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

Male and female, arteriosclerotic (breeder) and nonarteriosclerotic (virgin), Sprague-Dawley rats were made severely diabetic with alloxan. Two weeks later experimental animals had both carotid arteries ligated to induce a state of acute cerebral ischemia. After six weeks of cerebral ischemia either with or without severe diabetes the animals were killed. Animals which survived either the acute induction of diabetes or cerebral ischemia did not manifest any new episodes of cerebral ischemia. Subjects with combined diabetes and cerebral ischemia manifested the greatest loss in body weight, adrenal hypertrophy and thymus gland involution, increased levels of serum CPK and SGOT, but decreased SGPT and LDH, hyperglycemia and hypertriglyceridemia, and the most extensive cerebral edema. It is suggested that diabetic rats may have a greater predilection toward cerebrovascular accidents because the diabetic state contributes not only to an exacerbation of atherosclerosis, but also complicates any condition of cerebrovascular ischemia by creating extracerebral edema.
Stroke
PMID:Chronic diabetes followed by chronic cerebral ischemia induced by bilateral carotid artery ligation in arteriosclerotic versus nonarteriosclerotic rats. 117 43

We report an autopsy case of infant death due to heat stroke. On a winter day, a 52-day-old female baby was placed under a Japanese electric foot warmer with a coverlet (kotatsu) on an electric carpet warmer in a heated room at home. After about 5 h, the mother noticed that the baby was unconscious and took her to a hospital. Spontaneous respiration, however, was already absent, and the pupils were dilated. The trunk was hot; body temperature was 41.3 degrees C. The skin of the whole body was dry. Autopsy revealed second-degree burn injuries on the left side of the face and the dorsum of the left hand. Numerous marked petechiae and ecchymoses were found in the thymus (capsule and parenchyma), pleurae (visceral and parietal), pericardial cavity (internal and external surfaces), epicardium, and beneath the serosa at the origin of the aorta. In addition, there was congestion in various organs, edema in the brain and lungs, and hemorrhage in the lungs. Histopathologically, macrophages without hemosiderin granules were present in the alveoli. When the heating conditions at the accident were reproduced experimentally, the temperature in the electric kotatsu warmer rose to 50-60 degrees C. Thus, we concluded that misuse of the electric kotatsu caused heat stroke in this infant.
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PMID:An autopsy case of infant death due to heat stroke. 147 26

Poly(ADP-ribose) synthetase has been purified 2,000-fold to apparent homogeneity from human placenta. The purification procedure involves affinity chromatography with 3-aminobenzamide as the ligand. The purified enzyme absolutely requires DNA for the catalytic activity and catalyzes poly(ADP-ribosyl)ation of the synthetase itself (automodification) and histone H1. Mg2+ enhances both the automodification and poly(ADP-ribosyl)ation of histone H1. The enzyme is a monomeric protein with a pI of 10.0 and an apparent molecular weight of 116,000. The sedimentation coefficient and Strokes radius are 4.6 S and 5.9 nm, respectively. The frictional ratio is 1.82. Amino acid analysis and limited proteolysis with papain and alpha-chymotrypsin indicate that the human placental enzyme is very similar to the enzyme from calf thymus, although some differences are noted. Mouse antibody raised against the placental enzyme completely inhibits the activity of enzymes from human placenta and HeLa cells and cross-reacts with the enzymes from calf thymus and mouse testis. Immunoperoxidase staining with this antibody demonstrates the intranuclear localization of the enzyme in human leukemia cells. All these results indicate that molecular properties as well as antigenic determinants of poly(ADP-ribose) synthetase are highly conserved in various animal cells.
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PMID:Purification and characterization of poly (ADP-ribose) synthetase from human placenta. 243 82

1. Prostacyclin elicits potent vasodilation and inhibition of platelet aggregation through binding to its membrane receptor. The impairment of prostacyclin receptor activity is implicated in various human cardiovascular diseases. We recently succeeded in molecular cloning of cDNA for the mouse, rat, and human prostacyclin receptors. 2. In the present study, we examined the mRNA expression of the prostacyclin receptor in various rat tissues, and further investigated its gene expression in the hypertrophied cardiac ventricles of stroke-prone spontaneously hypertensive rats (SHRSP). 3. In rat tissues, a single RNA band of approximately 3.7 kb was detected by northern blotting analysis using rat prostacyclin receptor cDNA as a probe. In adult Wistar rats, abundant mRNA expression was observed in the aorta, lung and spleen. Substantial amounts of transcript were expressed in the heart, pancreas, thymus and stomach. In contrast, no mRNA expression was detected in the brain. 4. We further examined the mRNA expression of the prostacyclin receptor in the ventricles of 21 week old SHRSP. The ventricles of SHRSP showed remarkable hypertrophy, compared with those of age-matched Wistar-Kyoto (WKY) rats. The expression of prostacyclin receptor mRNA in the hypertrophied ventricles of SHRSP was almost equivalent to that in the ventricles of WKY. 5. The present study revealed the gene expression of the prostacyclin receptor in various rat tissues, and further demonstrated the receptor mRNA expression in hypertensive cardiac hypertrophy. The present study will give a clue to investigate the clinical implication of prostacyclin and its receptor.
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PMID:Gene expression of prostacyclin receptor in the hypertrophied heart of spontaneously hypertensive rats. 907 86

Data on the development of three experimental models of hemorrhagic stroke in mice are reported. The models differ in the extent of damage. From the standpoint of the immunopharmacological investigation, most adequate model is provided by the light acute brain circulation disorder (LABCD). In the LABCD model, the hemorrhagic stroke is characterized by reduction in the thymus weight, inhibition of the antibody (hemolysin) synthesis, and enhancement of the delayed type hypersensitivity response. The new antistroke drug cerebral decreased (especially after intranasal administration) the level of lethality in experimental animals and improved the immunological indices.
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PMID:[Effect of Cerebral on the immune system in experimental hemorrhagic stroke]. 1210 85

An anterior mediastinal cystic lesion in an 11-year-old mongrel dog was examined. The dog showed dysbasia and vomiting due to megaoesophagus, and anterior mediastinal round mass lesion, approximately 35 mm in diameter, was found by X ray. Based on clinical examinations, the dog was diagnosed as acquired myasthenia gravis and was successfully controlled by anticholinesterase treatment for approximately 4 months. The dog died of thermic stroke and was necropsied. Grossly, fatty tissues with cysts containing yellowish fluid and white nodules were found in the anterior mediastinal area. Histopathologically, multiple cysts, neoplastic tissues, and atrophic thymus were found within the examined tissues. The cysts were lined by thin wall consisting of ciliated long cuboidal and non-ciliated round cells and were filled with eosinophilic colloidal fluid. Some extended cysts contained neoplastic foci within their lumen and walls. The neoplastic tissues consisted of mixed population of large epithelial cells with abundant clear cytoplasm and large oval nuclei, and lymphocytes. Immunohistochemically, proliferating epithelial cells were intensely positive for keratin and cytokeratin, and more than half number of infiltrating lymphocytes were intensely positive for CD3 suggesting T cells. All these findings indicate the neoplastic lesion is thymoma and multiple cysts are considered as thymic or brachial cleft cysts.
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PMID:Thymoma and multiple thymic cysts in a dog with acquired myasthenia gravis. 1218 22

Age-related changes in hematological values, serum biochemical constituents, and weights of various organs in both sexes of the Spontaneously Hypertensive (SHR/Izm), Stroke-prone SHR (SHRSP/Izm), and Wistar Kyoto (WKY/Izm) rat strains, bred under SPF conditions, were examined to obtain fundamental data. The body weights from 3-30 weeks and systolic blood pressure from 6-30 weeks in each strain were measured every week. At the ages of 8, 16, and 30 weeks, the hematological values (erythrocyte, hemoglobin, hematocrit, leucocyte, thrombocyte), serum biochemical constituents (total protein, GOT, GPT, ALP, BUN, creatinine, glucose, total Ca and phosphorus, and ionized Ca, Na, K, and Cl were measured. Also, the organs, brain, heart, lung, thymus, liver, spleen, pancreas, bilateral kidneys, adrenal glands, testes/ovaries, digestive tract, and muscle (soleus) were weighed. The age-related changes as well as the strain and sex differences in each measured item were examined. The body weights of each strain increased, but rate of the increase was less in SHR and SHRSP, and was lowest in SHRSP. The blood pressure of SHR and SHRSP elevated with age, and showed higher in SHRSP than SHR, while that of WKY did not change. There were many strain differences in most measured items at each time point, particularly at 30 weeks. In SHRSP, high values of BUN, creatinine, total and ionized Ca, weights of brain, heart, liver, kidney and digestive duct were observed at most time points indicating that this strain's abnormality of calcium metabolism may be related to functions of the kidney and digestive duct as well as hypertension.
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PMID:Age-related changes in blood pressure, hematological values, concentrations of serum biochemical constituents and weights of organs in the SHR/Izm, SHRSP/Izm and WKY/Izm. 1499 46

The past few decades have revealed that cell death can be precisely programmed with two principal forms, apoptosis and necrosis. Besides pathophysiological alterations, physiologic processes, such as the pruning of neurons during normal development and the involution of the thymus, involve apoptosis. This review focuses on the role of inter- and intracellular signaling systems in cell death, especially in the nervous system. Among neurotransmitters, glutamate and nitric oxide have been most extensively characterized and contribute to cell death in excitotoxic damage, especially in stroke and possibly in neurodegenerative diseases. Within cells, calcium, the most prominent of all intracellular messengers, mediates diverse forms of cell death with actions modulated by many proteins, including IP3 receptors, calcineurin, calpain, and cytochrome c.
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PMID:Cell signaling and neuronal death. 1687 82

Infarction size and infections are important determinants of stroke outcome in humans. Bacterial infections are promoted by stroke-induced immunodeficiency which in experimental stroke is mainly characterized by extensive lymphocyte apoptosis and dysfunction. Pharmacological inhibition of caspases may improve stroke outcome not only by reducing apoptotic brain damage but also by attenuating stroke-induced immunodeficiency. We investigated the effects of systemic administration of the novel, non-toxic caspase-inhibitor quinolyl-valyl-O-methylaspartyl-[-2,6-difluorophenoxy]-methyl ketone (Q-VD-OPH) on stroke-induced neuronal and lymphocyte apoptosis, susceptibility to infections, and mortality in a murine model of stroke induced by middle cerebral artery occlusion (MCAO). Q-VD-OPH reduced ischemic brain damage and stroke-induced programmed cell death in thymus and spleen, decreased susceptibility to post-stroke bacteremia, and improved survival. Therefore, Q-VD-OPH may be a promising therapeutic agent in stroke.
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PMID:Protection from brain damage and bacterial infection in murine stroke by the novel caspase-inhibitor Q-VD-OPH. 1758 6

Antioxidants specifically addressed to mitochondria have been studied for their ability to decelerate aging of organisms. For this purpose, a project has been established with participation of several research groups from Belozersky Institute of Physico-Chemical Biology and some other Russian research institutes as well as two groups from the USA and Sweden, with support by the "Mitotechnology" company founded by "RAInKo" company (O. V. Deripaska and Moscow State University). This paper summarizes the first results of the project and estimates its prospects. Within the framework of the project, antioxidants of a new type (SkQ) were synthesized comprising plastoquinone (an antioxidant moiety), a penetrating cation, and decane or pentane linker. Using planar bilayer phospholipid membranes, we selected SkQ derivatives with the highest penetrating ability, namely plastoquinonyl-decyl-triphenylphosphonium (SkQ1), plastoquinonyl-decyl-rhodamine 19 (SkQR1), and methylplastoquinonyl-decyl-triphenylphosphonium (SkQ3). Anti- and prooxidant properties of these substances and also of ubiquinone and ubiquinonyl-decyl-triphenylphosphonium (MitoQ) were tested on isolated mitochondria. Micromolar concentrations of cationic quinones are found to be very strong prooxidants, but in lower (sub-micromolar) concentrations they display antioxidant activity. The antioxidant activity decreases in the series SkQ1=SkQR1>SkQ3>MitoQ, so the window between the anti- and prooxidant effects is smallest for MitoQ. SkQ1 is rapidly reduced by complexes I and II of the mitochondrial respiratory chain, i.e. it is a rechargeable antioxidant. Extremely low concentrations of SkQ1 and SkQR1 completely arrest the H2O2-induced apoptosis in human fibroblasts and HeLa cells (for SkQ1 C1/2=1.10(-9) M). Higher concentrations of SkQ are required to block necrosis initiated by reactive oxygen species (ROS). In mice, SkQ1 decelerates the development of three types of accelerated aging (progeria) and also of normal aging, and this effect is especially demonstrative at early stages of aging. The same pattern is shown in invertebrates (drosophila and daphnia). In mammals, the effect of SkQs on aging is accompanied by inhibition of development of such age-related diseases as osteoporosis, involution of thymus, cataract, retinopathy, etc. SkQ1 manifests a strong therapeutic action on some already developed retinopathies, in particular, congenital retinal dysplasia. With drops containing 250 nM SkQ1, vision is recovered in 50 of 66 animals who became blind because of retinopathy. SkQ1-containing drops instilled in the early stage of the disease prevent the loss of sight in rabbits with experimental uveitis and restore vision to animals that had already become blind. A favorable effect is also achieved in experimental glaucoma in rabbits. Moreover, the pretreatment of rats with 0.2 nmol SkQ1 per kg body weight significantly decreases the H2O2-induced arrhythmia of the isolated heart. SkQ1 strongly reduces the damaged area in myocardial infarction or stroke and prevents the death of animals from kidney infarction. In p53-/- mice, SkQ1 decreases the ROS level in the spleen cells and inhibits appearance of lymphomas which are the main cause of death of such animals. Thus, it seems reasonable to perform clinical testing of SkQ preparations as promising drugs for treatment of age-related and some other severe diseases of human and animals.
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PMID:A biochemical approach to the problem of aging: "megaproject" on membrane-penetrating ions. The first results and prospects. 1820 23


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