Our previous study indicated that bone marrow stromal cells(BMSCs) treatment exerted adverse effects after stroke in type 1 diabetic rats(T1DM),the possible mechanisms by which BMSCs treatment exacerbated blood-brain ...
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Our previous study indicated that bone marrow stromal cells(BMSCs) treatment exerted adverse effects after stroke in type 1 diabetic rats(T1DM),the possible mechanisms by which BMSCs treatment exacerbated blood-brain barrier(BBB) leakage and functional outcomes remain *** this study,we investigated whether the highmobility group box 1(HMGB1)/receptor for advanced glycation endproducts(RAGE) axis signaling in contributed to the adverse effects in type 1 diabetic stroke caused by BMSCs *** 1 diabetes mellitus(T1 DM) rats were subjected to middle cerebral artery occlusion(MCAo) and 24 hours later were treated with:(1) phosphate-bufferedsaline;(2) BMSCs(3 × 106);(3) Gly(Glycyrrhizin,an HMGB1 inhibitor,4 mg/kg) and(4) BMSCs(3 × 106) + Gly(4 mg/kg) starting at 24 hours after MCAo and monitored for 14 *** tests,immunostaining,and western blot were *** monotherapy of stroke in T1DM rats significandy increased HMGB1 and RAGE expression in the ischemic brain when compared to T1DM-MCAo control ***,BMSCs monotherapy exacerbated functional *** monotherapy and combination of Gly and BMSCs treatment significantly improve functional outcomes and reduce the levels of HMGB1 and RAGE in the ischemic brain when compared to T1DM control or BMSCs monotherapy *** HMGB1/RAGE axis signaling may play a vital role in BMSCs treatment induced functional impairments after stroke in T1DM *** of the HMGB1/RAGE axis signaling pathway by Gly may attenuate the adverse effects induced by BMSCs treatment in T1DM-MCAo rats.
Objectives:The aim of this study was to investigate whether serum neurofilaments(Nfs),neuron-specific enolase(NSE) and S100 calcium binding protein B(S100 B) in patients with chronic insomnia disorder(CID) were:(1) hi...
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Objectives:The aim of this study was to investigate whether serum neurofilaments(Nfs),neuron-specific enolase(NSE) and S100 calcium binding protein B(S100 B) in patients with chronic insomnia disorder(CID) were:(1) higher than those in healthy individuals;(2) lower in post-therapy CID patients than free-therapy patients;(3)associated with their impaired functions,including poor sleep quality,and reduced cognitive function(comprehensive cognition and memory performance in a specific task).Methods:Forty insomniac outpatients were categorized into free-therapy CID group(ft-CID,n = 40) and among forty insomniac outpatients,twenty-four patients were selected after six months treatment as re-visiting CID group(rv-CID,n = 24).Twenty demographically similar healthy subjects who accompanied the patients or had a medical examination were selected as negative *** subjects were assessed with the polysomnography(PSG) for 2 consecutive nights,On the morning following the second night,they completed a series of questionnaires assessing and neuropsychological tests,Pittsburgh Sleep Quality Index(PSQI),the 17-item Hamilton Depression Rating Scale(HAMD-17),the 14-item Hamilton Anxiety Scale(HAMA-14),and the Chinese-Beijing Version of Montreal Cognitive Assessment(MoCA-C).The special memory was evaluated with the Nine Box Maze *** Nfs,NSE and S100 B levels were quantified with a quantitative sandwich enzyme-linked immunosorbent assay(ELISA).Results:① Compared to the controls,the PSQI,HAMD-17,HAMD-S,HAMA-S,HAMA-17 and MoCA-C scores were significantly higher in the ft-CID and rv-CID group(Ps < 0.01).The differences in PSQI,HAMD-17,HAMD-S,HAMA-S and HAMA-17 scores between the ft-CID and rv-CID groups were significant(Ps <0.01),but the difference in MoCA scores between the rv-CID group and HC group(Ps > 0.05) was insignificant.② The ft-CID group and the rv-CID group had higher serum NfH,NfL and S100 B than the HC group(Ps < 0.05).Furthermore,the rv-CID patients had lower
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