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artemin/inflamație

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ArticoleStudii cliniceBrevete
Pagină 1 din 33 rezultate
BACKGROUND Pathologies that affect the bone marrow have a significant inflammatory component; however, it is not clear how inflammatory mediators affect nociceptive nerve terminals within the marrow cavity. METHODS In this study, an in vivo bone-nerve preparation was used to directly record the

GDNF, Neurturin, and Artemin Activate and Sensitize Bone Afferent Neurons and Contribute to Inflammatory Bone Pain.

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Pain associated with skeletal pathology or disease is a significant clinical problem, but the mechanisms that generate and/or maintain it remain poorly understood. In this study, we explored roles for GDNF, neurturin, and artemin signaling in bone pain using male Sprague Dawley rats. We have shown

Heart Failure Risk Associated With Rheumatoid Arthritis-Related Chronic Inflammation.

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Background Inflammation may contribute to incident heart failure (HF). Rheumatoid arthritis (RA), a prototypic inflammatory condition, may serve as a model for understanding inflammation-related HF risk. Methods and Results Using the Vanderbilt University Medical Center electronic health record, we

Artemin transiently increases iNOS expression in primary cultured trigeminal ganglion neurons.

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Artemin, a member of the glial cell line-derived neurotrophic factor family, is an important cytokine and a critical participant in trigeminal pain disorders such as tongue pain and migraine. However, the mechanisms underlying artemin's activity are largely unknown. In the present study, we used

[Inhibitory effect of artemin on endotoxin-induced nitric oxide synthesis].

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OBJECTIVE To investigate the effect of Artemin on LPS-induced nitric oxide synthesis in macrophages. METHODS 1. Nitrite oxide (NO) production of RAW 264.7 cells was induced by LPS or LPS in combination with interferon-gamma (IFN gamma) in the presence or absence of Artemin. The amount of NO in the

Intramuscular nerve damage in lacerated skeletal muscles may direct the inflammatory cytokine response during recovery.

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The expression of inflammatory cytokines and growth factors in surgically repaired lacerated muscles over a 12-week recovery phase was investigated. We hypothesized that these expression levels are influenced by both neural and muscular damage within lacerated muscles. Microarrays were confirmed
Bladder sensation is mediated by lumbosacral dorsal root ganglion neurons and is essential for normal voiding and nociception. Numerous electrophysiological, structural, and molecular changes occur in these neurons following inflammation. Defining which neurons undergo these changes is critical for

Distribution of artemin and GFRalpha3 labeled nerve fibers in the dura mater of rat: artemin and GFRalpha3 in the dura.

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OBJECTIVE We examined the distribution of artemin and its receptor, glial cell line-derived neurotrophic factor family receptor alpha3 (GFRalpha3), in the dura mater of rats. BACKGROUND Artemin, a member of the glial cell line-derived neurotrophic factor family, is a vasculature-derived growth

Differential contribution of SNARE-dependent exocytosis to inflammatory potentiation of TRPV1 in nociceptors.

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Potentiation of the pain-integrator ion channel transient receptor potential vanilloid type 1 (TRPV1) underlies thermal hyperalgesia mediated by a variety of proinflammatory factors. Two complementary mechanisms of TRPV1 inflammatory sensitization have been proposed, namely a decrease of its

The aryl hydrocarbon receptor AhR links atopic dermatitis and air pollution via induction of the neurotrophic factor artemin.

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Atopic dermatitis is increasing worldwide in correlation with air pollution. Various organic components of pollutants activate the transcription factor AhR (aryl hydrocarbon receptor). Through the use of AhR-CA mice, whose keratinocytes express constitutively active AhR and that develop

Artemin growth factor increases nicotinic cholinergic receptor subunit expression and activity in nociceptive sensory neurons.

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BACKGROUND Artemin (Artn), a member of the glial cell line-derived growth factor (GDNF) family, supports the development and function of a subpopulation of peptidergic, TRPV1-positive sensory neurons. Artn (enovin, neublastin) is elevated in inflamed tissue and its injection in skin causes transient

The neurotrophic factor artemin influences the extent of neural damage and growth in chronic pancreatitis.

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OBJECTIVE Chronic pancreatitis is characterised by severe abdominal neuropathic pain, perineural inflammatory cell infiltrations and intrapancreatic neural growth. Artemin was recently shown to eliminate neuropathic pain and reverse neurochemical damage after nerve injury. The role of artemin and

The emerging role of miR-223 as novel potential diagnostic and therapeutic target for inflammatory disorders.

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Since their discovery of more than a decade ago, microRNAs have been demonstrated to have profound effects on almost every aspect of biology. Specific microRNAs have emerged as key players in disease biology by playing crucial role in disease development and progression. This review draws attention

Inflammatory and neuropathic cold allodynia are selectively mediated by the neurotrophic factor receptor GFRα3.

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Tissue injury prompts the release of a number of proalgesic molecules that induce acute and chronic pain by sensitizing pain-sensing neurons (nociceptors) to heat and mechanical stimuli. In contrast, many proalgesics have no effect on cold sensitivity or can inhibit cold-sensitive neurons and

Peripherally increased artemin is a key regulator of TRPA1/V1 expression in primary afferent neurons.

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BACKGROUND Artemin, a member of the glial cell line-derived neurotrophic factor family, is known to have a variety of neuronal functions, and has been the subject of attention because it has interesting effects, including bi-directional results in modulation in neuropathic and inflammatory pain. It
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