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Based on the differential fluorescence (live cells fluoresce green and dead cells orange) exhibited when intercalated with AO, the live/dead cells can be easily differentiated
The optimal AO concentration for enhanced sensitive differentiation has been optimized as 001%. These studies offer a promising application for rapid differentiation and quantification of live/dead cells in the case of cytotoxic treatment/therapies within several minutes.Brain-derived neurotrophic factor redistribution in the dorsal root ganglia correlates with neuropathic pain inhibition after resiniferatoxin treatment.BACKGROUND CONTEXT: Brain-derived neurotrophic factor (BDNF) and its cognate receptor, the tyrosine kinase B (TrkB), are normally expressed in neurons and implicated in multiple pathological conditions. Brain-derived neurotrophic factor is produced in the central nervous system microglia in response to noxious stimuli and appear to potentiate central sensitization. Resiniferatoxin (RTX) is an excitotoxic agonist of the vanilloid receptor 1 (VR1), a cation channel protein considered an integrator for nociception.

Resiniferatoxin, administered into the dorsal root ganglia (DRG), selectively eliminates the VR1-positive neurons and improves tactile allodynia in a neuropathic pain rat PURPOSE: The goal of the present study was to evaluate the role of BDNF in RTX-induced neuropathic pain suppression.STUDY DESIGN: The study design was a sciatic nerve injury animal model with METHODS: Resiniferatoxin was injected into the DRG of the L3-L6 spinal nerves after the rats displayed tactile allodynia and thermal hyperalgesia produced by a photochemical injury to the sciatic nerve. Behavioral testing and immunohistochemical and mRNA analysis of the DRG were performed to determine RESULTS: Brain-derived neurotrophic factor expression in the DRG of neuropathic rats was upregulated in the small- and medium-size neurons, whereas the upregulation was observed in the large-size neurons of non-neuropathic rat DRG. A high-dose RTX injection in the DRG of neuropathic rats led to elimination of both thermal hyperalgesia and tactile allodynia and also upregulated BDNF in the large-size neurons, similar to the nonallodynic rats. Tyrosine kinase B changes CONCLUSION: Resiniferatoxin injection in the DRG of neuropathic rats upregulates BDNF expression in the same pattern as in the large-size neurons of non-neuropathic rats. Therefore, BDNF upregulation may have pain suppressive effects. These effects are likely mediated by TrkB.

A zebrafish retinal graded photochemical stress model.INTRODUCTION: In order to develop a model for investigating the genes that contribute to retinal degeneration, we examined the early graded photochemical stress response in the adult zebrafish (Danio rerio) retina and investigated the role of an NMDA inhibitor, thiokynurenate.METHODS: Following intravitreal injection of rose bengal (6 or 12 mg/mL), light 400 nM thiokynurenate. Learn more and electron microscopic analysis was performed at 2 and 4 h and gene expression analysis was carried out at 2, 4 and RESULTS: Light and electron microscopy demonstrated a graded photochemical response in photoreceptor, nuclear, and ganglion cell layer thickness. Increased vacuolation of the inner plexiform layer was also observed. The inhibitor produced a distinct lesion pattern. Cellular stress genes were elevated in low and high lesions, while some homeobox gene expression was reduced with DISCUSSION: The phenotypic and genetic changes observed from this model can serve as a basis for understanding the pathology of retinal oxidative and cellular stress.

These changes may aid our understanding of aging and macular Ozone affects breathing and pulmonary surfactant function in mice.The effect on breathing of BALB/c mice immediately following ozone exposure (2 ppm) for 0, 2, 4, 6, and 8 h was studied with a whole body plethysmograph. Whether such exposure affected the normal function of pulmonary surfactant of maintaining airway patency was evaluated with a capillary surfactometer. Respiratory rate in mice that were not exposed was 358+/-16 (mean+/-S.E.) breaths/min and decreased to 202+/-10 after 6 h exposure. The mean pressure change caused by breathing diminished significantly, indicating a reduced tidal volume.

BAL fluid from controls maintained patency for 88+/-2% of the study time, 120 s, implying a good surfactant function, but the ozone exposure caused the surfactant to lose its capability of maintaining patency (P < 0001). This decaying surfactant function of the BAL fluid coincided with an increasing protein concentration in the fluid of exposed animals (16+/-04 mg/ml in the 8-h group) as compared to controls (04+/-04 mg/ml, P < 0001). Learn more is concluded that leakage of plasma proteins into the airway lumen was probably the main reason for the surfactant dysfunction, which may have contributed to the Aromatization and 19-hydroxylation of androgens by rat brain cytochrome P-450.The oxidative metabolism of androgens in the rat brain includes aromatization preceded by the requisite 19-hydroxylation. We have examined the transformation of [19-C3H3]androstenedione and [4-14C]testosterone by the semipurified cytochrome P-450 fraction of the rat brain.
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