任督灸用于新冠肺炎的预防和后期体质的恢复

邪正相争强者胜。人体阳气盛衰决定着个体对新型冠状病毒肺炎(简称“新冠肺炎”)的易感性及预后、转归情况。任督灸作为艾灸疗法中的一种特色大灸,以施灸面积广、火力大、持久深透且隔铺药物为特点,通过艾药结合的方式作用于任督二脉,可最大程度调整五脏六腑及全身气血,扶助人体阳气,提高抗御新型冠状病毒的能力。任督灸可根据个体的身体状态,辨证施以不同的药物。谨守病机,随证加减,以灸促药,以药强灸。一则可以温补元气,提升人体正气;二则可以温化寒湿,改变人体寒湿的环境状态;三则对证施药纠偏,恢复患者阴阳平衡的状态,营造不利于病毒生存的体内环境。在新冠肺炎防控中,任督灸可以发挥“未病先防”“愈后防复”的重要作用。     

A calcium-dependent protease as a potential therapeutic target for Wolfram syndrome

Wolfram syndrome is a genetic disorder characterized by diabetes and neurodegeneration and considered as an endoplasmic reticulum (ER) disease. Despite the underlying importance of ER dysfunction in Wolfram syndrome and the identification of two causative genes, Wolfram syndrome 1 (WFS1) and Wolfram syndrome 2 (WFS2), a molecular mechanism linking the ER to death of neurons and β cells has not been elucidated. Here we implicate calpain 2 in the mechanism of cell death in Wolfram syndrome. Calpain 2 is negatively regulated by WFS2, and elevated activation of calpain 2 by WFS2-knockdown correlates with cell death. Calpain activation is also induced by high cytosolic calcium mediated by the loss of function of WFS1. Calpain hyperactivation is observed in the WFS1 knockout mouse as well as in neural progenitor cells derived from induced pluripotent stem (iPS) cells of Wolfram syndrome patients. A small-scale small-molecule screen targeting ER calcium homeostasis reveals that dantrolene can prevent cell death in neural progenitor cells derived from Wolfram syndrome iPS cells. Our results demonstrate that calpain and the pathway leading its activation provides potential therapeutic targets for Wolfram syndrome and other ER diseases.The endoplasmic reticulum (ER) takes center stage for protein production, redox regulation, calcium homeostasis, and cell death (1, 2). It follows that genetic or acquired ER dysfunction can trigger a variety of common diseases, including neurodegenerative diseases, metabolic disorders, and inflammatory bowel disease (3, 4). Breakdown in ER function is also associated with genetic disorders such as Wolfram syndrome (5–8). It is challenging to determine the exact effects of ER dysfunction on the fate of affected cells in common diseases with polygenic and multifactorial etiologies. In contrast, we reasoned that it should be possible to define the role of ER dysfunction in mechanistically homogenous patient populations, especially in rare diseases with a monogenic basis, such as Wolfram syndrome (9).Wolfram syndrome (OMIM 222300) is a rare autosomal recessive disorder characterized by juvenile-onset diabetes mellitus and bilateral optic atrophy (7). Insulin-dependent diabetes usually occurs as the initial manifestation during the first decade of life, whereas the diagnosis of Wolfram syndrome is invariably later, with onset of symptoms in the second and ensuing decades (7, 10, 11). Two causative genes for this genetic disorder have been identified and named Wolfram syndrome 1 (WFS1) and Wolfram syndrome 2 (WFS2) (12, 13). It has been shown that multiple mutations in the WFS1 gene, as well as a specific mutation in the WFS2 gene, lead to β cell death and neurodegeneration through ER and mitochondrial dysfunction (5, 6, 14–16). WFS1 gene variants are also associated with a risk of type 2 diabetes (17). Moreover, a specific WFS1 variant can cause autosomal dominant diabetes (18), raising the possibility that this rare disorder is relevant to common molecular mechanisms altered in diabetes and other human chronic diseases in which ER dysfunction is involved.Despite the underlying importance of ER malfunction in Wolfram syndrome, and the identification of WFS1 and WFS2 genes, a molecular mechanism linking the ER to death of neurons and β cells has not been elucidated. Here we show that the calpain protease provides a mechanistic link between the ER and death of neurons and β cells in Wolfram syndrome.     

Effect of Multivitamin Supplementation on Measles Vaccine Response among HIV-Exposed Uninfected Tanzanian Infants

Immunization and nutritional interventions are mainstays of child health programs in sub-Saharan Africa, yet few published data exist on their interactions. HIV-exposed (but uninfected) infants enrolled in a randomized placebo-controlled trial of multivitamin supplements (vitamins B complex, C, and E) conducted in Tanzania were sampled for an assessment of measles IgG quantity and avidity at 15 to 18 months. Infants were vaccinated between 8.5 and 12 months of age, and all mothers received high-dose multivitamins as the standard of care. Of 201 HIV-exposed infants who were enrolled, 138 (68.7%) were seropositive for measles. There were no effects of infant multivitamin supplementation on measles seroconversion proportions, IgG concentrations, or IgG avidity (P > 0.05). The measles seroconversion proportion was greater for HIV-exposed infants vaccinated at 10 to 11 months of age than for those vaccinated at 8.5 to 10 months (P = 0.032) and greater for infants whose mothers had a CD4 T-cell count of <200 cells/μl than for infants whose mothers had a CD4 T-cell count of >350 cells/μl (P = 0.039). Stunted infants had a significantly decreased IgG quantity compared to nonstunted infants (P = 0.012). As for measles avidity, HIV-exposed infants vaccinated at 10 to 11 months had increased antibody avidity compared to those vaccinated at 8.5 to 10 months (P = 0.031). Maternal CD4 T-cell counts of <200 cells/μl were associated with decreased avidity compared to counts of >350 cells/μl (P = 0.047), as were lower infant height-for-age z-scores (P = 0.016). Supplementation with multivitamins containing B complex, C, and E does not appear to improve measles vaccine responses for HIV-exposed infants. Studies are needed to better characterize the impact of maternal HIV disease severity on the immune system development of HIV-exposed infants and the effect of malnutrition interventions on vaccine responses. (This study has been registered at ClinicalTrials.gov under registration no. NCT00197730.)     

非典型抗精神病药诱发代谢综合征和加重认知障碍相关机制的研究进展

认知障碍是精神分裂症的核心症状。非典型抗精神病药物治疗容易诱发患者的代谢综合 征,而代谢综合征又可进一步加重患者的认知障碍。引起以上临床表现的内在机制主要包括脑源性神 经因子机制、胰岛素抵抗机制、肠道菌群机制、免疫炎症机制和微血管病变机制。基于非典型抗精神病 药物、代谢综合征和认知障碍之间存在复杂联系,现就 3 者的关系及已发现的生物学机制予以综述。     

Associations of Body Mass Index and Waist Circumference with 3-Year All-Cause Mortality Among the Oldest Old: Evidence from a Chinese Community-Based Prospective Cohort Study

Objective

Current international and national guidelines for body mass index (BMI) and waist circumference (WC) have been recommended to all adults. However, whether recommendations applied to the oldest old (aged 80+) is poorly known. The study objective was to investigate the relation of BMI and WC with 3-year all-cause mortality among the oldest old.

壳聚糖的化学改性及其衍生物的抗氧化活性研究进展

摘 要壳聚糖是一种天然无毒的生物聚合物,主要经甲壳素的脱乙酰作用制得,具有良好的生物相容性、独特的抗氧化活性及生物可降解性等。由于壳聚糖在中性和碱性溶液中溶解性较差,其应用受到了一定限制,通常对其进行多种改性,拓宽其应用范围,提高其利用价值。近年来具有抗氧化能力的壳聚糖及壳聚糖衍生物表现出了优越的医用价值。本文综述了几种壳聚糖常用的改性方法,并介绍了壳聚糖及其衍生物作为抗氧化剂应用的研究进展。     

健脾清热化湿方联合美沙拉秦治疗脾虚湿热型缓解期溃疡性结肠炎的单病例随机对照试验

背景缓解期溃疡性结肠炎（UC）患者病程长,需长期维持治疗,中医药治疗缓解期UC具有一定的疗效。健脾清热化湿方治疗缓解期UC的疗效还不确切。目的采用单病例随机对照试验,评价健脾清热化湿方联合美沙拉秦对比美沙拉秦治疗脾虚湿热型缓解期UC患者的疗效和安全性。方法于2020年6月至2021年3月,在广州中医药大学第一附属医院门诊纳入1例缓解期UC患者。采取自身对照的方式,共进行4轮次无洗脱期的随机对照试验,每一轮次包括试验期和对照期两个治疗期,每个治疗期干预1个月,共8个治疗期。受试者在试验期服用健脾清热化湿方颗粒与美沙拉秦,在对照期服用美沙拉秦。比较两个治疗期的中医证候评分（TCMSS）、Bristol粪便性状量表（BSFS）、腹痛和腹泻视觉模拟评分（VAS）、炎症性肠病简明健康量表（SHS）评分及安全性。结果4轮次试验后,试验期腹泻、腹胀、肢体倦怠评分及TCMSS总分的改善程度优于对照期（P<0.05）。4轮次试验后,试验期BSFS评分和腹泻VAS评分的改善程度优于对照期,腹痛VAS评分的改善程度劣于对照期（P<0.05）。4轮次试验后,试验期SHS评分的改善程度优于对照期（P<0.05）。患者在4个周期均无不良反应发生。结论健脾清热化湿方联合美沙拉秦可改善脾虚湿热型缓解期UC患者的临床症状,且安全性较高。     

不同医用磁共振成像设备在中枢神经系统的临床图像质量评价与比较研究

目的对不同型号医用MRI成像设备进行中枢神经系统的临床图像质量评价与比较研究。材料与方法根据美国放射学会2013年颁布的MRI图像质量认证指南,共收集全国40余家医疗机构的531例中枢神经系统平扫MRI图像,对其4个常见序列进行临床图像质量Likert 5级评分;并将样本分为国产组与进口组,以及1.5 T组与3.0 T组进行比较研究。结果 3.0 T组大多数图像质量评价指标优于1.5 T组(P<0.05)。1.5 T组中,进口亚组大多数指标优于国产亚组(P<0.05);3.0 T组中,国产与进口亚组大多数指标差异无统计学意义。1.5 T组中,选取国产设备(联影)与进口设备(西门子、GE)分别比较,国产设备部分指标优于进口设备,部分指标仍与进口设备有一定差距。结论在中枢神经系统MRI临床图像质量中,3.0 T设备总体优于1.5 T设备,国产设备在某些方面优于进口设备,但整体水平仍与进口设备有一定差距。