-function||we can use X in eXogenously as indicator for 2(ii) in MHC 2||Mnemonic||Verified||08/31/19 8:57 AM||Mohamed||Menofyemail@example.com|
|204||101||Immunology||Cellular||Differentiation of T cells||As per information on p. 102||Minor change to diagram. For Th17: add inhibited by IFN-gamma and IL-4. For Treg: add inhibited by IL-6.||Spelling/formatting||I agree we should add this to the next edition. However, it shouldn't be part of the errata. -Victor Martinez||Verified||Agree. We should be consistent -Scott||Yes, on annotate, it looks like there has been an effort to add in these cytokines, but there also seems to be some concern of over-population/over-crowding of the diagram.|
I think it would be nice to have these for consistency, but maybe we can work with the illustration team to find a layout that works better. Maybe arrows coming from the helper T cell could all be parallel instead of coming out radially? It may be easier to read the cytokines that way.
|This would be something for the illustration team to address. Please add a note to annotate with Illustration team tagged. -VV||Prelim accept by 2 authors + 1 editor||01/20/19 6:57 PM||Charles||de Leeuwfirstname.lastname@example.org|
|205||101||Immunology||Cellular||Differentiation of T cells||Mnemonic||To remember which section of the thymus (cortex or medulla) is involved in positive vs negative T cell selection, think of the letter “t” as a plus sign (+) and the letter “l” as a minus sign (-). Clarifying image attached.||Mnemonic||Could not understand the "t" as a (+) sign and "I" as a (-) sign- Priyesh||Verified||Reject.|
I think the "t" as "+" and "I" as "-" is clever, but I'm not sure where the letter I is coming from here?
|Agree, reject. -VV||Reject by 2 authors + 1 editor||02/10/19 10:39 AM||Matthew J.||Christensenemail@example.com|
|206||101||Immunology||Cellular||Differentiation of T cells||None needed||Add in the down-regulators of Th17 cells and Treg cells as indicated on page 102. That is, add a red -IL4 and IFN-gamma for Th17 cells and a red -IL-6 for Tre cells onto the diagram.||Mnemonic||Verified||08/06/19 12:33 PM||Abhishek||Gamifirstname.lastname@example.org|
|207||101||Immunology||Lymphocytes||Differentiation of T cells||first aid||we can use O in pOsitive selection as indicator for cOrtex ,, and E in nEgative selection as indicator for mEdulla||Mnemonic||Verified||08/31/19 9:09 AM||Mohamed||Menofyemail@example.com|
|208||101||Immunology||Cellular||Important cytokines||First Aid Usmle Step 1 2019, page 102||I suggest to add new column "Cytokines" into the table "Differentiation of T-cells" for visual perception of the information located on the next page (102).||Clarification to current text||09/04/19 12:09 PM||Alsu||Zagorulkofirstname.lastname@example.org|
|209||102||Immunology||Cellular||Cytotoxic T cells||https://www.hindawi.com/journals/bmri/2010/764542/||They also fight against intracellular Listeria||High-yield addition to next year||Verified||Reject.|
CTLs are important for immunity against intracellular pathogens in general. I don't think knowing listeria as a CTL target specifically is HY.
|Agree with Connie, reject. -VV||Reject by 2 authors + 1 editor||03/01/19 8:13 PM||Ala||Jamalemail@example.com|
|210||102||Immunology||Lymphocytes||Macrophage-lymphocyte interaction||https://www.ncbi.nlm.nih.gov/pubmed/7751026||Macrophages, dendritic cells, and other APCs release IL-12, which stimulates T cells to differentiate into Th1 subtype. Th1 cells secrete IFN-gamma, which enhances the ability of monocytes and macrophages to kill microbes they ingest. This function is also enhanced by interaction of T cell CD40L with CD40 on macrophage. (This also explains how macrophages favour differentiation into Th1)||Clarification to current text||It is already covered on that section, however, we could consider adding this to the next edition for completeness. -Victor Martinez||Verified||On the fence. We already state that Th1 cells are induced by IL-12 in the chart, so I'm not sure it is completely necessary to add that into the macrophage-lymphocyte interaction section. However, it does complete the story a little better, which I think could be helpful to include.|
Would not consider this something to address urgently, but might be worth considering for 2020!
|I agree with Connie. This is already covered. We could include this information here again but risk unnecessary repetition.|
However, this could consider for the 2020 edition as there is space on this page.
|Agree, the chart does a great job of summarizing the function. Would not recommend addition again.||Reject by 2 authors + 1 editor||01/27/19 3:38 AM||Arpit||Jainfirstname.lastname@example.org|
|211||102||Immunology||Cellular||T cell subsets||USMLE WORLD QBANK FOR STEP 1, QUESTION ID 762||As TH1 cells secrets interferon gamma and interleukin 2 it also secretes Lymphotoxin B||Minor erratum||I don't think lymphotoxin B is HY at all, but I don't have access to UW and don't know if this is being presented as extraneous info or not.|
Unless someone else can verify, I think it's too LY because it's not central to T cell function and also goes by several other names (TNFC)
|Agree with Connie, not convinced that it's HY enough for purposes of Step 1. Would not recommend addition to the text. -VV||Reject by 2 authors + 1 editor||04/01/19 3:55 PM||Muhanad||Shaibemail@example.com|
|212||102||Immunology||Cellular||T cells||FA 2019 page 102 & 108||Mnemonics to help keep straight the cytokines/interferons secreted by Th cells||Mnemonic||Verified||05/06/19 10:28 PM||Emily||Tuttfirstname.lastname@example.org|
|213||105||Immunology||Immune Responses||Immunoglobulin isotypes||https://www.uptodate.com/contents/the-humoral-immune-response||Maternal IgG starts to wane by birth and is almost completely gone by 6 months of age. It does not "start to wane after 6 months". As it is stated on page 110, the half-life of preformed antibodies is around 3 weeks.||Major erratum||Verified||Faculty input needed.|
The submitter is correct about the half-life of passively transferred IgG, and they are correct with the UTD reference, which says that "maternal IgG is largely cleared from an infant's circulation by 6 months of age." The reference given is an old paper from 1982.
However, more recent literature all states that passively acquired maternal Abs have distinct half-lives in infants, with pertussis-specific IgG waning by 4 mo, but measles remain protective at 6 mo and is still detectable by 1 year, dengue is still present in 82% of babies at 4 mo and 28% at 6 mo, but mean duration of rubella ab is 2.1 mo and varicella is 2.4 mo.
I want to say that our current text is fine given the large range of IgG half-lives, but UTD says otherwise, so faculty input might be nice!
|Would greatly appreciate faculty input per Connie's well-sourced comment. -VV EDIT: Please change "(provides infants with passive immunity that starts to wane after 6 months of age)" to "(provides infants with passive immunity that starts to wane after birth)"||Prelim accept by 2 authors + 1 editor||Anthony DeFranco||suggested change OK except change "starts to wane by birth" to "starts to wane after birth" (maternal IgG in the infant wanes because no longer supplied via placenta). This is the boards level concept for students, reality is slightly more complicated (as indicated by the additional research, probably as some antibody, mostly IgA is present I'm mother's milk and can provide some protection), but impossible/undesirable in a book of this kind to include minor qualifications of this type||Accept||01/07/19 3:17 AM||Panagiotis||Kaparaliotisemail@example.com|
|214||105||Immunology||Immune Responses||Immunoglobulin isotypes||NAD||Mature, naive B-cells express only IgM and IgD prior to activation. Mature, naive B-cells are "Mature" and "Dumb" (M and D)||Mnemonic||Verified||06/08/19 2:50 AM||Mehreen||Alifirstname.lastname@example.org|
|215||106||Immunology||Immune Responses||Complement||-||C5b activates MAC mnemonic: Big-MAC; B from Big is to remember it's C5b not C5a||Mnemonic||It is catchy since almost everyone knows McDonald's. We should add this to the next edition. -Victor Martinez.||Verified||I like this one,Suggest consideration for 2020. -Scott||Yes, but is this HY? C5b-9 as MAC is definitely HY, but I feel like it's always presented as C5-9 or C5b-9, and we don't really have to identify the individual components, and I haven't seen anything requiring differentiation of C5b-9 from C5a-9.|
Maybe editor input? It's a cute mnemonic, but I wouldn't include it unless it's HY bc of crowding.
|Inclined to reject. We have a really nice mnemonic for C5a to help remember it's use. Additionally, questions usually present with C5-9 rather than identifying the specific component. Recommend no changes. -VV||Reject by 2 authors + 1 editor||01/20/19 5:47 PM||Hasan||Alarouriemail@example.com|
|216||106||Immunology||Immune Responses||Complement||https://www-ncbi-nlm-nih-gov.www.libproxy.wvu.edu/pubmed/11257302||C1-Like Complex should be clarified in the image to be "MBL Complex". This is important, because MBL deficiencies have been described and are testable items for STEP (see next errata)||Minor erratum||08/18/19 9:25 PM||Joseph||McGuirefirstname.lastname@example.org|
|217||107||Immunology||Physiology||Complement disorders||https://www.ncbi.nlm.nih.gov/pmc/articles/PMC15187/||"decay-acclerating factor" should be replaced with "decay-accelerating factor"||Spelling/formatting||Agree, minor spelling error -Victor Martinez||Verified||Agree - spelling error. Change to decay-accelerating factor as suggested. - Sarah||Agree with Sarah, change typo.|
|Haha, good catch! But doesn't really need to be on published errata, defer to 2020. Please replace "decay-acclerating factor" with "decay-accelerating factor" -VV||Prelim accept by 2 authors + 1 editor||12/23/18 11:07 PM||Joshua||Tayloremail@example.com|
|218||107||Immunology||Pharmacology||Complement disorders||https://www.uptodate.com/contents/ace-inhibitor-induced-angioedema?search=kallikrein%20inhibitor&source=search_result&selectedTitle=4~22&usage_type=default&display_rank=4 - https://www.uptodate.com/contents/ace-inhibitor-induced-angioedema?search=kallikrein%20inhibitor&source=search_result&selectedTitle=4~22&usage_type=default&display_rank=4||Benefit in the treatment of ACE inhibitor-induced angioedema: ECALLANTIDE : recombinant protein that inhibits plasma kallikrein.||High-yield addition to next year||Verified||UTD even says that available studies on this drug are conflicting. Ecallantide is literally under the section labeled, "therapies of unproven efficacy." I don't think this is HY, and the conflicting studies means that this won't be tested.|
|Agree, reject. No changes.||Reject by 2 authors + 1 editor||02/19/19 12:06 AM||Lissette||Orozcofirstname.lastname@example.org|
|219||107||Immunology||Immune Responses||Complement disorders||was in a Uworld answer explanation but can also be read here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2952982/||early complement disorders: add that it's not any recurrent infection but it's again especially the "encapsulated" bacteria!||High-yield addition to next year||06/07/19 10:54 AM||Noam Leander||Degneremail@example.com|
|220||107||Immunology||Immune Responses||Complement disorders||https://www-ncbi-nlm-nih-gov.www.libproxy.wvu.edu/pmc/articles/PMC2952982/ or https://www.uptodate.com/contents/inherited-disorders-of-the-complement-system?search=Complement%20system%20disorders&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1||There are several complement disorders not listed here that have been described in the literature, but the high-yield ones not included in the book (according to Boards and Beyond as well as Pathoma) are MBL deficiencies (MBL gene affected; susceptible to meningitis caused by Neiserria meningitidis), C3 deficiencies (susceptible to recurrent infection with encapsulated bacteria & type III hypersensitivity syndromes), C3 Nephritic Factor (autoantibody), and hypocomplementemia. Others have been described in the attached article, but aren't considered high-yield to other STEP resources yet.||Major erratum||08/18/19 9:42 PM||Joseph||McGuirefirstname.lastname@example.org|
|221||108||Immunology||Immune Responses||Important cytokines||https://www-ncbi-nlm-nih-gov.www.libproxy.wvu.edu/gene/3576||IL-8 is now commonly referred to as CXCL8. Questions sometimes refer to IL-8 as CXCL8 without acknowledgement that it was formerly called IL-8.||Minor erratum||08/18/19 9:14 PM||Joseph||McGuireemail@example.com|
|222||109||Immunology||Immune Responses||Respiratory burst (oxidative burst)||https://www.uptodate.com/contents/chronic-granulomatous-disease-pathogenesis-clinical-manifestations-and-diagnosis?search=chronic%20granulomatous%20disease&source=search_result&selectedTitle=1~117&usage_type=default&display_rank=1||Under respiratory burst diagram it states that "phagocytes of patients with CGD can utilize H2O2" when it should be cannot utilize H2O2.||Minor erratum||Reject, the wording is correct GCD patients can utilize H2O2 generated by organisms, ultimately change this H2O2 into reactive oxygen species. -Victor Martinez||Verified||Reject.|
Text as is is correct. Patients with CGD cannot make their own H2O2, but they CAN utilize H2O2 generated by invading organisms.
|Agree with Connie and Victor. No changes. -VV||Reject by 2 authors + 1 editor||01/25/19 5:28 PM||Nidhi||Shahfirstname.lastname@example.org|
|223||110||Immunology||Immune Responses||Cell surface proteins||n/a||NK cells are KILLER at 16 yrs (CD 16) and caught at 56 yrs (CD 56 - suggestive marker)||Mnemonic||Verified||07/10/19 10:00 PM||A||Pandeyemail@example.com|
|224||111||Immunology||Immune Responses||Vaccination||It's Mnemonic||*in*activated vaccine = typhoid (V*i* polysaccharide, *in*tramuscular).||Mnemonic||Reject. I agree with Scott. It is not HY. -Victor Martinez||Verified||Reject. Not HY. -Scott||Reject, not HY.|
|Reject. -VV||Reject by 2 authors + 1 editor||01/05/19 4:28 PM||Moatasem||Al-Janabifirstname.lastname@example.org|
|225||111||Immunology||Immune Responses||Vaccination||Plotkin SA, Cam NB. A New Typhoid Vaccine Composed of the Vi Capsular Polysaccharide. Arch Intern Med. 1995;155(21):2293–2299. doi:10.1001/archinte.1995.00430210041007||The Vi typhoid vaccine is a subunit vaccine NOT an inactivated vaccine. Since it is composed of a capsular polysaccharide antigen and not the whole inactivated bacterium, it is by definition a subunit vaccine (similar to strep pneumo and H. influenza).||Minor erratum||Agree with the student. Typhoid Vi vaccine is made of the polysaccharide capsule from the bacteria. Therefore, it should be under the subunit classification. -Victor Martinez||Verified||CDC defines as an inactivated vaccine. Would not recommend any changes to the text. -VV https://www.cdc.gov/vaccines/hcp/vis/vis-statements/typhoid.html||Reject by 2 authors + 1 editor||02/07/19 11:52 AM||Daniel||Badinemail@example.com|
|226||111||Immunology||Immune Responses||Vaccination||https://www.vaccines.gov/basics/types||I’ve always had a hard time remembering the live versus killed vaccines. I came up with two “stories” to help remember them. Live attenuated vaccine Mnemonic – The small, type A, yellow chicken named Sabin received his flu mist and MMR before rotating at BCG. Meaning – small (smallpox), type (typhoid oral) A (adenovirus), yellow (yellow fever) chicken (varicella – chicken pox), Sabin (Polio oral), flu mist (influenza), MMR (MMR), rotating (rotavirus), BCG (BCG) Killed or inactivated vaccine Mnemonic – A hippo named Salk contracted rabies from the flu shot. Meaning – A hippo (hepatitis A), Salk (Polio IM), rabies (rabies), flu shot (influenza IM) *The only one missing from this is typhoid Vi, but assuming one understands there is a typhoid oral and IM (Vi polysaccharide) vaccine, it should be fine.||Mnemonic||Verified||06/04/19 2:29 PM||Blake||Wallfirstname.lastname@example.org|
|227||111||Immunology||Immune Responses||Vaccination||https://www.uptodate.com/contents/treatment-and-prevention-of-enteric-typhoid-and-paratyphoid-fever#H14||On page 111, the Vi polysaccharide typhoid vaccine is given as an example of a killed/inactivated vaccine. It is actually a subunit vaccine||Major erratum||09/24/19 12:30 PM||Muhammad Shariq||Usmanemail@example.com|
|228||112||Immunology||Immune Responses||Hypersensitivity types||n/a||Under hypersensitivity type II I would match the formatting of type I. In the first part just say "Antibodies bind to cell surface antigens causing:" Keep the part with Cellular destruction, Inflammation and cellular dysfunction, but add on the square bullet point as seen in the HS type I.||Spelling/formatting|