meningitis/tyrosine

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Increased expression of tyrosine phosphatase SHP2 in experimental pneumococcal meningitis: correlation with tumor necrosis factor-alpha and cerebrospinal fluid pleocytosis.

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Protein tyrosine phosphatase SHP2 plays a crucial role in the development of the central nervous system. To explore the expression and possible role of SHP2 during the course of bacterial meningitis, this article reports a juvenile rat bacterial meningitis model established by direct intracisternal

Tyrosine kinase inhibition reduces inflammation in the acute stage of experimental pneumococcal meningitis.

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Bacterial meningitis is an acute inflammatory disease of the central nervous system with a mortality rate of up to 30%. Excessive stimulation of the host immune system by bacterial surface components contributes to this devastating outcome. In vitro studies have shown that protein tyrosine kinase

Oxidative stress in bacterial meningitis in humans.

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OBJECTIVE To study reactive nitrogen species-mediated oxidative brain damage and antioxidant defenses in patients with acute bacterial meningitis. METHODS Nitrotyrosine (a widely used marker for the formation of reactive nitrogen species, such as peroxynitrite) and the lipid peroxidation product

Delayed diagnosis of X-linked agammaglobulinaemia in a boy with recurrent meningitis.

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X-linked agammaglobulinaemia (XLA) is a rare inherited primary immunodeficiency disease characterized by the B cell developmental defect, caused by mutations in the gene coding for Bruton's tyrosine kinase (BTK), which may cause serious recurrent infections. The diagnosis of XLA is

Entry of Neisseria meningitidis into mammalian cells requires the Src family protein tyrosine kinases.

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Neisseria meningitidis, the causative agent of meningitis and septicemia, is able to attach to and invade a variety of cell types. In a previous study we showed that entry of N. meningitidis into human brain microvascular endothelial cells (HBMEC) is mediated by fibronectin bound to the outer

Reactive nitrogen species contribute to blood-labyrinth barrier disruption in suppurative labyrinthitis complicating experimental pneumococcal meningitis in the rat.

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Sensorineural hearing damage is a frequent complication of bacterial meningitis, affecting as many as 30% of survivors of pneumococcal meningitis. There is a substantial body of evidence that oxidants, such as reactive nitrogen species (RNS), are central mediators of brain damage in experimental

Fcγ receptor I alpha chain (CD64) expression in macrophages is critical for the onset of meningitis by Escherichia coli K1.

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Neonatal meningitis due to Escherichia coli K1 is a serious illness with unchanged morbidity and mortality rates for the last few decades. The lack of a comprehensive understanding of the mechanisms involved in the development of meningitis contributes to this poor outcome. Here, we demonstrate that

Development of brain injury in mice by Angiostrongylus cantonensis infection is associated with the induction of transcription factor NF-kappaB, nuclear protooncogenes, and protein tyrosine phosphorylation.

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Eosinophilic meningitis or meningoencephalitis caused by Angiostrongylus cantonensis is endemic to the Pacific area of Asia, especially Taiwan, Thailand, and Japan. Although eosinophilia is an important clinical manifestation of A. cantonensis infection, the role of eosinophils in the progress of

Redundant roles for Met docking site tyrosines and the Gab1 pleckstrin homology domain in InlB-mediated entry of Listeria monocytogenes.

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The bacterial pathogen Listeria monocytogenes causes food-borne illnesses leading to gastroenteritis, meningitis, or abortion. Listeria induces its internalization into some mammalian cells through interaction of the bacterial surface protein InlB with host Met receptor tyrosine kinase. Binding of

Protein Oxidation Biomarkers and Myeloperoxidase Activation in Cerebrospinal Fluid in Childhood Bacterial Meningitis.

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The immunological response in bacterial meningitis (BM) causes the formation of reactive oxygen and nitrogen species (ROS, RNS) and activates myeloperoxidase (MPO), an inflammatory enzyme. Thus, structural oxidative and nitrosative damage to proteins and DNA occurs. We aimed to asses these events in

Prognostic factors and clinical outcome of patients with lung adenocarcinoma with carcinomatous meningitis.

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BACKGROUND In recent years, the incidence of carcinomatous meningitis (CM) in lung adenocarcinoma has been rising. However, it remains unclear which treatment strategies improve the outcome of these patients. METHODS We retrospectively reviewed data for 67 lung adenocarcinoma patients diagnosed with

Carcinomatous meningitis in a patient with Her2/neu expressing bladder cancer following trastuzumab and chemotherapy: a case report and review of the literature.

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BACKGROUND Targeted therapies may impact the natural history of bladder cancer based upon their pharmacokinetics. The Her2/neu receptor tyrosine kinase, overexpressed by half of all primary urothelial carcinomas, has recently been examined as a therapeutic target in bladder cancer in a prospective

Successful treatment of carcinomatous meningitis with gefitinib in a patient with lung adenocarcinoma harboring a mutated EGF receptor gene.

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Carcinomatous meningitis is a severe complication of lung cancer. Although treatment with gefitinib, a tyrosine kinase inhibitor of epidermal growth factor (EGF) receptor, has been reported to be highly effective against lung cancers harboring a mutated EGF gene, its effect against carcinomatous

Gefitinib is also active for carcinomatous meningitis in NSCLC.

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Carcinomatous meningitis (CM) and spinal cord metastases (SCM) are uncommon, yet fatal complication for patients with non-small cell lung cancer (NSCLC). Gefitinib, developed to inhibit the tyrosine kinase of the epidermal growth factor receptor (EGFR), represents the first new treatment modality

Dynamic changes of hepatocyte growth factor in eosinophilic meningitis caused by Angiostrongylus cantonensis infection.

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Hepatocyte growth factor (HGF) is a member of the angiogenic growth factor family, which exerts a variety of effects on epithelial, endothelial, and neuronal cells by binding to the c-MET receptor tyrosine kinase. It was reported that HGF attenuates cerebral ischemia-induced increase in permeability

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