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)

Ischemia-induced biliary tract lesions, called ischemic cholangitis, often lead to strictures of biliary ducts and cholestasis. Causes of ischemic changes of the biliary tract can be found in the arterial blood supply or in the peribiliary capillary plexus. Known examples are thrombosis after transplantation, intraoperative ligation, or the application of chemotherapeutic drugs. Rarely, such changes are due to inflammation of the blood vessels, such as occurs in polyarteritis nodosa or giant cell arteritis. We present a report of a 49-year old man with leucocytoclastic vasculitis after viral infection, influenza vaccination, and antibiotic treatment, leading to florid ischemic cholangitis. We conclude that hypersensitivity vasculitis must be included in the differential diagnosis of cholestasis and cholangitis.
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PMID:Florid ischemic cholangitis due to leucocytoclastic vasculitis. 1506 28

Viral myocarditis is a disease with a high morbidity and mortality. The pathogenesis of this disease remains poorly characterized, with components of both direct virus-mediated and secondary inflammatory and immune responses contributing to disease. Apoptosis has increasingly been viewed as an important mechanism of myocardial injury in noninfectious models of cardiac disease, including ischemia and failure. Using a reovirus murine model of viral myocarditis, we characterized and targeted apoptosis as a key mechanism of virus-associated myocardial injury in vitro and in vivo. We demonstrated caspase-3 activation, in conjunction with terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling and annexin binding, in cardiac myocytes after myocarditic viral infection in vitro. We also demonstrated a tight temporal and geographical correlation between caspase-3 activation, histologic injury, and viral load in cardiac tissue after myocarditic viral infection in vivo. Two pharmacologic agents that broadly inhibit caspase activity, Q-VD-OPH and Z-VAD(OMe)-FMK, effectively inhibited virus-induced cellular death in vitro. The inhibition of caspase activity in vivo by the use of pharmacologic agents as well as genetic manipulation reduced virus-induced myocardial injury by 40 to 60% and dramatically improved survival in infected caspase-3-deficient animals. This study indicates that apoptosis plays a critical role in mediating cardiac injury in the setting of viral myocarditis and is the first demonstration that caspase inhibition may serve as a novel therapeutic strategy for this devastating disease.
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PMID:Caspase inhibition protects against reovirus-induced myocardial injury in vitro and in vivo. 1545 24

Clinical experience of Perftoran (commercial drug of low concentrated perfluorocheminal emulsion) applications is presented in some statistical data and in brief analysis of clinical trials and following clinical studies described in the Russian scientific literature. Observed data allow us to suppose that Perftoran facilitates oxygen delivery together with remaining red blood cells at blood replacements and will have more wider area for application than just a blood substitute. Its infusion alleviates symptoms of ischemia at different types of occlusion vessels disease, improves grafting in plastic surgery, diminishes inflammation and prevents rejection of transplants, activates detoxication functions of liver, inhibits retro-virus infection development. Local PF applications is able to accelerate wounds and ulcers healing.
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PMID:Clinical results of Perftoran application: present and future. 1576 64

This investigation was carried out on 851 consecutive judicial autopsies of drug addicts who died mostly of heroin overdose from 1977 to 1996. Research of anti-HIV/HBV/HCV antibodies was performed, and histologic sections were retrospectively reviewed. More than 65% were HBV/HCV-positive and about 17% HIV-positive; females were HIV-positive more often than males. Intracranial microhemorrhages were frequently found; cerebral infectious diseases were rare. Inflammatory heart lesions, myocardial fibrosis, and acute ischemia were common. Interstitial nephritis (found in about 8%) was more frequent in females, in older patients, and in those carrying HIV infection; glomerular sclerosis was detected in about 12%. Acute bronchitis and/or pneumonia was demonstrated in 12%, without significant association with HIV infection; pulmonary hemorrhages, foreign body granulomas, and food aspiration were also commonly seen; hyperplasia of pulmonary perivascular lymphatic tissue was rather characteristic. Liver was carrying steatosis in 66.3% and/or hepatitis in 64.5%; acute hepatitis was more frequent in females, chronic hepatitis in older subjects and in those proven positive for hepatotropic viruses; cirrhosis occurred more often in older patients, in those carrying virus infection, and in consumers of nonnarcotics drugs such as ethanol. No pathologic finding was clearly related to drug abuse; therefore, during autopsy, drug addiction can be suspected, but anamnestic and circumstantial data are needed to lead pathologists to request toxicologic analysis to ascertain the cause of death. The present investigation emphasizes that, in addition to the risk of death by overdose, the high incidence of acute and chronic diseases could seriously undermine the health status of heroin and/or other drug consumers.
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PMID:Histopathological findings in 851 autopsies of drug addicts, with toxicologic and virologic correlations. 1589 41

Plasma and myocardial levels of proinflammatory cytokines such as tumor necrosis factor(TNF)-alpha, interleukin 1beta, and interleukin 6 are elevated in patients with heart failure. Not only viral infection but also cardiac overload, ischemia, and neuro-humoral factors stimulate systemic and myocardial production of these cytokines. Administration of proinflammatory cytokines directly depresses myocardial contractility in vitro and in vivo. In addition, TNF and interleukin induce myocardial apoptosis and promote cardiac hypertrophy and fibrosis, suggesting that these cytokines are involved in the progression of cardiac remodeling. Vasoactive peptides such as endothelin and adrenomedullin also have cytokine-like functions in the heart, acting as autocrine and paracrine factors. Thus, proinflammatory cytokines and these peptides play important roles in the pathogenesis and pathophysiology of heart failure.
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PMID:[Pathophysiological role of cytokines in heart failure]. 1668 63

Epidemiologic studies demonstrate significant environmental impact of maternal viral infection and obstetric complications on the risk of schizophrenia and indicate their detrimental influences on brain development in this disorder. Based on these findings, animal models for schizophrenia have been established using double stranded RNA, bacterial lipopolysaccharides, hippocampal lesion, or prenatal/perinatal ischemia. Key molecules regulating such immune/inflammatory reactions are cytokines, which are also involved in brain development, regulating dopaminergic and GABAergic differentiation, and synaptic maturation. Specific members of the cytokine family, such as interleukin-1, epidermal growth factor, and neuregulin-1, are induced after infection and brain injury; therefore, certain cytokines are postulated to have a central role in the neurodevelopmental defects of schizophrenia. Recently, to test this hypothesis, a variety of cytokines were administered to rodent pups. Cytokines administered in the periphery penetrated the immature blood-brain barrier and perturbed phenotypic neural development. Among the many cytokines examined, epidermal growth factor (or potentially other ErbB1 ligands) and interleukin-1 specifically induced the most severe and persistent behavioral and cognitive abnormalities, most of which were ameliorated by antipsychotics. These animal experiments illustrate that, during early development, these cytokine activities in the periphery perturbs normal brain development and impairs later psychobehavioral and/or cognitive traits. The neurodevelopmental and behavioral consequences of prenatal/perinatal cytokine activity are compared with those of other schizophrenia models and cytokine interactions with genes are also discussed in this review.
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PMID:Recent progress in animal modeling of immune inflammatory processes in schizophrenia: implication of specific cytokines. 1683 94

The liver is the largest internal organ in the body, responsible for over 500 metabolic, regulatory, and immune functions. Loss of liver function leads to liver failure which causes over 25,000 deaths/year in the United States. Efforts in the field of hepatic tissue engineering include the design of bioartificial liver systems to prolong patient's lives during liver failure, for drug toxicity screening and for the study of liver regeneration, ischemia/reperfusion injury, fibrosis, viral infection, and inflammation. This chapter will overview the current state-of-the-art in hepatology including isolated perfused liver, culture of liver slices and tissue explants, hepatocyte culture on collagen "sandwich" and spheroids, coculture of hepatocytes with non-parenchymal cells, and the integration of these culture techniques with microfluidics and reactor design. This work will discuss the role of oxygen and medium composition in hepatocyte culture and present promising new technologies for hepatocyte proliferation and function. We will also discuss liver development, architecture, and function as they relate to these culture techniques. Finally, we will review current opportunities and major challenges in integrating cell culture, bioreactor design, and microtechnology to develop new systems for novel applications.
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PMID:Integration of technologies for hepatic tissue engineering. 1719 68

Irrespective of the morphological features of end-stage cell death (that may be apoptotic, necrotic, autophagic, or mitotic), mitochondrial membrane permeabilization (MMP) is frequently the decisive event that delimits the frontier between survival and death. Thus mitochondrial membranes constitute the battleground on which opposing signals combat to seal the cell's fate. Local players that determine the propensity to MMP include the pro- and antiapoptotic members of the Bcl-2 family, proteins from the mitochondrialpermeability transition pore complex, as well as a plethora of interacting partners including mitochondrial lipids. Intermediate metabolites, redox processes, sphingolipids, ion gradients, transcription factors, as well as kinases and phosphatases link lethal and vital signals emanating from distinct subcellular compartments to mitochondria. Thus mitochondria integrate a variety of proapoptotic signals. Once MMP has been induced, it causes the release of catabolic hydrolases and activators of such enzymes (including those of caspases) from mitochondria. These catabolic enzymes as well as the cessation of the bioenergetic and redox functions of mitochondria finally lead to cell death, meaning that mitochondria coordinate the late stage of cellular demise. Pathological cell death induced by ischemia/reperfusion, intoxication with xenobiotics, neurodegenerative diseases, or viral infection also relies on MMP as a critical event. The inhibition of MMP constitutes an important strategy for the pharmaceutical prevention of unwarranted cell death. Conversely, induction of MMP in tumor cells constitutes the goal of anticancer chemotherapy.
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PMID:Mitochondrial membrane permeabilization in cell death. 1723 44

After kidney transplantation thrombotic microangiopathy (TMA) may recur in patients with previous hemolytic uremic syndrome or may develop de novo. De novo TMA has been reported to occur in less than 1% of renal transplant recipients by large registries, but single center series reported an incidence of the disease as high as 14-20%. A number of factors may predispose to posttransplant TMA, including ischemia-reperfusion injury, acute rejection, viral infection. Immunosuppressive treatment can also contribute to the development of de novo TMA. Calcineurin inhibitors may cause or aggravate endothelial lesions through their pronecrotic, vasoactive and profibrotic activity. Anti-mTOR agents may delay the repair of the endothelial damage through their interference with endothelial growth factor. Usually, TMA develops in the early posttransplant period but may also occur later. Clinically, TMA is characterized by progressive renal failure and hypertension. Microangiopathic hemolytic anemia and thrombocytopenia may occur in about 60% of cases. Histologically, TMA may be localized to glomeruli or may involve arteries or both. The prognosis depends on the timely diagnosis and on histological picture. Treatment is based on the removal of inciting factors. Early plasmapheresis could improve clinical signs and symptoms and rescue renal function in a number of patients. Anecdotal successes have also been reported with intravenous immunoglobulins and rituximab.
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PMID:De novo thrombotic microangiopathy. An underrated complication of renal transplantation. 1759 67

Lymphoma is a systemic disease. It is not uncommon to be found involved in digestive or central nervous system. However, lymphoma involved in these two systems at the same time is rare. The clinical feature of a case of lymphoma with gastrointestinal bleeding and limbs weakness was investigated and the literature was reviewed. The patient came to our hospital with melena and hematemesis. She was diagnosed as gastric ulcer by gastroscopy and biopsy showed lymphoma. Two days after she came to hospital, the patient presented with progressing limbs weakness. Magnetic resonance imaging (MRI) showed irregular abnormal signals in T2-T4 vertebra, which was enhanced obviously. A strip abnormal signal could be seen in spinal cord and involved in neighboring centrum and ribbing. The lesion extended to paravertebral tissue. The final diagnosis was lymphoma involved in stomach and spinal cord. Diseases presented with both upper digestive tract bleeding and symptoms of central nervous system were rare, including malignancies, virus infection and some therapy. Lymphoma was one of the causes. On the other hand, spinal cord ischemia might occur after gastrointestinal bleeding. Thus, doctors should examine the patients carefully to diagnose these diseases.
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PMID:[A case of upper gastrointestinal bleeding and paraplegia]. 1765 79


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