基于互联网平台的髋关节置换患者健康教育实证分析

目的：探讨互联网平台应用于髋关节置换患者健康教育的效果,利用现代技术手段创造新的健康教育模 式。方法：整群抽取2013年3-8月300例髋关节置换手术患者按时间段分为两组进行前瞻性研究,对照组采用传统教 育模式,试验组在对照组的基础上将多媒体素材传到互联网关节登记系统或导入电脑,辅以视频教育,分析两组患 者知信行的变化关系,评价其对焦虑水平、满意度和术后并发症等的影响程度。结果：试验组患者术后健康教育知 识、态度、行为依从性、满意度及并发症均优于对照组,术后焦虑水平低于对照组,两组比较差异均有统计学意义 (P<0.05)。结论：基于互联网关节登记系统及电脑视频教育的应用可改变患者的知信行,降低患者焦虑水平,增加患 者满意度,具有临床使用和推广价值。     

孕晚期干预支持对初产妇产时认知行为及分娩质量的影响

目的：探讨孕晚期干预支持在初产妇分娩中的应用效果。方法100例初产妇随机分为观察组和对照组各50例,对照组给予常规对症支持护理,观察组在对照组的基础上主要给予干预支持护理,比较两组产时认知行为及自然分娩率、阵痛发作、产程、会阴侧切、产后出血、并发症等分娩结局。结果观察组孕妇分娩态度、应对行为、分娩知识的得分及自然分娩率、满意度都明显高于对照组,两组比较,差异有统计意义（P＜0．05）;观察组产程时间、剖宫产率、阵痛发作、并发症均明显低于对照组,两组比较,差异有统计学意义（ P＜0．05）。结论孕晚期干预支持对初产妇产时认知行为及分娩质量有良好帮助,能减轻初产妇焦虑情绪水平,提高其自然分娩率,减少其剖宫产率及并发症,提升母婴安全,提高初产妇对护理的满意度。     

论常燕生以“生物史观”为基础的新法治主义

为适应近代中国的救亡需求,新法家主要代表常燕生融合西方进化论学说和中国古代法家的法治思想,创生出有机生物史观和国家主义法治思想。以此为基础,常燕生大力提倡文化启蒙,主张建构近代民族国家,呼吁走渐进改良式的救亡道路。常燕生的思想因而带有明显的济世救亡的工具主义特质。批判性地反思其缺陷和不足,镜鉴其菁华,必大有益于当世“法治中国”建设。     

绞股蓝正丁醇提取物对快速老化小鼠学习记忆的影响及其机制

目的研究绞股蓝正丁醇部位对阿尔茨海默病(AD)模型小鼠学习记忆的影响。方法采用Morris水迷宫方法对小鼠记忆行为进行检测;采用ELISA法测定SOD、GSH-PX和MDA的含量;采用HE法染色观察对小鼠大脑海马组织的影响。结果绞股蓝正丁醇部位能改善老年痴呆小鼠的学习记忆能力;能促进SOD和GSH-PX生成,抑制MDA的生成。结论绞股蓝正丁醇部位可提高AD小鼠的抗氧化能力,从而起到防治AD的作用。     

慢性乙型肝炎的抗病毒研究进展

慢性乙型肝炎是由乙型肝炎病毒(hepatitis B virus,HBV)引起的全球性传染病,HBV感染是我国肝硬化、原发性肝癌的重要原因。目前,干扰素类与核苷(酸)类似物抗病毒药物已广泛应用于临床,在一定程度上抑制了病毒的复制并控制了疾病的发展,但仍未从根本上清除病毒;各种治疗性疫苗在抗HBV方面也取得了一定疗效,但临床效果不佳。目前不少研究结果表明,生物免疫治疗可以成功清除体内的HBV,从而为乙肝的治疗带来新的希望。     

香菇多糖结构修饰研究进展

目的　对香菇多糖化学结构的修饰方法及其生物活性进行系统总结。方法　通过查阅近年来中英文相关文献,对香菇多糖已经报道的化学结构修饰方法及修饰后的生物活性进行了系统分析,总结阶段性进展。结果　香菇多糖结构修饰方法有化学修饰,包括硫酸化、羧甲基化、磷酸化及与金属离子螯合法等,物理修饰和生物修饰法等。不同的修饰方法对香菇多糖的生物活性有较大的影响。结论　结构修饰及其药理活性的深入研究仍是香菇多糖一个重要的研究方向。     

The Role of Serotonin (5-HT) in Behavioral Control: Findings from Animal Research and Clinical Implications

The neurotransmitters serotonin and dopamine both have a critical role in the underlying neurobiology of different behaviors. With focus on the interplay between dopamine and serotonin, it has been proposed that dopamine biases behavior towards habitual responding, and with serotonin offsetting this phenomenon and directing the balance toward more flexible, goal-directed responding. The present focus paper stands in close relationship to the publication by Worbe et al. (2015), which deals with the effects of acute tryptophan depletion, a neurodietary physiological method to decrease central nervous serotonin synthesis in humans for a short period of time, on the balance between hypothetical goal-directed and habitual systems. In that research, acute tryptophan depletion challenge administration and a following short-term reduction in central nervous serotonin synthesis were associated with a shift of behavioral performance towards habitual responding, providing further evidence that central nervous serotonin function modulates the balance between goal-directed and stimulus-response habitual systems of behavioral control. In the present focus paper, we discuss the findings by Worbe and colleagues in light of animal experiments as well as clinical implications and discuss potential future avenues for related research.     

Lipopolysaccharide-Induced Depressive-Like Behavior is Associated with α1-Adrenoceptor Dependent Downregulation of the Membrane GluR1 Subunit in the Mouse Medial Prefrontal Cortex and Ventral Tegmental Area

Background:

Chronic stress-induced depressive-like behavior is relevant to inflammatory immune activation. However, the neurobiological alterations in the brain following the central inflammatory immune activation remain elusive.

Methods:

Therefore, we investigated the neurobiological alterations during depressive-like behavior induced in mice by systemic administration of lipopolysaccharide (LPS; 1.2mg/kg administered twice at a 30-min interval via intraperitoneal injection).

Results:

At 24h after the second administration of LPS, an increased immobility time in the tail suspension test and the forced swimming test were observed, as well as reduced sucrose preference. Protein levels of the AMPA receptor GluR1 were significantly decreased at the plasma membrane in the medial prefrontal cortex (mPFC) and ventral tegmental area (VTA), while levels of the GluR2 were increased at the plasma membrane in the nucleus accumbens (NAc) at 24h after LPS. However, total GluR1 and GluR2 protein levels in the mPFC, VTA, and NAc were not affected by LPS. Moreover, LPS facilitated release of noradrenaline in the mPFC and VTA, but not in the NAc. Consistently, systemic administration of prazosin, an α₁-adrenoceptor antagonist, blocked the LPS-induced downregulation of the membrane GluR1 subunit in both the mPFC and VTA and also blocked the upregulation of the membrane GluR2 subunit in the NAc. Intracerebroventricular administration of prazosin 30min before LPS injection abrogated the LPS-induced depressive-like behaviors. In opposition, administration of propranolol, a β-adrenoceptor antagonist, did not affect the LPS-induced downregulation of GluR1, the upregulation of GluR2, or the depressive-like behavior.

Conclusions:

These results suggest that LPS-activated α₁-adrenoceptor-induced downregulation of membrane GluR1 in the mPFC and VTA is associated with inflammation-induced depressive-like behavior.     

Acute Nicotine Administration Increases BOLD fMRI Signal in Brain Regions Involved in Reward Signaling and Compulsive Drug Intake in Rats

Background:

Acute nicotine administration potentiates brain reward function and enhances motor and cognitive function. These studies investigated which brain areas are being activated by a wide range of doses of nicotine, and if this is diminished by pretreatment with the nonselective nicotinic receptor antagonist mecamylamine.

Methods:

Drug-induced changes in brain activity were assessed by measuring changes in the blood oxygen level dependent (BOLD) signal using an 11.1-Tesla magnetic resonance scanner. In the first experiment, nicotine naïve rats were mildly anesthetized and the effect of nicotine (0.03–0.6mg/kg) on the BOLD signal was investigated for 10min. In the second experiment, the effect of mecamylamine on nicotine-induced brain activity was investigated.

Results:

A high dose of nicotine increased the BOLD signal in brain areas implicated in reward signaling, such as the nucleus accumbens shell and the prelimbic area. Nicotine also induced a dose-dependent increase in the BOLD signal in the striato-thalamo-orbitofrontal circuit, which plays a role in compulsive drug intake, and in the insular cortex, which contributes to nicotine craving and relapse. In addition, nicotine induced a large increase in the BOLD signal in motor and somatosensory cortices. Mecamylamine alone did not affect the BOLD signal in most brain areas, but induced a negative BOLD response in cortical areas, including insular, motor, and somatosensory cortices. Pretreatment with mecamylamine completely blocked the nicotine-induced increase in the BOLD signal.

Conclusions:

These studies demonstrate that acute nicotine administration activates brain areas that play a role in reward signaling, compulsive behavior, and motor and cognitive function.     

Sedentary behavior is associated with chronic obstructive pulmonary disease: A generalized propensity score-weighted analysis

Chronic obstructive pulmonary disease (COPD) is the fourth and third leading cause of death worldwide and in China, respectively. Sedentary behavior has been shown to increase the risk of respiratory disease, such as asthma. However, the relationship between sedentary behavior and COPD is unclear. This study aimed to investigate the association between sedentary behavior and COPD.Data was extracted from the 2018 a large-scale cross-sectional study of Chronic Disease and Lifestyle Population Survey in Sichuan Province of China, in which sedentary behavior and chronic diseases were self-reported according to medical records. The association between sedentary behavior on risk of COPD was estimated using multivariable regression model in non-matching cohorts and generalized propensity score-weighted (GPSW)cohorts, respectively, controlling for potential confounders.Individuals who remained sedentary for more than 7 hours per day were more likely to have COPD than the control group (<3 hours) both in conventional multivariate logistic regression analysis (OR = 2.020, 95%CI: 1.575–2.585, P < .001) and GPSW analysis (OR = 2.381, 95%CI: 1.778–3.188, P < .001). After GPSW and the sensitivity analysis using refined smoking variable further found a dose-effect between sedentary behavior and COPD, with 1.242 (95%CI: 1.006–1.532, P < .05) times risk of COPD in those sedentary behavior of more than 5 hours per day (GPSW) and 1.377 (95%CI: 1.092–1.736, P < .05) times risk in those sedentary behavior above 5 hours per day (sensitivity analysis), comparing with the control group.Sedentary behavior is independently associated with increased risk of COPD, adjusting for other confounders. The findings of this study have important implications for future research and public health guidance. Reducing sedentary time may have a significant role in COPD prevention.