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

The effect of steady-state increases in systemic arterial pressure on the duration of left ventricular ejection time was studied in 11 normal male subjects. Methoxamine, a pressor amine of predominantly vasoconstrictor activity but lacking significant inotropic effect, was administered intravenously resulting in an average increase in mean arterial pressure of 27 mm Hg. Heart rate was held constant by high right atrial pacing, and there was no significant change in cardiac output. During methoxamine infusion, when stroke volume, heart rate, and inotropic state were held constant, left ventricular ejection time increased as mean arterial pressure increased. There was a highly significant correlation between the increase in mean systolic blood pressure and the prolongation of left ventricular ejection time (r = 0.870). In one subject, an increase in mean systolic pressure of 75 mm Hg prolonged left ventricular ejection time 55 msec, producing paradoxical splitting of the second heart sound. The prolongation of left ventricular ejection time during infusion was not blocked by the prior intravenous administration of atropine sulfate or propranolol hydrochloride, thus ruling out both vagal inhibition of the left ventricle and reflex withdrawal of sympathetic tone as its cause. In three subjects, left ventricular end diastolic pressure was measured and found to be significantly increased. This finding suggests that the normal left ventricle maintains a constant stroke volume in the presence of an increased pressure load by the Frank Starling mechanism. This study concludes that arterial pressure must be included as a prime determinant of left ventricular ejection time along with stroke volume, heart rate, and inotropic state in intact man.
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PMID:The effect of steady-state increases in systemic arterial pressure on the duration of left ventricular ejection time. 1669 43

Aged individuals exhibit reduced functional recovery after stroke. We examined the expression profile in aged animals of a recently identified group of growth-associated genes that underlies post-stroke axonal sprouting in the young adult. Basal levels of most growth-promoting genes are higher in aged cortex compared with young adult, and are further induced after stroke. Compared with the young adult, these genes are induced at later time points after stroke. For growth-inhibitory molecules, myelin-associated glycoprotein and ephrin A5 are uniquely induced in the aged brain; chondroitin sulfate proteoglycans and oligodendrocyte myelin glycoprotein are induced at earlier time points; and Nogo-A, semaphorin IIIa and NG2 decline in aged vs. young adult after stroke. The aged brain does not simply have a reduction in growth-associated molecules after stroke, but a completely unique molecular profile of post-stroke axonal sprouting.
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PMID:Growth-associated gene and protein expression in the region of axonal sprouting in the aged brain after stroke. 1678 55

Kynurenine 3-monooxygenase (KMO) is an NADPH-dependent flavoprotein hydroxylase that catalyzes the conversion of l-Kynurenine (L-Kyn) to 3-hydroxykynurenine (3OHKyn). The reaction is central to the tryptophan degradative pathway and takes place within microglial cells defining cellular concentrations of the N-methyl-d-aspatate (NMDA) receptor agonist quinolinate and antagonist kynurenate. The influence over the cellular concentrations of these NMDA receptor effectors makes KMO an attractive target for the treatment of ischemic stroke. Pseudomonas fluorescens str 17400, expresses five activities of tryptophan catabolism including that of KMO. The KMO gene from P. fluorescens was cloned into the pET-17b plasmid using incorporated NdeI and XhoI restriction sites. This construct yielded PfKMO to 20% of total cell protein after 12h of expression at 22 degrees C without induction by isopropyl-beta-thiogalactopyranoside (IPTG). The enzyme could be readily purified using ammonium sulfate fractionation and ion exchange chromatography, resulting in pure KMO with a turnover number of 5.0 s(-1). PfKMO activity was dependent on the reduction state of the enzyme. Preparation and storage benefited from the presence of a reductant such as dithiothreitol or beta-mercaptoethanol. The loss of activity was found to be directly related to the oxidation of thiols as measured by dinitrothiobenzoate assay. Steady-state assays monitoring the consumption of dioxygen were used to measure apparent kinetic parameters and ligand perturbation of flavin fluorescence was used to determine a Kd value for both L-Kyn and the inhibitor m-nitrobenzoylalanine. PfKMO is offered as prototypical bacterial form of the enzyme to serve as a viable platform on which to base future KMO studies.
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PMID:Heterologous expression and purification of kynurenine-3-monooxygenase from Pseudomonas fluorescens strain 17400. 1697 76

When a patient with migraine has a stroke, all other causes of stroke should be ruled out before the stroke is attributed to migraine. Migraine mimics that present with headaches and stroke, including arteriovenous malformation and cervical carotid artery dissection, should be considered. Patent foramen ovale is a risk factor for both migraine and stroke and should be ruled out with transesophageal echocardiography. A patient with migraine with aura with persistent focal neurologic deficits in the distribution of the typical aura can be diagnosed with migrainous stroke. Patients with migraine with aura with persistent focal neurologic deficits can be treated pharmacologically with intravenous verapamil or magnesium sulfate to relieve the symptoms in familial hemiplegic migraine and sporadic hemiplegic migraine. Prophylactic treatment should be administered to patients with frequent attacks of migraine with aura to prevent recurrence. Oral verapamil is recommended for patients with familial hemiplegic migraine and may be effective in patients with sporadic hemiplegic migraine. Endovascular closure of patent foramen ovale has been reported to prevent recurrence of migraine with aura. The role of patent foramen ovale closure remains controversial pending completion of controlled randomized trials.
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PMID:Interactions between migraine and stroke. 1703 72

Acute leukemia is a rare malignancy of pregnancy. When it develops, there are many complications to consider and management becomes exceedingly difficult. We report a case of acute myelogenous leukemia presenting as preeclampsia and fetal demise at 36 weeks of gestation. A 30-year-old multigravida presented with intrauterine fetal demise at 36 weeks' gestation, hypertension, and thrombocytopenia. The patient received platelet and packed red blood cell transfusion, with concurrent prophylactic magnesium sulfate and dexamethasone treatment. Following labor induction, the patient delivered a nonviable female fetus and suffered a stroke postpartum. Peripheral smear and flow cytometry revealed the patient had acute myeloid leukemia with prominent monocytic differentiation. The patient expired on postpartum day six. Acute leukemia during the pregnancy is associated with an unfavorable outcome.
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PMID:Acute myelogenous leukemia mimicking a hemolysis, elevated liver enzymes, and low platelets syndrome during pregnancy: case report and review of the literature. 1709 46

The ECM (extracellular matrix) is a complex molecular framework that provides physical support to cells and tissues, while also providing signals for cell growth, migration, differentiation and survival. The ECM of the CNS (central nervous system) is unusual in that it is rich in CSPGs (chondroitin sulfate proteoglycans), hyaluronan and tenascins. The CSPGs are widely expressed throughout the developing and adult CNS and have a role in guiding or limiting neurite outgrowth and cell migration. Alterations in the synthesis or breakdown of the ECM may contribute to disease processes. Here, we examine changes in the brain-specific CSPGs, brevican and phosphacan, following transient middle cerebral artery occlusion, a model of stroke in the rat. We have investigated their expression at various time points as well as their spatial relationship with ADAMTS-4 (a disintegrin and metalloprotease with thrombospondin motifs 4). The co-localization of ADAMTS or its activity may indicate a functional role for this matrix-protease pair in degeneration/regeneration processes that occur in stroke.
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PMID:Brevican and phosphacan expression and localization following transient middle cerebral artery occlusion in the rat. 1763 24

Taste is always accompanied by tactile stimulation, but little is known about how touch interacts with taste. One exception is evidence that taste can be "referred" to nearby tactile stimulation. It was recently found (Lim J, and Green BG. 2007. The psychophysical relationship between bitter taste and burning sensation: evidence of qualitative similarity. Chem Senses. 32:31-39) that spatial discrimination of taste was poorer for bitterness than for other tastes when the perceived intensities were matched. We hypothesized that this difference may have been caused by greater referral of bitterness by touch. The present study tested this hypothesis by comparing localization of quinine sulfate and sucrose under conditions that minimized and maximized the opportunity for referral. In both conditions, stimulation was produced by 5 cotton swabs spaced 1 cm apart and arranged in an arc to enable simultaneous contact with the front edge of the tongue. Only one swab contained the taste stimulus, whereas the rest were saturated with deionized water. In both conditions, the swabs were stroked up-and-down against the tongue 5 times. Subjects were asked to identify which swab contained the taste stimulus 1) 5 s after the fifth stroke (touch-removed condition) and 2) immediately at the end of the fifth stroke, with the swabs still in contact with the tongue (touch-maintained condition). Ratings of taste intensity were obtained to assess the possible effect of perceived intensity on spatial localization. Taste localization was surprisingly accurate, especially for sucrose, with errors of localization in the range of 1 cm or less. For both stimuli, localization tended to be poorer when the tactile stimulus was present while subjects made their judgments, but the difference between conditions was significant only for the lower concentration of quinine. The results are discussed in terms of both the surprisingly good spatial acuity of taste and the possibility of having a close perceptual relationship between touch and bitter taste.
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PMID:Tactile interaction with taste localization: influence of gustatory quality and intensity. 1796 29

To understand the fates of human mesenchymal stem cells (hMSCs) following transplantation into a rodent model of middle cerebral artery occlusion (MCAo), magnetic resonance imaging (MRI) techniques were employed, hMSCs were labeled with ferumoxides (Feridex)--protamine sulfate complexes, which were visualized and examined by MRI up to 10 weeks following transplantation. Migration of the transplanted cells to the infarcted area was further confirmed by histological methods. We found that the hMSCs transplanted in MCAo models possess the capacity to migrate to the infarcted area extensively in both ipsilateral and contralateral injections, exhibiting a pathotropism. We also analyzed the detailed migration patterns of transplanted hMSCs. We speculate that the extensive migratory ability of hMSCs may represent a therapeutic potential for developing efficient cell transplantation strategies in stroke.
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PMID:In vivo tracking of human mesenchymal stem cells in experimental stroke. 1835 Oct 16

Ischemic brain injury causes tissue damage and neuronal death. The deficits can often be permanent because adult neurons fail to regenerate. One barrier to neuronal regeneration is the formation of the glial scar, a repair mechanism that is otherwise necessary to seal off necrotic areas. The process of gliosis has been well described, but the mechanisms regulating the robust production of scar components after injury remain poorly understood. Here we show that the early growth response 1 transcriptional factor (Egr-1, also called Krox24, Zif268, and NGFI-A) is expressed in astrocytes in the ventricular wall, corpus callosum, and striatum of normal mouse brain. After experimental stroke caused by permanent occlusion of the middle cerebral artery, Egr-1 was expressed long term in reactive astrocytes that accumulate around the injury site. Gain- and loss-of-function studies in primary astrocytes indicated that Egr-1 regulates the transcription of chondroitin sulfate proteoglycans genes, the main extracellular matrix proteins of the glial scar. Egr-1 bound to a site within the phosphacan promoter and transactivated its expression. Egr-1-deficient mice accumulated lower levels of phosphacan RNA and protein than wild-type mice after stroke, but there were no measurable differences in neurite outgrowth toward the infarct area between the two groups. Our findings suggest that Egr-1 is an important component of the transcriptional network regulating genes involved in gliosis after ischemic injury.
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PMID:Egr-1 regulates expression of the glial scar component phosphacan in astrocytes after experimental stroke. 1855 77

Ischemia-reperfusion (I/R) injuries are implicated in a large array of pathological conditions such as myocardial infarction, cerebral stroke, and hepatic, renal, and intestinal ischemia, as well as following cardiovascular and transplant surgeries. The hallmark of these pathologies is excessive inflammation. Toll-like receptors (TLRs) are recognized as one of the main contributors to pathogen-induced inflammation and, more recently, injury-induced inflammation. Endogenous ligands such as low-molecular hyaluronic acid, fibronectin, heat shock protein 70, and heparin sulfate were all found to be cleaved in the inflamed tissue and to activate TLR2 and TLR4, initiating an inflammatory response even in the absence of pathogens and infiltrating immune cells. In this review, we discuss the contribution of TLR activation in hepatic, renal, cerebral, intestinal, and myocardial I/R injuries. A greater understanding of the role of TLRs in I/R injuries may aid in the development of specific TLR-targeted therapeutics to treat these conditions.
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PMID:Toll-like receptors in ischemia-reperfusion injury. 1900 78


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