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)

In this study we examined multiple serial liver biopsy specimens from liver transplant recipients to determine the pathological features of hepatitis C virus-induced hepatitis. Hepatitis C virus infections acquired after transplantation and previous infections that recurred in patients after transplantation were confirmed by the results of the polymerase chain reaction. Of 43 patients infected with the hepatitis C virus, 18 had a mild form of chronic hepatitis. Four patients had hepatitis that progressed to focal bridging fibrosis or cirrhosis. There were no significant clinical or pathological differences between infections acquired after transplantation and recurrent infections (as determined by polymerase chain reaction) except that acquired infections more often developed into hepatitis. Findings indicative of hepatitis C infection included portal and parenchymal mononuclear infiltrates of varying degrees, acidophilic necrosis and swollen hepatocytes. Other common findings included lymphoid aggregates, bile duct damage and fatty change. Atypical pathological conditions included extensive hepatocyte swelling or acidophilic necrosis with minimal inflammation mimicking ischemia and ductal or ductular damage and proliferation with mixed portal infiltrates mimicking rejection or obstruction. We conclude that in transplant recipients infection by the hepatitis C virus usually produces a mild disease state, but the diagnosis of hepatitis can be difficult to make because indicators of hepatitis may mimic those of rejection, ischemia, obstruction or other hepatic infections. Serial biopsy specimens with persistent pathology and polymerase chain reaction may be necessary to define the presence of a hepatitis C virus lesion.
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PMID:Hepatitis C viral infection in liver transplant recipients. 138 15

During their life span, leukocytes adhere transiently to one another, to other cell types, such as vascular endothelial cells, and to extracellular matrix proteins. This adhesiveness is mediated by families of specific cell surface adhesion molecules, namely, integrins, immunoglobulin superfamily molecules, and selectins. Adhesion is required for leukocyte-mediated cytotoxicity, phagocytosis, chemotaxis, and induction of lymphocyte proliferation and maturation. It also participates in recirculation and homing of lymphocytes into lymphoid organs and in leukocyte migration from the vascular compartment to extravascular tissues. Adhesion underlies the beneficial or detrimental role of leukocytes in immune and inflammatory responses. In animals, blocking monoclonal antibodies to adhesion molecules dramatically reduce vascular and tissue injury in several organs following ischemia-reperfusion, and delay renal allograft rejection. Moreover, expression of particular adhesion molecules is induced or increased in cells which are targets for allergic or autoimmune reactions and in inflamed tissues. On the other hand, a congenital deficiency of the CD11/CD18 integrins (Leu-CAMs) leads to recurrent, and sometimes fatal, bacterial infections, and lack of particular cell-adhesion molecules on Burkitt's lymphoma cells may enable these cells to escape immunosurveillance.
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PMID:Leukocyte adhesion in host defense and tissue injury. 183 Aug 30

Histological preparations of the spleen obtained from 64 corpses of persons of both sex and various age died from traumas, asphyxia, acute cardiac ischemia have been investigated. Microscopical anatomy of the spleen lymphoid formations has been described at various age periods, as well as structural interrelations of periarterial lymphoid muffs and lymphoid nodules with each other, with arteries and trabeculae. The periarterial lymphoid muffs embrace the splenic arteries immediately as they leave the trabeculae and get into the periarterial zones of the lymphoid nodules. The data have been obtained on relative contents of the main splenic structural components and on size of the lymphoid nodules and their germinative centers at various age in accordance with the modern age periodization, intensity of the age factor influence on these parameters is demonstrated. Problems of morphofunctional interrelations of certain splenic structures are discussed.
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PMID:[Lymphoid formations of the spleen in persons of different ages]. 336 50

We assessed the structural and functional evolution of small intestinal transplant rejection in a rat model by use of 1-micron section, electron microscopic, and in vitro electrophysiologic techniques to study jejunal mucosa 3, 6, and 9 d posttransplantation. The earliest structural abnormalities detected in jejunal loops transplanted from Lewis X Brown Norway F1 hybrids into Lewis rats occurred within 3 d posttransplantation and consisted of focal endothelial cell injury of the microvasculature and focal injury of crypt epithelial cells. Both alterations were associated with adjacent infiltration of large lymphoid cells, and both markedly progressed and became rather diffuse over the following 6 d. In contrast, villus absorptive cells were not markedly altered in structure until the 9th postoperative day. As compared with host jejuna, allograft jejunal epithelium demonstrated multiple functional abnormalities. Transepithelial resistance declined progressively by days 6 and 9 (both P less than 0.05), although baseline transepithelial spontaneous potential difference was only affected at day 9 (P less than 0.01). Stimulated absorption by allograft jejuna, as assessed by measuring electrical response to mucosal glucose, was not significantly diminished until day 9 (P less than 0.05). In contrast, stimulated secretion assessed by measurement of electrical response to serosal theophylline was diminished by day 6 (P less than .01). These data suggest that the earliest epithelial injury during rejection, as judged both structurally and functionally, occurs in the crypt and is paralleled by endothelial injury at the level of the microvasculature. Thus, the primary targets for rejection are most likely endothelial cells and crypt epithelial cells. In contrast, structural and functional impairment of villus epithelium is detectable only at substantially later times during rejection and are most likely secondary processes related to either ischemia produced by microvascular injury or decreased epithelial regenerative ability secondary to crypt injury. Last, we show that the detrimental structural and functional sequellae of jejunal transplantation across the major histocompatibility complex in this model is strikingly ameliorated with cyclosporine therapy.
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PMID:Structural and functional evolution of jejunal allograft rejection in rats and the ameliorating effects of cyclosporine therapy. 397 15

Within 3-6 hr after the reestablishment of the circulation, a characteristic pathology developed in renal homotransplants. Blood monocytes and lymphocytes adhered to large thin-walled vessels of the septa carrying interlobular arteries, traversed their walls, and aggregated in the connective tissue spaces around them. Within 3 days, the number and size of the extravascular cells markedly increased, filling the septa completely and spreading from them centrifugally to occupy the intertubular spaces throughout the cortex. The composition of these aggregates at first was a mixture of lymphocytes and monocytes, and later consisted of large blast cells, macrophages, a few plasma cells, and polymorphonuclear leukocytes. Mitotic activity was seen 2 days after surgery among the large blast cells and increased to a maximal level a day later. Coevally with these changes, the thin-walled septal vessels, intertubular veins and capillaries, and finally, arteries and arterioles, in that order, were damaged. Focal injury of tubules was slight 24 hr after homografting; widespread cortical necrosis had developed 5-7 days later. At no time up to 7 days were concentrations of immunoglobulins detected by fluorescence microscopy in the transplanted kidneys. The morphologic manifestations and temporal sequences of renal homograft destruction suggested that several mechanisms acted synergistically to eliminate the transplant. The initial injury appeared to be the result of an interaction between host lymphoid cells and target endothelium, a phenomenon akin to allogeneic inhibition; followed by spreading ischemia; additional contact injury to tubules; and nonspecific inflammation associated with necrobiotic tissue.
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PMID:Renal homotransplantation in rats. I. Allogeneic recipients. 486 33

Neuropathological findings were described in a 9-day-old female infant who died of the vitamin B12 non-responsive (mut0) type of methylmalonic acidemia (MMA). Widespread karyorhectic fragments of varying size and shape were noted throughout the brain, in particular densely accumulated in the cerebellar granular layers and the layer IV of the striate cortex. Bilateral or symmetrical necrotic foci were observed in various regions of the grey matter: Sommer's sector of the hippocampus, basal ganglia, thalamus, hypothalamus and brainstem. In the cerebral cortex small spongy necrotic foci were scattered mainly in the depths of gyri. Alzheimer type II astrocytes appeared in the preserved zone of the caudate nucleus. Myelinated nerve fibers in the brainstem were spongy or vacuolated, whereas peripheral myelin sheaths of cranial nerves were intact. Multiple hemorrhagic foci were noted in the cerebellum, predominantly the granular layers. The lymphoid tissue in the spleen and the thymus was hypoplastic. It may be difficult to explain exactly the mechanisms of the pathological changes observed here on routine light microscopy; the outcome of systemic ischemia/hypoxia before death cannot be completely ignored. But, it is suggested that widespread karyorhexis may occur selectively in specific cells (or cell groups), including immature neurons and other cellular components (glial and/or mesenchymal cells) among the patients with the mut0 type of MMA.
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PMID:Methylmalonic acidemia: brain lesions in a case of vitamin B12 non-responsive (mut0) type. 852 25

The selectins are carbohydrate-binding cell adhesion molecules acting in the vascular system. They mediate the docking of leukocytes to the blood vessel wall and the rolling of these cells along the endothelial cell surface. These adhesion phenomena initiate the entry of leukocytes into sites of inflammation as well as the migration of recirculating lymphocytes into secondary lymphoid tissues. Blocking selectin function with antibodies or oligosaccharides has proven to be beneficial in various animal models of inflammation and models of ischemia/reperfusion damage. This has raised much interest in the identification of the physiological ligands of the selectins. Several glycoprotein ligands have been identified, some of which can even be selectively isolated from cellular detergent extracts using a selectin as an affinity probe. Four of these "high affinity" ligands have been cloned. The structural requirements of their interaction with the selectins is discussed.
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PMID:Ligand-specificity of the selectins. 880 82

Parameters related to hepatic oxidative stress, cell injury, and liver histology were determined in control rats and in animals treated with 3,3',5-triiodothyronine (T3), after in vitro perfusion under normoxic or ischemia-reperfusion conditions. Thyroid calorigenesis was found concomitantly with higher rates of hepatic O2 consumption and thiobarbituric acid reactive substances (TBARS) formation, glutathione (GSH) depletion, enhanced TBARS/GSH ratio as indicator of oxidative stress, and higher sinusoidal lactate dehydrogenase (LDH) efflux compared to control values, assessed under normoxic conditions. Perfused livers from control animals subjected to ischemia-reperfusion exhibited significant increases in the TBARS/GSH ratio and in the sinusoidal LDH efflux over values obtained under normoxic conditions, concomitantly with the appearance of small foci of necrotic cells in centrilobular and midzonal areas of the liver lobule. These parameters were further modified in the liver of hyperthyroid rats subjected to ischemia-reperfusion, with elevations in the TBARS/GSH ratio and in the sinusoidal LDH efflux largely exceeding the sum of effects elicited by hyperthyroidism or ischemia-reflow alone. In this situation, liver injury was more pronounced than in control rats, being characterized by multifocal areas of necrotic cells, irregularly distributed in the hepatic lobule, with lymphoid and macrophagic reaction. It is concluded that the concurrence of the hepatic mechanisms related to the oxidative stress underlying thyroid calorigenesis and ischemia-reoxygenation exacerbates liver injury, which seems to be mediated by potentiation of the prooxidant state of the organ.
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PMID:Potentiation of ischemia-reperfusion liver injury by hyperthyroidism in the rat. 916 93

This review illustrates the changing paradigms in the understanding of the pathogenesis of pneumatosis intestinalis. Although many theories have been evoked, pragmatically there appear to be four major clinical and diagnostic imaging considerations. The most common and most emergent life-threatening cause of intramural bowel gas is the result of bowel necrosis due to bowel ischemia, infarction, necrotizing enterocolitis, neutropenic colitis, volvulus, and sepsis. In the stomach, intramural gas can be caused by emphysematous gastritis or ingestion of caustic agents. These situations represent surgical emergencies. Pneumatosis is found secondary to mucosal disruption presumably due to over-distention from peptic ulcer, pyloric stenosis, annular pancreas, and even to more distal obstruction. Disruption can also be caused by ulceration, erosions, or trauma, including the trauma of child abuse. Disruption can also be iatrogenic from intracatheter jejunal feeding tubes, stent perforation, sclerotherapy, or surgical or endoscopic trauma. In these cases, the gas may be focal or linear. Treatment depends on the extent of the disruption and the underlying cause. A more subtle form of mucosal disruption may occur due to mucosal erosions and also to defects in intestinal crypts secondary to acute and subclinical enteritides that allow intraluminal bacterial gas under pressure to percolate into the bowel wall layers, particularly the submucosa (29). Pneumatosis, often linear or cystic in appearance, is seen with increased frequency in patients who are immunocompromised because of steroids, chemotherapy, radiation therapy, or AIDS. In these cases, the pneumatosis may result from intraluminal bacterial gas entering the bowel wall due to increased mucosal permeability caused by defects in bowel wall lymphoid tissue. Clinical and imaging findings are important in the differentiation of this transient pneumatosis from fulminant life-threatening causes in this subset of patients. A pulmonary cause must still be considered in cases of chronic obstructive pulmonary disease, asthma, and cystic fibrosis. It can occur with barotrauma and after chest tube placement. It may relate to increased intrathoracic pressure associated with retching and vomiting. The possibility remains that occasionally the origin of pneumatosis intestinalis will remain cryptogenic--caused but unexplained.
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PMID:Pneumatosis intestinalis: a review. 953 Feb 94

Each year, thousands of peoples die, suffering from an anatomical or functional loss of their intestine; these patients would benefit from bowel transplantation; the difficulties of bowel transplantation are as follows: 1. the physiological characteristics of the small bowel, and the fact that denervation, lymphatics interruption and ischemia, independently from rejection, may disturb its function; 2. secondly, the organ is septic; thus, its transplantation causes major infectious problems; 3. at last, the immunological characteristics of the intestinal allograft. Bowel transplantation causes a two-way immunological conflict, not only a standard rejection response, but also a graft-versus-host disease, similar to that observed after bone marrow transplantation; this reaction is caused by the lymphoid tissue conveyed within the bowel graft. The introduction of a new immunosuppressive molecule, FK 506, in combination with profound antibiotic prophylactic regimens, decontamination protocols and vigorous anti-viral protection (against cytomegalovirus and Epstein-Barr), have significantly improved the results. Bowel transplantation has recently reached clinical application. The one-year survival rate of intestinal grafts reaches now 70%. Still, there is no doubt that, due to its microbiological and immunological characteristics, the small bowel will remain the most challenging abdominal organ to transplant.
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PMID:[Intestinal transplantation: a clinical reality in 1998]. 976 Jul 59


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