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排序方式: 共有8501条查询结果,搜索用时 31 毫秒
31.
Emilio Domínguez‐Salazar Gabriela Hurtado‐Alvarado Fernanda Medina‐Flores Javik Dorantes Oscar Gonzlez‐Flores Arturo Contis‐Montes de Oca Javier Velzquez‐Moctezuma Beatriz Gmez‐Gonzlez 《Journal of sleep research》2020,29(3)
Sleep loss increases blood–brain barrier permeability. As the blood–brain barrier and the blood–tissue barriers in the reproductive tract (blood–testis and blood–epididymis barriers) share common characteristics, we hypothesized that sleep restriction may also modify their barrier function. Previous reports showed that sleep loss decreased sperm viability and progressive fast mobility, which may be a consequence of altered blood–testis and blood–epididymis barrier. Therefore, we quantified changes in blood–testis and blood–epididymis barrier after sleep loss and related them to male fertility. Adult male Wistar rats were sleep restricted using the multiple‐platform technique in a protocol of 20 hr daily sleep deprivation plus 4 hr of sleep recovery in the home‐cage. At the 10th day, barrier permeability assays were performed with Na‐fluorescein, 10 kDa Cascade blue‐dextrans and Evans blue, and the expression of tight junction proteins, actin and androgen receptor was quantified. At the 10th day of sleep restriction and after sleep recovery days 1–7, males were placed with sexually receptive females, sexual behaviour was tested, and the percentage of pregnancies was calculated. Sleep restriction increased the barrier permeability to low‐ and high‐molecular‐weight tracers, and decreased the expression of tight junction proteins, actin and androgen receptor. Concomitantly, sleep restriction reduced the percentage of ejaculating males and the number of pregnancies. Sleep recovery for 2–3 days progressively re‐established fertility, as indicated by a higher percentage of ejaculating males and impregnated females. In conclusion, chronic sleep loss alters fertility concomitantly with the disruption of the blood–tissue barriers at the reproductive tract, the mechanism involves androgen signalling. 相似文献
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目的 探讨血脑屏障通透性与接受溶栓治疗的急性脑梗死患者预后的相关性。方法 纳入绵阳市盐亭县人民医院在2018年5月-2019年5月收治的急性脑梗死且接受溶栓治疗的患者共76例,随访3个月,根据预后情况分为预后良好组和预后不佳组,比较2组患者临床资料、实验室检查指标水平、血脑屏障通透性等。结果 所有研究对象随访3个月后共有8例患者失访,其中mRs评分为良好(0~1分)共32例,为预后良好组,余为预后不佳组(2~6分)共36例; 2组患者性别、BMI、梗死部位、冠心病史、高血压病史、糖尿病史、高脂血症史、脑卒中史、发病时间、吸烟史、饮酒史、家族史、应用药物、基线NIHSS评分、Cr,BUN,HDLc,LDLc,PLT,HGB,APTT,DD、空腹血糖、糖化血红蛋白水平均无明显差异(P>0.05); 预后良好组患者年龄、房颤史的比例、UA水平与预后不佳组比较均有明显差异(P<0.05); 2组患者AUC无明显差异(P>0.05); 预后良好组患者Ktrans及VP与预后不佳组比较均有明显差异(P<0.05); 进行logistics回归分析显示年龄(OR=1.190,P=0.026)、Ktrans(OR=1.104,P=0.005)为预后不佳的危险因素,VP(OR=0.556,P=0.022)为保护因素。结论 血脑屏障通透性为影响接受溶栓治疗的急性脑梗死患者预后的相关因素。 相似文献
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36.
Joël Jovanovic Xuan Liu Despina Kokona Martin S. Zinkernagel Andreas Ebneter 《Glia》2020,68(3):574-588
The role of microglia in retinal inflammation is still ambiguous. Branch retinal vein occlusion initiates an inflammatory response whereby resident microglia cells are activated. They trigger infiltration of neutrophils that exacerbate blood–retina barrier damage, regulate postischemic inflammation and irreversible loss of neuroretina. Suppression of microglia-mediated inflammation might bear potential for mitigating functional impairment after retinal vein occlusion (RVO). To test this hypothesis, we depleted microglia by PLX5622 (a selective tyrosine kinase inhibitor that targets the colony-stimulating factor-1 receptor) in fractalkine receptor reporter mice (Cx3cr1gfp/+) subjected to various regimens of PLX5622 treatment and experimental RVO. Effectiveness of microglia suppression and retinal outcomes including retinal thickness as well as ganglion cell survival were compared to a control group of mice with experimental vein occlusion only. PLX5622 caused dramatic suppression of microglia. Despite vein occlusion, reappearance of green fluorescent protein positive cells was strongly impeded with continuous PLX5622 treatment and significantly delayed after its cessation. In depleted mice, retinal proinflammatory cytokine signaling was diminished and retinal ganglion cell survival improved by almost 50% compared to nondepleted animals 3 weeks after vein occlusion. Optical coherence tomography suggested delayed retinal degeneration in depleted mice. In summary, findings indicate that suppression of cells bearing the colony-stimulating factor-1 receptor, mainly microglia and monocytes, mitigates ischemic damage and salvages retinal ganglion cells. Blood–retina barrier breakdown seems central in the disease mechanism, and complex interactions between different cell types composing the blood–retina barrier as well as sustained hypoxia might explain why the protective effect was only partial. 相似文献
37.
The gut microbiota plays an important role in the occurrence and development of neuroimmunological diseases. Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune disease of the central nervous system that is characterized by the peripheral production of the disease-specific serum autoantibody aquaporin-4 (AQP4)-IgG. Recently, accumulating evidence has provided insights into the associations of gut microbiota dysbiosis and intestinal mucosal barrier destruction with NMOSD, but the underlying pathogenesis remains unclear. Thus, a microbiota intervention might be a potential therapeutic strategy for NMOSD by regulating the gut microbiota, repairing the intestinal mucosal barrier, and modulating intestinal immunity and peripheral immunity. 相似文献
38.
《Brain & development》2020,42(3):264-269
ObjectiveSome pediatric patients with autoimmune encephalitis (AE) experience sequelae in spite of immunotherapy. In this study, we aimed to evaluate the association of serum matrix metallopeptidase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) levels with the neurological prognosis of AE.MethodsWe retrospectively included 13 patients with AE who had been referred to Saitama Children’s Medical Center from February 2011 to May 2019. We compared serum MMP-9 levels, TIMP-1 levels, and MMP-9/TIMP-1 ratio in the acute period (within 30 days from the onset of AE) and subacute period (30-day period following the acute period). We also compared these biomarker levels between patients with (group A) and without sequelae (group B). Sequelae were evaluated at discharge or the last visit.ResultsGroup A (median age, 7.8 years; range, 5.3–10.7 years) and group B (median age, 13.3 years; range, 11.1–15.4 years) had 6 patients each; 1 patient was excluded because the time of AE onset was unknown. In the acute period, there were no significant differences in MMP-9 levels, TIMP-1 levels, and MMP-9/TIMP-1 ratio between groups A and B. In the subacute period, serum MMP-9/TIMP-1 ratio was higher in group A than in group B (p < 0.01). There were no significant differences in MMP-9 and TIMP-1 levels between groups A and B.ConclusionsPatients with sequelae of AE showed a high MMP-9/TIMP-1 ratio in the subacute period. Our study demonstrates that elevation of serum MMP-9/TIMP-1 ratio in the subacute period may be a predictive factor of sequelae of AE. 相似文献
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Leila H. Shayegan BA Laura E. Levin MD Eloise R. Galligan MD Anne W. Lucky MD Anna L. Bruckner MD Elena Pope MD Irene Lara-Corrales MD Karen Wiss MD Catherine C. McCuaig MD Maria C. Garzon MD Lawrence F. Eichenfield MD Kristen P. Hook MD John C. Browning MD MBA Lawrence A. Schachner MD Marissa J. Perman MD Leslie Castelo-Soccio MD PhD Moise L. Levy MD Sharon A. Glick MD Kimberly D. Morel MD 《Pediatric dermatology》2020,37(2):326-332