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)

The neuropathological characteristics and alteration of the dopamine D2 receptor (D2R) were investigated in 27 cases of hypoxic-ischemic basal ganglia necrosis (BGN) by means of neuropathological and immunohistochemical methods. Perinatal hypoxic-ischemic BGN manifested neuronal karyorrhexis as well as eosinophilia, karyorrhexis being more predominant in preterm infants and eosinophilia more predominant in full-term infants. Immunoreactivity to D2R was detected in the cytoplasm and dendrites of small and large neurons in the basal ganglia, and increased with neuronal maturation during the late gestational period in normal human basal ganglia. The number of D2R-positive neurons was smaller in all cases of acute BGN than that in controls, the areas of decreased D2R-positive neurons corresponding to the damaged regions observed on HE staining. Furthermore, neurons showed high expression of D2R in a few cases of remote BGN, suggesting some plasticity as to the recovery of D2R. Thus, the neuropathological characteristics of perinatal hypoxic-ischemic BGN may be related to neuronal maturation during different developmental stages in each region, and D2R development may play a role in the basal ganglia vulnerability to hypoxic-ischemia.
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PMID:Neuropathological characteristics and alteration of the dopamine D2 receptor in hypoxic-ischemic basal ganglia necrosis. 954 80

A flock of 15-wk-old tom turkeys experienced an acute onset of paresis and ataxia in 75% of the birds after handling. Cartilaginous emboli were found in the spinal cord vasculature from one of five turkeys at this initial presentation. Most of the flock recovered within 6 days, but 3% remained paretic. Myelomalacia was present in three turkeys that failed to recover. Two of these turkeys had cartilaginous and osseous emboli within the medullary spaces of the vertebral bodies, internal vertebral venous sinuses, and spinal cord. The third turkey had vascular and spinal cord necrosis consistent with thrombosis and resultant ischemia. These changes suggest that turkeys may be susceptible to a syndrome analogous to fibrocartilaginous embolism of the spinal cord in mammals. The articular cartilage of the vertebral body endplate may be the source of the emboli. The turkeys with emboli had articular cartilage defects consisting of matrix eosinophilia, chondrocyte loss, multicellular cluster formation, cartilage detachment, and cartilage clefts. Cartilaginous emboli in the spinal cord should be considered as a potential cause for acute paresis and ataxia, especially in flocks with preexisting abnormalities of the vertebral articular cartilage surfaces.
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PMID:Intravascular cartilaginous emboli in the spinal cord of turkeys. 964 39

Cholesterol emboli are being increasingly recognized as an important cause of renal dysfunction in an aging US population. Irregularly shaped atheroemboli typically cause partial obstruction of small renal vessels resulting in ischemia. A vasculitis-like picture often evolves with an inflammatory reaction and giant cell formation. Cholesterol emboli may be temporally related to vascular manipulation, anticoagulant, or thrombolytic drug use. Spontaneous cases have been reported. Patients with cholesterol emboli may present with a spectrum of acute renal failure varying from mild and asymptomatic to life-threatening disease. The differential diagnosis includes radiocontrast nephropathy, endocarditis with left-sided emboli, vasculitis, and thrombotic emboli. The physical examination findings suggestive of cholesterol emboli include extrarenal emboli and livedo reticularis. The urinalysis is typically unremarkable. Some patients have hematuria and/or non-nephrotic proteinuria. Serology and hematology results may suggest an inflammatory-like picture with elevated erythrocyte sedimentation rate, hypocomplementemia, eosinophilia, and eosinophiluria. In the setting of a clear precipitating factor and suggestive physical findings, cholesterol emboli can be established purely on clinical grounds. Demonstration of cholesterol crystals by biopsy of the kidney, skin (if lesion present), or muscle is diagnostic in unexplained cases. The kidney is the organ most frequently involved in this order. Therapy is supportive with particular emphasis on management of hypertension and hypercholesterolemia.
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PMID:Atheroembolic Renal Disease. 1186 88

Apoptotic and necrotic cell death may act in concert in focal cerebral ischemia. This study explored the temporal and spatial pattern of apoptosis and necrosis in a novel photothrombotic ring stroke model with or without spontaneous reperfusion. Adult male Wistar rats were subjected to a ring-shaped laser irradiation beam simultaneously with intravenous erythrosin B infusion. The presence and attributes of apoptosis and necrosis in the anatomically well-defined cortical region at risk and ring-lesion region were verified under light microscopy with TUNEL, Hoechst 33342, and hematoxylin and eosin staining. Cells exhibiting apoptotic morphology with chromatin condensation and apoptotic bodies and necrotic ghost appearance were observed. The occurrence of apoptosis and necrosis in the ischemic regions was confirmed by electron microscopy and gel electrophoresis, in which DNA isolated from the lesion area revealed both a ladder and a smear. Double staining with TUNEL and the cell markers NeuN, glial fibrillary acidic protein, and ED-1 revealed that the majority of apoptotic cells were of neuronal origin. Cells exhibiting pyknosis/eosinophilia, apoptosis, or ghost appearance were quantified by stereological means. In subregions with severe ischemia, the peak appearance of apoptotic cells started earlier, i.e., at 24 h, than the peak of necrotic cells, and the high concentration of the apoptotic cells remained as long as that of necrotic cells, i.e., until 72 h post-ischemia. The ratio of apoptotic to necrotic cells was approximately 1:2. Therefore, apoptosis may be an important contributor to neuronal cell death in brain regions with severely reduced blood flow after thrombo-embolic stroke.
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PMID:Long-lasting neuronal apoptotic cell death in regions with severe ischemia after photothrombotic ring stroke in rats. 1241 Mar 94

A-25-year-old man was admitted because of a painless tumor of the scrotum. The patient denied a history of exogenous material injection and trauma in the scrotum. Physical and radiological examination revealed a mass in the scrotum, and blood laboratory tests showed no significant findings except for mild eosinophilia (5.6%). Resection of the mass was performed. The mass was isolated and located in the subcutaneous tissue of the scrotum. The mass was rectangular and symmetrical, and measured 65 x 45 x 15 mm. Histologically, the mass was composed of adipose tissue with fibrosis. Many epithelioid granulomas with multinucleated giant cells of foreign body and Langhans' types and heavy infiltrates of lymphocytes and eosinophils were recognized. Characteristically, the lesion showed broad coagulative and lytic necrosis. Congestion and edema suggestive of ischemia were seen in some areas. Special stains for acid-fast bacteria, gram-positive bacteria and fungi failed to detect any microorganisms. Polymerase chain reaction for mycobacterium tuberculosis revealed no reaction products. Immunohistochemically, the majority of lymphocytes were CD45RO-positive T cells, and S-100 protein-positive cells and CD68-positive macrophages were scattered in small amounts. The appearances were typical for sclerosing lipogranuloma except for the necrosis. Although the pathological mechanism of the broad necrosis is unclear, the necrosis might be the result of ischemia. Our case suggests that primary sclerosing lipogranuloma of the scrotum might show broad necrosis, and that T-cell-mediated immune response might play a part in the formation of lipogranuloma.
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PMID:Primary sclerosing lipogranuloma with broad necrosis of the scrotum. 1258 42

To distinguish recent ischemic myocardial changes in myocardial infarction-prone Watanabe heritable hyperlipidemic (WHHLMI) rabbits from general postmortem myocardial degeneration, we examined hearts of WHHLMI rabbits after sudden death and postmortem hearts of non-atherogenic rabbits. Hearts of 8 WHHLMI rabbits were excised within 30 min of sudden death and hearts of 27 non-atherosclerotic rabbits were excised at designated periods after sacrifice. A large number of myocardial cells from WHHLMI rabbits exhibited features characteristic of ischemia (intercellular gap, intracellular edema, eosinophilia, disappearance of myocardial cells, indistinct nuclei, wavy myocardial fibers) simultaneously at regions close to proximal occluded coronary arteries. Although postmortem hearts of non-atherosclerotic rabbits exhibited similar characteristics, several features characteristic of autolyzed myocytes were also randomly observed in the left ventricle wall. Each feature was detected independently in myocardial cells or regions of the ventricle wall. In conclusion, we found several unique characteristics associated with myocardial infarction which enable discrimination between recent ischemic myocardial changes and myocardial degeneration following death.
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PMID:Discrimination of recent ischemic myocardial changes in WHHLMI rabbits from the findings of postmortem degeneration. 1636 18

We report a 22 years old male with chronic allergic rhinitis, who presented with asthma, prolonged fever, eosinophilia, cutaneous vasculitis, subcutaneous nodules, polyarthritis, ulcers in the nasal mucosa and external auditory canal, hematuria, proteinuria, renal failure, severe hypertension, pulmonary infiltrates and mesenteric ischemia with a perforation of the sigmoid colon. Arteriography showed multiple aneurysmae of intrarenal arteries and a skin biopsy showed a leukocytoclastic vasculitis. A diagnosis of Churg-Strauss syndrome was made. He was initially treated with steroids and cyclophosphamide but abandoned therapy. Eighteen years after the onset of the disease, he required hemodialysis. Eight months after being on dialysis, he suffered a reactivation of the disease with lung hemorrhage and finally died, due to an upper gastrointestinal bleeding caused by a duodenal ulcer.
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PMID:[Late reactivation of Churg-Strauss syndrome]. 1653 66

Roux en Y hepatojejunostomy is the surgery of choice for bile duct repair. Anastomotical dysfunction after reconstruction has several etiopathologies. Besides technical factors, ischemia of the duct is responsible for late obstruction. Bile colonization with secondary stones and sludge can also be identified as a cause. An unusual cause of anastomotical dysfunction secondary to ascaris biliary infestation after biliary reconstruction is reported herein. The patient had intermittent cholangitis and eosinophilia. At operation, the worm was found obstructing the anastomosis.
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PMID:An unusual cause of bilioenteric anastomotic dysfunction after iatrogenic bile duct injury. 1680 20

Homeostasis of the reduction-oxidation (redox) state is critical to protection from oxidative stress in the lungs. Therefore, the lungs have high levels of antioxidants, including glutathione, heme oxygenase, and superoxide dismutase. The numbers of inflammatory cells -- particularly eosinophils -- are increased in the airways of asthma patients, and these pulmonary inflammatory cells release large amounts of harmful reactive oxygen species and reactive nitrogen species. Human thioredoxin 1 (TRX1) is a redox-active protein of approximately 12 kDa that contains a (32)Cys-Gly-Pro-(35)Cys sequence necessary for its activity. The strong reducing activity of the sequence results from the cysteine residues acting as proton donors and cleaving disulfide (S-S) bonds in the target protein. Endogenous or exogenous TRX1 or both protect the lungs against ischemia-reperfusion injury, influenza infection, bleomycin-induced injury, or lethal pulmonary inflammation caused by interleukin-2 and interleukin-18. We showed that exogenous TRX1 inhibits airway hyperresponsiveness and pulmonary inflammation accompanied by eosinophilia in mouse models of asthma. Recently, we reported that exogenous TRX1 improves established airway remodeling in a prolonged antigen-exposure mouse asthma model. Exogenous and endogenous TRX1 also prevents the development of airway remodeling. Here, we discuss the role and clinical benefits of TRX1 in asthma.
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PMID:Redox-regulated mechanisms in asthma. 1817 61

The present study aims to explore whether Mg infusion has a preventive effect on ischemia-reperfusion injury in rats. A total of 20 Sprague-Dawley-type adult male rats were used. In group 1 (control), 0.9% isotonic solution was administered. In group 2 (experiment), magnesium sulfate (0.5 mg per 100 g) was administered. Ischemia was induced for 15 min for the two groups. Magnesium (Mg), interleukin 8 (IL-8), and malondialdehyde levels were analyzed in blood, while edema, neutrophil infiltration, eosinophilia, loss of striation, and nucleolization were evaluated in histopathological examination. Mg levels in the experiment group were higher than those in the control group after ischemia-reperfusion (p < 0.05). In the control group, postischemia and postreperfusion IL-8 values were higher than preoperative values (p < 0.05). As for eosinophilia and loss of striation values, these were higher in the experiment group after ischemia-reperfusion than the values in the control group (p < 0.05). Histopathologically, Mg infusion cannot prevent the tissue injury triggered in ischemia-reperfusion periods. Eosinophilia can be one of the major and earliest markers of ischemia-reperfusion injury.
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PMID:Preventive role of magnesium on skeletal muscle ischemia-reperfusion injury-an experimental study. 1880 32


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