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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Astroprotein (an astrocyte-specific cerebroprotein) levels in cerebrospinal fluid (CSF) were determined by radioimmunoassay in 47 stroke patients. (Astroprotein is immunologically identical to glial fibrillary acidic protein.) Astroprotein levels in CSF increased markedly in acute cases of intracerebral hemorrhage and slightly to moderately in some acute cases of subarachnoid hemorrhage and cerebral infarction. In intracerebral hemorrhage, CSF astroprotein levels in the acute stage of the ictus reflected the size of the lesion and were used to estimate the clinical outcome. In subarachnoid hemorrhage and cerebral infarction, CSF astroprotein levels were related to the general neurological state. Evidence obtained indicated that fundamentally different destructive and/or degenerative processes in the brain may be involved in intracerebral hemorrhage, subarachnoid hemorrhage and cerebral infarction and that determination of CSF astroprotein may have clinical significance in stroke patients.
Stroke
PMID:Levels in stroke patients of CSF astroprotein, an astrocyte-specific cerebroprotein. 52 9

Histopathologic changes in the thalamus of 23 rats after somatosensory cortical infarction produced by middle cerebral artery occlusion were examined using the Fink-Heimer silver staining method, immunohistochemistry with antibodies against glial fibrillary acidic protein and laminin, and conventional stains. Middle cerebral artery occlusion produced cortical infarcts in the lateral parietal region, with variable involvement of the frontoparietal parasagittal sensorimotor cortex. Within 3 days after occlusion, massive terminal degeneration but no neuronal changes were apparent in the ipsilateral thalamus. By 1 week after occlusion, abnormal neurons with darkly stained, shrunken nuclei and atrophic perikarya were present in the ipsilateral thalamic nuclei. These neurons were densely argyrophilic in Fink-Heimer sections. Rats with small lateral parietal cortical lesions had degenerating neurons limited to the medial ventroposteromedial nucleus. Large lesions involving the parasagittal sensorimotor cortex resulted in widespread neuronal damage in the ventroposteromedial, ventroposterolateral, intralaminar, and posterior nuclear regions but nowhere else. Immunoreactivity to laminin antibody decreased, and astrocytic proliferation was abundant in affected thalamic areas. These findings are consistent with retrograde neuronal degeneration due to thalamocortical fiber damage in ischemic cortical regions. Such lesions remote from the infarct may influence functional recovery in patients with stroke.
Stroke 1990 May
PMID:Neural damage in the rat thalamus after cortical infarcts. 169 45

Intraventricular hemorrhage, or hemorrhage into the germinal matrix tissues of the developing brain, remains a common problem of preterm infants. The "risk period" for this insult is the first 3-4 postnatal days. We hypothesized that this risk period for hemorrhage is related to rapid perinatal maturation of the germinal matrix vasculature and employed the newborn beagle pup model for the study of this maturation. Newborn beagle pups (n = 30) were anesthetized and systemically perfused with buffered formalin; the brains were removed and prepared for immunohistochemical study. Sections stained with Bandeiraea lectin demonstrated that there was no difference in germinal matrix vessel density between postnatal days 1 and 4. Germinal matrix sections were also stained for antibodies to alpha-smooth muscle actin, collagen IV, collagen V, desmin, factor VIII-related antigen, fibronectin, glial fibrillary acidic protein, laminin, transferrin, and vimentin. Vasculature staining by alpha-smooth muscle actin was not noted until postnatal day 10, and differential staining was detected for antibodies to laminin and collagen V. Quantification of staining intensity by confocal microscopy demonstrated a significant increase in both extracellular matrix components at postnatal day 4 compared with day 1 (p less than 0.05 for both). These basement membrane proteins may add sufficient structural integrity to germinal matrix vessels to prevent capillary rupture and thus intraventricular hemorrhage.
Stroke 1991 Mar
PMID:Beagle pup germinal matrix maturation studies. 200 9

Traumatic or stroke-like injuries of the cerebral cortex result in the rapid retrograde degeneration of thalamic relay neurons that project to the damaged area. Although this phenomenon has been well documented, neither the basis for the relay neuron's extreme sensitivity to axotomy nor the mechanisms involved in the degenerative process have been clearly identified. Physiological and biochemical studies of the thalamic response to cortical ablation indicate that pathological overexcitation might contribute to the degenerative process. The responses of thalamic projection neurons, protoplasmic astrocytes, and inhibitory thalamic reticular neurons in adult mice were examined from one to 120 days following ablation of the somatosensory cortex as part of an investigation of the role of excitotoxicity in thalamic retrograde degeneration. The responses of thalamic neurons to cortical ablation were compared with those produced by intracortical injection of the convulsant excitotoxin kainic acid, since the degeneration of neurons in connected brain structures distant to the site of kainic acid injection is also thought to occur via an excitotoxic mechanism. Within two days after either type of cortical injury, protoplasmic astrocytes in affected regions of the thalamic ventrobasal complex and the medial division of the posterior thalamic nuclei became reactive and expressed increased levels of immunohistochemically detectable glial fibrillary acidic protein. Within the affected regions of the ventrobasal complex an increased intensity of puncta positive for glutamate decarboxylase immunoreactivity, presumably due to an increase in its content within the terminals of the reciprocally interconnected thalamic reticular neurons, was also evident. These immunohistochemically detectable alterations in the milieu of the damaged thalamic neurons preceded the disappearance of the affected relay neurons by at least two days following cortical ablation and by seven to 10 days following intracortical kainic acid injection. Regions of the thalamus containing reactive astrocytes corresponded very closely to the regions undergoing retrograde degeneration. Protoplasmic astrocytes in these areas remained intensely reactive up to 60 days after cortical injury. Levels of glutamate decarboxylase were only transiently elevated in the degenerating regions of the ventrobasal complex following cortical ablation and returned to normal by 14 days. Increased glutamate decarboxylase immunoreactivity was transiently seen through the entire ventrobasal complex following intracortical kainic acid injection but was markedly more intense in degenerating regions. These patterns of labeling did not return to normal until 50 days after intracortical kainic acid injection, well after the death of the relay neurons. Cortical ablation and intracortical kainic acid injection produce similar alterations in thalamic neuronal and glial populations.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Thalamic retrograde degeneration following cortical injury: an excitotoxic process? 216 45

Brain injury, including ischemia, changes normal astrocytes into reactive species that hypertrophy and begin to proliferate. Understanding the mechanisms that underlie these changes could lead to new abilities to promote regeneration and retard neural degeneration after ischemia. Because ionic changes occur after nonneural cells are exposed to mitogens, we have begun to examine the ionic changes that may trigger reactive gliosis. We showed that two changes thought to be important for mitogenesis, elevation of interstitial potassium or intracellular pH, are correlated with reactive gliosis as indicated by increased immunohistochemical staining for glial fibrillary acidic protein. This relation was seen after activation of cerebral cortex by recurrent spreading depression but not by physiologic stimulation. Deoxyribonucleic acid synthesis occurs in fibroblasts only when intracellular potassium exceeds 90 mM, a level seen in astrocytes only during spreading depression. Thus, our results support the contention that a threshold level of potassium (and pH) must be exceeded in eukaryotic cells before proliferation or anabolism will proceed.
Stroke 1990 Nov
PMID:Ionic concomitants of astroglial transformation to reactive species. 223 80

The brain lesions in spontaneously hypertensive stroke-prone rats (SHRSP) are characterised by multifocal microvascular damage, breakdown of the blood-brain barrier, massive extravasation of plasma constituents and severe brain oedema, with consequent spongy and cystic tissue destruction in the cerebral cortex and basal ganglia as well as loosening of the white matter. In this paper we analyse in greater detail the pathogenetic mechanisms by which the spongy and cystic lesions are formed and the response of astrocytic cells. For this purpose, tracer (Evans blue)-stained brain lesions were examined in 8-month-old SHRSP immunohistochemically and electron microscopically. Sponginess of the neuropil in small lesions and at the periphery of larger lesions was due to swollen neuronal and astrocytic cell processes, i.e. at this stage the oedema was mainly intracellular. Cystic lesions were formed in the grey matter both by expansion of the extracellular space (ECS) containing protein-rich oedema fluid, and by rupture and subsequent loss of massively swollen cellular elements. In the white matter small slit-formed cysts along the fibre tracts were also formed by the expansion of ECS. In apparently recent lesions astrocytes displayed cyto-plasmic oedema but otherwise were still fairly normal. In more chronic lesions increased numbers of enlarged astrocytes with prominent staining for glial fibrillary acidic protein were present. Their distribution corresponded well to the spread of oedema, i.e. they were prominent around the leaky vessels in the grey matter, in the subpial zone and in the white matter. In the reparative phase the grey matter cysts became lined by astrocytic processes, a new glia limitans. Profuse sheets of glial processes in the neuropil around the cysts reestablished the compactness of the brain parenchyma.
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PMID:Cyst formation and glial response in the brain lesions of stroke-prone spontaneously hypertensive rats. 318 37

Immunochemical studies of gamma gamma-neuron specific enolase (NSE), parvalbumin (PV), S-100 protein (S-100) and acidic fibrillary glial protein (GFAP) were studied in the cerebrospinal fluid and blood serum in 7 patients with ischemic cerebral stroke, aged 57 to 81 years. Cerebrospinal fluid and the first blood sample were taken on the first or second day of the disease. Further blood samples were taken once a week till the end of patients hospitalization, ending by patients discharge or death. Immunochemical identification of proteins under study were performed with Western-blotting technique. It was found that all proteins studied were present in both cerebrospinal fluid and blood serum on the first two days of the disease in small quantities. The blood content of both NSE and PV increased significantly during the first week of the disease. Both proteins disappeared from the blood serum between the second and fourth disease weeks. S-100 protein and GFAP contents in the blood reached significantly high level within the time interval between second and fifth disease weeks, and remained at a relatively high level till patients' death. In all cases computed tomography study and/or brain autopsy revealed extensive ischemic foci localized within areas supplied by the middle cerebral artery. No clear-cut correlation between extensiveness of the ischemic cerebral damage and the content of the proteins studied in both cerebrospinal fluid and blood serum was found. However, our data indicate that serial studies of the above proteins in patients with ischemic stroke may be useful in monitoring the progress of the disease, and occasionally in the prognosis at least in some cases.
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PMID:Immunochemical analysis of some proteins in cerebrospinal fluid and serum of patients with ischemic strokes. 798 25

Accumulation of glial fibrillary acidic protein xk(G-FAP) in reactive astrocytes is a characteristic neuropathologic feature of ischemic brain injury. We examined injury-induced changes in GFAP mRNA and protein in a well-characterized model of focal hypoxic-ischemic injury in perinatal rodent brain. Postnatal Day (PND) 7 rats underwent right carotid artery ligation followed by 2.5 h exposure to 8% oxygen, which results in injury to ipsilateral cortex, hippocampus, and striatum in the majority of animals. Using Northern analysis, we assayed GFAP mRNA in samples from the lesioned and contralateral hemispheres of animals killed 1 h to 14 days later, and from animals treated with the neuroprotective glutamate antagonist MK-801. GFAP immunoreactivity in tissue homogenates from the lesioned and contralateral hemispheres was also compared with an immunoblot assay. One and 4 h posthypoxia GFAP mRNA expression was barely detectable. In the lesioned cortex, increased GFAP mRNA was detected at 24 h postinjury; over the next 2 weeks GFAP mRNA was consistently higher (at least 2-fold) in lesioned than in contralateral cortex. In contrast, in lesioned hippocampus and striatum, consistent increases in GFAP mRNA were first detected on PND 12. Immunoassays of GFAP demonstrated early (PND 8) and sustained (to PND 21) up to 10-fold increases in lesioned cortex, hippocampus, and striatum. In this perinatal stroke model regionally specific increases in GFAP mRNA expression and GFAP immunoreactivity are detected in the first 2 weeks after hypoxic-ischemic injury; intrinsic properties of glia and/or neurons in different brain regions may influence the timing and magnitude of stimulation of this response.
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PMID:Hypoxic-ischemic brain injury stimulates glial fibrillary acidic protein mRNA and protein expression in neonatal rats. 815 21

Cell cultures were derived from adult human brain biopsies [from cortical gray (cultures 9-HB-G and 33-HB-G) and white (culture 14-HB-W) and stroke-injured white matter (culture 33-HB-IW)]. The morphology and growth rate of cultured cells were examined and correlated with the presence of vimentin and glial fibrillary acidic protein (GFAP). The cultures from various brain matters differed in cell morphology and rate of growth but not in GFAP and vimentin staining. Cells of primary and rapidly proliferating cultures were GFAP-negative and vimentin-positive. Spontaneous growth deceleration occurred in culture 14-HB-W within passages 5 to 10 and in cultures 9-HB-G, 33-HB-G, and 33-HB-W within passages 17 to 20. This deceleration, as well as the successive complete growth arrest, were accompanied by an appearance of GFAP-positive cells and an elevated intensity for vimentin staining. We propose that GFAP-positive astrocytes originate from glial precursor cells that migrate from the explants and differentiate under prolonged subcultivation.
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PMID:Appearance of GFAP-positive cells in adult human brain cultures spontaneously decelerated in growth. 845 9

The potential cerebroprotective effects of recombinant human basic fibroblast growth factor (rhbFGF) were evaluated in a feline model of acute cerebral ischemia using high-speed magnetic resonance imaging (MRI) in conjunction with immunohistology. The neuroprotective efficacy of three doses of rhbFGF was evaluated in a unilateral middle cerebral artery (MCA) occlusion/reperfusion model. Ten h following a 2 h period of MCA occlusion in control (vehicle-treated) animals, cerebral perfusion in the ischemic hemisphere was 58 +/- 17% of the contralateral normal hemisphere. Corresponding ischemic/normal perfusion ratios in rhbFGF-treated groups were not significantly different: 54 +/- 16% (14 micrograms/kg/h dose), 40 +/- 19% (42 micrograms/kg/h dose) and 75 +/- 8% (125 micrograms/kg/h dose). Triphenyltetrazolium chloride histopathological assessment demonstrated brain damage in vehicle-treated animals comprising 31 +/- 15% of the hemisphere; in rhbFGF-treated groups injury was not significantly different: 19 +/- 4% (14 micrograms/kg/h rhbFGF), 24 +/- 6% (42 micrograms/kg/h rhbFGF) and 16 +/- 10% (125 micrograms/kg/h rhbFGF). Immunohistochemical analysis of brain sections using glial fibrillary acidic protein (GFAP) revealed that in animals that showed marked perfusion deficits throughout the entire experiment (regardless of treatment), GFAP staining was elevated contralateral to the occlusion and absent ipsilaterally. While some tendency towards protection is found, particularly at higher doses of rhbFGF, it must be concluded that in the chosen stroke model and time interval, the doses used did not significantly improve reperfusion or confer significant cerebroprotective benefit. Non-invasive high-speed MRI was found to be useful for evaluation of putative cerebroprotective agents.
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PMID:Evaluation of recombinant human basic fibroblast growth factor (rhbFGF) as a cerebroprotective agent using high speed MR imaging. 861 13


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