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Sivu 1 alkaen 36 tuloksia
Increased blood-brain barrier permeability and brain edema after focal cerebral ischemia induced by hyperlipidemia: role of lipid peroxidation and calpain-1/2, matrix metalloproteinase-2/9, and RhoA overactivation.
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OBJECTIVE
Hyperlipidemia is a highly prevalent risk factor for ischemic stroke. Its impact on brain injury and blood-brain barrier permeability, so far, has not been assessed in animal models of ischemic stroke.
METHODS
Wild-type and apolipoprotein E(-/-) mice, fed with normal or cholesterol-rich
The Rho guanine nucleotide exchange factor P-Rex1 as a potential drug target for cancer metastasis and inflammatory diseases.
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Phosphatidylinositol 3,4,5-trisphosphate (PIP3)-dependent Rac exchanger 1 (P-Rex1) is a guanine nucleotide exchange factor (GEF) for Rac small GTPases and the Rac-related GTPase RhoG. P-Rex1 plays an important role in cell migration and relays intracellular signals generated through
Anthrax edema toxin inhibits endothelial cell chemotaxis via Epac and Rap1.
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Angiogenesis involves the assembly of endothelial cells into capillaries from a pre-existing vasculature. Because abnormal angiogenesis is a hallmark of many cancers, it is critical to find factors that control this process. Endothelial cells are enriched in the anthrax receptor; we therefore
Effects on Anti-Inflammatory, DNA Binding and Molecular Docking Properties of 2-chloroquinolin-3-yl-methylene-pyridine / pyrazole Derivatives and their Palladium(II) Complexes
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Two new sets of Schiff bases 2-chloroquinolin-3-yl-methylene-pyridin-2-amine (CMPA) and 2-chloroquinolin-3-yl-methylene-pyrazole-5-amine-3-thole (CMPT) and their respective palladium (II) complexes have been synthesised and characterized with the aid of elemental analysis, IR, 1H
Differential inhibition of adenylyl cyclase isoforms and soluble guanylyl cyclase by purine and pyrimidine nucleotides.
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Mammals express nine membranous adenylyl cyclase isoforms (ACs 1-9), a structurally related soluble guanylyl cyclase (sGC) and a soluble AC (sAC). Moreover, Bacillus anthracis and Bacillus pertussis produce the AC toxins, edema factor (EF), and adenylyl cyclase toxin (ACT), respectively.
Late-onset ornithine transcarbamylase deficiency in two families with different mutations in the same codon.
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We report on late-onset ornithine transcarbamylase (OTC) deficiency in two families with mutations in the same codon, but different base substitutions. Onset of symptoms showed great variation, and five hemizygotes finally died. Clinical diagnosis was late and difficult. In family A, 1 patient also
Association Between Acute Inflammatory Cells and Mutation in ICAM-1 Gene With Injury Severity and Outcome Among Traumatic Cerebral Hemorrhagic Contusion
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Background: Acute inflammation in the brain after trauma is mediated by acute inflammatory cells (neutrophils) that contributes to ischemic brain damage, neurological deterioration, and poor outcome. Migration of neutrophils to brain is
Crucial role of phospholipase C epsilon in skin inflammation induced by tumor-promoting phorbol ester.
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In two-stage skin chemical carcinogenesis, phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) acts as a promoter essential for clonal expansion of the initiated cells carrying the activated ras oncogenes. Although protein kinase C (PKC) isozymes are the main targets of TPA, their role in tumor
Final report on the safety assessment of octoxynol-1, octoxynol-3, octoxynol-5, octoxynol-6, octoxynol-7, octoxynol-8, octoxynol-9, octoxynol-10, octoxynol-11, octoxynol-12, octoxynol-13, octoxynol-16, octoxynol-20, octoxynol-25, octoxynol-30, octoxynol-33, octoxynol-40, octoxynol-70, octoxynol-9 carboxylic acid, octoxynol-20 carboxylic acid, potassium octoxynol-12 phosphate, sodium octoxynol-2 ethane sulfonate, sodium octoxynol-2 sulfate, sodium octoxynol-6 sulfate, and sodium octoxynol-9 sulfate.
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Octoxynols are ethoxylated alkylphenols in which the size of the molecule is related to the number of moles of ethylene oxide used in synthesis. Reactions are performed at elevated temperature, under pressure, and in the presence of NaOH. It is possible that the synthesis may leave trace amounts of
Synthesis and pharmacochemical study of new Cu(II) complexes with thiophen-2-yl saturated and alpha,beta-unsaturated substituted carboxylic acids.
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Copper complexes with thiophen-2-yl saturated and alpha,beta-unsaturated carboxylic acids as ligands were prepared, characterized and pharmacochemically studied. The available evidence supports a dimeric structure for the complexes of the general formula [Cu2(L)4(MeOH)2] where L are the anions of
Structural modeling of a novel CAPN5 mutation that causes uveitis and neovascular retinal detachment.
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CAPN5 mutations have been linked to autosomal dominant neovascular inflammatory vitreoretinopathy (ADNIV), a blinding autoimmune eye disease. Here, we link a new CAPN5 mutation to ADNIV and model the three-dimensional structure of the resulting mutant protein. In our study, a kindred with
Mutant NADH dehydrogenase subunit 4 gene delivery to mitochondria by targeting sequence-modified adeno-associated virus induces visual loss and optic atrophy in mice.
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OBJECTIVE
Although mutated G11778A NADH ubiquinone oxidoreductase subunit 4 (ND4) mitochondrial DNA (mtDNA) is firmly linked to the blindness of Leber hereditary optic neuropathy (LHON), a bona fide animal model system with mutated mtDNA complex I subunits that would enable probing the pathogenesis
Epac/Rap and PKA are novel mechanisms of ANP-induced Rac-mediated pulmonary endothelial barrier protection.
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Acute lung injury, sepsis, lung inflammation, and ventilator-induced lung injury are life-threatening conditions associated with lung vascular barrier dysfunction, which may lead to pulmonary edema. Increased levels of atrial natriuretic peptide (ANP) in lung circulation reported in these
Loss of Gadd45a does not modify the pulmonary response to oxidative stress.
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It is well established that exposure to high levels of oxygen (hyperoxia) injures and kills microvascular endothelial and alveolar type I epithelial cells. In contrast, significant death of airway and type II epithelial cells is not observed at mortality, suggesting that these cell types may express
Monozygotic twins with CAPN5 autosomal dominant neovascular inflammatory vitreoretinopathy.
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BACKGROUND
The purpose of this study was to describe the clinical findings in a set of monozygotic twins with autosomal dominant neovascular inflammatory vitreoretinopathy (ADNIV) over a 23-year period.
METHODS
A pair of female twins were examined between 26 and 49 years of age. The concordance and
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