Disease relevance of Brain Infarction

• Since a host of diseases produce an abnormal blood-brain/cerebrospinal fluid (blood-brain/CSF) permeability allowing C protein extravasation, we investigated if C activation occurs in CSF in vitro and in CNS in vivo during subarachnoid hemorrhage (SAH) or brain infarction [1].
• We determined whether elevated homocysteine levels and the methylene tetrahydrofolate reductase (MTHFR) C677T polymorphism are risk factors for SVD as a whole, and for two different SVD subtypes: isolated lacunar infarction and ischaemic leukoaraiosis [2].
• BACKGROUND AND PURPOSE: The extent of brain infarction after local cerebral ischemia is frequently assessed with the mitochondrial activity indicator 2,3,5-triphenyltetrazolium chloride (TTC) [3].
• Patients with atherothrombotic infarction had higher total serum cholesterol and low density lipoprotein cholesterol concentrations than patients with lacunar infarction [4].
• Twenty-four to 48 hours after middle cerebral artery occlusion, brain infarction volumes after ischemia were significantly larger in MBP-JE mice than in wild-type controls and were accompanied by increased local transmigration and perivascular accumulation of macrophages and neutrophils [5].

Psychiatry related information on Brain Infarction

• BACKGROUND AND PURPOSE: Cerebral microangiopathy, indicated on MRI by lacunar infarctions (LI) and deep white matter lesions (DWML), is said to lead to vascular dementia [6].

High impact information on Brain Infarction

• The combined use of barbiturates and radiolabeled deoxyglucose may enhance the identification of recent brain infarction in experimental animals and in man [7].
• Brain infarction and the clinical expression of Alzheimer disease [8].
• Does ethanol intoxication promote brain infarction in young adults [9]?
• Plasminogen activator inhibitor genotype and brain infarction [10].
• The renin-angiotensin-aldosterone system has functions that may contribute to brain infarction (BI) [11].

Chemical compound and disease context of Brain Infarction

• All groups received preischemic glucose loading (2 gm/kg) to promote brain infarction [12].
• Postischemic loading with histidine, a precursor of histamine, alleviates both brain infarction and delayed neuronal death [13].
• On the other hand, no subjects in the cilostazol group showed silent brain infarction or strokes during the study period [14].
• Lacunar infarctions due to cholesterol emboli [15].
• The blood flow change by acetazolamide in the cerebral cortex was significantly lower in the multiple lacunar infarctions group than in the single lacunar infarction group [16].

Biological context of Brain Infarction

• CONCLUSIONS: Impairments in the protein C pathway and endogenous fibrinolysis may contribute to the increased risk for brain infarction after recent (< or = 1 week) infection/inflammation [17].
• METHODS: Cerebral blood flow was measured by the 133Xe inhalation method in 55 patients (mean +/- SD age, 62 +/- 11 years; 39 with brain infarction and 16 with hemorrhage) and 10 control subjects (mean +/- SD age, 61 +/- 9 years) [18].
• The transcription factor E2F1 is known to mediate apoptosis in isolated quiescent and postmitotic cardiac myocytes, and its absence decreases the size of brain infarction following cerebral ischemia [19].
• In conclusion, cilostazol treatment decreases ischemic brain infarction in association with inhibition of apoptotic and oxidative cell death [20].
• We propose that ion-transport characteristics of astroglia account for the observed relationship of [H+]o to tissue lactate during complete ischemia and suggest that brain infarction develops after plasma membranes in brain cells can no longer transport ions to regulate [H+] [21].

Anatomical context of Brain Infarction

• Allopurinol and dimethylthiourea reduce brain infarction following middle cerebral artery occlusion in rats [22].
• The circulating white blood cells of patients with brain infarction were labelled in vitro with Indium-111 tropolonate; the cells were reinjected to study the inflammatory process by gamma camera imaging [23].
• RESULTS: Brain MRI disclosed an isolated lacunar infarction in the dorsal caudal intralaminar nuclei of the thalamus [24].
• The findings suggest that naloxone, acting through a blockade of mu opioid receptor activation, is beneficial to cerebral I/R insult in terms of reducing brain infarction, neutrophil accumulation, and chemokine expression [25].
• TM is ubiquitous throughout the systemic microcirculation but is reduced in brain regions predisposed to lacunar infarction [26].

Gene context of Brain Infarction

• To better understand the interaction of pro- and antiinflammatory acute phase processes in brain infarction, plasma levels of IL-1RA, IL-6, and acute phase proteins including fibrinogen and c-reactive protein (CRP) were measured within 4 +/- 2 days of onset in 50 patients with acute ischemic stroke and in 20 age-matched healthy controls [27].
• The ischaemic leukoaraiosis group had a different endothelial marker profile, with lower levels of TFPI (P = 0.01) and a higher TF/TFPI ratio (P = 0.01) compared with the isolated lacunar infarction group [28].
• BACKGROUND AND PURPOSE: We initiated the present study to evaluate the clinical value of consecutive concentration determinations of S-100 and glial fibrillary acidic proteins in cerebrospinal fluid from patients with brain infarction [29].
• The highest CA II concentrations were found in patients with brain infarction (median 66.5 micrograms L-1, n = 20), whereas the control patients had markedly lower values (median 7.8 micrograms L-1, n = 97) [30].
• Well-characterized antisera were therefore used to examine the neuronal expression of CDK2, CDK4 and cyclins A, D1 and E in sections of brain from patients who had experienced cardiac arrest or focal brain infarction, and died 3.5 h to 9 days later [31].
• Our results indicate that the SNP in the AGTRL1 gene is associated with the susceptibility to brain infarction [32].

Analytical, diagnostic and therapeutic context of Brain Infarction

• Single-photon emission computed tomography with thallium-201-labeled diethyldithiocarbamate was performed in 26 consecutive patients less than or equal to 24 hours after a supratentorial brain infarction [33].
• The vascular anatomy was studied by latex infusion, brain infarction by vital staining, the size of the ischemic penumbra by imaging of ATP and protein synthesis, and blood flow by laser-Doppler flowmetry [34].
• First, NMDA antagonism by ifenprodil and its derivative is an effective approach for tissue sparing in animal models of stroke and brain infarction [35].
• METHODS: In the present work, we have determined the HFE genotypes for C282Y and H63D in subjects from two case-control studies: the ECTIM and GENIC studies, designed to identify genetic variants associated with myocardial and brain infarction, respectively [36].
• The cerebrovascular acetazolamide reactivity in the cerebral cortex and the cerebral white matter was significantly lower in the leuko-araiosis with lacunar infarction group than in the leuko-araiosis without lacunar infarction group and the control group [37].

References