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Elevated blood plasma levels of epinephrine, norepinephrine, tyrosine hydroxylase, TGFβ1, and TNFα associated with high-altitude pulmonary edema in an Indian population.
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Biomarkers are essential to unravel the locked pathophysiology of any disease. This study investigated the role of biomarkers and their interactions with each other and with the clinical parameters to study the physiology of high-altitude pulmonary edema (HAPE) in HAPE-patients (HAPE-p) against
Protection against LPS-induced pulmonary edema through the attenuation of protein tyrosine phosphatase-1B oxidation.
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One hallmark of acute lung injury is the disruption of the pulmonary endothelial barrier. Such disruption correlates with increased endothelial permeability, partly through the disruption of cell-cell contacts. Protein tyrosine phosphatases (PTPs) are known to affect the stability of both
Polymorphisms of the tyrosine hydroxylase gene in subjects susceptible to high-altitude pulmonary edema.
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OBJECTIVE
A blunted hypoxic ventilatory response (HVR) has been observed in some sufferers of high-altitude pulmonary edema (HAPE), and was proposed as a potential mechanism in its pathogenesis. Tyrosine hydroxylase (TH) is a rate-limiting enzyme in the carotid body responding to hypoxia to
[Palpebral edema secondary to treatment by a specific inhibitor of tyrosine kinase: Glivec. A case report].
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Iatrogenic causes for palpebral edema are rarely suspected and must be specifically sought. The authors report a case of palpebral edema in a patient treated with a specific inhibitor of the BCR-ABL tyrosine kinase (Glivec) for chronic myeloid leukemia. Histopathological analysis of specimens of the
Treatment of diabetic macular edema with an inhibitor of vascular endothelial-protein tyrosine phosphatase that activates Tie2.
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OBJECTIVE
AKB-9778 is a small-molecule competitive inhibitor of vascular endothelial-protein tyrosine phosphatase (VE-PTP) that promotes Tie2 activation and reduces vascular leakage and neovascularization in mouse models. The purpose of this study was to test the safety, tolerability,
AZD2171, a pan-VEGF receptor tyrosine kinase inhibitor, normalizes tumor vasculature and alleviates edema in glioblastoma patients.
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Using MRI techniques, we show here that normalization of tumor vessels in recurrent glioblastoma patients by daily administration of AZD2171-an oral tyrosine kinase inhibitor of VEGF receptors-has rapid onset, is prolonged but reversible, and has the significant clinical benefit of alleviating
Development of hygromas or severe edema during treatment with the tyrosine kinase inhibitor STI571 is not associated with platelet-derived growth factor receptor (PDGFR) gene polymorphisms.
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STI571 is active against Bcr/Abl-, c-kit- and platelet-derived growth factor receptor (PDGFR)-driven malignancies. Mild to moderate edema is common, whereas severe edema, body cavity effusions and subdural hygromas are rarely observed. These effects have been suggested to involve inhibition of PDGFR
Bradykinin- and substance P-induced edema formation in the hamster cheek pouch is tyrosine kinase dependent.
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The purpose of this study was to determine whether protein tyrosine kinase, a ubiquitous family of intracellular signaling enzymes that regulates endothelial cell function, modulates bradykinin- and substance P-induced increase in macromolecular efflux from the intact hamster cheek pouch
[Incorporation of L-3H-tyrosine by neuroglia in experimental brain edema].
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Astrocyte swelling and protein tyrosine nitration in hepatic encephalopathy.
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Hepatic encephalopathy (HE) is a neuropsychiatric syndrome during the course of acute or chronic liver disease. It is functional in nature, potentially reversible and precipitated by rather heterogeneous factors. Current evidence suggests that HE is the consequence of a low grade chronic glial edema
SH2 domain-containing protein tyrosine phosphatase 2 and focal adhesion kinase protein interactions regulate pulmonary endothelium barrier function.
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Enhanced protein tyrosine phosphorylation is associated with changes in vascular permeability through formation and dissolution of adherens junctions and regulation of stress fiber formation. Inhibition of the protein tyrosine phosphorylase SH2 domain-containing protein tyrosine phosphatase 2 (SHP2)
Expression of functional tyrosine kinases on immortalized Kaposi's sarcoma cells.
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Kaposi's sarcoma (KS) is the most frequent malignant lesion in patients with AIDS and is characterized by spindle cell proliferation, inflammatory cell infiltration, angiogenesis, edema, and invasiveness. KS origin is still debated. The complex aspect of this disease is probably supported by
Therapeutic hypothermia attenuates brain edema in a pig model of cardiac arrest: Possible role of the angiopoietin-Tie-2 system.
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OBJECTIVE
This study aimed to clarify whether therapeutic hypothermia protects against cerebral edema following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) in a porcine model via regulating the angiopoietin-Tie-2 ligand-receptor system.
METHODS
Male pigs were randomized into the
Earlier diagnosis of progressive disease during bevacizumab treatment using O-(2-18F-fluorethyl)-L-tyrosine positron emission tomography in comparison with magnetic resonance imaging.
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Antiangiogenic treatment using bevacizumab in brain tumor patients may cause difficulties in the diagnosis of tumor progression (ie, nonenhancing tumor progression). Newly defined criteria for treatment assessment and diagnosis of tumor progression (ie, RANO [Response Assessment in Neuro-Oncology]
Preclinical activity of ABT-869, a multitargeted receptor tyrosine kinase inhibitor.
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ABT-869 is a structurally novel, receptor tyrosine kinase (RTK) inhibitor that is a potent inhibitor of members of the vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) receptor families (e.g., KDR IC50 = 4 nmol/L) but has much less activity (IC50s > 1 micromol/L)
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