Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using microangiography combined with benzidine stains, we studied the development of vessels in the meninges, cortex, and white matter in 30 neonates, 16 infants and children, and eight neonates with periventricular leukomalacia. The vessels of the deep white matter, especially the ventriculofugal arteries, are useful as an index of cerebrovascular maturity. The lesions of primary leukomalacia utilizing the combined radiographic-histological techniques are localized to the ends of ventriculofugal arteries or between medullary arteries. The infants with leukomalacia have either poorly developed vessels or severe clinical complications producing ischemia or both.
 ...
PMID:Development of cerebrovascular architecture and its relationship to periventricular leukomalacia. 61 67

Hypoxia-ischemia induced by unilateral carotid ligation followed by either 15 (moderate) or 90 (severe) min exposure to 8% oxygen was associated with induction of IGF-BP 2 mRNA expression. A specific rat IGF-BP 2 cDNA probe was used to determine the IGF-BP 2 mRNA distribution in brain sections using in situ hybridization. Untreated control rats and the non-ligated hemisphere in experimental rats expressed IGF-BP 2 mRNA in the choroid plexus, meninges and more weakly in the thalamus, hippocampus and cortical layer 5. Increased expression in experimental rats was limited to regions known to have neuronal damage. Three days after the moderate insult the signal was increased in the CA1/2 region of the hippocampus and thalamus of the ligated side. Three days after the severe insult IGF-BP 2 expression was found surrounding the infarcted regions while by 5 days after severe insult the whole infarcted volume showed induction. The results suggest a role for the IGFs in the post-asphyxial response. IGF-BP 2 may alter the bio-availability of IGF 1 or 2 or modulate their actions in the area of infarction, and thus promote cerebral repair and recovery.
 ...
PMID:Expression of insulin-like growth factor-binding protein 2 (IGF-BP 2) following transient hypoxia-ischemia in the infant rat brain. 127 50

We used a cytochemical technique for the detection of superoxide in cerebral inflammation and ischemia-reperfusion in anesthetized cats. The technique is based on the oxidation of Mn2+ to Mn3+ by superoxide; Mn3+, in turn, oxidizes diaminobenzidine. The oxidized diaminobenzidine forms an osmiophilic electron-dense product that is detected by electron microscopy. The reagents, manganese chloride (2 mM) and diaminobenzidine (2 mg/ml), were placed topically on the brain surface of anesthetized cats equipped with cranial windows. Inflammation was induced by topical carrageenan with or without phorbol 12-myristate 13-acetate to activate leukocytes. In inflammation, superoxide was detected in the plasma membrane and in the phagocytic vacuoles of leukocytes. In ischemia-reperfusion, superoxide was identified in the meninges in association with blood vessels. It was located primarily in the extracellular space and occasionally in endothelial and vascular smooth muscle cells. In both inflammation and ischemia, the reaction product was eliminated by superoxide dismutase or by the omission of either manganese or diaminobenzidine. It was unaffected by sodium azide, which inhibits peroxidases. No superoxide was detected in the brain parenchyma. The findings confirm the generation of superoxide is cerebral ischemia-reperfusion and show that it is produced in cerebral vessels.
 ...
PMID:Cytochemical detection of superoxide in cerebral inflammation and ischemia in vivo. 132 63

Plain and Gd-DTPA-enhanced MR images of the brain were obtained in 18 consecutive patients with meningitis (eight with tuberculous, five with bacterial, three with viral, and two with fungal infections); the MR images were compared with CT scans. MR images were obtained on a 2.0-T superconducting unit with both T1- and T2-weighted pulse sequences before injection and with a T1-weighted sequence after injection of Gd-DTPA (0.1 mmol/kg) in all patients. In tuberculous meningitis, MR imaging depicted ischemia/infarct, hemorrhagic infarct of basal ganglia, meningeal enhancement at either basal cistern or convexity surface of brain, and associated small granulomas in a few more patients than CT did. In bacterial meningitis, primary foci of extracranial inflammation (i.e., mastoid, paranasal sinuses) and adjacent intracranial lesions including localized dural inflammation, subdural fluid collection, and/or brain parenchymal lesions were demonstrated much better on MR than on CT. Otherwise, MR images generally matched the CT scan. Although the plain MR images, both T1- and T2-weighted, were the most sensitive in delineating ischemia/infarct, hemorrhage, and edema, they were not as specific as Gd-DTPA-enhanced T1-weighted images and postcontrast CT scans in defining the active inflammatory process of the meninges and focal lesions precisely. We conclude that if Gd-DTPA is used, MR imaging appears to be superior to CT in the evaluation of patients with suspected meningitis. Precontrast MR is needed to delineate ischemia/infarct, edema, and subacute hemorrhage.
 ...
PMID:Gd-DTPA-enhanced MR imaging of the brain in patients with meningitis: comparison with CT. 210 19

Plain and Gd-DTPA-enhanced MR images of the brain were obtained in 18 consecutive patients with meningitis (eight with tuberculous, five with bacterial, three with viral, and two with fungal infections); the MR images were compared with CT scans. MR images were obtained on a 2.0-T superconducting unit with both T1- and T2-weighted pulse sequences before injection and with a T1-weighted sequence after injection of Gd-DTPA (0.1 mmol/kg) in all patients. In tuberculous meningitis, MR imaging depicted ischemia/infarct, hemorrhagic infarct of basal ganglia, meningeal enhancement at either basal cistern or convexity surface of brain, and associated small granulomas in a few more patients than CT did. In bacterial meningitis, primary foci of extracranial inflammation (i.e., mastoid, paranasal sinuses) and adjacent intracranial lesions including localized dural inflammation, subdural fluid collection, and/or brain parenchymal lesions were demonstrated much better on MR than on CT. Otherwise, MR images generally matched the CT scan. Although the plain MR images, both T1- and T2-weighted, were the most sensitive in delineating ischemia/infarct, hemorrhage, and edema, they were not as specific as Gd-DTPA-enhanced T1-weighted images and postcontrast CT scans in defining the active inflammatory process of the meninges and focal lesions precisely. We conclude that if Gd-DTPA is used, MR imaging appears to be superior to CT in the evaluation of patients with suspected meningitis. Precontrast MR is needed to delineate ischemia/infarct, edema, and subacute hemorrhage.
 ...
PMID:Gd-DTPA-enhanced MR imaging of the brain in patients with meningitis: comparison with CT. 210 81

Computerized tomography in 134 patients with traumatic epilepsy allowed to reveal different changes in the brain tissue, meninges and CSF spaces. Early stages were characterized by signs of meningeal adhesions. With increased duration of the disease these changes were supplemented by signs brain atrophy in the form of dilatation of the subarachnoidal spaces, internal hydrocephalus. CSF cysts were diagnosed in 5 patients, porencephaly in 2, ischemia foci in the brain in 9 patients.
 ...
PMID:[The results of computed tomography in patients with traumatic epilepsy]. 251 89

In this study we present a method to achieve a complete transection of optic nerve axons in adult rat, while preserving the vasculature and retaining the continuity of the meninges. Under deep anesthesia, the optic nerve of adult rat is exposed. Using specially designed instruments built from disposable glass microsampling pipettes, a small opening is created in the meninges of the optic nerve, 2-3 mm behind the eye globe. A glass dissector is introduced through the opening and is used to cut all the axons through the whole width of the nerve. Complete transection of the optic nerve axons was achieved, while retaining the continuity of the meninges and avoiding damage to the nerve's vascular supply. Transection was confirmed by transillumination showing a complete gap in the continuity of the nerve axons, and by both morphological and electrophysiological criteria. Nerve transection performed by the conventional technique leads to neuroma formation and hampers regeneration. Crush injury may cause nerve ischemia, which is detrimental to axonal recovery. Both of these disadvantages are avoided by the method of transection presented here. The opening created in the 'meningeal tube' can be used to inject substances that may be of benefit in recovery, rescue and/or regeneration of the injured axons. The model is particularly suitable for in vivo studies on nerve regeneration, and especially for screening of putative therapeutic agents.
 ...
PMID:Complete transection of rat optic nerve while sparing the meninges and the vasculature: an experimental model for optic nerve neuropathy and trauma. 898 77

In order to elucidate the mechanism(s) of neuronal protection by hypothermia against ischemic damage, we examined the effect of lowering temperature on the microglial activation that is thought to cause the development of ischemia-induced neuronal damages. Cultured microglia from neonatal rats were measured for microglial activation by the following indices: production of superoxide and nitric oxide by the methods of acetyl-cytochrome c reduction and nitrite accumulation in the culture medium, respectively, and cell proliferation evaluated by [3H]thymidine uptake. At 30 degrees C, superoxide production induced by phorbol ester was approximately as low as 30% of the control at 37 degrees C, and nitric oxide production after addition of lipopolysaccharide was decreased to approximately 25% of the control. The time course of nitric oxide production indicates that the induction of nitric oxide synthase seemed to be significantly suppressed by lowering temperature. In addition, the proliferation of microglia was remarkably inhibited at 30 degrees C. The level of proliferation in the hypothermic condition is much lower in microglia (14% of the control) than those in astrocytes cultured from brain cortices (96%) and fibroblasts cultured from brain meninges (53%), suggesting that the microglial activation is highly susceptible to lowering temperature. The present study indicates that hypothermia potently inhibits proliferation, superoxide and nitric oxide production of cultured microglia and that the hypothermic protection against postischemic neuronal damage might be, at least in part, due to the suppression of microglial activation.
 ...
PMID:Hypothermic suppression of microglial activation in culture: inhibition of cell proliferation and production of nitric oxide and superoxide. 930 Apr 14

COX-2 expression, an inducible form of cyclooxygenase was studied in human brain after ischemia-reperfusion. Previously, a prominent COX-2 upregulation was described in neurons few hours or days after ischemia but little is known about COX-2 expression in non-neuronal cells participating in post-ischemic inflammation. Aim of the study was to examine COX-2 expression in activated glial cells of individuals, who died two or more weeks after resuscitation. In the cerebral cortex of these individuals ischemic necrosis was more or less widespread. In some brain areas numerous microglial cells were found. At the centre of the necrosis high expression of COX-2 was detected in macrophages, polymorphic cells and leukocytes. At the margin of necrosis hypertrophic astrocytes were COX-2 immunopositive. Expression of COX-2 was observed also in the wall of blood vessels of necrotic brain areas and in meninges. The results of the study suggest that in the late period after global ischemia reactive and hypertrophic astrocytes and macrophages may be the major sources of prostaglandins in the human brain.
 ...
PMID:Expression of cyclooxygenase-2 in astrocytes of human brain after global ischemia. 1046 24

In two series of experimental occlusion of the middle cerebral artery (MCA) in mice, the time course and the evolution of morphological changes were followed. Both series comprised control animals used in experiments for the screening of neuroprotective and therapeutic effects after focal ischemia. In both series the left MCA was permanently occluded and the animals were sacrificed by perfusion fixation at certain time intervals following occlusion. In the first series the follow up was continued until the 30th day after ischemia. In the second, the observation period was extended to two months. The general question was addressed, whether or not such experimental settings can contribute to the understanding of cellular (necrosis vs apoptosis) and tissue (resorption vs scar) reaction. In the two series the technical procedures were only slightly different. Nevertheless, the development of morphological sequelae was at variance. Differences in tissue reaction in both sets revealed features that were rarely observed in previous protocols. In the first series, infarct areas were different in size, often a central part near the meninges was preserved and gave rise to a prominent mesenchymal reaction. In the second series, infarcts had almost constant size and mesenchymal reaction changes were minimal. The end product in both series, however, was a shallow groove much smaller than the primary well-demarcated defect. We conclude that minor technical variations of MCA occlusion in the mouse demonstrate the variability of occlusion sequelae due to collateral irrigation known from human cerebral pathology. On the cellular level, neuronal death is obviously completed during the first 24 hours in the infarct core. Thus, the mechanism of neuronal damage can only be best observed by morphology at the transition between completed territorial necrosis and unchanged tissue: shrunken neuronal perikarya develop into pycnotic nuclei, that may be interpreted as apoptosis. A second area of partial damage is marked by gliosis. Astrocytic reaction extended far beyond the infarct border, even to the contralateral hemisphere and could represent a component of size compensation.
 ...
PMID:Morphology of tissue damage caused by permanent occlusion of middle cerebral artery in mice. 1108 90


1 2 Next >>