gliosis/phosphatase

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Inhibition of Protein Tyrosine Phosphatase 1B Improves IGF-I Receptor Signaling and Protects Against Inflammation-Induced Gliosis in the Retina.

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OBJECTIVE Insulin-like growth factor-I receptor (IGF-IR) signaling mediates retinal growth and survival and its failure may contribute to aggravate diabetic retinopathy (DR). Protein tyrosine phosphatase 1B (PTP1B) negatively modulates IGF-IR signaling, but its involvement in inflammation during DR

Neonatal nutritional programming induces gliosis and alters the expression of T-cell protein tyrosine phosphatase and connexins in male rats.

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Changes to neonatal nutrition result in long-lasting impairments in energy balance, which may be described as metabolic programing. Astrocytes, which are interconnected by gap junctions, have emerged as important players in the hypothalamic control of food intake. In order to study the effects of

CDC25B, Ki-67, and p53 expressions in reactive gliosis and astrocytomas.

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OBJECTIVE To investigate the expression of CDC25B, which is a member of the cyclin-dependent kinase activating phosphatase family, in diffuse astrocytoma (DA), anaplastic astrocytoma (AA), glioblastoma multiforme (GBM), pilocytic astrocytoma (PA) and reactive gliosis (RG). Also, to study the

Calcineurin A beta deficiency ameliorates HFD-induced hypothalamic astrocytosis in mice.

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ᅟ: Astrocytosis is a reactive process involving cellular, molecular, and functional changes to facilitate neuronal survival, myelin preservation, blood brain barrier function and protective glial scar formation upon brain insult. The overall pro- or anti-inflammatory impact of reactive astrocytes

Midkine regulates amphetamine-induced astrocytosis in striatum but has no effects on amphetamine-induced striatal dopaminergic denervation and addictive effects: functional differences between pleiotrophin and midkine.

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Midkine (MK), a neurotrophic factor with important roles in survival and differentiation of dopaminergic neurons, is upregulated in different brain areas after administration of different drugs of abuse suggesting MK could modulate drugs of abuse-induced pharmacological or neuroadaptative effects.

Activity of acid phosphatase and TPP-ase at a fine structure level in the neuroglia as related to myelination of the brain.

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An ultrastructural investigation of the activity of acP and TPP-ase in the neuroglia of different developmental stages of the rabbit corpus callosum was performed. The observations made, lead to following conclusions: 1. The strongest demonstration of end products of acP activity was observed in the

Increased expression of phosphatase and tensin homolog in reactive astrogliosis following intracerebroventricular kainic acid injection in mouse hippocampus.

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A phosphatase and tensin homolog (PTEN) has been known to play multiple biological roles. However, role of PTEN in astrocyte activation is not clear yet. In the present study, the expression pattern of PTEN in the process of reactive gliosis was immunohistochemically examined in

Reactive oxygen species regulate prosurvival ERK1/2 signaling and bFGF expression in gliosis within the retina.

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OBJECTIVE Gliosis is the response of glial cells within retinal tissue to injury. It can be beneficial in the short term, but if the response is extended it can lead to scar formation, which contributes to blindness. Phosphorylation of extracellular signal regulated kinase 1/2 (ERK1/2) is considered

Systemic inflammation without gliosis mediates cognitive deficits through impaired BDNF expression in bile duct ligation model of hepatic encephalopathy.

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Chronic liver disease per se induces neuroinflammation that contributes to cognitive deficits in hepatic encephalopathy (HE). However, the processes by which pro-inflammatory molecules result in cognitive impairment still remains unclear. In the present study, a significant increase in the activity

Glycosaminoglycan levels and proteoglycan expression are altered in the hippocampus of patients with mesial temporal lobe epilepsy.

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Extracellular matrix proteoglycans (PGs) and glycosaminoglycans (GAGs) play a crucial role in cell differentiation and synaptogenesis by modulating neurite outgrowth. The chondroitin sulfate (CS)-rich PG, the receptor protein tyrosine phosphatase zeta/beta (RPTP zeta/beta), has been related to

Protective effect of the leaves of Vitex negundo against ethanol-induced cerebral oxidative stress in rats.

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The present study investigated the effect of the various fractions of hydromethanolic extract of the leaves of Vitex negundo (Verbenaceae) against ethanol-induced cerebral oxidative stress in rats. Cerebral oxidative stress was induced by the administration of 20% ethanol (5 ml/100 gbw) for a period

Neuropathological features of frontotemporal dementia and parkinsonism linked to chromosome 17q21-22 (FTDP-17): Duke Family 1684.

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Frontotemporal dementia with parkinsonism (FTDP-17) is an autosomal dominant disorder that presents clinically with dementia, extrapyramidal signs, and behavioral disturbances in mid-life and progresses to death within 5 to 10 years. Pathologically, the disorder is characterized by variable neuronal

In situ hybridization of mRNA expression for IP3 receptor and IP3-3-kinase in rat brain after transient focal cerebral ischemia.

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Loss of intracellular calcium homeostasis has been regarded an important factor underlying neuron cell death after cerebral ischemic insult. In the brain, a major mechanism for regulation of intracellular calcium is through the signal transduction pathway involving hydrolysis of

Medulla oblongata transcriptome changes during presymptomatic natural scrapie and their association with prion-related lesions.

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BACKGROUND The pathogenesis of natural scrapie and other prion diseases is still poorly understood. Determining the variations in the transcriptome in the early phases of the disease might clarify some of the molecular mechanisms of the prion-induced pathology and allow for the development of new

Neurohepatic toxicity of subacute manganese chloride exposure and potential chemoprotective effects of lycopene.

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Excess manganese (Mn) is potentially toxic resulting in a permanent neurodegenerative disorder, clinically known as "manganism" that is distinctive for hepaticencephalopathy. The present study was designed to explore the toxic impacts of subacute Mn exposure on brain and liver tissues, and the

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