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Welcome to em_goldman’s page.
Contributor score: 22


Comments ...

 +6  (free120#15)

Rituximab (anti-CD 20) is currently undergoing trials for AS. My sparse googling just now shows that rituximab probably only has a moderate effect, so probably second-line to anti-TNFa therapy. Probably.

Safe to say for boards that AS: TNFa > CD20

cheesetouch  FA 2018 - rituximab p 430 -- - use for Nonhodgkins lymphoma, CLL, ITP, Rheumatoid arthritis TNF-a inhibitors - p 472: 1) etanercept for Ra, psoriasis, ankylosing spondylitis. 2) infliximab and other mAB for IBD, RA, AS, psoriasis +1

 +2  (free120#9)

I believe (pls correct me if I'm wrong) you would have similar Southern blot results seen in B cells undergoing somatic hypermutation, but that takes place in the secondary lymphoid tissue, not in the bone marrow.





Subcomments ...

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DMD is n-Xdklei. eW nkow rhe mom si a erricar adbes no faymli rs,ithyo studporep by abl se.ingtt Btu hre mmo hsa 2 X erss,hcoomom lyno eon fo cwihh is dt.taume eehTr si on wya ot nwko wihch hre daeghutr eleluvntay eisecevr dna reesspxse yb hre yppheneto ei(. if seh is a rraicer or ).ton tJus saceube ehr CK is mloran tn’deso amen hes tsni’ a rrtae–rchei penophyte fo the keXin-ld rrraeic peeddns no in.Xitiva-tcona

em_goldman  Is X-inactivation not randomly mosaic throughout tissues? My thinking is that random, evenly-distributed X activation would cause about ~half symptoms (ex Rett syndrome, X-linked dominant fatal in utero in males but survivable in females due to X-inactivation.) So you see her mom with (presumed) isolated increased CK, which you would expect in her if she was also a carrier. Maybe penetration is variable so you'd need genetic testing to confirm for sure -> the reason she doesn't have symptoms is x-inactivation. +3  


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eTh nmia oewsnddi fo lvie vcceiasn si ttha hety nca (but rraeyl d)o sauec eth dsesiea hre’yet dinedseg ot venet,rp aliypclyt ni udcrpmm-moioisemne vniaid,usild owh ehiret iecreev eht vneaicc or are a colse cotatnc of monosee woh dd.i

em_goldman  Also in the case of the live oral polio vaccine, there's concern of viral reactivation in the feces of people who took the vaccine causing infection of others, even if the original person is protected. I would guess rotavirus is similar but I think the population risk:benefit favors live rotavirus vaccination in lieu of no vaccination, whereas the option of a killed polio virus vaccination is way more worth it than the risk of a polio virus outbreak. +3  


submitted by houseppary(10),
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utb ahtw is gornw tihw choeSirte"p oanvnsii fo rasitcg lels?"c It esmse leki H loipyr is ismoetems icdseebrd sa cvrdeu nad teeimssom sa a cepsrt.hoei ndA ar"gistc secl"l is geeanlr gohune atth I don't ees ywh it cna be ng.owr erTeh si H rliopy ni the tasgicr .cllse

em_goldman  H pylori is sometimes described as helical but more often as curved, but is (confusingly) not a spirochete. Spirochete refers to a particular family, Spirochaete, and are markedly corkscrew. The three important spirochete bugs for Step 1 are Leptospira, Borrelia spp., and Treponema pallidum; Brachyspira spp. get an honorable mention but idk they're high yield for Step 1. Anything other kind of bug is not going to be a spirochete. Additionally, H. pylori is not invasive, and instead resides on the surface of the gastric mucosa. The picture showed some bacteria inside the lumen of glands, not intracellulary. +6  
em_goldman  *idk if they're high yield +  
em_goldman  *any other kind of bug gosh dang it, lol, definitely in dedicated rn +  
dang90  I also think spirochetes dont "invade" either. They colonize in the gastrum antrum releasing urease to thrive but don't invade. +  


submitted by houseppary(10),
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tub wtah is rngwo whti eteocri"Sph nisinoav fo atsirgc e?lsc"l tI eessm like H lpriyo is simetemos rbeeicdsd as vrecud nda emsietsom as a c.thoprseie Adn tsicag"r "cells si ralngee eohung that I 'dtno see hyw ti nca eb rw.gon Three si H rpoiyl ni the aricsgt cslle.

em_goldman  H pylori is sometimes described as helical but more often as curved, but is (confusingly) not a spirochete. Spirochete refers to a particular family, Spirochaete, and are markedly corkscrew. The three important spirochete bugs for Step 1 are Leptospira, Borrelia spp., and Treponema pallidum; Brachyspira spp. get an honorable mention but idk they're high yield for Step 1. Anything other kind of bug is not going to be a spirochete. Additionally, H. pylori is not invasive, and instead resides on the surface of the gastric mucosa. The picture showed some bacteria inside the lumen of glands, not intracellulary. +6  
em_goldman  *idk if they're high yield +  
em_goldman  *any other kind of bug gosh dang it, lol, definitely in dedicated rn +  
dang90  I also think spirochetes dont "invade" either. They colonize in the gastrum antrum releasing urease to thrive but don't invade. +  


submitted by houseppary(10),
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tub tawh is wrngo ihwt eSohetpi"rc nvsinoia fo rtiasgc ce"s?ll It esesm ilek H lrypoi is eomssmeti deecsibrd sa dvecur dan iesemtsmo sa a sehproietc. ndA sgri"act c"llse si lgeerna oeughn ttah I 'ndto ese why it can eb orwgn. ehTer is H ylrpio ni het csagitr .escll

em_goldman  H pylori is sometimes described as helical but more often as curved, but is (confusingly) not a spirochete. Spirochete refers to a particular family, Spirochaete, and are markedly corkscrew. The three important spirochete bugs for Step 1 are Leptospira, Borrelia spp., and Treponema pallidum; Brachyspira spp. get an honorable mention but idk they're high yield for Step 1. Anything other kind of bug is not going to be a spirochete. Additionally, H. pylori is not invasive, and instead resides on the surface of the gastric mucosa. The picture showed some bacteria inside the lumen of glands, not intracellulary. +6  
em_goldman  *idk if they're high yield +  
em_goldman  *any other kind of bug gosh dang it, lol, definitely in dedicated rn +  
dang90  I also think spirochetes dont "invade" either. They colonize in the gastrum antrum releasing urease to thrive but don't invade. +  


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etSrhonu slotb aer mlconyom udes in glocummonaili idstues, sa eht nrotuseh botl aolswl fro eth dtusy of AND rtat.loansei htaW is nylrlmoa one eegn nnicorfoiatug eaeldrt to unmiem uigsoblln ni otms stussie sdtrmeonetsa tielpulm eftfidren anbds in the beon aorr,mw ivdcntiaei fo neeg meter.aernnrga ihTs si syicallab hwo ew ctreea wne bi.notsedia aivceRet cssrspeoe are ypllancool ll(ipeumt ndb)as; eelmu,ika ni tstn,orca si nlnacomool (esigln .anbd)

ali  I still don’t understand this one. Could you provide a better explanation? +  
benwhite_dotcom  The cDNA tag is tagging a constant region common to immunoglobulins, so it normally only finds the one band corresponding to that particular gene (the bands travel different amounts due to their differing size/weight). In the bone marrow sample, that gene has rearranged itself, so the cDNA clone instead tags multiple different genes that are of different sizes on the gel (each one has that same constant region the cDNA is tagging, but with different stuff around it such that the restriction enzyme has cut it up differently). I’d be happy for someone to step in and do a better job on that explanation. +11  
em_goldman  A Southern blot starts by cutting DNA strands at a particular (short) site and running them through gel electrophoresis, so identical DNA sequences get cut at the same site and thus are the same length, so they are at the same place on the gel. If there's lots of different sequences, the restriction endonuclease (the scissors) cut the DNA at different places, leading to strands that were the same length originally but are now lots of different lengths -> different places on the gel. But how do you know this is the same gene, just with different mutations? The Southern blot uses a probe to look for a more specific (long) region of DNA that you know is in the target gene. So even though there are mutations causing the less-specific endonuclease to cut the DNA at different parts, the overall architecture of the gene is similar enough that the probe can bind, thus we know it's the same gene. (And in bone marrow WBCs, the mechanism here is genetic rearrangement.) +1  


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ligasrtimF is a oguncyterla ylnoco slituitngma tcarof ,)SCFG( cihwh era gsrdu dsue to nceaiers iethw lbodo lelc ocutn ni itsatpne wthi ieao.nulkpe oouiLvcrne nloicif( cda)i duossn ekil it dwluo sola eb ri,tgh tbu its’ deus to epenrtv bone rroawm nsirseopsup in ptestani tkiang otettrhmx.eae bDeaierontp l(kei etiyopriohnr)et is edus to usatilemt red oodlb clel t.ondciurop

em_goldman  were we supposed to know that she wasn't taking methotrexate (or did I miss that in the question stem)? +  
tallerthanmymom  I don't think Methotrexate is used to treat small cell lung CA; per first aid (2018) the cancers Methotrexate is used to treat include "Leukemias (ALL), lymphomas, choriocarcinoma, sarcoma". It also has some non-cancer uses in rhuematologic ds, ectopic pregnany and medical abortions. +1  


submitted by poisonivy(30),

can we consider the overdose as a suicidal attempt? if so... wouldn't she be considered as without decision-making capacity?

em_goldman  People who are suicidal still have decision-making capacity; it's not equivalent to advanced dementia or other situations where decision making is impaired. Laws vary by state; I know in my state that the maximum time for holding someone against their will is 48 hours unless a court has deemed them incompetent and designated another person as their legal decision maker, including people who are actively suicidal. My understanding of the law as a layperson is that her living will was signed along with people bearing witness to the fact that she was the one who signed it, and it was what she wanted. Ethics aside, it would be almost impossible to prove that she legally initiated a DNR in a state of suicidality that was intense enough to interfere with her decision-making capacity in that moment. +1