Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Presentation of a case of disseminated intravascular coagulation with micro-angiopathic hemolytic anemia, associated with a micro-carcinoma of the prostate. In the absence of other etiology it is postulated that the carcinoma was responsible for the hematological disturbance in spite of its small size andlack of either metastases or mucin secretion. The unusual discovery in this disease of bony necroses of the vertebrae, which are attributed to ischemia following micro-thromboses, is also discussed.
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PMID:[Disseminated intravascular coagulation with microangiopathic hemolytic anemia and bone necrosis associated with a prostatic microcarcinoma]. 70 6

Cystic adventitial disease consists of a collection of clear gelatinous material within an aberrant synovial-type cyst located in the subadventitial plane of the wall of a major artery. Recurrent minor trauma is presumed to potentiate mucin production and enlargement of the cyst with resultant arterial occlusion and symptoms of ischemia. It occurs most commonly in the popliteal artery in young men; forty-seven such patients have been reported on. Extrapopliteal disease is distinctly less frequent, occurring three times in the external iliac, three times in the radial, once in the ulnar, and once in the common femoral artery. Surgical therapy of choice is evacuation of the gelatinous material and abrasion of the lining of the cyst. Grafting is occasionally necessary. Long-term results are excellent and recurrence is uncommon.
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PMID:Cystic adventitial disease of the common femoral artery. 115 24

Cystic changes of gastric mucosal glands have been described mainly after gastric operations, and like intestinal metaplasia and dysplasia, they may represent a premalignant condition. Their association with gastritis raises the possibility of their being secondary to the inflammatory process. Enterogastric reflux of duodenal contents, local chronic ischemia, and inflammatory reaction as a result of gastric surgery and suture at gastroenterostomy have been considered responsible for this lesion. In 18 of 157 consecutive patients (11.5%) who underwent endoscopic gastric biopsy within a year we found cystic changes of gastric mucosal glands. Cystic changes were present in 43% of 30 patients after gastric operation for duodenal ulcer disease, within an average of 8.4 years in contrast to only 4% of patients with an intact stomach. This change is statistically significant (Z = 1.97, (p less than 0.05) and suggests that there is a cause-and-effect link between the operation and the development of cystic lesions. In three patients we traced the original operative specimen, and in none did we find cystic changes. All the cases were associated with chronic gastritis; mild dysplasia was found in four (22%). The cystic glands were shown (by alcian blue-periodic acid-schiff staining) to secrete neutral mucin like normal gastric glands, and unlike dysplastic glands or intestinal metaplasia where acid mucin is characteristic. Thus, our findings suggest an inflammatory cause for the cystic glandular change (reactive, hyperplastic change of glands), and suggest that it is probably not a preneoplastic state.
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PMID:Cystic changes in gastric glands after gastric surgery and in the intact stomach. 191 56

The initial effect of anticancer therapy, such as radiation and chemotherapy, is on the rapidly proliferating cells of the oral epithelium. As a consequence, the epithelium may show atrophy and ulceration. The sites of these alterations are related to the rate of epithelial proliferation. Regions of rapid proliferation, such as the oral lining mucosa, show a greater frequency of ulceration than masticatory mucosa or skin. Subsequent changes in the mucosa reflect damage to connective tissue, including fibroblasts and blood vessels. This results in hyalinization of collagen, hypovascularity, and ischemia. Indirect effects of anticancer therapy may include granulocytopenia and reduced salivary secretion, so that the protective mucin coating of the epithelium is compromised. These changes result in tissue with reduced barrier function and impaired ability to heal and to resist entry of pathogens, thus increasing the risk of systemic infections.
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PMID:Oral complications of cancer therapies. Mucosal alterations. 234 90

A total of 512 colectomy and endoscopic biopsy specimens were reviewed to define the prevalence and possibly the significance of dystrophic goblet cells (DGCs) in neoplastic and nonneoplastic colonic diseases. As compared with an incidence of 1% in disease-free specimens, DGCs were observed in 38% of cases of inflammatory bowel disease, 23% of colonic malignancies, 30% of nonneoplastic polyps, 22% of adenomas, and 8% of cases showing acute self-limited colitis. In contrast, no dystrophic cells were seen in a group of miscellaneous diseases including diverticulitis, diverticulosis, abscesses, fistulas, ischemia, pseudomembranous colitis, melanosis coli, amyloidosis, shock, and mechanical trauma. Although dystrophic cells occur in association with dysplasia and carcinoma, their presence in nonpremalignant lesions, including acute self-limited colitis, raises doubt as to their diagnostic significance. Histochemical studies of the mucin composition in DGCs were unrevealing, failing to show any differences between DGCs and their morphologically normal counterparts in the same region of the colon.
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PMID:The incidence and carbohydrate histochemistry of dystrophic goblet cells in colon. 323 12

While it is well established clinically that urinary tract infection in the presence of outflow obstruction may be associated with difficulty in eradicating bacteria, it is not clear whether this is secondary to the presence of residual urine volume or other local effects of the obstruction such as attenuation of the intrinsic antibacterial defense mechanisms of the mucosal surface. Experiments in our laboratory and others over the past several years have demonstrated that the primary antibacterial defense mechanism of the bladder is the antiadherence effect of the bladder surface mucin layer. Additional studies have shown that heparin can duplicate this antiadherence activity of bladder mucin. The present report demonstrates that one hour of overdistension or ischemia and one week of partial outlet obstruction cause a functional defect in the intrinsic antiadherence effect of the bladder mucosa as evidenced by increased bacterial adherence. This defect can be reversed by heparin exposure prior to bacterial challenge. These results indicate that partial outlet obstruction and its potential sequelae such as overdistension and, particularly, mucosal ischemia, have dramatic adverse effects on the intrinsic antiadherence defense mechanism of the bladder. These effects can be reversed by intravesical exposure to an exogenous anionic polyelectrolyte (heparin).
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PMID:Heparin inhibition of increased bacterial adherence following overdistension, ischemia and partial outlet obstruction of the rabbit urinary bladder. 352 24

In this study, the kinetics of copper-zinc superoxide dismutase (CuZn-SOD) in experimentally induced ischemia-reperfusion injury of the canine jejunum were examined using immunohistochemical procedures, and evaluated as an index for the viability of transplants. A pedicled jejunal graft was subjected to arterial reperfusion after clamping the supplying blood vessels for 30 min. Under nonischemic conditions, some of the goblets in the goblet cells and the mucin covering the surface of the villi were stained positively with luxol fast blue, von Kossa, and immunohistochemistry for CuZn-SOD. Between 5 and 30 min after reperfusion, the appearance of goblets with positive immunoreaction for CuZn-SOD in the intestinal glands and the disappearance of these goblets in the villi were observed in the grafts of animals that received arterial reperfusion after 30 min of clamping of the arteries and veins at room temperature. Thereafter, the former disappeared gradually and the latter returned toward the nonischemic condition. The administration of allopurinol led to a decrease in tissue damage and a significantly higher number of goblets with positive immunoreaction for CuZn-SOD than in untreated animals. Furthermore, the goblets in the intestinal glands showed a negative reaction for CuZn-SOD 5 to 30 min after reperfusion. Preservation at 4 degrees C during ischemia revealed similar results to those observed in the animals given allopurinol. Thus, the distribution and intensity of CuZn-SOD positive goblets seems to be a useful indicator for the evaluation of tissue damage induced by free radicals mediating ischemia-reperfusion injury.
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PMID:The kinetics of copper-zinc superoxide dismutase in experimentally induced ischemia-reperfusion injury of the canine jejunum. 763 26

Endothelial activation is central to the pathophysiology of glomerulonephritis, vasculitis, allograft rejection, ischemia-reperfusion injury and thrombotic angiopathies. Major advances in endothelial biology during the past year have emphasized the importance of selectin, mucin, integrin, and immunoglobulin-like adhesion molecules in leukocyte trafficking in glomerular inflammation, and have defined novel mechanisms by which leukocyte-endothelial cell interactions are regulated by inflammatory mediators and cytokines. These breakthroughs have already spawned experimental immunosuppressive strategies that should antecede the development of novel, potent and specific therapies for common renal diseases.
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PMID:The endothelium in glomerular inflammation. 764 26

In orthotopic liver transplantation, extended cold ischemia of the graft may induce cell damage, particularly in biliary epithelium. We have investigated the effects of a cold University of Wisconsin (UW) solution on cultured human gallbladder biliary epithelial cells (GBEC) exposed or not exposed to stagnant bile. In UW solution, morphological alterations of cultured GBEC were not prominent under light microscopy after 16 hours at 4 degrees C, being more striking after 24 to 48 hours. Ultrastructural examination of GBEC showed a condensation of chromatin at the periphery of the nuclei after 16 hours in cold UW solution. Both protein and DNA syntheses were strikingly reduced in these cells. After rewarming in standard Williams' medium at 37 degrees C for 24 hours, cultured GBEC exhibited both normal morphology and function. As in both freshly isolated and routinely cultured GBEC, rewarmed cells expressed various mucin genes, namely MUC1, MUC3, MUC4, MUC5AC, and MUC5B genes, whereas MUC2 mRNAs were barely detectable. A dramatic decline in the steady-state mRNA levels of both MUC3 and MUC5B was found in cultured GBEC versus freshly isolated cells. Addition of bile into UW solution at 4 degrees C had no significant effect on GBEC morphology and DNA and protein syntheses. When bile was added during the rewarming period, both protein and DNA syntheses were strongly reduced. Addition of bile during either storage in UW solution or rewarming period induced increased steady-state MUC2, MUC3 and MUC5AC mRNA levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:UW-preservation of cultured human gallbladder epithelial cells: phenotypic alterations and differential mucin gene expression in the presence of bile. 780 58

This study was undertaken to elucidate the role of autonomic denervation in the pathogenesis of acute acalculous cholecystitis. In Experiment I, the gallbladder was denervated by performing either celiac neurotomy (sympathetic denervation) or truncal vagotomy (parasympathetic denervation), or both, in dogs. In Experiment II, 45-min ischemia and 90-min reperfusion of the gallbladder with or without autonomic denervation were performed by simultaneously occluding the middle hepatic artery and superior mesenteric vein. Celiac neurotomy, and truncal vagotomy, or both, did not cause cholecystitis. Sympathetic denervation, however, decreased the amount of mucin in the gallbladder mucosa and parasympathetic denervation caused reduction of the tissue blood flow, as well as the accumulation of lipid peroxide and xanthine oxidase in the gallbladder mucosa. These changes were most remarkable 1-2 weeks after denervation and were alleviated 4 weeks after denervation. Ischemia-reperfusion 2 weeks after denervation caused more severe cholecystitis than ischemia-reperfusion alone. The most severe inflammation developed in animals that received both celiac neurotomy and truncal vagotomy. These results suggest that autonomic denervation alone does not induce acute cholecystitis, but that it plays an important role in the progression of the inflammatory process in ischemia-reperfusion injury.
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PMID:Experimental study of the pathogenesis of acute acalculous cholecystitis: role of autonomic denervation. 806 1


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