Longer time spent in bed attempting to sleep is associated with rapid renal function decline: the Dongfeng–Tongji cohort study

Introduction: Prospective evidence on the relation between time in bed and renal dysfunction remains limited. We aimed to investigate the association of time spent in bed attempting to sleep (TSBS) with renal function decline in a middle-aged and elderly Chinese population.

Methods: About 16,733 eligible participants with a mean age of 62.3 years at baseline were included. Rapid renal function decline was defined as (baseline eGFR???revisit eGFR)/years of follow-up ≥5?mL/min per 1.73 m²/year. A total of 1738 study participants experienced rapid renal function decline after a median 4.6-year follow-up. Logistic regression models were used for multivariate analyses.

Results: The adjusted odds ratio (OR) of rapid renal function decline was 1.18 (95% CI: 1.02, 1.37) for TSBS ≥9?h/night compared with TSBS 7 to <8?h/night. This association remained significant (OR?=?1.19, 95% CI: 1.03, 1.38) after further adjustment for sleep quality, midday napping and usage of sleeping pills. Particularly, the association appeared to be prominent in individuals with diabetes.

Conclusions: Longer TSBS (≥9?h) was independently associated with an increased risk of rapid renal function decline. Our findings emphasized the importance to have optimal TSBS.

• Key messages

• Our study firstly investigated the association between time spent in bed attempting to sleep (TSBS) and renal dysfunction in Chinese adults.

• Compared with individuals TSBS 7 to <8?h, individuals with TSBS ≥9?h had 19% increased risk for rapid renal function decline after adjustment for multivariate confounders.

• The association appeared to be prominent in individuals with diabetes.

     

成人麻痹性斜视病因分析及手术治疗

目的：观察和探讨成人麻痹性斜视的类型和手术矫正效果。
　　方法：回顾性分析了我院2010－06／2013－06成人麻痹性斜视临床病例46例,将所有病例分为水平斜视组和垂直斜视组,其中水平斜视为主者26例,包括外直肌麻痹16例,内直肌麻痹10例;垂直斜视为主者20例,包括上斜肌麻痹7例,上直肌麻痹8例,下直肌麻痹2例,双上转肌麻痹3例。发病原因：先天性者9例,车祸等外伤所致19例,鼻部或颅脑手术史8例,原因不明者10例。手术方式包括直肌后徙术、直肌缩短术、直肌部分移位术或直肌联结术、下斜肌部分切除术、下斜肌后徙转位术等。采用SPSS10．0统计软件对两组的疗效进行卡方检验,同时对水平斜视组的两种术式改善麻痹眼运动情况进行t检验。
　　结果：末次随访时水平斜视组治愈、好转和无效者分别为20例（77％）,5例（19％）,1例（4％）;垂直斜视组分别为15例（75％）,3例（15％）和2例（10％）,两组间统计无显著性差异（P＞0．05）;麻痹眼的眼球运动得到改善。水平斜视中所用的两种术式,均能改善麻痹眼的眼球运动,分别为3．76±0．91,3．72±0．84mm,统计学上无显著性差异（P＝0．93）。
　　结论：成人麻痹性斜视病情复杂,根据不同麻痹肌及麻痹程度不同,采用不同的手术方式,术后可获得眼位的美容正位,改善代偿头位和主要注视野的复视。     

豚鼠早期实验性近视眼视网膜色素上皮细胞bFGF表达变化的研究

目的：研究豚鼠早期实验性近视眼视网膜色素上皮(retinal pigment epithelial,RPE)细胞前部及后极部碱性成纤维细胞生长因子(basic fibroblast growth factor,bFGF)的改变,探索近视的发病机制。

方法：两周龄豚鼠30只随机分为A组、B组、C组,每组10只,再随机选取5只10眼正常两周龄豚鼠不作任何干预,作为正常对照眼。选取任意眼戴一-10.00D凹透镜,分别饲养6、15、30d后除去镜片,验光及测眼轴长度确定近视形成后,采用细胞酶消化法培养豚鼠的前部及后极部RPE细胞,取3～6代RPE细胞进行免疫细胞化学、实时荧光定量PCR、Western-blot蛋白印迹法检查前部及后极部RPE细胞中bFGF表达变化。

结果：bFGF的表达定位于细胞浆和细胞核。免疫细胞化学、实时荧光定量PCR、Western-blot蛋白印迹法结果均表明：A、B、C三组实验眼和对照眼前部及后极部RPE细胞均有bFGF的表达,实验组前部及后极部与对照组相应前部及后极部比较,实验组中bFGF的阳性率低于对照组,差异有统计学意义(P<0.05); 而且,随着诱导时间的推移,实验组的阳性率逐渐降低,差异有统计学意义(P<0.05),对照组的阳性率不变,差异无统计学意义(P>0.05); 但实验组和对照组各组自身前部及后极部比较,差异无统计学意义(P>0.05)。

结论：实验组前部及后极部与对照组相应前部及后极部比较,bFGF的表达显著低于对照组。     

脂联素对小鼠氧诱导视网膜病变的保护作用

目的：观察脂联素对C57BL/6J小鼠氧诱导视网膜病变的影响。

方法：将新生C57BL/6J小鼠随机分为3组,分别为常氧对照组、生理盐水注射氧诱导视网膜病变(oxygen-induced retinopathy,OIR)组和脂联素注射OIR组。将后两组小鼠于生后第7d(P7)至P12置于体积分数75%±2%高氧氧箱中以诱导OIR模型。脂联素注射OIR模型组在P7～P15每天接受腹腔注射重组鼠脂联素蛋白(3.0μg/g),生理盐水注射OIR组则于上述相同时间点注射同等剂量的生理盐水。三组小鼠均于P17时取右眼行视网膜铺片和Lectin染色,观察视网膜中央无血管区及病理性新生血管的情况; 取左眼行视网膜切片和HE染色,观察视网膜组织病理学变化; 应用Western-blot测定左眼视网膜组织中iNOS、nNOS、eNOS的表达; 取右眼视网膜组织定量检测ROS/RNS含量以及NO水平。

结果：脂联素注射OIR组小鼠视网膜中央无血管区面积较生理盐水注射OIR组明显减少(t=7.304,P<0.01),病理性新生血管数目明显减少(t=2.654,P<0.01); 脂联素注射OIR组小鼠视网膜组织ROS含量较生理盐水注射组明显降低(t=13.349,P<0.01); 脂联素注射OIR组小鼠视网膜组织NO含量明显高于生理盐水注射组(t=3.023,P<0.01),iNOS表达明显低于生理盐水注射组(t=5.112,P<0.01),eNOS表达明显高于生理盐水注射组(t=7.421,P<0.01),nNOS的表达无统计学差异(t=1.074,P>0.01)。

结论：脂联素可以通过激活内源性eNOS促进生理性NO生成,同时又能抑制ROS/RNS的产生,在OIR进程中发挥视网膜血管的保护作用。     

A simple hydrazone as a multianalyte (Cu2+, Al3+, Zn2+) sensor at different pH values and the resultant Al3+ complex as a sensor for F−

A new colorimetric and fluorescence molecular chemosensor based on triazole hydrazone can be used as a multi-probe for selective detection of Al³⁺, Zn²⁺, and Cu²⁺ by monitoring changes in the absorption and fluorescence spectral patterns. Results show that Al³⁺ and Zn²⁺ ions can induce remarkable fluorescence enhancement at pH 6.0 and pH 10.0, respectively, while the addition of Cu²⁺ ions leads to a significant UV-visible absorption enhancement in the visible range at pH 6.0. In addition, the resultant Al³⁺ complex could act as an ‘on–off’ fluorescence sensor for F⁻. The fluorescence sensor was also used to monitor intracellular Al³⁺, Zn²⁺, and F⁻ in Hela cells.

A fluorescent probe for Al³⁺ and Zn²⁺ was synthesised, and the resultant Al³⁺-complex was used for the detection of F⁻.     

浅谈应急条件下饮用水水质的快速评估

目的开展应急条件下饮用水水质快速评估,保障饮水安全,为饮用水卫生应急工作提供参考。方法参考世界卫生组织饮水安全计划、美国环保局等发达国家的经验作法并结合我国实情,开展水质快速评估工作。结果应用饮用水水质快速评估方法进行现场卫生学调查,筛选水质敏感指标,对饮水危害因素进行定量评估分析。结论饮用水水质快速评估能够保障短期内水质安全,满足应急供水需求,具有一定的实践价值。     

广东省某地区不同年龄段人群镉负荷水平研究

目的探究广东省某地区不同年龄段人群镉负荷水平,利用基准剂量法评估不同年龄段人群尿NAG及尿β2MG相应的尿镉参考剂量,以此对不同年龄段人群尿镉可接受阈值进行研究。方法对该地区开展基于大样本人群调查的环境流行病学研究,采集当地常住居民的尿液样本,共获得872例(男性375例,女性497例)有效样本。并以我国环境镉污染健康危害区判定标准值为肾功能损害发生临界值,应用BMDS软件对不同年龄段人群进行尿镉基准剂量估算。结果以尿NAG为效应指标的BMDL值为低年龄组4.25μg/g肌酐,高年龄组4.05μg/g肌酐;以尿β2MG为效应指标的BMDL值为低年龄组1.70μg/g肌酐,高年龄组1.58μg/g肌酐。结论在镉污染健康风险评价中,尿β2MG比尿NAG更为敏感,高年龄组人群尿镉可接受阈值低于低年龄组。在长期镉暴露过程中,高年龄组人群可能比低年龄组人群更容易发生肾功能损害。     

Involvement of neuronal TGF-β activated kinase 1 in the development of tolerance to morphine-inducedantinociception in rat spinal cord

Background and Purpose

Tolerance induced by morphine and other opiates remains a major unresolved problem in the clinical management of pain. There is now good evidence for the importance of MAPKs in morphine-induced antinociceptive tolerance. A member of the MAPK kinase kinase family, TGF-β activated kinase 1 (TAK1) is the common upstream kinase of MAPKs. Here, we have assessed the involvement of TAK1 in the development of tolerance to morphine-induced analgesia.

Experimental Approach

The effects of an antagonist of TAK1 on morphine tolerance were investigated in vivo using the Randall–Selitto test, and the mechanism was investigated using Western blot and immunohistochemistry. The expression of TAK1 after chronic morphine exposure was also evaluated in vitro by immunohistochemistry.

Key Results

Chronic intrathecal morphine exposure up-regulated protein levels and phosphorylation of spinal TAK1. TAK1 immunoreactivity was co-localized with the neuronal marker NeuN. Intrathecal administration of 5Z-7-oxozeaenol (OZ), a selective TAK1 inhibitor, attenuated the loss of morphine analgesic potency and morphine-induced TAK1 up-regulation. Furthermore, OZ decreased the up-regulated expression of spinal p38 and JNK after repeated morphine exposure. In vitro studies demonstrated that sustained morphine treatment induced TAK1 up-regulation, which was reversed by co-administration of OZ. A bolus injection of OZ showed some reversal of established morphine antinociceptive tolerance.

Conclusions and Implications

TAK1 played a pivotal role in the development of morphine-induced antinociceptive tolerance. Modulation of TAK1 activation by the selective inhibitor OZ in the lumbar spinal cord may prove to be an attractive adjuvant therapy to attenuate such tolerance.