Associations of childhood adversity and adulthood trauma with C-reactive protein: A cross-sectional population-based study

Mounting evidence highlights specific forms of psychological stress as risk factors for ill health. Particularly strong evidence indicates that childhood adversity and adulthood trauma exposure increase risk for physical and psychiatric disorders, and there is emerging evidence that inflammation may play a key role in these relationships. In a population-based sample from the Health and Retirement Study (n = 11,198, mean age 69 ± 10), we examine whether childhood adversity, adulthood trauma, and the interaction between them are associated with elevated levels of the systemic inflammatory marker high sensitivity C-reactive protein (hsCRP). All models were adjusted for age, gender, race, education, and year of data collection, as well as other possible confounds in follow-up sensitivity analyses. In our sample, 67% of individuals had experienced at least one traumatic event during adulthood, and those with childhood adversity were almost three times as likely to have experienced trauma as an adult. Childhood adversities and adulthood traumas were independently associated with elevated levels of hsCRP (β = 0.03, p = 0.01 and β = 0.05, p < 0.001, respectively). Those who had experienced both types of stress had higher levels of hsCRP than those with adulthood trauma alone, Estimate = −0.06, 95% CI [−0.003, −0.12], p = 0.04, but not compared to those with childhood adversity alone, Estimate = −0.06, 95% CI [0.03, −0.16], p = 0.19. There was no interaction between childhood and adulthood trauma exposure. To our knowledge, this is the first study to examine adulthood trauma exposure and inflammation in a large population-based sample, and the first to explore the interaction of childhood adversity and adulthood trauma with inflammation. Our study demonstrates the prevalence of trauma-related inflammation in the general population and suggests that childhood adversity and adulthood trauma are independently associated with elevated inflammation.     

Insights on the pathophysiology of Alzheimer's disease: The crosstalk between amyloid pathology,neuroinflammation and the peripheral immune system

Alzheimer's disease (AD) is the most common form of dementia, whose prevalence is growing along with the increased life expectancy. Although the accumulation and deposition of amyloid beta (Aβ) peptides in the brain is viewed as one of the pathological hallmarks of AD and underlies, at least in part, brain cell dysfunction and behavior alterations, the etiology of this neurodegenerative disease is still poorly understood. Noticeably, increased amyloid load is accompanied by marked inflammatory alterations, both at the level of the brain parenchyma and at the barriers of the brain. However, it is debatable whether the neuroinflammation observed in aging and in AD, together with alterations in the peripheral immune system, are responsible for increased amyloidogenesis, decreased clearance of Aβ out of the brain and/or the marked deficits in memory and cognition manifested by AD patients. Herein, we scrutinize some important traits of the pathophysiology of aging and AD, focusing on the interplay between the amyloidogenic pathway, neuroinflammation and the peripheral immune system.     

糖脂稳态失衡性动脉粥样硬化与血管衰老

血管衰老是严重影响人类健康和生活质量的最常见老年疾病之一,可发生于全身多种血管,如主动脉、冠状动脉、脑内血管以及周围血管等。动脉粥样硬化(atherosclerosis,AS)是血管衰老的主要病理基础,多种危险因素可促进AS的发生发展。糖脂稳态失衡引发的AS与老年性血管衰老密切相关,在老年血管性疾病的发生发展中发挥了重要作用。糖脂稳态失衡性AS作为血管病变的发病基础,如何参与血管衰老,二者之间如何相互影响,是目前学术界研究的热点。本文就糖脂稳态失衡性AS与血管衰老的相关性及其研究进展进行简要综述,以期帮助临床重新认识血管衰老并对其进行早期干预。     

健脾益肾方联用中药灌肠对改善慢性肾衰竭患者免疫功能的效果观察

目的:观察健脾益肾方联合中药灌肠对改善慢性肾衰竭患者免疫功能的效果。方法:将65例慢性肾衰竭患者随机分为两组,治疗组33例给予健脾益肾方和中药灌肠;对照组32例仅予中药灌肠。治疗前后检查患者肾功能三项、血红蛋白、免疫球蛋白IgA、IgG、IgM及血清补体C3、C4水平,并观察食欲、睡眠及二便情况等。结果:健脾益肾方与中药灌肠联用能更显著地降低肾功能三项,提升血红蛋白、血清补体C3及免疫球蛋白IgG、IgM水平,两组比较有显著性差异(P<0.05,P<0.01)。结论:健脾益肾方与中药灌肠联用能明显改善慢性肾衰竭患者的临床症状,保护肾功能,调节其免疫功能状态,从而治疗及延缓肾衰竭。     

树突状细胞与移植免疫耐受研究新进展

树突状细胞(DC)的生物学功能和免疫学特性是目前医学免疫学的研究热点之一。随着对DC免疫/耐受关系的进一步认识,最大限度地发挥其耐受潜能,从而探寻诱导移植免疫耐受新的治疗方法。     

Bioinformatics-based SARS-CoV-2 epitopes design and the impact of spike protein mutants on epitope humoral immunities

BackgroundEpitope selection is the key to peptide vaccines development. Bioinformatics tools can efficiently improve the screening of antigenic epitopes and help to choose the right ones.ObjectiveTo predict, synthesize and testify peptide epitopes at spike protein, assess the effect of mutations on epitope humoral immunity, thus provide clues for the design and development of epitope peptide vaccines against SARS-CoV-2.MethodsBioinformatics servers and immunological tools were used to identify the helper T lymphocyte, cytotoxic T lymphocyte, and linear B lymphocyte epitopes on the S protein of SARS-CoV-2. Physicochemical properties of candidate epitopes were analyzed using IEDB, VaxiJen, and AllerTOP online software. Three candidate epitopes were synthesized and their antigenic responses were evaluated by binding antibody detection.ResultsA total of 20 antigenic, non-toxic and non-allergenic candidate epitopes were identified from 1502 epitopes, including 6 helper T-cell epitopes, 13 cytotoxic T-cell epitopes, and 1 linear B cell epitope. After immunization with antigen containing candidate epitopes S_206-221, S_403-425, and S_1157-1170 in rabbits, the binding titers of serum antibody to the corresponding peptide, S protein, receptor-binding domain protein were (415044, 2582, 209.3), (852819, 45238, 457767) and (357897, 10528, 13.79), respectively. The binding titers to Omicron S protein were 642, 12,878 and 7750, respectively, showing that N211L, DEL212 and K417N mutations cause the reduction of the antibody binding activity.ConclusionsBioinformatic methods are effective in peptide epitopes design. Certain mutations of the Omicron would lead to the loss of antibody affinity to Omicron S protein.     

急性心肌梗塞患者血气和酸碱变化及其临床意义

对９１例首次急性心肌梗塞患者进行动脉血气分析。结果表明：①２５．２％（２３／９１）患者ＰａＯ２＜８．００ｋＰａ（１ｋＰａ＝７．５ｍｍＨｇ），４０．６％（３７／９１）患者ＰａＯ２＜９．３３ｋＰａ。ＰａＯ２＜９．３３ｋＰａ的３７例中１１例死亡，病死率明显高于ＰａＯ２＞９．３３ｋＰａ者（Ｐ＜０．０５）。ＰａＯ２＜８．００ｋＰａ的１１例患患者中９例死亡，病死率明显高于ＰａＯ２８．００～９．３３ｋＰａ者（Ｐ＜０．０１）。②９１例患者中８２例发生不同类型酸碱失衡（９０．１％），３８例混合型酸碱失衡者１３例死亡，病死率明显高于单纯性酸碱失衡者（Ｐ＜０．０１）。ｐＨ＞７．５００者１４例中９例死亡，病死率明显高于ｐＨ７．３００～７．５００者（Ｐ＜０．０１）。③９１例患者ｐＨ为７．４６５±０．０６９。提示：动脉血气分析有利于对心肌梗塞患者的预后和病情判断及指导治疗。     

生物免疫系统对信息安全的启示

生物免疫系统是一种高度分布性的自适应系统,它具有完善的机制来抵御外来病原体的入侵.它具有动态平衡性、分布性、自适应性、多样性等特点.本文探讨了这些特点为信息安全系统所带来的启示.     

抗CD47单克隆抗体(B6H12)对人树突状细胞成熟及其功能的影响

为阐明可溶性的抗CD47单克隆抗体(B6H12)对树突状细胞(DC)的免疫调控作用及分子机理.联合应用 rhGM-CSF、IL-4、细菌脂多糖(LPS)在体外诱导扩增人外周血单核细胞来源的DC,并在培养体系中添加抗CD47单 克隆抗体(B6H12);采用透射电镜观察DC形态,流式细胞术检测DC膜表面分子的表达;ELISA法检测DC释放的 IL-12 P70水平;BrdU-ELISA法检测DC刺激同种异型淋巴细胞增殖,凝胶电泳迁移率改变实验(EMSA)检测NF-κB 结合活性变化。结果发现:①经抗CD47单克隆抗体(B6H12)处理的DC,膜表面标记(CD80、CD86、CD1a、CD83、 DR)的表达显著地低于未加B6H12单克隆抗体DC组(P<0.05);其释放IL-12 P70蛋白质的能力及刺激同种异 型淋巴细胞增殖的能力也显著低于对照组(P<0.01)。②与未加B6H12单克隆抗体DC组相比,B6 H12单克隆抗 体处理DC组的NF-κB活性显著降低(P<0.05),并且这种抑制作用随单克隆抗体浓度增大而增强。结论:可溶 性的抗CD47单克隆抗体通过抑制NF-κB的结合活性,影响着DC向成熟发育及功能。