Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty-two patients with ischemic stroke were studied over time (1st-12th day) for the activity of enzymes and isoenzymes of energy metabolism (CPK, LDH, SDH). It has been shown that the brain-specific CPK BB-isoenzyme may serve as a marker of the severity and extension of brain damage while the aerobic LDH fractions may be useful in evaluation of the reversibility of hypoxic changes in the brain. The authors consider the employment of the studied enzymes for the prognosis of vascular and tissue damage.
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PMID:[Diagnostic and prognostic role of organ-specific plasma enzymes in the acute period of cerebral circulatory disorders]. 382 84

Five cases of subdural hematoma from arterial rupture (SDH-AR) are described and other 39 reported cases are reviewed. The average age of the patient is 59 and male to female ratio is 2:1. Fifty two percent of the patients have history of recent head injuries most of which are trivial. A very few patient have initial loss of consciousness. Approximately half of the patients with history of head trauma have long lucid interval (average of 7 days). Those patients without history of head trauma have spontaneous onset of the symptoms and some of the have acute onset of headache and loss of consciousness, simulating cerebrovascular accident. Natural history of the SDH-AR is progressing deterioration of the symptoms, resulting in coma and death. Skull fracture is seldom demonstrated in the patients with SDH-AR. Angiography shows and extracerebral avascular mass over the cerebral convexity with marked midline shift. In 3 cases including our 2 cases, extravasation of the contrast medium from the cortical artery is observed and this is a useful finding for making diagnosis of this disease. Computerized tomography reveals high density extracerebral mass with remarkable mass effect. Craniotomy discloses subdural clot and spurting arterial rupture from a branch of the cortical artery around the Sylvian fissure. In some cases, subarachnoid hemorrhage is observed but in none of the cases, cerebral contusion or laceration is present. It is presumed that the mechanism of the arterial rupture is gliding movement of the brain within the skull upon injury, tearing an arterial twig with dural attachment. Hypertension, arteriosclerosis and brain atrophy may be important contributing factors to this mechanism. Pseudoaneurysm of the cortical artery caused by closed head injury is also associated with this mechanism and may explain delayed sudden onset of the symptoms in some patients with SDH-AR.
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PMID:[Subdural hematoma from arterial rupture -mechanism of arterial rupture in minor head injury]. 713 4

Several members of a three-generation kindred from Sardinia were affected by a maternally inherited syndrome characterized by features of both myoclonus epilepsy with ragged-red fibers (MERRF) and mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS). Clinically, symptoms such as myoclonus epilepsy, neural deafness and ataxia were variably associated with stroke-like episodes and/or migrainous attacks. Morphologically, numerous MELAS-associated SDH-stained vessels were observed in muscle biopsies, either alone or in combination with ragged-red fibers, the morphological hallmark of MERRF. Sequence analysis of the mtDNA tRNA genes revealed the presence of a single, heteroplasmic T-->C transition at nt 8356, in the region of the tRNA(Lys) gene corresponding to the T-psi-C stem. The T-->C(8356) transition was exclusively found in the maternal lineage of our family, and the relative amount of the mutant mtDNA species in muscle was correlated with the severity of the clinical presentation. Therefore, we propose that the T-->C(8356) transition is responsible for the mitochondrial encephalomyopathy found in our family, and must be added to the expanding list of the pathogenetically relevant mutations of human mtDNA.
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PMID:A MERRF/MELAS overlap syndrome associated with a new point mutation in the mitochondrial DNA tRNA(Lys) gene. 806 54

We report three members of a family, who exhibited a phenotype similar to 'myoclonus epilepsy with ragged-red fibers' but had a genotype usually associated with 'mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes'. The patients, a 48-year-old female, and her two sons, aged 21 and 19 respectively, presented with photo-reactive syncopal episodes, disturbances of gait and writing, dysarthria and finger tremor since the 3rd and 2nd decade of life, respectively, that were accompanied also by numbness and weakness of the extremities. Subsequently, cerebellar ataxia and myoclonus were also noted. Electromyography revealed both myogenic and neurogenic muscular changes, and nerve conduction studies demonstrated a sensory-motor neuropathy. Biopsy showed ragged-red fibers with strongly stained SDH-positive vessels in skeletal muscles, and a marked loss of myelinated fibers of the sural nerves. Mitochondrial (mt) DNA analyses of peripheral blood, muscles and nerves revealed that all members had a heteroplasmic np3271 (T-C) point mutation in the mitochondrial tRNA-Leu gene (UUR). This family is unique, in that all patients presented with a myoclonus epilepsy with ragged-red fibers-like phenotype and had a distinctive peripheral neuropathy, while the detected mtDNA 327l (T-C) mutation has been reported to date only in rare cases of mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes
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PMID:A mitochondrial encephalo-myo-neuropathy with a nucleotide position 3271 (T-C) point mutation in the mitochondrial DNA. 1140 19

Only one case of acute spontaneous subdural haematoma (ASSDH) has been reported following transsphenoidal surgery, whereas, another case of chronic SDH has been reported. We present a patient with pituitary apoplexy, who was treated by transsphenoidal surgery. 8 days postoperative he developed an ASSDH requiring immediate surgical evacuation. This case documents the third occurrence of SDH as a complication of transsphenoidal surgery and is the first report of ASSDH that required immediate surgical evacuation.
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PMID:Acute spontaneous subdural haematoma after transsphenoidal surgery. 1634 29

Oxidative stress is implicated as a major cause of aging and age-related diseases, such as Parkinson's and Alzheimer's, as well as ischemia-reperfusion injury in stroke. The mitochondrial electron transport chain is the principal source of reactive oxygen species within cells. Despite considerable medical interest, the molecular mechanisms that regulate reactive oxygen species formation within the mitochondrion remain poorly understood. Here, we report the isolation and characterization of a Drosophila mutant with a defect in subunit b of succinate dehydrogenase (SDH; mitochondrial complex II). The sdhB mutant is hypersensitive to oxygen and displays hallmarks of a progeroid syndrome, including early-onset mortality and age-related behavioral decay. Pathological analysis of the flight muscle, which is amongst the most highly energetic tissues in the animal kingdom, reveals structural abnormalities in the mitochondria. Biochemical analysis shows that, in the mutant, there is a complex II-specific respiratory defect and impaired complex II-mediated electron transport, although the other respiratory complexes remain functionally intact. The complex II defect is associated with an increased level of mitochondrial hydrogen peroxide production, suggesting a possible mechanism for the observed sensitivity to elevated oxygen concentration and the decreased lifespan of the mutant fly.
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PMID:Hypersensitivity to oxygen and shortened lifespan in a Drosophila mitochondrial complex II mutant. 1705 19

Mitochondrial encephalomyopathy, lactacidosis and stroke-like episode (MELAS) syndrome is a phenotypically and genetically heterogeneous mitochondrial disorder with a clinical onset between the first and third decade. The clinical hallmark is the stroke-like-episode, which mimicks ischemic stroke but is usually transient and non-disabling in nature. The morphological equivalent on MRI is a T2-hyperintensity, predominantly over the temporo-parieto-occipital region, not confined to a vascular territory, which is also hyperintense on diffusion weighted imaging and on apparent diffusion coefficient sequences (vasogenic edema, stroke-like lesion). Additional features include seizures, cognitive decline, psychosis, lactic acidosis, migraine, visual impairment, hearing loss, short stature, diabetes, or myopathy. Muscle biopsy typically shows ragged-red fibers, COX-negative fibers, SDH hyperreactivity, and abnormally shaped mitochondria with paracristalline inclusions. The diagnosis is confirmed by demonstration of a biochemical respiratory chain defect or one of the disease-causing mutations, of which 80 % affect the mitochondrial tRNALeu gene.
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PMID:[MELAS syndrome as a differential diagnosis of ischemic stroke]. 1901 24

The m.3302A>G mutation in the mitochondrial tRNA(Leu(UUR)) gene has been identified in only 12 patients from 6 families, all manifesting adult-onset slowly progressive myopathy with minor central nervous system involvement. An 11-year-old boy presented with progressive proximal-dominant muscle weakness from age 7years. At age 10, he developed recurrent stroke-like episodes. Mitochondrial myopathy, encephalopathy, lactic acidosis, plus stroke-like episodes (MELAS) was diagnosed by clinical symptoms and muscle biopsy findings. Mitochondrial gene analysis revealed a heteroplasmic m.3302A>G mutation. Histological examination showed strongly SDH reactive blood vessels (SSVs), not present in previous cases with myopathies due to the m.3302A>G mutation. These findings broaden the phenotypic spectrum of this mutation.
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PMID:MELAS phenotype associated with m.3302A>G mutation in mitochondrial tRNA(Leu(UUR)) gene. 2358 2

We here report a 39-year-old woman of short stature with sensorineural deafness, who suddenly developed status epilepticus. T2-weighed image of brain magnetic resonance imaging (MRI) revealed a high signal lesion in the left temporal area, the distribution of which was not compatible with any particular arterial supply. Lactate and pyruvate were elevated in the serum and cerebrospinal fluid. As the mitochondrial gene analysis revealed the m.3243A>G mutation, diagnosis of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episode (MELAS) was made. In the histochemical study of a biopsied muscle, the intramuscular blood vessels reacted strongly with SDH (SSV), but the SSV was negative for cytochrome c oxidase (COX), the findings characteristic of myoclonic epilepsy with ragged-red fibers (MERRF). This is the first case of MELAS in which the muscle histochemistry showed positive SSV unassociated with increased COX.
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PMID:[A case of MELAS associated with histochemical findings of muscles characteristic of MERRF]. 2696 Feb 69

Increased number of population with heart stroke/attack is attributed to sedentary lifestyle and consumption of high-sugar diets, especially fructose. The objective of this study is to investigate the cardio-protective activity of aqueous extract of Phyllanthus amarus (PAAE) against high-fructose (HF) diet induced cardiac damage in Wistar rats. Male Wistar rats were randomly assigned into five groups of six animals each: Control (C), Control treated with PAAE (C+PAAE), High fructose diet fed (F), High fructose diet fed treated with PAAE (F+PAAE) and High fructose diet fed treated with Pioglitazone (F+Pio). PAAE was orally administered at a dosage of 200mg/kg body weight/day to C+PAAE and F+PAAE group rats for 60days. Pioglitazone (10mg/kg body weight/day) was used to compare the efficacy of PAAE. After 60days, heart and aorta samples were collected for biochemical and histological analysis. Co-administration of PAAE along with HF-diet for 60days prevented the increase in levels of cardiac and aortic lipids i.e., total lipids, triglycerides, total cholesterol and free fatty acids and decreased phospholipids. Further, enhanced activities of cardiac aldose reductase (15.3%) and sorbital dehydrogenase (6.9%) and decreased activity of creatine kinase (35.6%) in group-F were also prevented by PAAE treatment with the recovery of 126% for AR, 122% for SDH and 118% for CK. PAAE treatment showed protection from HF-diet induced increase in stress markers (LPO and PO), decreased non-enzymatic (GSH and Vit-C) and enzymatic (GR, GPx, GST, SOD, and CAT) antioxidants in the heart and aorta. Histopathological examination of the heart and aorta indicated that PAAE/Pio treatment reduced fat deposition and necrosis. The present study clearly indicates the cardio protection efficacy of PAAE against HF-diet induced oxidative stress in rats.
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PMID:Cardioprotective effect of Phyllanthus amarus against high fructose diet induced myocardial and aortic stress in rat model. 2894 83


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