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)

Partial resection of the liver is the only curative treatment for patients with hepatocellular carcinoma associated with severe cirrhosis of the liver. Surgical hemostasis on the cut surface of the cirrhotic liver appears very difficult because of the resultant deep cavity and the marked hemorrhagic diathesis. However, by using the microcrystalline collagen powder and the fibrinogen tissue adhesive, complete hemostasis and prevention of postoperative bleeding can be obtained, with minimal blood loss and hepatic ischemia.
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PMID:Use of microcrystalline collagen powder and fibrinogen tissue adhesive for hemostasis and prevention of rebleeding in patients with hepatocellular carcinoma associated with cirrhosis of the liver. 246 32

We studied 23 patients suffering cerebral ischemia who also had laboratory evidence of either a lupus anticoagulant (LA) or an abnormal anticardiolipin antibody (ACA). Four patients had lupus or a lupus-like illness, three had drug-induced lupus, and 16 had no overt evidence of collagen-vascular disease. Cerebral ischemic events were multiple in 71% of the patients; two patients presented with multi-infarct dementia. Recognized cerebrovascular disease risk factors were present in 57% of the patients. The partial thromboplastin time was prolonged in only 35% of the patients. An LA was identified in 15 of 21 patients tested, and an elevated ACA titer was identified in 10 of 12 patients tested. Simultaneous assays for LA and ACA were discordant in eight of 10 patients tested. LA- and ACA-associated brain ischemia is often recurrent, but other risk factors for cerebrovascular disease are often present. The laboratory findings in such patients may display considerable heterogeneity.
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PMID:Lupus anticoagulants, anticardiolipin antibodies, and cerebral ischemia. 249 72

It has been suggested that complex ventricular arrhythmias commonly occur in hypertensive patients with left ventricular hypertrophy. We have previously demonstrated that coronary artery ligation in anesthetized spontaneously hypertensive rats (SHR) and their normotensive controls (WKY) resulted in a significantly increased incidence and duration of ventricular fibrillation in SHR compared with WKY. The object of the present study was to characterize the structural and electrophysiological abnormalities in hypertrophied hearts, associated with the occurrence of arrhythmias. We used a double tissue bath in which a ventricular strip was exposed simultaneously to normal and to altered conditions (low pH, hypoxia and high potassium). Electrical activity recorded using standard micro-electrode techniques showed the occurrence of arrhythmias in all preparations and the development of major alterations in conduction (a conduction block appeared at 11 +/- 1 mn in SHR vs 16 +/- 1 mn in WKY, p less than 0.05), and maximal upstroke velocity (Vmax values before and 3 mn after the beginning of ischemia were 229 +/- 12 to 46 +/- 7 v/s for the SHR and 227 +/- 10 to 106 +/- 12 v/s for the WKY; p less than 0.001). These changes were associated in hypertrophied ventricles with a marked sub-endocardial collagen fibrosis as estimated by the use of automated image analysis (subendocardial collagen density = 4.39 +/- 0.34 p. 100 in SHR vs 1.66 +/- 0.15 p. 100 in WKY; p less than 0.001). Action potential duration measured using conventional glass micro-electrodes in a single chamber tissue bath revealed a highly significant difference (p less than 0.001) in APD 90 p. 100 of papillary muscles between SHR (114.7 +/- 2.8 ms) and WKY (76.9 +/- 1.7 ms). The addition of tetra-ethylammonium to block potassium channels induced triggered activity arising from early afterdepolarizations only in muscles hypertrophied SHR hearts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hypertensive myocardial hypertrophy and rhythm disorders: 2 possible origins]. 253 Sep 53

More efficient methods of islet isolation must be developed for islet transplantation to become clinically routine. During collagenase dispersal of human pancreas, an amorphous, viscous, gellike material often develops and entraps large numbers of islets, thereby reducing the yield. When donor human pancreas is minced and treated with collagenase, the gel forms most abundantly if the digestion temperature is less than 35 degrees C and if pH falls below 7.2 +/- 0.2. Gel formation appears to be proportional to warm- or cold-ischemia time and may be related to tissue trauma during collection. Once gel has formed, trapped islets cannot be released by filtration, dilution, DNase, incubation temperature, or pH adjustment. These characteristics suggest that the material is gelatin derived from collagen released enzymatically from pancreatic stroma. We demonstrate that gelation is greatly reduced or eliminated when 1) the incubation medium includes glycerol--a common gelatin solvent--at 5% (vol/vol), 2) the minced tissue-to-total incubation volume ratio is greater than or equal to 1:10, 3) free-islet exposure to pancreatic digestion products is minimized by frequent separation of islets, and 4) collagenase concentration is optimized by titration. Gelation is also minimized by maintaining 5) incubation temperature at 38 +/- 1 degree C and 6) pH in the range 7.7-7.9. Variations in these physical and chemical conditions were analyzed by determining islet yields (stereoscopic microscope counts of serially diluted samples) and by insulin radioimmunoassay of acid alcohol extracts of isolated islets after separation through discontinuous Ficoll gradients. When isolation conditions are optimized as stated, we typically recover 3.3 +/- 1.0 x 10(4) islets/g pancreas, corresponding to greater than 10(6) islets per donor.
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PMID:Factors influencing isolation of islets of Langerhans. 264 35

Membranous and endochondral ossification processes are insufficient to describe all the aspects observed in the growing skeleton. The presence of chondroid tissue that we have identified by means of all modern histological techniques, including those able to detect the different types of collagen, has also to be explained. Present in the mandibular symphysis of either the human or cat fetuses, chondroid tissue has also been observed in the other parts of the mandible, in the sutural areas of the skull and in all the bones of both axial and appendicular skeleton. The differentiation of the mesenchyme into chondroid tissue could probably be related with mechanical forces exerted simultaneously in opposite directions or with a transient ischemia.
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PMID:Skeletal growth and chondroid tissue. 269 51

Magnetic resonance imaging (MRI) studies were performed on 27 patients with vascular lesions of the central nervous system before and after embolization with either IBCA, polyvinyl alcohol foam particles, Avitene (microfibrillar collagen) or balloons. Thirteen pial brain arteriovenous malformations (AVMs), 3 brain AV fistulas, 2 giant aneurysms, 5 dural AVMs, 1 vertebro-vertebral fistula and 3 meningiomas were studied. The pre-embolization MR demonstrated the nidus and venous drainage of all pial AVMs. MR failed to detect 3 out of 5 dural AVMs using only spin echo sequences. A draining vein alone was seen in the remaining two cases. MR was superior to CT in detecting contiguous parenchymal changes such as atrophy, reversible ischemia, and mass effect in the pre-embolization studies. Following embolization, MR demonstrated partial or complete obliteration of the vascular nidus in all 13 pial AVMs. The embolized area was seen as an area of increased signal consistent with thrombus where previously there had been signal void. Ischemic or edematous changes in the brain parenchyma following embolization were seen on MR more easily than on CT scans. MR was accurate in the assessment of aneurysm patency, degree of thrombosis and balloon position in both giant aneurysms, and AV fistulae. These MR findings had an impact on patient management. MR will be an increasingly useful tool in the diagnosis and management of a number of neurovascular diseases requiring endovascular intervention.
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PMID:Neurovascular lesions and endovascular therapy: the role of MR. 279 27

The arteriograms of sixty-two patients with chronic ischemia of the hand and fingers were reviewed. Twelve patients were considered to have Raynaud's disease. Thoracic outlet syndrome caused ischemic symptoms in thirteen patients. Arteriosclerosis obliterans affected twenty-two patients. The signs of arteriosclerosis are described including irregular constrictions, multiple occlusions and the corkscrew pattern of the collateral arteries. The differential diagnosis includes thromboangiitis obliterans and collagen vasculitis.
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PMID:[Arteriographic data in chronic ischemia of the hand. Study of 62 cases]. 286 65

Unstable coronary artery disease (CAD) might be related to obstructions of coronary blood flow by platelet aggregates. In 121 men and 43 women admitted to the coronary care unit with suspected unstable CAD, blood samples for tests of platelet function were obtained within 24 hours after admission. Platelet reactivity was tested in vitro in platelet rich plasma as the aggregability towards ADP 1 microM and collagen 1 mg/ml and as the sensitivity to prostacyclin (PSP). The levels of beta-thromboglobulin and platelet factor 4 were determined ex vivo in platelet poor plasma. Patients who developed a nontransmural myocardial infarction (n = 39) or had signs of myocardial ischemia at an exercise test performed within a week (n = 39) were considered to have unstable CAD while patients without signs of ischemia constituted the control group. In the acute phase the PSP was reduced in patients with unstable CAD without any difference between genders. The aggregability towards ADP was higher in women than men but otherwise there were no differences between groups or sexes in any other test in the acute phase. After 12 months there were no differences in PSP between the groups but women had a lower PSP than men. Thus, in the acute phase of unstable CAD, the platelet sensitivity to the inhibitory effects of prostacyclin was reduced which might contribute to the risk for further platelet aggregation, coronary occlusion and myocardial infarction.
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PMID:Platelet reactivity in unstable coronary artery disease. 295 54

There are conflicting views on the pathogenesis of the intestinal malfunction seen in infants with gastroschisis. It has been variously ascribed to abnormalities of ganglion cells and smooth muscle elements, intestinal ischemia, and the "peel" which invests the serosa of the intestine. Review of the clinical and experimental literature showed only limited information on the histology of the eviscerated human intestine. In order to add to this data base, and to further investigate the pathogenesis of the intestinal malfunction from a histologic standpoint, we reviewed surgical and autopsy material from our experience with 105 neonates with gastroschisis. Ten specimens were satisfactory for evaluation from a standpoint of tissue integrity. The specific mural components of mucosa, submucosa, muscularis, and ganglion cells were examined and found to be either normal, or to show nonspecific abnormalities that varied from case to case, and were related mostly to intestinal infarction due to compromise of the gut at the site of the gastroschisis defect. In six patients, this progressed to atresia formation. The most consistent abnormalities were found in the serosal layer with its peel. Using special stains, the peel was found to be composed largely of fibrin and collagen. Based on this study, we feel that edema and ischemic changes, though often present, are much less prominent than the peel, as the leading histologic abnormality of the intestine of gastroschisis. Squamous epithelial cells were seen in the peel in four cases, suggesting that the peel had been "appliqued" onto the serosa of the herniated fetal gut.
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PMID:Histology of the intestine in human gastroschisis--relationship to intestinal malfunction: dissolution of the "peel" and its ultrastructural characteristics. 297 19

As part of a study of the interactions between myocardial cells and extracellular matrix during healing of necrotic lesions, we have examined the fate of myocyte basal lamina (BL) after injury with ischemia, freeze-thawing, or isoproterenol. Using light and electron microscopy, and antibodies to three BL-associated antigens, we found that the BL of necrotic myocytes remained largely intact and continued to delineate the myocyte compartment from connective tissue space. Inflammatory cells entered the myocyte compartment through holes in the acellular BL and removed cell debris. The holes may have been produced by inflammatory cells and/or by the stretching force of the beating heart. After removal of debris, some BL sheaths of necrotic myocytes collapsed, resulting in spatial approximation of vessels. Interstitial cells deposited collagen and elastic fibers in the connective tissue space and within portions of the myocyte compartment. The acellular myocyte BL, collapsed or not, retained normal antigen staining for type IV collagen, laminin, and heparan sulfate for about 10 days, then showed diminished staining in patchy areas. These areas may correspond to BL disruption and degradation in conjunction with fibrosis, although a substantial amount of acellular BL remained in situ and became embedded in scar tissue. At least two types of granulo-vesicular bodies, measuring 25 to 60 and 60 to 160 nm respectively, were associated with the acellular BL; these were of unknown origin and function. The study shows that the fate of acellular BL in injured myocardium is similar to the fate of BL in other injured tissues; however, the appearance of holes in acellular BL, within hours after injury, is unusual and may enhance scar tissue formation. Whether the acellular BL contributes to regeneration of myocardium, as do acellular BLs in other injured tissues, remains to be determined.
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PMID:Basal lamina of rat myocardium. Its fate after death of cardiac myocytes. 333 5


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