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)

Ischemic preconditioning is a phenomenon that describes how a sublethal ischemic insult can induce tolerance to subsequent ischemia. This phenomenon has been observed after focal or global ischemia in different animal models. However, the hypothesis that bacterial infection might lead to neuronal tolerance to injury has not been investigated. To mimic cerebral bacterial infection, we injected bacterial lipopolysaccharide (LPS) in the right dorsal hippocampus, followed 24 hours later by an excitotoxic lesion using kainic acid in the mouse model. Quantification of lesion size after cresyl violet counterstaining revealed that LPS pretreatment afforded neuroprotection to CA3 neurons against KA challenge. To investigate the events underlying this protection, we studied the cytokine profile induced after LPS injection. Interleukin (IL)-1 beta and transforming growth factor beta 1 (TGF-beta 1) were the main cytokines expressed at 24 hours after LPS injection. Because IL-1 beta has been described as deleterious in acute injury, we decided to investigate the function of TGF-beta 1. An adenovirus expressing a constitutively active form of TGF-beta 1 was injected intracerebrally 1 week before the induction of excitotoxic lesion, and neuronal protection was observed. To confirm the neuroprotective role of TGF-beta 1, the TGF-beta 1 adenovirus was replaced by recombinant human TGF-beta 1 protein and total neuroprotection was observed. Furthermore, the antibody-mediated blocking of TGF-beta 1 action prevented the protective effect of pretreatment with LPS. We have demonstrated in vivo that the cerebral tolerance phenomenon induced by LPS pretreatment is mediated by TGF-beta 1 cytokine.
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PMID:Transforming growth factor-beta 1-mediated neuroprotection against excitotoxic injury in vivo. 1452 28

Cholestasis is a common sequela of liver transplantation. Although the majority of cases remain subclinical, severe cholestasis may be associated with irreversible liver damage, requiring retransplantation. Therefore, it is essential that clinicians be able to identify and treat the syndromes associated with cholestasis. In this review, we consider causes of intrahepatic cholestasis. These may be categorized by time of occurrence, namely, within 6 months of liver transplantation (early) and thereafter (late), although there may be an overlap in their causes. The causes of intrahepatic cholestasis include ischemia/reperfusion injury, bacterial infection, acute cellular rejection, cytomegalovirus infection, small-for-size graft, drugs for hepatotoxicity, intrahepatic biliary strictures, chronic rejection, hepatic artery thrombosis, ABO blood group incompatibility, and recurrent disease. The mechanisms of cholestasis in each category and the clinical presentation, diagnosis, treatment, and outcome are discussed in detail.
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PMID:Intrahepatic cholestasis after liver transplantation. 1452 93

Mammalian hibernation has been reported to increase resistance to various harmful events such as low body temperature, severe ischemia, bacterial infection, irradiation, and muscle disuse, and to prolong the lifespan of the mammal. Therefore, hibernation mechanisms are thought to play a critical role in maintaining healthy organisms. Although the application of this physiological phenomenon to medical fields has strongly been desired, it has been prevented by a poor understanding of the hibernation mechanism. In order to clarify how mammalian hibernation is controlled in organisms, we have looked for a physiological signal of hibernation and found marked changes in cardiac calcium regulation associated with a circannual hibernation. Focusing on these changes, we initially discovered a molecular marker of hibernation, hibernation-specific proteins (HP), of which production in the liver and the blood content are controlled by an endogenous circannual rhythm responsible for hibernation. Our recent studies on HP regulation have revealed that circannual signals for the timing of hibernation are transmitted through the neuroendocrine system and that HP are actively transported into the cerebrospinal fluid (CSF) prior to the onset of hibernation. This suggested that hibernation is controlled by HP in the brain and its regulation system. Based on these results, the future medical application of these results is discussed.
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PMID:[Investigation of mechanisms of mammalian hibernation and its possible application in medical treatment]. 1513 27

Heat shock proteins (Hsps) are molecular chaperones that assist intracellular folding, assembly and translocation of proteins in prokaryotic and eukaryotic cells. A variety of stresses including hyperthermia, radiation, heavy metals, ischemia, anoxia and reoxygenation have been shown to increase the expression of Hsps. Likewise, bacterial infection represents a stress for the host cell. In this study, expression of the constitutive (Hsp73) and inducible (Hsp72) isoforms of Hsp70 and Hsp90 was monitored in brain, heart, liver and skeletal muscle from the western painted turtle Chrysemys picta bellii diagnosed with Septicemic Cutaneous Ulcerative Dermatitis (SCUD). This disease is caused by a gram-negative bacterium probably belonging to the Citrobacter spp. The expression of Hsp73 increased 1.8-fold in brain and liver, 2.2-fold in heart but did not change in skeletal muscle; Hsp72 expression increased 5.5-fold in brain and 3-fold in liver but did not change in heart or skeletal muscle; Hsp90 expression increased 9-fold in brain, 2.7-fold in heart and 2.4-fold in skeletal muscle but did not change in liver. These results suggest a tissue-specific Hsp response during bacterial infection and a role for Hsps in immunopathological events in reptiles.
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PMID:Bacterial infection and tissue-specific Hsp72, -73 and -90 expression in western painted turtles. 1545 Aug 61

Emphysematous gastritis (or phlegmonous gastritis) and gastric emphysema (or gastric pneumatosis) are variations of conditions associated with the presence of intramural air in the stomach. The presence of air in the gastric wall is a very rare clinical condition, associated with bacterial infection, increased intragastric pressure from gastric outlet obstruction, gastric mucosal disruption or air dissection from the mediastinum. In adults, this can occur in the setting of instrumentation-related injury, gastric outlet obstruction by gastric, duodenal or pancreatic malignancies or bowel ischemia. Here we describe a case of gastric emphysema related to repeated biliary stenting and partial duodenal obstruction in a patient with inoperable periampullary cancer, and provide the first description of the endoscopic ultrasonographic findings of gastric emphysema in the literature. In our case, endoscopic ultrasound showed a band of bright echogenicity arising from the submucosa layer, representing air in the gastric wall.
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PMID:Endoscopic ultrasonographic appearance of gastric emphysema. 1578 59

We evaluated an association of nonreassuring fetal heart rate (FHR) patterns and subsequent cerebral palsy (CP) in pregnancies with intrauterine bacterial infection. Among 10,030 infants born during 1995 to 2000, 139 were complicated with acute intrauterine bacterial infection in labor. The FHR patterns 2 hours immediately before delivery were interpreted according to the guidelines of the National Institute of Child Health and Human Development. The correlations between the FHR patterns and umbilical blood gases, as well as FHR patterns and CP were studied. Statistics included unpaired t test, contingency table with chi (2) and Fisher test, and one-way analysis of variance with Bonferroni/Dunn test. Fifteen infants (11%) developed CP at 2 years or older. Nonreassuring FHR patterns including recurrent late deceleration, severe variable deceleration, and prolonged deceleration occurred in 24% of pregnancies with intrauterine infection. Incidence of CP was not different according to the FHR deceleration patterns or umbilical pH values. Multiple logistic regression analysis revealed that fetal tachycardia (OR, 11; 95% CI, 1.8 to 67) and lower gestational age (< 34 weeks; OR, 9.4; 95% CI, 0.96 to 93) was associated with CP in intrauterine infection. Nonreassuring FHR patterns were increased in intrauterine infection. CP occurred more frequently and was associated with tachycardia and lower gestational age, but not with FHR deceleration patterns or acidemia, suggesting different pathophysiology from acute hypoxia-ischemia.
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PMID:Association of nonreassuring fetal heart rate patterns and subsequent cerebral palsy in pregnancies with intrauterine bacterial infection. 1590 11

Bacterial infection is implicated in the selective CNS white matter injury associated with cerebral palsy, a common birth disorder. Exposure to the bacterial endotoxin LPS produced death of white matter glial cells in isolated neonatal rat optic nerve (RON) (a model white matter tract), over a 180-min time course. A delayed intracellular Ca(2+) concentration ([Ca(2+)](i)) rise preceded cell death and both events were prevented by removing extracellular Ca(2+). The cytokines TNF-alpha or IL-1beta, but not IL-6, mimicked the cytotoxic effect of LPS, whereas blocking either TNF-alpha with a neutralizing Ab or IL-1 with recombinant antagonist prevented LPS cytotoxicity. Ultrastructural examination showed wide-scale oligodendroglial cell death in LPS-treated rat optic nerves, with preservation of astrocytes and axons. Fluorescently conjugated LPS revealed LPS binding on microglia and astrocytes in neonatal white and gray matter. Astrocyte binding predominated, and was particularly intense around blood vessels. LPS can therefore bind directly to developing white matter astrocytes and microglia to evoke rapid cell death in neighboring oligodendroglia via a calcium- and cytokine-mediated pathway. In addition to direct toxicity, LPS increased the degree of acute cell death evoked by ischemia in a calcium-dependent manner.
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PMID:Acute lipopolysaccharide-mediated injury in neonatal white matter glia: role of TNF-alpha, IL-1beta, and calcium. 1597 42

Patients with pulmonary insufficiency due to scleroderma have long been considered suboptimal candidates for lung transplantation. This has been supported by small single-center experiences that did not reflect the entire U.S. experience. We sought to evaluate the outcome of patients with scleroderma who underwent lung transplantation. We conducted a retrospective review of 47 patients with scleroderma who underwent lung transplantation at 23 U.S. centers between 1987 and 2004 and were reported to the United Network for Organ Sharing. Women constituted 57% of the patients. The mean age was 46 years. Twenty-seven patients received single lung transplants (57%), and the remaining received double lung transplants. The mean cold ischemia time was 4.1 hours. There were 7 early deaths (< or =30 days) and 17 late deaths (> 30 days). The causes of early death were primary graft failure and a cardiac event in two patients each and bacterial infection and stroke in one patient each. Late mortality was due to infection in seven patients, respiratory failure in three, malignancy in two, and multisystem organ failure, rejection, pulmonary hypertension, and a cardiac event in one patient each. The causes of early and late death were not recorded for two patients. One patient received a second transplant owing to graft failure of the first. Twenty-three patients (49%) were alive at a mean follow-up of 24 months. The Kaplan-Meier 1- and 3-year survival rates were 67.6% and 45.9% respectively, which are not significantly different from those of 10,070 patients given transplants for other lung conditions during the same period (75.5% and 58.8% respectively, P = 0.25). Donor gender, recipient's age, and type of transplant did not affect survival. In carefully selected patients with scleroderma who have end-stage lung disease, lung transplantation is a valid life-saving therapeutic option. Available data suggest acceptable short-term morbidity and mortality and a long-term survival similar to that of patients given transplants for other lung conditions.
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PMID:Outcomes of lung transplantation in patients with scleroderma. 1622 54

Long pentraxin 3 (PTX3) is a newly discovered acute phase protein produced at the sites of infection and inflammation by tissue cells, macrophages, monocytes, and dendritic cells. PTX3 plays an important role in preventing infection of certain fungi, bacteria, and viruses in the lung. Recombinant PTX3 has been proposed as a potential antifungal molecule for therapy. However, under certain experimental conditions, such as intestinal ischemia-reperfusion, high volume mechanical ventilation, or severe bacterial infection, increased expression of PTX3 is associated with more severe lung injury. Therefore, it is necessary to further explore the sources of PTX3 in the lung and the regulatory mechanisms of its expression. It is also essential to further determine how PTX3 binds to pathogens, complement, and apoptotic cells, and to determine whether PTX3 has a specific receptor in targeted cells. These studies will provide insight into the pathological processes of pulmonary infection and acute lung injury and provide potential novel therapeutic strategies to control pulmonary infections without severe lung injury.
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PMID:Long pentraxin 3 in pulmonary infection and acute lung injury. 1727 44

Calciphylaxis is a rare, but potentially life-threatening condition usually observed in patients with end-stage chronic renal disease and characterized by small- and medium-sized blood vessel calcification leading to tissue ischemia. The clinical features are primarily cutaneous, consisting of skin necrosis and ulceration, mostly located in the lower extremities. We report a case of a 56-year-old woman with a previous history of renal disease and atypical lobular hyperplasia of the right breast, who developed painful skin necrosis on both breasts. Differential diagnosis comprises acute bacterial infection with ulceration, cutaneous vasculitis, cancer and calciphylaxis.
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PMID:Calciphylaxis of the breast: a rare disease in the differential diagnosis of breast cancer. 1854 Nov 4


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