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Contributor score: 172


Comments ...

 +0  (nbme23#31)
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I kitnh I nfduo tahw eth isdasee swa, hughot I olhnyest have no aedi hwy yhte oudwl ttse hist rreaht naht AXL. e’reTsh a dicnotnoi lclaed senaiTtrn blmigieolnuagopaymHma fo aIcynfn. tI neprsest owl/w ounulgnbloimmi velsel tpso 6 otnshm nad nca rntspee wamls/l ylpmh nodse dan itsnslo in yncnfia BTU o/w ayn hoter sifgdnni fo rraiymp eficoinmuyeidmcn dnuilgcin acddseree ntu.ocs

serH’e an atilcre atobu :ti r/ryseino.:-nd-ioli/psnpei-a-coasscefce/aiyiaietmpsmomednmutnpyaaimpur/o/regtrietgiaby-m/ams-utsgcnlehfmna-fmtiripeiiynouhcbf

uYo yilidfente ’tond eend to kown eth eiasesd to get het trrcoec srenwa nesic het klin of lack fo mumolsibnlniuog wdolu cleu you noti the kacl fo amgiernl e,snecrt but I ithnk hits is erom ielykl ntha AXL isnce yeerv oecsru I aedr epismil tath B lelc counst era nare 0 in eht slscica entaesinptro lsnsu(e mI’ simnisg a anosre ywh ktcoeueyl onctu iw/fdf ’wltnuod show a intniafsgci recdseae in lsyoycmhtep deu to -orzenrae B )cslle. Just awtend to ptu shit eehr ni acse htreo eelpop lraet aecm wgr,oinnde ohguth I aym sltli be or.wgn

keycompany  I think we are all overthinking this question (and it is remarkably simple). I don't think this question is testing us on any of the UFAP immunodeficiency syndromes, per say. What they are really asking is "what would also be absent if there are no immunoglobulins and everything else is normal"? The answer is absent germinal centers b/c that's where Ig is synthesized. I think they put all other aspects of the history in this stem just to help you rule out any of the other answers. +9

 +8  (nbme24#25)
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Yuo onwk ts’i an edvolpene rusvi encis it ’tsneod hodl up to iacd ro ingbe .dride uoY owkn ti aecuss a vrefe dna a gho,uc wiehl afcfgeint the .alrxyn Only siurv eyroagct ttah sfit lal ttah oinf is het nsivrocuaor (esascu SRA)S rofm htta tli.s

zelderonmorningstar  EBV doesn’t cause fever and cough? +
zelderonmorningstar  Wow, just checked First Aid and it doesn’t list “cough” as a symptom of EBV. +4
drdoom  EBV is not a “respiratory virus”; it’s a *B cell virus*. Even though you might associate it with the “upper respiratory tract” (=kissing disease), it doesn’t cause respiratory inflammation since that’s not its trope. B cells are its trope! That’s why EBV is implicated in Burkitt Lymphoma, hairy leukoplakia and other blood cancers. (EBV is also known as “lymphocryptovirus” -- it was originally discovered “hiding” in *lymphocytes* of monkeys.) So, EBV = think B cells. +20
fulminant_life  EBV does cause pharyngeal and laryngeal inflammation along with fever, malaise, and cough and LAD. The only thing that pointed me away from mono and towards coronavirus was the patients age. +5
nbmehelp  Can someone explain what not holding up to acid or being dried has to do with being enveloped? +
yb_26  @nbmehelp, the envelope consists of phospholipids and glycoproteins => heat, acid, detergents, drying - all of that can dissolve the lipid bilayer membranes => viruses will loss their infectivity (because they need an envelope for two reasons - to protect them against host immune system, and to attach to host cells surface in order to infect them) +6
lowyield  @yb_26 does that mean that non-enveloped viruses hold up better to acid/dryness? +1
rina  yes enveloped viruses are easier to kill (see post from drsquarepants: https://www.nbmeanswers.com/exam/nbme23/1161). also i think the "when dried" might refer to the fact that coronavirus is spread by respiratory droplets (don't even need to read first aid can just read the news at this point!) +2

 +17  (nbme24#34)
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uaesceB oyu rae s,uneip rheets’ eiednrasc pdaroel nigog ackb ot uyor rteah (no deen to kwor satiang ,ragiyvt oryu olbdo ’ntsi goploin in yoru esgl sa muhc heer)i.t As a tseulr, NAP is tercsede edu ot RA tschetr, aldigne to ierdisus adn a nuctidoer of bolod .eluomv

urachus  When the person is lying down (supine position), gravitational forces are similar on the thorax, abdomen and legs because these compartments lie in the same horizontal plane. In this position, venous blood volumes and pressures are distributed evenly throughout the body. https://www.cvphysiology.com/Cardiac%20Function/CF017 +
thelupuswolf  RAAS trumps ANP though, so the dec. in RAAS as said by colonelred_ is likely going to have more of an effect than ANP. +1
lola915  If you have an increase in ANP wouldn't natriuresis occur and cause a decrease in blood sodium? +1
mynamejeff  Because you are suprine, there's increased preload going back to your heart (no need to work against gravity, your blood isn't pooling in your legs as much). As a result, ANP is secreted due to RA stretch, leading to diuresis and a reduction of blood volume. +
sars  This is a "read my mind" question and complete it in 1.5 minutes. Thanks +

 +5  (nbme24#30)
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netiaPt has erndgaicoci skh,co fiileclpcyas eht LV icsen tis’ an areorint wlla IM tin’s nppgumi. yHtnselo oyu on’dt ende to nowk awth ahenpsp to VRP ot snawre orcertc icnse eht nyol cheico htat ash dienraces VSR dan deersadec PPWC is eht one dwacsr/deee VP.R mI’ ont latuseboly rues if uyo lucod uegfir it uot iegvn het ulavse in ocirdnceaig kh.sco Teh otqneaiu liiknng eht uvsael :is

VPR = mnupoa(yrl erartali srrpseue - w)dgee Ă· CO


 +13  (nbme24#29)
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aatlrPi tagsnois ahev eawk gstonai ctiaviyt on ertih now ush(t ni shit ecsa ti acsseu HR to nrci,esea nagdcrbie-re cef)tfe ubt wenh an culata gstanoi is pestnre ak(a whne ouy ear exscgiin,er uyo rae pudgircon EN dan E thta heva lufl osgna-bti ,fefctse) latpiar nsaogit yalctula vhae a limd aitagnonts teefcf u(tsh eth taerh etar a.ere)cessd

potentialdoctor1  Might be relevant to add that there are two beta-blockers that are actually partial beta-agonists (exert their blocking effects due to lesser effect when compared with endogenous catecholamines) ----> Pindolol and acebutolol +6
thelupuswolf  Key to note as madojo said that a partial agonist will compete with the full agonist in the presence of the full agonist, preventing the full agonist's maximum effect +

 +14  (nbme24#42)
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onneriicbtF si na rculexteaallr mrixta op,yecolrigtn lwehi inmla is na ateteenirdim famtnlie ttah asfcpeiiycll epvsdoir surtpop ot eht llec nlsec.uu nt’Do eocfsun nimla htiw minnila nci(ecse htase su ;laycler) inmnlia is ikle nc,ifironbte na MEC ncpiolgeyrot adn a aomjr otmpneonc of teh baasl naamli fo nbmeaets ebr.mnamse

masonkingcobra  Lamin looks like a "cross" and held up Jesus and the basal lamina is super important just like jesus (you bet there are people who believe this) https://answersingenesis.org/biology/microbiology/laminin-and-the-cross/ +17
dr.xx  blasphemy @masonkingcobra +1
luciana  I clearly confused lamin with laminin, now I know +2
almondbreeze  FA 2019 pg 48 lamin +1
almondbreeze  picked tubulin but i guess tubulin makes up microtubules and therefore is spherical +
gandon  I used to kill and rob people before I found Lamin. He died for my sins on the Cross and changed my life. +

 +15  (nbme24#24)
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heT seisead eher si roftucse pitsohbshaespa cdencyi.fie In i,t VI eoglcrly ro ertucfos ne’dots hlpe sbaeuec htob tnree the oosueenegnclisg waaypth lbewo ertoucfs atihopesha.psb tlaaescGo on het hetro nhda eetrsn oevab ti. I ’otdn nkhit yuo leyrla eedn to onkw iths to oceohs the rtcreco raswne iencs eht lccliani rciuept of asftgni ylhgyoiemapc tath si rcecdtreo /w seom tsro fo saugr tath anc eenrt hte eeongsoegcisunl tpahawy shuldo cuel ouy iton the griht s.nawer

neonem  I don't think you could have *totally* ruled out the other answers - I picked glycogen breakdown because it sounded kind of like Von Gierke disease (glucose-6-phosphatase) to me: characterized by fasting hypoglycemia, lactic acidosis, and hepatomegaly since you're not able to get that final step of exporting glucose into the blood. However, I guess in this case you wouldn't see that problem of glycerol/fructose infusion not increasing blood glucose. Nice catch. +16
vshummy  I think you were super smart to catch Von Gierke! Just to refine your answer b/c I had to look this up after reading your explanation, von gierke has a problem with gluconeogenesis as well as glycogenolysis. So they’d have a problem with glycerol and fructose but also galactose since they all feed into gluconeogenesis before glucose-6-phosphatase. Great thought process! +20
drmomo  glycerol and fructose both enter the pathway thru DHAP and glyceraldehyde-3-ph. Galactose enters thru Gal-1-ph to glu-1-ph conversion +2
linwanrun1357  In this cause (fructose bisphosphatase deficiency.,),fructose should help to increase serum glucose, bcz it can become into glucose-6-P by hexokinase. Therefore, this question makes me confused.... +
krewfoo99  According to uworld, fructose infusion will not increase blood glucose levels in Von Gierkes Disease as well +
atbangura  I believe Von Gierke is not a plausible answer choice because a galactose infusion would still not see an elevation in glucose levels. Remember, galactose could be converted to galactose 6 phosphate, but in order to complete gluconeogenesis and allow glucose to leave the Liver for an increase of its concentration in the blood, the patient would still need glucose 6 phosphatase which is eliminated in Von Gierke. +1
lilyo  So what disease is this??? I mean couldnt we have just answered the question based on the fact that the patient responds to galactose being infused and we know that galactose feeds into gluconeogenesis?? I am so confused. +1
djtallahassee  Its Hereditary Fructose intolerance right? gets sick after fructose and I guess glycerol can jump in via aldolase B on this pathway via page 74 of FA2019. It looked like a fructose thing to me so I just marked out the other ones and moved on. +1
paperbackwriter  @djtallahassee I was wondering same, but hereditary fructose intolerance also results in inhibition of glycogenolysis :/ confusing question. +
amt12d  A much simpler way to think about this, without trying to figure out a diagnosis, I looked at the time frame for when the child was presenting. He has eaten poorly for 3 days, by now, his glycogen breakdown is gone. His body would be trying to make glucose, therefore, gluconeogenesis is impaired, not glycogen breakdown. +2
tyrionwill  if fructose kinase is not available (fructose intolerence), then some fructose may go to F-6-P by hexokinase, then goes to G6P if gluconeogenesis is needed. however this patient's fructose kinase was intact, so no fructose would have go to F6P, so there would be no blood glucose increment after injection of fructose. +

 +32  (nbme24#28)
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taMs lcels dltegaa,uern rogpucdni emshaitin whhic atacsttr hiole.osipns The earyl getas of na rcleailg eitrnoac si smat llce i,teamdde tbu eht eatl sagte ungcl(idni sucmu onpiurd)cto si dedaimet by l.noosieshpi

atstillisafraud  Thanks for a good answer. This question made me feel like I was taking T21 pills +14
medguru2295  Thank you- I was really thinking this question had 2 correct answers... of course my dumbass picked Mast cells. +2
ajss  where do i find this info?? +
paperbackwriter  @ajss pg 112 of first aid 2019, under type I hypersensitivity. Immediate --> mast cells releasing histamine and tryptase, late--> eosinophils and leukotrienes recruited via chemokines +2
graciewacie9  Wow, i missed the fact that the question is asking for the RESULT of the reaction, NOT the cause of the reaction. Mast cells cause the initial reaction, eosinophils would be the result of the eosinophils. *facepalm +1
greentea733  @graciewacie9 SAME UGH +
lba9587  Pathophys (as far as I understand it)...Mast cell degranulates, thus the phospholipid bilayer et. Al are left behind and needs to be degraded. Who comes in? Our good friend eosinophils, as they contain Major Basic Protein (responsible from breakdown of expired mast cell). Note, you can tie this in to the delayed Leukotriene effects of an allergic rxn, as the bilayer is also broken down by arach. Acid. (See this link to support my credibility https://images.app.goo.gl/3cUF3ZVc7qy8uxAi9) +




Subcomments ...

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nCa aonnye lxeipan how 1c0m 20H etpiivso EEPP leads to kePa ynIstorarip A,P dEn lTaid ,AP kPae posnarityIr iPp dna ndE lTaid Ppi lal ibegn ipv?eoits

tea-cats-biscuits  In PEEP, bc of how mechanical ventilation works, all the inspiration part of breathing is done by the machine actively pushing air into the lungs. As a result, there is no negative pressures in the system compared to the normal lung which needs the negative inter-pleural pressure to draw air in. +24  
yotsubato  " As a result, there is no negative pressures in the system compared to the normal lung which needs the negative inter-pleural pressure to draw air in. " Thats totally what threw me off. TIL +  


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I dckpei MNDA ecasebu ist’ om,ltristuya ubt is tehre ayn derepe rnaeos for ist?h

tea-cats-biscuits  The Q is actually asking which of the receptors use Ca+ ions, and of the choices given only NMDA receptors do so. +13  


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I uhgtoht hatt the rapimry ettpyhcmasi ivreniotnan ot hte ahetr saw otuhghr .T-4T1 yhW uodlw atoinlustmi of tish ginagoln not ecffta nski sleevss ni eth uprep il?bm

methylased  Stellate ganglion --> sympathetics for sweat to skin in UE + head. Apparently also to increase HR (some cardiologists ablate stellate ganglion for tachy that cant be controlled by beta blockers). +  
tea-cats-biscuits  The stellate ganglion is a sympathetic ganglion, so it wouldn’t increase vasodilation in the skin of the upper extremity. Also in most people, the inferior cervical ganglion is fused with the first thoracic ganglion (T1), forming the stellate ganglion. +17  
sympathetikey  Got this wrong too. I think upper extremity skin vasodilation (which I picked) is probably more due to local metabolites. +  


submitted by hipster_do(6),
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’mI nigog ot asy its’ X eilndk lmneaagmugimlaaobi erahrt nath D,SCI btu eht efcirfndee teewnbe teshe otw rae yint btu sthi si ywh I ikhtn tis’ eth rre:ofm

  • Byo nrdeics(ae iskr tbu tohb AB nad ICSD aer x lk)dnei
  • rtucreneR alcrtiaeb conienfist utb od’nt iennomt aerirdha ro surthh ihhwc si in CISD
  • elniemiT is ftrae 6 ,tsmhno so eth oseht’rm tbandsoeii roew f.fo

DICS lsudoh be yiimdeealtm uacebse they sujt ’tnod heva het I2L .serrpecto VDCI sohsw pu ehnw ethyre’ -4020 sraey d.ol uoY get anbtes ngimrael cntrees ni obht. No iotnenm fo nabtes cihmyt ahwsdo chwhi si ni DSC.I

placebo079  “Uniformly” low is also a clue; in CVID they are not. +4  
tea-cats-biscuits  This makes sense, though what really threw me off was that in Classic Bruton’s Agammaglobulinemia there’s near-zero B counts though (or at least that’s what FA and UTD says, “Absent B cells in peripheral blood” FA 116, 2018). The Q says the leukocyte count was normal though. Wouldn’t the leukocyte count include lymphocytes in the differential? And wouldn’t lymphocytes be low due to the near complete lack of B cells in peripheral circulation if it was BA? +1  
partybrockk  @tea-cats-biscuits Bruton’s is a failure of B cells to /MATURE/. So you get normal lymphocyte counts, decreased levels of immunoglobulins, and absent germinal centers. +5  
tea-cats-biscuits  @partybrockk That makes sense to me, but I keep getting hung up on how that’s not what either FA or UTD says about the classic lab findings of XLA. UTD specifically says this: “Laboratory findings include hypogammaglobulinemia/agammaglobulinemia, deficient antibody responses to immunizations, and absent or markedly reduced B cells in the blood,” and I previously quoted FA. I suppose it doesn’t really matter, but it’s definitely a bit frustrating unless I’m missing something about how absent B cells in the blood wouldn’t correlate to a decreased lymphocyte count ... +3  
temmy  please correct me if i am wrong cos i might be but my logic was there is decreases immunoglobulin uniformly meaning the B cells are uniformly absent and since they develop in the germinal center, the germinal center will be absent. +2  
almondbreeze  Picked 'decreased # of CD4 lymphocytes'.. ->Both CD4 and CD8 T lymphocytes were affected; the decrease was most pronounced for naĂŻve T cells. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809006/) +  


submitted by hipster_do(6),
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Im’ ggion ot say s’it X lednik uagmmaalimlgeaobni rtareh tnah DSIC, ubt het inedrffeec nebtwee ehste two aer tiyn but sith si yhw I tikhn ’sti eth ofem:rr

  • Boy reec(iadsn skir tbu thob BA adn DISC era x i)nldek
  • cnReretru creitaabl nfiecstion ubt ’ndot nimonet airhadre ro uhthsr chhwi si in DICS
  • eeimilnT is farte 6 nhs,omt os hte ehs’motr sbeiidtona erow f.of

CDSI shduol eb dlimyaetmie eseaubc ehyt tjus odn’t hvae eth I2L rpceerts.o VIDC wssoh up ehwn tyr’ehe 00-24 asyre old. Yuo gte banset eglrmani eetcrns ni bo.ht No mneonti fo anestb myhcti asodwh hicwh is in S.DIC

placebo079  “Uniformly” low is also a clue; in CVID they are not. +4  
tea-cats-biscuits  This makes sense, though what really threw me off was that in Classic Bruton’s Agammaglobulinemia there’s near-zero B counts though (or at least that’s what FA and UTD says, “Absent B cells in peripheral blood” FA 116, 2018). The Q says the leukocyte count was normal though. Wouldn’t the leukocyte count include lymphocytes in the differential? And wouldn’t lymphocytes be low due to the near complete lack of B cells in peripheral circulation if it was BA? +1  
partybrockk  @tea-cats-biscuits Bruton’s is a failure of B cells to /MATURE/. So you get normal lymphocyte counts, decreased levels of immunoglobulins, and absent germinal centers. +5  
tea-cats-biscuits  @partybrockk That makes sense to me, but I keep getting hung up on how that’s not what either FA or UTD says about the classic lab findings of XLA. UTD specifically says this: “Laboratory findings include hypogammaglobulinemia/agammaglobulinemia, deficient antibody responses to immunizations, and absent or markedly reduced B cells in the blood,” and I previously quoted FA. I suppose it doesn’t really matter, but it’s definitely a bit frustrating unless I’m missing something about how absent B cells in the blood wouldn’t correlate to a decreased lymphocyte count ... +3  
temmy  please correct me if i am wrong cos i might be but my logic was there is decreases immunoglobulin uniformly meaning the B cells are uniformly absent and since they develop in the germinal center, the germinal center will be absent. +2  
almondbreeze  Picked 'decreased # of CD4 lymphocytes'.. ->Both CD4 and CD8 T lymphocytes were affected; the decrease was most pronounced for naĂŻve T cells. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809006/) +  


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yhW is het wrsnea scaedrede oldbo uelvom sa ooedpsp ot dradcseee psaalm mdoius neonctnitroca?

tea-cats-biscuits  I think it might just be what NBME feels “decreased plasma sodium concentration” means, since through the mechanism that BV is lowered in bedrest, you would definitely have a decreased plasma sodium concentration compared to not-bedrest. However you won’t be presenting with any pathologic signs of hyponatremia because the Na+ would still be maintained in normal limits. Low blood volume is the cause of one of the main pathologic states associated w/bedrest -- cardiac deconditioning and postural hypotension once out of bedrest. Seems like poor wording though. +3  
mnemonia  Remember that changes in sodium concentration over a long period time need to be due to a water dysregulation problem (like SIADH, polydipsia, HF, etc.). Here we just have physiologically increased effective circulating volume, and the body will compensate by diuresing, and since Na+ (and K+) are regulated ions, their plasma levels will not fluctuate. +4  


submitted by colonelred_(86),
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ooedLk ti pu dna dnouf hatt ebsucea ue’ryo ni a speniu npoiitso orf a gonl meit u’eryo gnigo ot ahev airendces nvesou nuertr chhwi delas to dseraceni .OC hsTi liveygenta deesfakbc on ,RSAA gnaidle ot sdeacrdee orsateel.ndo sA a tsul,re eo’uyr gogni ot evah rcainseed iiuesdrs hcwih sdlea to deseeacdr oobld dna spamla volme.u

medstruggle  Doesn’t supine position compress IVC leading to decreased venous return? (This is the pathophys of supine hypotension syndrome.) There was a UWorld questions about this ... +3  
tea-cats-biscuits  @medstruggle *Supine position* decreases blood pooling in the legs and decreases the effect of gravity. *Supine hypotension syndrome*, on the other hand, seems specific to a pregnant female, since the gravid uterus will compress the IVC; in an average pt, there wouldn’t be the same postural compression. +6  
welpdedelp  this was the exact same reasoning I used, but I thought the RAAS would inactivate which would lead to less aldosterone and less sodium retention +3  
yotsubato  You gotta be preggers to compress your IVC +4  
nwinkelmann  Could you also think of it in a purely "rest/digest" vs "fight/fright/flight" response, i.e. you're PNS is active, so your HR and subsequently your CO is less? But the explanation given above does make sense. Also because I think just saying someone is one bed rest leaves a lot up for interpretation, maybe not with this patient because his pelvis is broken, but lots of people on bed rest aren't lying flat.... ? +1  
urachus  wouldnt low aldosterone cause low plasma sodium? choice B +4  
kpjk  could it be that, while low aldosterone levels decrease plasma sodium levels- there is also decrease in blood volume(plasma),so there wont be a decrease in the "concentration" of sodium +4  
almondbreeze  FA 2019 pg 306 on Lt heart failure induced orthopnea - Shortness of breath when supine: increased venous return from redistribution of blood +  
almondbreeze  if there was no HF, it would lead to increased CO --> decreased aldosterone +  


submitted by stapes2big(9),
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I’m nto rseu outba hist neo utb eth ayw I tuhogth abotu it wsa tath sicen het cndcefnoei etavlnri ilceundd 1, ti saw otn tsciinnfiag. ndA tshu p aeuvl umts eb above 050.

tea-cats-biscuits  That makes sense! +  
asapdoc  Had the same reasoning +11  
jkan  I get that it's not significant, but why is it 0.05<p<1 and not p>1.0 +8  
jkan  nvm, it's can't be greater than 1 because then it would have a negative% confidence interval which cannot happen (Think if p>0.05 means at least 95% within confidence interval) +9  
charcot_bouchard  p=0.05 means theres 5% chance null hypothesis is true. p=1 means theres 100% chance null hypothesis is true. >1 means >100% chance which isnt possible. +11  
wowo  p is a probability, so can't be greater than 1 +7  
noname  @charcot_bouchard, that is not a good interpretation of p-value. A better interpretation of p=0.05 would be: If in reality there is no increase in risk (RR=1), and if we replicated the same study of the same sample size many different times, then we would expect to find a risk ratio of (X) only about 5% of the time. +1  


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Why si avnletteiar sicinlpg or t-toctiprsasprnaionl moaiicdifnto ie?crtrnoc

tea-cats-biscuits  You just have to know that POMC is a pro-protein that must be cleaved; not sure if there’s anything in the stem that would really have given it away. +1  
mcl  Dunno if this helps, but it says "this protein" (singular) is the precursor of two different protein products. This must mean that the modification occurs after the protein is made, which means after transcription and splicing has already happened. +28  
ngman  Also I believe mRNA refers to after the splicing already occurs. If the protein products are from the same mRNA then it can't be alternate splicing. +1  
medschul  They're cleaved by tissue-specific proteases +  
duat98  I think: Alternative splicing occurs with hnRNA not mRNA. You get mRNA from alternatively splicing the hnRNA. an mRNA can only make 1 type of protein. Since the question says the 2 proteins comes from the same mRNA it cannot be alternative splice or post transcriptional mod. FA 2018 page 43 has a good illustration. +6  
tadki38097  Just general testing taking strategy i guess, but for this question i was torn between post-transcriptional and post-translational, but then i saw that alternative splicing was also a choice...because alternative splicing IS a post-transcriptional modification you know it has to be post-translational because you can't select two answer choices. +