Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using an ultrastructural immunoperoxidase technique, the distribution of endogenous albumin in the rat glomerulus was delineated under normal and abnormal hemodynamic conditions. Superficial glomeruli in anesthetized Munich-Wistar rats were rapidly fixed in situ by applying glutaraldehyde to the renal surface. Fixed tissue slices were treated with anti-rat albumin Fab fragments conjugated to horseradish peroxidase (HRP), and were then subjected to the Graham-Karnovsky ultrastructural peroxidase localization procedure. During normal blood flow, dense reaction product specific for albumin was largely confined to the glomerular capillary lumen and endothelial fenestrae, with only small amounts detectable in the lamina rara interna, and none deeper in the basement membrane (GBM) or in the urinary space. If cortical tissue was subjected to routine immersion fixation, or if fixation was performed in situ after ligation of the renal artery, reaction product was detected throughout the GBM and in the urinary space. If fixation was performed in situ after ligation of the renal artery and vein (or artery, vein and ureter), reaction product was found in the GBM and, in very large amounts, in the urinary space. If blood flow was restored for ten minutes after five minutes of renal pedicle (artery and vein) occlusion, the distribution of albumin returned to normal. Thus, glomerular barrier function depends upon the maintenance of normal blood flow conditions.
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PMID:Distribution of endogenous albumin in the rat glomerulus: role of hemodynamic factors in glomerular barrier function. 94 Feb 56

The distribution of endogenous immunoglobulin G (IgG) and exogenous catalase was delineated in the rat glomerulus under normal and abnormal hemodynamic conditions. IgG was identified by an ultrastructural immunoperoxidase technique using antirat IgG Fab fragments conjugated to horseradish peroxidase; catalase was identified by a cytochemical reaction. When superficial glomeruli in anesthetized Munich-Wistar rats were rapidly fixed in situ by dripping glutaraldehyde onto the renal surface, IgG and catalase were largely confined to the glomerular capillary lumen, with only small amounts in the lamina rara interna immediately beneath the endothelial fenestrae, and none deeper in the basement membrane (GBM) or in the urinary space. If cortical tissue was subjected to routine immersion fixation, or if fixation was performed in situ after ligation of the renal artery, IgG and catalase were found throughout the GBM but not in the urinary space. If fixation was performed in situ after ligation of the renal artery and vein (or artery, vein, and ureter), IgG and catalase were found in the GBM and in the urinary space. If blood flow was restored for 10 minutes after 5 minutes of occlusion of the renal artery and vein, the distribution of IgG and catalase returned to that seen during good blood flow, i.e. neither showed significant penetration beyond the endothelial layer. Thus, as was found previously for albumin, glomerular barrier function for IgG and catalase depends upon the maintenance of normal blood flow conditions. We propose that such conditions impose functional restrictions may be mediated by molecular sieving phenomena during normal ultrafiltration across the GBM, perhaps in association with concentration-polarization or charge effects or both. The epithelial slit pores may significantly modulate solute flux across the GBM by controlling the over-all rate of hydrodynamic flow during ultrafiltration.
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PMID:Glomerular permeability to proteins. Effects of hemodynamic factors on the distribution of endogenous immunoglobulin G and exogenous catalase in the rat glomerulus. 126 44

Hereditary colorectal cancer (CRC) is highly heterogeneous, both genotypically and phenotypically. The most frequently occurring hereditary colorectal cancer syndrome is Lynch syndrome, accounting for approximately 3% of the total colorectal cancer burden. Polyposis syndromes, such as familial adenomatous polyposis, account for a lesser percentage. Familial colorectal cancer, defined by family history, occurs in an estimated 20% of all colorectal cancer cases. With a worldwide annual colorectal cancer incidence of over one million, and annual mortality of over 600,000, hereditary and familial forms of colorectal cancer are a major public health problem. Lynch syndrome is attributable to DNA mismatch repair germline mutations, with the MSH2, MLH1, MSH6, and PMS2 genes being implicated. The characteristics of Lynch syndrome-associated colorectal tumors, including early age of onset and predilection to the proximal colon, mandate surveillance by colonoscopy beginning by age 20 to 25 and repeated every other year through age 40 and annually thereafter. Besides colorectal cancer, Lynch syndrome also predisposes to a litany of extracolonic cancers, foremost of which is endometrial cancer, followed by cancer of the ovary, stomach, renal pelvis and ureter, small bowel, hepatobiliary tract, pancreas, glioblastoma multiforme in the Turcot's variant, and sebaceous skin tumors in the Muir-Torre variant and, more recently identified, cancers of the breast and prostate. The most common polyposis syndrome is familial adenomatous polyposis, caused by mutations in the APC gene. Affected individuals have multiple colonic adenomas and, without treatment invariably develop colorectal cancer. Colonic surveillance with polypectomy may be pursued until the appearance of multiple colonic adenomas, at which time prophylactic colectomy should be considered. Extra-intestinal manifestations include desmoid tumor, hepatoblastoma, thyroid carcinoma, and medulloblastoma. Other polyposis syndromes include the hamartomatous polyp syndromes, including juvenile polyposis syndrome, Peutz-Jeghers syndrome, Cowden syndrome, and Bannayan-Ruvalcaba-Riley syndrome.
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PMID:Practical genetics of colorectal cancer. 2584 92