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)

Glycine encephalopathy (GE) is caused by an inherited deficiency of the glycine cleavage system (GCS) and characterized by accumulation of glycine in body fluids and various neurologic symptoms. Coma and convulsions develop in neonates in typical GE while psychomotor retardation and behavioral abnormalities in infancy and childhood are observed in mild GE. Recently, we have established a transgenic mouse line (low-GCS) with reduced GCS activity (29% of wild-type (WT) C57BL/6) and accumulation of glycine in the brain (Stroke, 2007; 38:2157). The purpose of the present study is to characterize behavioral features of the low-GCS mouse as a model of mild GE. Two other transgenic mouse lines were also analyzed: high-GCS mice with elevated GCS activity and low-GCS-2 mice with reduced GCS activity. As compared with controls, low-GCS mice manifested increased seizure susceptibility, aggressiveness and anxiety-like activity, which resembled abnormal behaviors reported in mild GE, whereas high-GCS mice were less sensitive to seizures, hypoactive and less anxious. Antagonists for the glycine-binding site of the N-methyl-D-aspartate receptor significantly ameliorated elevated locomotor activity and seizure susceptibility in the low-GCS mice. Our results suggest the usefulness of low-GCS mice as a mouse model for mild GE and a novel therapeutic strategy.
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PMID:Model mice for mild-form glycine encephalopathy: behavioral and biochemical characterizations and efficacy of antagonists for the glycine binding site of N-methyl D-aspartate receptor. 1841 41

We investigated whether renal function and microalbuminuria are independent predictors and whether any interaction exists between them, regarding future cardiovascular disease in hypertensive patients (n=10 881) followed for 4.5 years. The primary end points (PEs) were fatal and nonfatal myocardial infarction and stroke and other cardiovascular deaths. Creatinine and glomerular filtration rate (GFR), estimated using the formulas of the Modification of Diet in Renal Disease study group and Cockroft and Gault and in a subsample (n=4929) of microalbuminuria and interaction terms of microalbuminuria and renal function, were related to the risk of the PE using Cox proportional hazards model after full adjustment. Increased creatinine (P<0.001), decreased GFR from Cockroft and Gault (P=0.001), and decreased GFR from the Modification of Diet in Renal Disease study group (P=0.001) were all independent risk factors for the PE. Stepwise exclusion of patients with the poorest renal function excluded the possibility that the relationship between decreasing renal function and the PE was driven only by patients with severely impaired renal function. Microalbuminuria and all 3 of the indices of renal function predicted the PE independent of each other. There was a significant interaction between microalbuminuria and GFR from Cockroft and Gault (P=0.040) in prediction of the PE. Both renal function and microalbuminuria add independent prognostic information regarding cardiovascular risk in hypertensive patients. The cardiovascular risk associated with microalbuminuria increases with a decline in GFR, as demonstrated by a significant interaction between microalbuminuria and GFR from Cockroft and Gault. Because estimation of the total cardiovascular risk is essential for the aggressiveness of risk factor interventions, simultaneous inclusion of GFR and microalbuminuria in global cardiovascular risk assessment is essential.
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PMID:Interaction between renal function and microalbuminuria for cardiovascular risk in hypertension: the nordic diltiazem study. 1850 24

The availability of rapid imaging with multidetector CT systems and commercial analysis software has made perfusion imaging with CT an everyday technique, not only for the brain but also for other body organs. Perfusion imaging is usually performed as an adjunct to a conventional CT examination and is therefore particularly appropriate when a conventional CT is part of routine clinical protocols. The derived values are reproducible and have been validated against a range of reference techniques. Within neuroradiology, perfusion CT has attracted interest in the assessment of acute stroke but can also be used to assess secondary injury in head trauma and as an adjunct to CT angiography to evaluate cerebral spasm in subarachnoid haemorrhage. Within oncology, perfusion CT provides an imaging correlate for tumour vascularity that can be used to discriminate benign and malignant lesions, as an indicator of tumour aggressiveness, to reveal occult tumour and improve the delineation of tumours during radiotherapy planning, and as a functional assessment of tumour response to therapy. By exploiting the ability of CT systems to quantify contrast enhancement, CT perfusion imaging uses contrast media to assess vascular physiology and so improve diagnosis, prognosis, treatment selection and therapy monitoring.
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PMID:Perfusion imaging with computed tomography: brain and beyond. 1865 65

Mortality and morbidity remain high from neurologic emergencies, such as acute stroke, traumatic brain injury, and hypoxic-ischemic encephalopathy after cardiac arrest. Decisions regarding initial aggressiveness of care must be made at the time of presentation, and perceived prognosis is often used as part of this decision-making process. These decisions are predicated on the accuracy of early outcome prediction, however. Decisions to limit treatment early after neuroemergencies must be balanced with avoidance of self-fulfilling prophecies of poor outcome attributable to clinical nihilism. This article examines the role of prognostication early after neuroemergencies, the potential impact of early treatment limitations, and how these may relate to communication with patients and surrogate decision makers in the context of these acute neurologic events.
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PMID:Clinical nihilism in neuroemergencies. 1921 17

Stroke is the leading cause of disability in the United States and affects 15 million people worldwide. Studies performed in various parts of the world have found differences between sexes in stroke incidence, prevalence, mortality, and outcomes. Although men are at higher risk of stroke for most age groups below age 85 years, after this age the incidence reverses dramatically, with women being much more at risk. Furthermore, recent studies suggest that women have worse recovery than men post-stroke. Many aspects of recovery may influence this outcome, including sex-specific comorbidities, aggressiveness of acute treatment, prevention therapies, and varying degrees of social support and rates of depression. It is important to further define and investigate sex differences in stroke incidence, care, treatment, and outcomes to improve functional recovery in women.
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PMID:Stroke in women: disparities and outcomes. 2042 78

Steroid therapy is considered to improve clinical symptoms in hypertrophic pachymeningitis. We present a 70-year-old man with idiopathic hypertrophic pachymeningitis, whose clinical signs progressively worsened despite steroid therapy. He died of subarachnoid hemorrhage (SAH) with pituitary apoplexy 2 months after the admission regardless of improvement of laboratory data and magnetic resonance imaging appearance by one-and-half-month steroid therapy. Autopsy revealed thickened dura mater supporting the diagnosis of hypertrophic pachymeningitis. Brain parenchyma is generally not affected by the disease; however, histological investigation suggested that inflammation of the dura caused damage to superior hypophyseal artery resulting in SAH and apoplexy in the anterior lobe of the pituitary gland. The higher dose and the longer duration of steroid therapy should have achieved in our case although most laboratory data recovered within the normal range. The aggressiveness of hypertrophic pachymeningitis must be evaluated by clinical signs rather than by laboratory data or imaging examinations.
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PMID:A case of subarachnoid hemorrhage with pituitary apoplexy caused by idiopathic hypertrophic pachymeningitis. 2058 19

This study aimed to investigate the relationship between the expression of the molecular markers, extracellular matrix metalloproteinase inducer (EMMPRIN), galectin-3, and microvessel density (MVD) with MRI invasive features in invasive and noninvasive pituitary adenomas. MRI was performed preoperatively in 34 patients with histologically verified pituitary adenomas. The expression of EMMPRIN, galectin-3, and MVD was determined by using immunohistochemical techniques on excised surgical specimen from all patients. Correlative analyses between invasive MRI features and expression of EMMPRIN, galectin-3, and MVD were determined between invasive and noninvasive pituitary adenomas. Among MRI invasive features, adenoma crossing the lateral line (LL) of the internal carotid artery (ICA), percentage of intracavernous ICA encasement by the tumor over 50%, sphenoidal sinus invasion, irregular tumor shape, and bilateral ICA asymmetry correlated with increased expression of EMMPRIN and galectin-3 (P<.05), but tumor cystic necrosis and tumor apoplexy did not correlate with EMMPRIN and galectin-3 expression (P>.05). The invasive MRI features did not correlate with MVD expression. This study demonstrated that EMMPRIN and galectin-3 were associated with aggressiveness and invasion by pituitary adenoma. Furthermore, EMMPRIN and galectin-3 were two potential molecular markers for assessing the invasive potential of pituitary adenoma and may provide useful targets for molecular therapeutic strategy against invasive pituitary adenomas.
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PMID:The relationship between MRI invasive features and expression of EMMPRIN, galectin-3, and microvessel density in pituitary adenoma. 2151 51

Historically, humans have long sought to enhance their "athletic" performance to increase body weight, aggressiveness, mental concentration and physical strength, contextually reducing fatigue, pain, and improving recovery. Although regular training is the mainstay for achieving these targets, the ancillary use of ergogenic aids has become commonplace in all sports. The demarcation between ergogenic aids and doping substances or practices is continuously challenging and mostly based on perceptions regarding the corruption of the fairness of competition and the potential side effects or adverse events arising from the use of otherwise unnecessary ergogenic substances. A kaleidoscope of side effects has been associated with the use of doping agents, including behavioral, skeletal, endocrinologic, metabolic, hemodynamic, and cardiovascular imbalances. Among the various doping substances, the most striking association with thrombotic complications has been reported for androgenic anabolic steroids (i.e., cardiomyopathy, fatal and nonfatal arrhythmias, myocardial infarction [MI], intracardiac thrombosis, stroke, venous thromboembolism [VTE], limb arterial thrombosis, branch retinal vein occlusion, cerebral venous sinus thrombosis) and blood boosting (i.e., VTE and MI, especially for epoetin and analogs). The potential thrombotic complication arising from misuse of other doping agents such as the administration of cortisol, growth hormone, prolactin, cocaine, and platelet-derived preparations is instead speculative or anecdotal at best. The present article provides an overview on the epidemiological association as well as the underlying biochemical and biological mechanisms linking the practice of doping in sports with the development of thrombosis.
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PMID:Doping and thrombosis in sports. 2219 57

Strategic regions correspond to associative, limbic and paralimbic structures and related circuits, that underpin cognitive/behavioral functions. Strokes in these eloquent sites produce pictures of vascular dementia with syndromic features due to specific site lesion and/or interruption of their interconnections. This study aims at analysing subcortical strategic strokes that express similar cognitive/behavioral elements, by sharing common pathways. Patients (n=6) who attended in specialized ambulatory, were submitted to neuropsychological and neuroimaging assessments through MRI (GE Signa Horizon 1.5T) and brain SPECT (Millennium MG, ECD [TC-99m]). Stroke locations and respective main symptoms were: 1. anteromedian thalamus [L]: anterograde and retrograde amnesia (ARA), expression aphasia (EA), executive dysfunction (ED), apathy, and depression; 2. anterior thalamus [R]: ARA, inattention, apathy, and aggressiveness; 3. dorsomedian thalamus [L]: inattention, ED, anosognosia, and aggressiveness; 4. central paramedian thalamus [R]: EA, visual perception deficits (VPD), ED, infantility, and personality disorder; 5. caudate nucleus (ventral-head) [L]: VPD, ED, delirium, visual hallucinations, and personality disorder; and 6. anterior capsule [L]: VPD, ED, apathy, and depression. Vascular strategic syndromes connote the predominantly impaired cognitive/behavioral symptom of each site. Temporal and frontal disconnection symptoms were produced by disrupted MTT/hippocampal and IML/amygdala circuits expressing amnesic syndrome associated with heterogeneous dysexecutive syndrome, in all the cases, by disrupting frontal-basal ganglia-thalamus-cortical net, in three different levels of their pathway.
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PMID:Cognitive disconnective syndrome by single strategic strokes in vascular dementia. 2293 18

The function of subthalamic nucleus (STN) which is a part of the basal ganglia system is not clear, but it is hypothesized that this component might be involved in action selection. Unilateral damage to STN, which can commonly occur due to the small vessel stroke mainly, causes hemiballismus and sometimes hemichorea-hemiballismus. This paper deals with a 60-year-old patient with sudden onset of abnormal movements in his right limbs. He had increased appetite and hyperphagia and also developed mood and behavioral changes (aggressiveness, irritability, anxiety, and sometimes obscene speech). The magnetic resonance imaging revealed infarct area in left subthalamus. In our case, hemiballismus is caused by infarction in left subthalamic area. Occurrence of irritability, anxiety, and some behavioral changes such as aggressiveness and obscene speech can be explained by impairment of STN role in nonmotor behavior and cognitive function as a result of infarct.
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PMID:Hemiballismus, Hyperphagia, and Behavioral Changes following Subthalamic Infarct. 2312 61


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