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1. AABBE6. CEBAE11. DDDBA16. DECED21. BBDDB26. ADEDC31. DDEEE36. EEDAA41. BDCDB46. CDCBB 1.AACaspase-9 is an initiator caspase, encoded by the CASP9 gene. The aspartic acid specific protease caspase-9 has been linked to the mitochondrial death pathway. t is acti!ated d ring programmed cell death #apoptosis$. nd ction of stress signaling pathways %&'(SAP' ca ses release of cytochrome c from mitochondria and acti!ation of apaf-1 #apoptosome$, which in t rn clea!es the pro-en)yme of caspase-9 into the acti!e form.*.AAPrimary symptoms of C. par! m infection are ac te, watery, and non-bloody diarrhoea. C. par! m infection is of partic lar concern in imm nocompromised patients, where diarrhea can reach 1+1 per day. /ther symptoms may incl de anore0ia, na sea(!omiting and abdominal pain.nfection is ca sed by ingestion of spor lated oocysts transmitted by the fecal-oral ro tentamoeba histolytica is an anaerobic parasitic proto)oan.The acti!e #tropho)oite$ stage e0ists only in the host and in fresh loose feces2 cysts s r!i!e o tside the host in water, in soils, and on foods, especially nder moist conditions on the latter.http3(( pload.wikimedia.org(wikipedia(commons(c(cf(Tropho)oites4of4ntamo eba4...rocytes.%P5 http3((en.wikipedia.org(wiki(6ile3ntamoeba4histolytica4life4cycle-en.s!g5iardia lamblia is a flagellated proto)oan parasite that coloni)es and reprod ces in the small intestine, ca sing giardiasis. The giardia parasite attaches to the epitheli m by a !entral adhesi!e disc, and reprod ces !ia binary fission. 5iardiasis does not spread !ia the bloodstream, nor does it spread to other parts of the gastro-intestinal tract, b t remains confined to the l men of the small intestine.http3(( pload.wikimedia.org(wikipedia(commons(+(+7(5iardia4lamblia4S8479...74lores.:pg5iardia infection can occ r thro gh ingestion of dormant cysts in contaminated water, food, or by the faecal-oral ro te #thro gh poor hygiene practices$. The 5iardia cyst can s r!i!e for weeks to months in cold water, and therefore can be present in contaminated wells and water systems, especially stagnant water so rces s ch as nat rally occ rring ponds, storm water storage systems, and e!en clean-looking mo ntain streams.http3((en.wikipedia.org(wiki(6ile35iardia4life4cycle4en.s!gStrongyloides stercoralis is a nematode that can parasiti)e h mans. The ad lt parasitic stage li!es in t nnels in the m cosa of the small intestine.Strongyloides stercoralis is a nematode that can parasiti)e h mans. The ad lt parasitic stage li!es in t nnels in the m cosa of the small intestine. 8any people infected are s ally asymptomatic at first. Symptoms incl de dermatitis3 swelling, itching, lar!a c rrens, and mild hemorrhage at the site where the skin has been penetrated. f the parasite reaches the l ngs, the chest may feel as if it is b rning, and whee)ing and co ghing may res lt, along with pne monia-like symptoms #;ffler<s syndrome$. !ent ally, the intestines co ld be in!aded, leading to b rning pain, tiss e damage, sepsis, and lcers. n se!ere cases, edema may res lt in obstr ction of the intestinal tract as well as loss of peristaltic contractions.Strongyloidiasis in imm nocompetent indi!id als is s ally an indolent disease. =owe!er, in imm nocompromised indi!id als, strongyloidiasis can ca se a hyperinfecti!e syndrome #also called disseminated strongyloidiasis$ d e to the reprod cti!e capacity of the parasite inside the host. This hyperinfecti!e syndrome has a mortality rate of close to 9+>.http3((en.wikipedia.org(wiki(6ile3Strongyloides4stercorali)4lar!a.:pg?.@* microglob lin is a component of 8=C class molec les, which are present on all n cleated cells #e0cl des red blood cells$.8ice models deficient for the * microglob lin gene ha!e been engineered. These mice demonstrate that * microglob lin is necessary for cell s rface e0pression of 8=C class and stability of the peptide binding groo!e.n fact, in the absence of * microglob lin, !ery limited amo nts of 8=C class #classical and non-classical$ molec les can be detected on the s rface. n the absence of 8=C class , CB7 T cells cannot de!elop. #CB7 T cells are a s bset of T cells in!ol!ed in the de!elopment of ac ired imm nity.$ow le!els of * microglob lin can indicate non-progression of =D.e!els of beta-* microglob lin can be ele!ated in m ltiple myeloma and lymphoma,tho gh in these cases primary amyloidosis #amyloid light chain$ and secondary amyloidosis #Amyloid associated protein$ are more commonE.@@ Calcitriol , also called 1,*-dihydro0ycholecalciferol or 1,*-dihydro0y!itamin B?, is the hormonally acti!e form of !itamin B with three hydro0yl gro ps.t increases the le!el of calci m #Ca*F$ in the blood by #1$ increasing the ptake of calci m from the g t into the blood, #*$ decreasing the transfer of calci m from blood to the rine by the kidney, and#?$ increasing the release of calci m into the blood from bone.Calcitriol is prod ced in the cells of the pro0imal t b le of the nephron in the kidneys by the action of *-hydro0y!itamin B? 1-alpha-hydro0ylase .consistent se of CS6-PCG for =SD serology established a diagnosis in the ma:ority of ac te aseptic meningitis patients. .CCsophageal !arices are e0tremely dilated s b-m cosal !eins in the lower esophag s. They are most often a conse ence of portal hypertension, commonly d e to cirrhosis2 patients with esophageal !arices ha!e a strong tendency to de!elop bleeding. The ma:ority of blood from the esophag s is drained !ia the esophageal !eins, which carry deo0ygenated blood from the esophag s to the a)ygos !ein, which in t rn drains directly into the s perior !ena ca!a. These !eins ha!e no part in the de!elopment of esophageal !arices. The remaining blood from the esophag s is drained into the s perficial !eins lining the esophageal m cosa, which drain into the coronary !ein #left gastric !ein$, which in t rn drains directly into the portal !ein. These s perficial !eins #normally only appro0imately 1mm in diameter$ become distended p to 1* cm in diameter in association with portal hypertension.http3(( pload.wikimedia.org(wikipedia(commons(b(b(sophageal4!arices...4- 4wale.:pg H.BC leads to the formation of small blood clots inside the blood !essels thro gho t the body. As the small clots cons me coag lation proteins and platelets, normal coag lation is disr pted and abnormal bleeding occ rs from the skin #e.g. from sites where blood samples were taken$, the gastrointestinal tract, the respiratory tract and s rgical wo nds. The small clots also disr pt normal blood flow to organs #s ch as the kidneys$, which may malf nction as a res lt. The acti!ation of the coag lation cascade yields thrombin that con!erts fibrinogen to fibrin2 the stable fibrin clot being the final prod ct of hemostasis. The fibrinolytic system then f nctions to break down fibrinogen and fibrin. Acti!ation of the fibrinolytic system generates plasmin #in the presence of thrombin$, which is responsible for the lysis of fibrin clots. The breakdown of fibrinogen and fibrin res lts in polypeptides called fibrin degradation prod cts #6BPs$ or fibrin split prod cts #6SPs$. n a state of homeostasis, the presence of plasmin is critical, as it is the central proteolytic en)yme of coag lation and is also necessary for the breakdown of clots, or fibrinolysis.7.@@p? is a t mor s ppressor protein that in h mans is encoded by the TP?
