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A total of 258 cases of elderly patients with herpes zoster were divided into treatment group (n =128) and control group (n =130).The treatment group received a once daily dose of narrowband ultraviolet irradiation plus oral acyclovir 0.8 g,5 times a day.However,the control group received a once daily dose of infrared therapy plus the same oral acyclovir.At Day 9,the effective rates of treatment and control groups were 91.7％ (117/128) vs.74.6％ (97/130) (P＜0.05).Also,in terms of pain relief time (2.56 ± 1.51) vs.(5.44 ±4.06) days,crusting time (4.51 ±0.48) vs.(6.11 ± 1.81) days and healing time (5.65 ±0.56) vs.(9.28 ±0.21) days,the treatment group was better than those of the control group (P ＜0.01).
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The study is to investigate the effect of angiotensin II (Ang II) and its receptor blockers on migration and endothelin-1 (ET-1) expression of rat vascular adventitial fibroblast subpopulations. Vascular adventitial fibroblasts were individually expanded by using cloning rings, and the effects of Ang II on the migration of adventitial fibroblast subpopulations were evaluated by Transwell. Fluorescence quantitative-PCR detected the expression of preproET-1 mRNA induced by Ang II, and its receptor antagonists losartan and PD-123319. The concentration of ET-1 was determined by ELISA. It showed that spindle shaped and epithelioid shaped cells were isolated by using cloning rings, named as spindle cells and round cells. RT-PCR showed that fibroblast subpopulations did not have leukocytes, endothelial cells and smooth muscle cells, namely pure cell lines. Compared with respective control cells, two subpopulations had transferring ability. Ang II significantly improved round cells migration in a concentration-dependent manner, and had no obvious influence on spindle cells migration. Ang II (1 x 10(-8) - 1 x 10(-6) mol x L(-1)) significantly increased the expression of preproET-1 mRNA in round cells (P < 0.01), and had no significant effect on the expression of preproET-1 mRNA in spindle cells. Losartan blocked the expression of preproET-1 mRNA induced by Ang II in round cells, and had no significant effect on the expression of preproET-1 mRNA in spindle cells. The effects of Ang II and ET-1 receptor inhibitors on the release of ET-1 were similar to the expression of preproET-1 mRNA. The results indicate that there are two cell subpopulations: round cells and spindle cells in rat vascular adventitial fibroblasts. Ang II significantly improved cells migration, and increased the expression of ET-1 in round cell subpopulation. It suggested that there may be different migratory mechanisms in two cell subpopulations, and the two subpopulations may play a different role in vascular remodeling and reparative process.
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Objective To evaluate the role of δ opioid receptor in the brain injury following asphyxial cardiac arrest-resuscitation in rats.Methods Ninety-six pathogen-free male Sprague-Dawley rats,weighing 300-350 g,were randomly divided into 4 groups (n =24 each):sham operation group (group S),asphyxial cardiac arrest-resuscitation group (group M),δ opioid receptor agonist BW373U86 group (group B) and δ opioid receptor antagonist naltrindole group (group N).Cardiac arrest was induced by clamping the tracheal tube for 8 min.Mechanical ventilation with pure oxygen was performed.Epinephrine 0.02 mg/kg and 5％ NaHCO3 1 mg/kg were injected intravenously as soon as chest compression was started.Appearance of spontaneous breathing and MAP ＞ 50 mm Hg (lasting for more than 10 min) were considered to be signs of successful recovery of spontaneous circulation (ROSC).BW373U86 and naltrindole 1 mg/kg were injected via the femoral vein immediately after ROSC in groups B and N,respectively,while the equal volume of normal saline was given instead in groups S and M.Neurological deficit score (NDS) was evaluated at 3,24 and 72 h after ROSC.The rats were then sacrificed,brains were isolated and the hippocampus was obtained for detection of the expression of brain-derived neurotrophic factor (BDNF)and tyrosine receptor kinase B (TrkB)mRNA by RT-PCR.The histological grading (HG) of neurons and number of survival neurons in hippocampal CA1 region were determined at 72 h after ROSC.Results Compared with group S,the expression of BDNF and TrkB mRNA was significantly up-regulated,HG was increased,and NDS and the number of survival neurons were decreased in groups M,B and N (P ＜ 0.05).Compared with group M,the expression of BDNF and TrkB mRNA was significantly up-regulated in group B,the expression of BDNF and TrkB mRNA was down-regulated in group N,and HG was significantly decreased,and NDS and the number of survival neurons were increased in groups B and N (P ＜ 0.05).NDS was significantly lower,the number of survival neurons was smaller,the expression of BDNF and TrkB mRNA was lower,and HG was higher in group N than in group B (P ＜ 0.05).Conclusion Activation of δ opioid receptor can reduce the brain injury following asphyxial cardiac arrest-resuscitation in rats and the mechanism may be related to up-regulation of BDNF and TrkB after activation of δ opioid receptor.
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Objective To investigate the effect of isoflurane preconditioning on the expression of 5-lipoxy-genase (5-LOX) during focal cerebral ischemia-reperfusion (I/R) in rats.Methods Thirty-nine male adult Sprague-Dawley rats weighing 250-300 g were randomly divided into 3 groups (n =13 each):sham operation group (group S); focal cerebral I/R group (group I/R); isoflurane preconditioning group (group Ⅰ).Focal cerebral I/R was produced by mid-cerebral artery occlusion in anesthetized rats.The rats inhaled 2 h of 2％ isoflurane and focal cerebral I/R was produced 24 h later in group I.The neurological deficits were scored at 24 h of reperfusion.The animals were then sacrificed.The brains were immediately removed for determination of the infarct size.The expression of 5-LOX,myeloid differentiation factor88 (MyD88) and nuclear factor kappa B (NF-κB) protein and mRNA was detected using Western blot and RT-PCR respectively.Results Compared with group S,the neurological deficit score was significantly increased,the infarct size was enlarged in groups I/R and I,the expression of 5-LOX,MyD88 and NF-κB protein and mRNA was up-regulated in group I/R,and the expression of 5-LOX mRNA and MyD88 protein and mRNA was up-regulated in group I (P ＜ 0.05).Compared with group I/R,the neurological deficit score was significantly lower,the infarct size was smaller,and the expression of 5-LOX,MyD88 and NF-κB protein and mRNA was lower in group I (P ＜ 0.05).Conclusion Isoflurane preconditioning can reduce focal cerebral I/R injury by down-regulating the expression of 5-LOX and inhibiting MyD88/NF-κB signaling pathway in rats.
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Objective To investigate the effect of isoflurane preconditioning on Toll-like receptor 4 (TLR4)-myeloid differentiation factor 88 (MyD88) signaling pathway in ischemic penumbra following focal cerebral ischemia-reperfusion (I/R) in rats.Methods Fifty-four healthy male SD rats,aged 3 months,weighing 250-280 g,were randomly divided into 3 groups (n =18 each):sham operation group (group S),I/R group and isoflurane preconditioning group (group IP).Focal cerebral I/R was induced by middle cerebral artery occlusion.In groups I/R and IP,a nylon thread with rounded tip was inserted into the right internal jugular vein and threaded cranially until resistance was met.The middle cerebral artery was occluded for 2 h,followed by 24 h reperfusion.In group IP,the animals inhaled 2.0％ isoflurane for 2 h,and middle cerebral artery occlusion was performed at 24 h after the end of preconditioning.Neurological deficit was scored at 24 h of reperfusion and then the rats were sacrificed.Five rats in each group were chosen and the brains removed for measurement of the cerebral infarct volume.The right cerebral ischemic penumbra was removed for detection of the expression of HSP60,TLR4,MyD88 protein and mRNA by Western blot analysis and real time-PCR.Apoptosis was detected in the ischemic penumbra in the left 3 rats in each group using TUNEL.Apoptosis index (AI) was calculated.Results Neurological deficit scores and AI were significantly increased,the cerebral infarct volume was significantly enlarged,and the expression of HSP60,TLR4,MyD88 protein and mRNA was up-regulated in groups I/R and IP as compared with group S ( P ＜ 0.05).Isoflurane preconditioning significantly reduced the cerebral infarct volume and decreased neurological deficit scores and AI,and down-regulated the expression of HSP60,TLR4,MyD88 protein and mRNA (P ＜ 0.05).Conclusion The mechanisn by which isoflurane preconditioning protects ischenic penumbra following focal cerebral I/R may be related to inhibition of TLR4-MyD88 signaling pathway.
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BACKGROUND: Acellular bladder submucosa is a natural extracellular matrix, which is mainly composed of collagen Ⅰ and Ⅲ. It is regarded as an ideal biological scaffold material. OBJECTIVE: To evaluate the biocompatibility of acellular bladder submucosa as a tissue engineered scaffold material. METHODS: Pig urinary bladder was immersed in the solution of PBS and sodium azide for a night, and the mucosa was removed. Acellular bladder submucosa was prepared using continuous hypotension, freeze-thawed treatment and NaOH spallation. The biocompatibility of acellular bladder submucosa was evaluated through histologic structure, DNA residual, cytotoxicity, cell adhesion, as well as subcutaneous inflammatory reactions. RESULTS AND CONCLUSION: The cell components were completely eliminated after deoellularization treatment, while the extracellular matrix was remained intact as normal bladder:According to MTT results, cytotoxicity of acellular bladder matrix was assigned to be the first grade. No DNA signal was observed after extraction, and the matrix also supported porcine smooth muscle cell attachment and proliferation. Subcutaneous implantation of the matrix indicated that the acellular bladder submucosa trigger no immunologic rejection reaction obviously. The results demonstrated that: the acellular bladder submucosa prepared here exhibits excellent biocompatibility, which can be used as substitution in tissue-engineering field.
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0.05). Phenylephrine induced contractile responses in a concentration-dependent manner in the dorsal detrusor strips, but not in the ventral detrusor strips. S-doxazosin, R-doxazosin and rac-doxazosin at 1 ?mol?L-1 antagonized the phenylephrine-induced contractile responses competitively in the dorsal detrusor strips, and their pKB values were 7.44?0.19, 7.39?0.14 and 7.38?0.30, respectively. Three pKB values of doxazosin and its enantiomers were not significantly different from each other. Electric field stimulation produced a steady contractile response that was completely inhibited by tetrodotoxin at 0.3 ?mol?L-1. S-doxazosin, R-doxazosin and rac-doxazosin significantly inhibited the contractile responses to electric field stimulation in the dorsal detrusor strips of the rabbit urinary bladder(P0.05). However, S-doxazosin, R-doxazosin and rac-doxazosin did not affect the responses to electric field stimulation in the ventral detrusor strips. Conclusion The pKB value of S-doxazosin against phenylephrine-induced contraction via-adrenoceptors is same to R-doxazosin and rac-doxazosin, and the three agents are able to inhibit the adrenergic contraction induced by electric field stimulation in dorsal detrusor strips of the rabbit urinary bladder.