中医神理论对健康状态的辨识

中医神理论是从古代哲学中发展演化而来的中医基础理论核心内容之一。文章通过神的概念、神的来源、神的分类、神的功能及神理论与健康状态的关系等方面介绍神理论。而健康是人类最基本的需求和权利,更是医学所追求的最高目标。"有诸内必形诸外"可以通过眼神、神情、气色、体态、舌象、脉象等外在表现出的特点判断神的状态从而达到判断人体健康状况的目的。     

一氧化碳中毒患者凝血功能变化及预后评估

目的探讨不同中毒程度的一氧化碳中毒(ACOP)患者凝血功能变化及对预后的评估价值。方法选取2015年1月至2017年12月中国人民解放军第三七一中心医院收治的61例ACOP患者,根据一氧化碳中毒诊断及分级标准,分为轻度组(35例)和中重组(26例),选取同期体检的30例健康者作为对照组,比较3组患者ICU住院时间(d)、机械通气时间(d)、碳氧血红蛋白含量(%)。同时检测并比较3组患者常规凝血功能指标[凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、凝血酶时间(TT)、纤维蛋白原(FIB)、D-二聚体(D-D)、纤维蛋白(原)降解产物(FDP)]及血栓弹力图(TEG)指标凝血反应时间(R)、血块形成时间(K)、血凝速率(Angle角)、血块强度(MA)、血凝综合指数(CI),分析各指标之间的相关性。所有ACOP患者随访28天,根据预后情况分为存活组(42例)和死亡组(19例),评估并比较两组患者凝血功能。结果两组患者在ICU住院时间(d)、机械通气时间(d)、碳氧血红蛋白含量(%)比较,差异均有统计学意义(P <0. 05)。3组患者常规凝血功能指标及TEG指标比较,差异均有统计学意义(P <0. 05)。中重组患者PT、APTT、TT短于轻度组患者,D-D、FDP水平高于轻度组,差异均有统计学意义(P <0. 05),中重组与轻度组患者FIB比较,差异无统计学意义(P>0. 05)。死亡组患者与存活组患者比较,PT、APTT、TT缩短,FIB、D-D、FDP水平升高,差异均有统计学意义(P <0. 05)。TEG指标中,轻度组患者与对照组患者比较,R值缩短,MA值升高,差异均有统计学意义(P <0. 05)。中重组患者R值、K值显著缩短(P <0. 05),Angle角、MA值、CI值显著升高(P <0. 05)。死亡组患者与存活组患者比较,R值、K值缩短(P <0. 05),Angle角、MA值、CI值升高,差异均有统计学意义(P <0. 05)。Pearson相关分析显示:TEG检测中R值分别与PT、APTT呈正相关(P <0. 05); K值与APTT呈正相关(P <0. 05),与FIB呈负相关(P <0. 05); Angle角分别与APTT呈负相关(P <0. 05),与FIB、D-D呈正相关(P <0. 05); MA值与FIB呈正相关(P <0. 05); CI值分别与PT、APTT呈负相关(P <0. 05),与FIB呈正相关(P <0. 05)。结论 ACOP患者凝血功能紊乱程度与患者病情严重程度相关。常规凝血功能指标与血栓弹力图指标具有相关性,两者对监测ACOP患者凝血功能对临床治疗具有指导意义。     

城市炭疽气溶胶恐怖事件医学处置效果评估方法

目的 构建一种炭疽气溶胶恐怖事件医学处置效果的量化评估方法。方法 首先构建炭疽暴露后医学干预的决策树模型、关键资源消耗配置模型及不同干预措施下人群状态转移模型,从而形成一个资源约束下炭疽事件医学处置效果的评估框架。然后基于离散事件仿真技术,以我国大城市遭受炭疽恐怖袭击为情景,分析评估52种干预策略对发病人数、峰值、死亡人数的影响。结果 干预效果对介入延迟时间和资源储备量2个因素均敏感。在仿真案例中,当介入延迟时间为事发后1 h时,将资源储备量从25%提高到100%可减少约59.91%的死亡人数;当介入延迟时间为事发后145时,将资源储备量从25%提高到100%只能减少约7.33%的死亡人数。干预策略对发病人数达到峰值的时间影响很小,最大值为10.52 d,最小值为9.67 d;对峰值人数影响较大,最大值为255 072人,最小值为103 943人。结论 建立了一种炭疽气溶胶恐怖事件医学处置效果的定量评估方法,在医学救援能力建设、应急策略选择方面具有一定的参考价值。     

舒降之对维持血透患者微炎症状态的影响

目的: 通过观察舒降之对维持性血液透析患者相关炎症和营养指标白介素-6(IL-6)、高敏C反应蛋白(hs-CRP)、白蛋白、前白蛋白、转铁蛋白的影响,了解其对维持性血液透析患者微炎症状态的作用,探讨他汀类药物在透析患者中应用指征.方法: 将34例稳定维持血液透析患者,随机分为实验组19例及对照组15例.实验期间实验组每位患者每日服用舒降之20 mg,对照组不服药,时间为2月,分别在实验开始、1月末、2月末检测患者血IL-6、CRP、前白蛋白、转铁蛋白及血脂浓度.实验结果采用t检验分析.结果:和实验前相比,实验结束时实验组IL-6明显升高、CRP明显降低、白蛋白与转铁蛋白升高 ,均具有统计学差异(P<0.01);而前白蛋白虽有一定幅度上升,但结果无统计学差异 .实验前后,总胆固醇、LDL浓度改变未显示出统计学差异.而实验结束时甘油三酯较1月末及实验开始时显著降低,结果具有统计学差异.对照组各项指标试验前后无明显改变.结论:舒降之可降低维持性血液透析患者血液CRP、IL-6浓度,升高转铁蛋白、白蛋白浓度,改善患者营养及微炎症状态,这种作用并不依赖于其调脂功能.     

气升式发酵罐发酵黄原胶的动力学

利用黄单孢菌研究了在50L气升式发酵罐发酵黄原胶的动力学,在logistic方程和Luedeking Piret方程的基础上,建立了两步发酵黄原胶的动力学模型,并对模型和实验数据进行了比较,进一步在200L相似结构的气升式发酵罐中的试验表明,该模型能较好的对发酵动力学进行描述.     

一种新型开菲尔奶制作工艺

将草莓汁、菠萝汁、白砂糖加入鲜牛奶中经杀菌冷却后接种开菲尔粒制作的发酵剂,25℃恒温发酵,采用正交试验法对其它工艺参数进行了研究.结果表明,草莓汁和菠萝汁的添加体积分数均为3%,白砂糖质量分数为8%,接种发酵剂体积分数4%,发酵16h后获得了一种口感、组织状态、风味俱佳的新型开菲尔奶.     

The redox state of the alarmin HMGB1 is a pivotal factor in neuroinflammatory and microglial priming: A role for the NLRP3 inflammasome

The alarmin high mobility group box-1 (HMGB1) has been implicated as a key factor mediating neuroinflammatory processes. Recent findings suggest that the redox state of HMGB1 is a critical molecular feature of HMGB1 such that the reduced form (fr-HMGB1) is chemotactic, while the disulfide form (ds-HMGB1) is pro-inflammatory. The present study examined the neuroinflammatory effects of these molecular forms as well as the ability of these forms to prime the neuroinflammatory and microglial response to an immune challenge. To examine the neuroinflammatory effects of these molecular forms in vivo, animals were administered intra-cisterna magna (ICM) a single dose of fr-HMGB1 (10 μg), ds-HMGB1 (10 μg) or vehicle and basal pro-inflammatory effects were measured 2 and 24 h post-injection in hippocampus. Results of this initial experiment demonstrated that ds-HMGB1 increased hippocampal pro-inflammatory mediators at 2 h (NF-κBIα mRNA, NLRP3 mRNA and IL-1β protein) and 24 h (NF-κBIα mRNA, TNFα mRNA, and NLRP3 protein) after injection. fr-HMGB1 had no effect on these mediators. These neuroinflammatory effects of ds-HMGB1 suggested that ds-HMGB1 may function to prime the neuroinflammatory response to a subsequent immune challenge. To assess the neuroinflammatory priming effects of these molecular forms, animals were administered ICM a single dose of fr-HMGB1 (10 μg), ds-HMGB1 (10 μg) or vehicle and 24 h after injection, animals were challenged with LPS (10 μg/kg IP) or vehicle. Neuroinflammatory mediators and the sickness response (3, 8 and 24 h after injection) were measured 2 h after immune challenge. We found that ds-HMGB1 potentiated the neuroinflammatory (NF-κBIα mRNA, TNFα mRNA, IL-1β mRNA, IL-6 mRNA, NLRP3 mRNA and IL-1β protein) and sickness response (reduced social exploration) to LPS challenge. fr-HMGB1 failed to potentiate the neuroinflammatory response to LPS. To examine whether these molecular forms of HMGB1 directly induce neuroinflammatory effects in isolated microglia, whole brain microglia were isolated and treated with fr-HMGB1 (0, 1, 10, 100, or 1000 ng/ml) or ds-HMGB1 (0, 1, 10, 100, or 1000 ng/ml) for 4 h and pro-inflammatory mediators measured. To assess the effects of these molecular forms on microglia priming, whole brain microglia were pre-exposed to these forms of HMGB1 (0, 1, 10, 100, or 1000 ng/ml) and subsequently challenged with LPS (10 ng/ml). We found that ds-HMGB1 increased expression of NF-κBIα mRNA and NLRP3 mRNA in isolated microglia, and potentiated the microglial pro-inflammatory response (TNFα mRNA, IL-1β mRNA and IL-1β protein) to LPS. fr-HMGB1 failed to potentiate the microglial pro-inflammatory response to LPS. Consistent with prior reports, the present findings demonstrate that the disulfide form of HMGB1 not only potentiates the neuroinflammatory response to a subsequent immune challenge in vivo, but also potentiates the sickness response to that challenge. Moreover, the present findings demonstrate for the first time that ds-HMGB1 directly potentiates the microglia pro-inflammatory response to an immune challenge, a finding that parallels the effects of ds-HMGB1 in vivo. In addition, ds-HMGB1 induced expression of NLRP3 and NF-κBIα in vivo and in vitro suggesting that the NLRP3 inflammasome may play role in the priming effects of ds-HMGB1. Taken together, the present results suggest that the redox state of HMGB1 is a critical determinant of the priming properties of HMGB1 such that the disulfide form of HMGB1 induces a primed immunophenotype in the CNS, which may result in an exacerbated neuroinflammatory response upon exposure to a subsequent pro-inflammatory stimulus.     

Intrinsic functional connectivity of insular cortex and symptoms of sickness during acute experimental inflammation

Task-based fMRI has been used to study the effects of experimental inflammation on the human brain, but it remains unknown whether intrinsic connectivity in the brain at rest changes during a sickness response. Here, we investigated the effect of experimental inflammation on connectivity between areas relevant for monitoring of bodily states, motivation, and subjective symptoms of sickness. In a double-blind randomized controlled experiment, 52 healthy volunteers were injected with 0.6 ng/kg LPS (lipopolysaccharide) or placebo, and participated in a resting state fMRI experiment after approximately 2 h 45 min. Resting state fMRI data were available from 48 participants, of which 28 received LPS and 20 received placebo. Bilateral anterior and bilateral posterior insula sections were used as seed regions and connectivity with bilateral orbitofrontal and cingulate (anterior and middle) cortices was investigated. Back pain, headache and global sickness increased significantly after as compared to before LPS, while a non-significant trend was shown for increased nausea. Compared to placebo, LPS was followed by increased connectivity between left anterior insula and left midcingulate cortex. This connectivity was significantly correlated to increase in back pain after LPS and tended to be related to increased global sickness, but was not related to increased headache or nausea. LPS did not affect the connectivity from other insular seeds. In conclusion, the finding of increased functional connectivity between left anterior insula and middle cingulate cortex suggests a potential neurophysiological mechanism that can be further tested to understand the subjective feeling of malaise and discomfort during a sickness response.     

Freezing of gait in Parkinson's disease is associated with altered functional brain connectivity

BackgroundPatients with Parkinson's disease (PD) may develop several gait disturbances during the course of illness and Freezing of gait (FOG) is one of them. Several neuroimaging studies have been conducted to identify the neural correlates of FOG but results have not been uniform. Resting state functional MRI (rs-fMRI) is relatively less explored in PD patients with FOG. This study aims to compare the whole brain resting state connectivity of PD patients with and without FOG using rs-fMRI.Methodsrs-fMRI was obtained for 28 PD patients (15 with and 13 patients without FOG) who were matched for various demographic and clinical characteristics. Seed to voxel analysis was performed at whole brain level and compared between the two groups.ResultsWhen compared to patients without FOG, the patients with FOG had reduced functional connectivity across multiple seeds. Major finding was reduced inter-hemispheric connectivity of left parietal opercular cortex with multiple regions of the brain primarily involving the primary somatosensory and auditory areas, which also negatively correlated with the FOGQ scores.ConclusionOur findings suggest that alterations in the resting state functional connectivity of the opercular parietal cortex may be one of the substrates of FOG. Reduced interhemispheric connectivity probably is the reason for impairment of control and coordination in bilateral leg movements while walking.     

The implication of frontostriatal circuits in young smokers: A resting‐state study

The critical roles of frontostriatal circuits had been revealed in addiction. With regard to young smokers, the implication of frontostriatal circuits resting‐state functional connectivity (RSFC) in smoking behaviors and cognitive control deficits remains unclear. In this study, the volume of striatum subsets, i.e., caudate, putamen, and nucleus accumbens, and corresponding RSFC differences were investigated between young smokers (n₁ = 60) and nonsmokers (n₂ = 60), which were then correlated with cigarette smoking measures, such as pack_years‐cumulative effect of smoking, Fagerström Test for Nicotine Dependence (FTND)‐severity of nicotine addiction, Questionnaire on Smoking Urges (QSU)‐craving state, and Stroop task performances. Additionally, mediation analysis was carried out to test whether the frontostriatal RSFC mediates the relationship between striatum morphometry and cognitive control behaviors in young smokers when applicable. We revealed increased volume of right caudate and reduced RSFC between caudate and dorsolateral prefrontal cortex (DLPFC), orbitofrontal cortex in young smokers. Significant positive correlation between right caudate volume and QSU as well as negative correlation between anterior cingulate cortex‐right caudate RSFC and FTND were detected in young smokers. More importantly, DLPFC‐caudate RSFC strength mediated the relationship between caudate volume and incongruent errors during Stroop task in young smokers. Our results demonstrated that young smokers showed abnormal interactions within frontostriatal circuits, which were associated with smoking behaviors and cognitive control impairments. It is hoped that our study focusing on frontostriatal circuits could provide new insights into the neural correlates and potential novel therapeutic targets for treatment of young smokers. Hum Brain Mapp 37:2013–2026, 2016. © 2016 Wiley Periodicals, Inc .