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目的 探讨老年难治性心力衰竭患者连续性肾脏替代治疗(continuous renal replacement therapy,CRRT)的效果及对血清C反应蛋白(Creactive protein,CRP)、半乳糖凝集素-3 (galectin-3,Gal-3)、氨基末端脑钠肽前体(N-terminal pro-bra...  相似文献   
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A century-long debate on bodily states and emotions persists. While the involvement of bodily activity in emotion physiology is widely recognized, the specificity and causal role of such activity related to brain dynamics has not yet been demonstrated. We hypothesize that the peripheral neural control on cardiovascular activity prompts and sustains brain dynamics during an emotional experience, so these afferent inputs are processed by the brain by triggering a concurrent efferent information transfer to the body. To this end, we investigated the functional brain–heart interplay under emotion elicitation in publicly available data from 62 healthy subjects using a computational model based on synthetic data generation of electroencephalography and electrocardiography signals. Our findings show that sympathovagal activity plays a leading and causal role in initiating the emotional response, in which ascending modulations from vagal activity precede neural dynamics and correlate to the reported level of arousal. The subsequent dynamic interplay observed between the central and autonomic nervous systems sustains the processing of emotional arousal. These findings should be particularly revealing for the psychophysiology and neuroscience of emotions.

“What Is an Emotion?” by William James (1), published more than a century ago, started the scientific debate on the nature of emotions. However, a shared and definitive theory of emotions is not in place yet, and the very definition of emotions and their nature is still a matter of debate. While more “classical” theories point to emotions as “the functional states of the brain that provide causal explanations of certain complex behaviors—like evading a predator or attacking prey” (2), other theories suggest how they are constructions of the world, not reactions to it (3). Namely, emotions are internal states constructed on the basis of previous experiences as predictive schemes to react to external stimuli.The role of bodily activity in emotions is often questioned. Despite the vast literature showing bodily correlates with emotions, a long-lasting debate about the relationship between bodily states and emotions persists (4). For instance, a feeling is defined as the subjective metarepresentation and labeling of physiological changes (such as an increase in heart rate, the increase of blood pressure, or changes in peristalsis) (5) that are strictly related to the body state on the one hand and to emotions on the other. To this extent, emotions are complex psychological phenomena in which feelings are interpreted and labeled. In a particular psychopathological condition known as alexithymia, individuals experience difficulties in experiencing and understanding emotions to various degrees (6). Indeed, some of these patients can perceive the physical changes connected to a feeling but are unable to label it as emotion, so that emotional experience is described only as its physical counterpart [e.g., described an experience as “I have my heart beating too fast” instead of “I’m fearful” (7)]. From a biological point of view the way in which physical changes become feelings and emotions is based on the interplay between the central and the autonomic nervous systems.The central nervous system (CNS) communicates with the autonomic nervous system (ANS) through interoceptive neural circuits that contribute to physiological functions beyond homeostatic control, from the emotional experience and the genesis of feelings (8) to decision making (9, 10). The debate about the role of the ANS in emotions can be condensed into two views: specificity or causation (4). The specificity view is related to the James–Lange theory, which states that bodily responses precede emotions’ central processing, meaning that bodily states would be a response to the environment, followed by an interpretation carried out by the CNS that would result in the feeling felt. However, causation theories represent an updated view of the James–Lange theory, suggesting that peripheral changes influence the conscious emotional experience; from a biological point of view this may reflect the fact that autonomic nervous signals from the body do influence perceptual activity in the brain (11, 12). In this regard, subjective perception may be influenced or shaped by ascending communication from visceral inputs to the brain (1315).Functional models of CNS and ANS interplay have described bidirectional dynamics in emotions (1618). In particular, the functional brain–heart interplay (BHI) involves brain structures that comprise the central autonomic network (CAN), which has been described as being in charge of autonomic control (19, 20). Moreover, the default mode network (DMN) has been found to be involved in autonomic control (21) and tasks of self-related cognition and interoception (22, 23), suggesting that the DMN participates in both ascending and descending communications with the heart. Finally, the constructed emotion theory suggests how DMN together with other intrinsic networks is crucial in the genesis of emotion and emotional experience (3).Psychophysiological studies have uncovered several correlates of different autonomic signals in the brain during emotional experiences (2427). To understand these correlations and the functional interactions between the heart and brain, various signal processing methods have been proposed to investigate functional BHI through noninvasive recordings (28). The study of emotions using these methods comprises the analysis of heartbeat-evoked potentials (29), nonlinear couplings (30), and information transfer modeling (31). However, the causative role of bodily inputs remains unknown (4) and, more specifically, the temporal and causal links between cortical and peripheral neural dynamics in both ascending and descending directions, i.e., from the brain to the body and from the body to the brain, are still to be clarified.In this study, we take a step forward in answering these scientific questions and investigate whether peripheral neural dynamics play a causal role in the genesis of emotions. We applied a mathematical model of functional BHI based on synthetic data generation (SDG) (32), estimating the directionality of the functional interplay using simultaneous electroencephalography (EEG) and electrocardiography (ECG) recordings gathered from healthy subjects undergoing emotion elicitations with video clips, the publicly available DEAP and MAHNOB datasets (33, 34). ECG series were analyzed to derive heart-rate variability (HRV) series, which result from the concurrent activity of the sympathetic and parasympathetic (vagal) branches of the ANS acting to regulate the heartbeat. We hypothesize that, from a neurobiological point of view, feelings and subsequent emotional experiences arise from the mutual interplay between brain and body, particularly in which the CNS integrates the afferent ANS information outflow, namely from-heart-to-brain interplay, which actually triggers a cascade of cortical neural activations that, in turn, modulate directed neural control onto the heart, namely from brain-to-heart interplay.  相似文献   
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Introduction:HIV confers increased risk of myocardial infarction (MI), but there has been little study of ischemic electrocardiogram (ECG) findings among people with HIV in sub-Saharan Africa.Objectives:To compare the prevalence of ischemic ECG findings among Tanzanians with and without HIV and to identify correlates of ischemic ECG changes among Tanzanians with HIV.Methods:Consecutive adults presenting for routine HIV care at a Tanzanian clinic were enrolled. Age- and sex-matched HIV-uninfected controls were enrolled from a nearby general clinic. All participants completed a standardized health questionnaire and underwent 12-lead resting ECG testing, which was adjudicated by independent physicians. Prior MI was defined as pathologic Q-waves in contiguous leads, and myocardial ischemia was defined as ST-segment depression or T-wave inversion in contiguous leads. Pearson’s chi-squared test was used to compare the prevalence of ECG findings among those with and without HIV and multivariate logistic regression was performed to identify correlates of prior MI among all participants.Results:Of 497 participants with HIV and 497 without HIV, 272 (27.8%) were males and mean (sd) age was 45.2(12.0) years. ECG findings suggestive of prior MI (11.1% vs 2.4%, OR 4.97, 95% CI: 2.71–9.89, p < 0.001), and myocardial ischemia (18.7% vs 12.1% OR 1.67, 95% CI: 1.18–2.39, p = 0.004) were significantly more common among participants with HIV. On multivariate analysis, ECG findings suggestive of prior MI among all participants were associated with HIV infection (OR 4.73, 95% CI: 2.51–9.63, p = 0.030) and self-reported family history of MI or stroke (OR 1.96, 95% CI: 1.08–3.46, p = 0.023).Conclusions:There may be a large burden of ischemic heart disease among adults with HIV in Tanzania, and ECG findings suggestive of coronary artery disease are significantly more common among Tanzanians with HIV than those without HIV.  相似文献   
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Background:The effects of omega-3 fatty acid on cardiovascular health obtained inconsistent results. A systematic review and meta-analysis were therefore conducted to assess the effects of omega-3 fatty acid supplementation for primary and secondary prevention strategies of major cardiovascular outcomes.Methods:The databases of PubMed, Embase, and the Cochrane library were systematically searched from their inception until September 2020. Relative risks (RRs) with 95% confidence intervals were used to assess effect estimates by using the random-effects model.Results:Twenty-eight randomized controlled trials involving 136,965 individuals were selected for the final meta-analysis. Omega-3 fatty acid was noted to be associated with a lower risk of major cardiovascular events (RR, 0.94; 95% CI, 0.89–1.00; P = .049) and cardiac death (RR, 0.92; 95% CI, 0.85–0.99; P = .022). However, no significant differences was noted between omega-3 fatty acid and the control for the risks of all-cause mortality (RR, 0.97; 95% CI, 0.92–1.03; P = .301), myocardial infarction (RR, 0.90; 95% CI, 0.80–1.01; P = .077), and stroke (RR, 1.02; 95% CI, 0.94–1.11; P = .694).Conclusions:Major cardiovascular events and cardiac death risks could be avoided with the use of omega-3 fatty acid. However, it has no significant effects on the risk of all-cause mortality, myocardial infarction, and stroke.  相似文献   
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于培养的新生大鼠海马神经细胞,应用fura2 荧光检测技术,观察了致疒间剂马桑内酯对单个海马神经细胞内钙离子浓度([Ca2+ ]i)的影响。培养液内马桑内酯浓度达10- 8m ol/L时可引起[Ca2+ ]i增加,[Ca2+ ]i随给药浓度的提高而升高。马桑内酯浓度达5×10- 8m ol/L时,[Ca2+ ]i维持于稳定的高水平上。当胞外无Ca2+时,马桑内酯仍可引起[Ca2+ ]i的升高;L型钙通道阻断剂verapam il不能阻断马桑内酯的上述作用。结果提示,海马神经细胞在致疒间剂作用下,发生Ca2+ 内流及胞内钙池释放现象。  相似文献   
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目的 研究中国人2型糖尿病合并高甘油三酯血症患者脂蛋白醒酶(1ipoprotein lipase,LPL)基因突变及对酶功能的影响,从脂代谢途径探讨引发糖尿病的遗传因素。方法 对高甘油三酯及血脂正常的2型糖尿病患者和正常人的LPL基因进行研究。利用PCR—SSCP、PCR—RFLP及DNA测序技术对LPL基因的启动子和10个外显子区域进行突变检测,针对特异位点进行体外定点突变和酶活力表达研究,利用网上工具平台Swiss-PDB Viewer对正常和突变蛋白进行二级结构模拟分析。结果 在177例高甘油三酯2型糖尿病患者中检测到4种错义突变:Ala71Thr、Val181IIe、Glyl88Glu和Glu242Lys,在正常血脂的糖尿病患者和健康人组中没有检出以上突变。这4种突变位于进化上高度保守的氨基酸位点,并分别在高度保守的外显子3、5及6区域。体内和体外酶活力研究表明,这4个突变均引起了酶活力降低甚至失活,其改变程度可以从它们所在序列的保守性、在酶功能结构城中的相对位置、相应的二级结构改变和氨基酸特性获得解释。结论 在受累个体中,LPL突变是引起患者血浆甘油三酯升高的直接原因,是其发展成2型糖尿病的遗传性易感因素。  相似文献   
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