BACKGROUND & AIMS: :Although the role of oxidative stress in maternal aging and infertility has been suggested, the underlying mechanisms are not fully understood. The present study is designed to determine the relationship between mitochondrial function and spindle stability in metaphase II (MII) oocytes under oxidative stress. MII mouse oocytes were treated with H2O2 in the presence or absence of permeability transition pores (PTPs) blockers cyclosporin A (CsA). In addition, antioxidant N-acetylcysteine (NAC), F0/F1 synthase inhibitor oligomycin A, the mitochondria uncoupler carbonyl cyanide 4-trifluoro-methoxyphenylhydrazone (FCCP) or thapsigargin plus 2.5 mM Ca2+ (Th+2.5 mM Ca2+) were used in mechanistic studies. Morphologic analyses of oocyte spindles and chromosomes were performed and mitochondrial membrane potential (DeltaPsim), cytoplasmic free calcium concentration ([Ca2+]c) and cytoplasmic ATP content within oocytes were also assayed. In a time- and H2O2 dose-dependent manner, disruption of meiotic spindles was found after oocytes were treated with H2O2, which was prevented by pre-treatment with NAC. Administration of H2O2 led to a dissipation of DeltaPsim, an increase in [Ca2+]c and a decrease in cytoplasmic ATP levels. These detrimental responses of oocytes to H2O2 treatment could be blocked by pre-incubation with CsA. Similar to H2O2, both oligomycin A and FCCP dissipated DeltaPsim, decreased cytoplasmic ATP contents and disassembled MII oocyte spindles, while high [Ca2+]c alone had no effects on spindle morphology. In conclusion, the decrease in mitochondria-derived ATP during oxidative stress may cause a disassembly of mouse MII oocyte spindles, presumably due to the opening of the mitochondrial PTPs.

背景与目标： : 尽管已经提出了氧化应激在孕产妇衰老和不育中的作用，但其潜在机制尚未完全了解。本研究旨在确定氧化应激下中期II (MII) 卵母细胞线粒体功能与纺锤体稳定性之间的关系。在存在或不存在通透性过渡孔 (ptp) 阻滞剂环孢菌素A (CsA) 的情况下，用H2O2处理MII小鼠卵母细胞。此外，在机理研究中使用了抗氧化剂N-乙酰半胱氨酸 (NAC)，F0/F1合酶抑制剂寡霉素A，线粒体解偶联羰基氰化物4-三氟-甲氧基苯腙 (FCCP) 或thapsigargin加2.5 mM Ca2 (Th 2.5 mM Ca2)。进行了卵母细胞纺锤体和染色体的形态学分析，并测定了卵母细胞内线粒体膜电位 (DeltaPsim)，胞质游离钙浓度 ([Ca2] c) 和胞质ATP含量。以时间和H2O2剂量依赖性的方式，在用H2O2处理卵母细胞后发现了减数分裂纺锤体的破坏，而NAC预处理可以防止这种破坏。施用H2O2导致DeltaPsim消散，[Ca2] c增加和细胞质ATP水平降低。卵母细胞对H2O2处理的这些有害反应可以通过与CsA预孵育来阻断。与H2O2相似，寡霉素A和FCCP都消散了DeltaPsim，降低了细胞质ATP含量并分解了MII卵母细胞纺锤体，而单独的高 [Ca2] c对纺锤体形态没有影响。总之，氧化应激过程中线粒体衍生的ATP的减少可能会导致小鼠MII卵母细胞纺锤体的分解，这可能是由于线粒体PTPs的打开所致。

BACKGROUND & AIMS: OBJECTIVE:To investigate the relation between measures of pain threshold and symptoms of distress to determine if fibromyalgia is a discrete construct/ disorder in the clinic.

METHODS:627 patients seen at an outpatient rheumatology centre from 1993 to 1996 underwent tender point and dolorimetry examinations. All completed the assessment scales for fatigue, sleep disturbance, anxiety, depression, global severity, pain, functional disability, and a composite measure of distress constructed from scores of sleep disturbance, fatigue, anxiety, depression, and global severity-the rheumatology distress index (RDI).

RESULTS:In regression analyses, the RDI was linearly related to the count of tender points (r2 = 0.30). Lesser associations were found between the RDI and dolorimetry measurements (r2 = 0.08). The RDI was more strongly correlated with the two measures of pain threshold than any of the individual fibromyalgia symptom variables. In partial correlation analyses, all of the information relating to symptom variables was contained in the tender point count, and dolorimetry was not independently related to symptoms.

CONCLUSION:Tender points are linearly related to fibromyalgia variables and distress, and there is no discrete enhancement or perturbation of fibromyalgia or distress variables associated with very high levels of tender points. Although fibromyalgia is a recognisable clinical entity, there seems to be no rationale for treating fibromyalgia as a discrete disorder, and it would seem appropriate to consider the entire range of tenderness and distress in clinic patients as well as in research studies. The tender point count functions as a 'sedimentation rate' for distress, and is a better measure than the dolorimetry score.

背景与目标： 目的 : 研究疼痛阈值的测量与痛苦症状之间的关系，以确定纤维肌痛是否是临床中的离散结构/疾病。
方法 : 在门诊风湿病中心1993年的627名患者1996年接受了压痛点和度日检查。全部完成乏力，睡眠障碍，焦虑，抑郁，整体严重程度，疼痛，功能障碍的评估量表，以及由睡眠障碍，乏力，焦虑，抑郁，和全球严重程度-风湿病困扰指数 (RDI)。
结果 : 在回归分析中，RDI与压痛点的计数呈线性关系 (r2 = 0.30)。在RDI和测年测量之间发现较小的关联 (r2 = 0.08)。与任何单个纤维肌痛症状变量相比，RDI与两种疼痛阈值的相关性更强。在偏相关分析中，与症状变量有关的所有信息都包含在压痛点计数中，并且度量法与症状没有独立关系。
结论 : 压痛点与纤维肌痛变量和困扰呈线性关系，并且没有与非常高的压痛点相关的纤维肌痛或窘迫变量的离散增强或扰动。尽管纤维肌痛是可识别的临床实体，但似乎没有理由将纤维肌痛作为一种离散性疾病进行治疗，并且在临床患者以及研究中考虑整个范围的压痛和困扰似乎是合适的。招标点计数起遇险的 “沉降率” 的作用，并且比dolorimetry评分更好。

BACKGROUND & AIMS: :Increased ammonia accumulation in the brain due to liver dysfunction is a major contributor to the pathogenesis of hepatic encephalopathy (HE). Fatal outcome of rapidly progressing (acute) HE is mainly related to cytotoxic brain edema associated with astrocytic swelling. An increase of brain ammonia in experimental animals or treatment of cultured astrocytes with ammonia generates reactive oxygen and nitrogen species in the target tissues, leading to oxidative/nitrosative stress (ONS). In cultured astrocytes, ammonia-induced ONS is invariably associated with the increase of the astrocytic cell volume. Interrelated mechanisms underlying this response include increased nitric oxide (NO) synthesis which is partly coupled to the activation of NMDA receptors and increased generation of reactive oxygen species by NADPH oxidase. ONS and astrocytic swelling are further augmented by excessive synthesis of glutamine (Gln) which impairs mitochondrial function following its accumulation in there and degradation back to ammonia ("the Trojan horse" hypothesis). Ammonia also induces ONS in other cell types of the CNS: neurons, microglia and the brain capillary endothelial cells (BCEC). ONS in microglia contributes to the central inflammatory response, while its metabolic and pathophysiological consequences in the BCEC evolve to the vasogenic brain edema associated with HE. Ammonia-induced ONS results in the oxidation of mRNA and nitration/nitrosylation of proteins which impact intracellular metabolism and potentiate the neurotoxic effects. Simultaneously, ammonia facilitates the antioxidant response of the brain, by activating astrocytic transport and export of glutathione, in this way increasing the availability of precursors of neuronal glutathione synthesis.

背景与目标： : 由于肝功能障碍，大脑中氨积累的增加是肝性脑病 (HE) 发病机理的主要原因。快速进展 (急性) HE的致命结果主要与星形细胞肿胀相关的细胞毒性脑水肿有关。实验动物中脑氨的增加或用氨处理培养的星形胶质细胞会在目标组织中产生活性氧和氮，从而导致氧化/亚硝化应激 (ONS)。在培养的星形胶质细胞中，氨诱导的ONS总是与星形细胞体积的增加有关。此响应的相关机制包括增加的一氧化氮 (NO) 合成，这部分与NMDA受体的激活以及NADPH氧化酶增加的活性氧生成有关。谷氨酰胺 (Gln) 的过度合成进一步加剧了ONS和星形细胞的肿胀，谷氨酰胺 (Gln) 在其中积累并降解回氨后会损害线粒体功能 (“特洛伊木马” 假说)。氨还在中枢神经系统的其他细胞类型中诱导ONS: 神经元，小胶质细胞和脑毛细血管内皮细胞 (BCEC)。小胶质细胞中的ONS有助于中枢炎症反应，而其在BCEC中的代谢和病理生理后果则演变为与HE相关的血管源性脑水肿。氨诱导的ONS导致mRNA的氧化和蛋白质的硝化/亚硝基化，从而影响细胞内代谢并增强神经毒性作用。同时，氨通过激活星形细胞的运输和谷胱甘肽的出口来促进大脑的抗氧化反应，从而增加了神经元谷胱甘肽合成前体的可用性。

BACKGROUND & AIMS: BACKGROUND:Diabetes mellitus (DM) is associated with hyperglycemia, inflammatory disorders and abnormal lipid profiles, currently the extracts from leaves of cynara scolymus has been discovered to treat metabolic disorders and has been stated by multitudinous scientists according to a good source of polyphenols compounds. The present study aimed to evaluate the protective effect of the ethanol leaves extract of C. scolymus in alloxan induced stress oxidant, hepatic-kidney dysfunction and histological changes in liver, kidney and pancreas of different experimental groups of rats. METHODS:We determinate the antioxidant activity by ABTS .+ and antioxidant total capacity (TAC) of all extracts of C. scolymus leaves, the inhibition of α-amylase activity in vitro was also investigated. Forty male Wistar rats were induced to diabetes with a single dose intraperitoneal injection (i.p.) of alloxan (150 mg/kg body weight (b.w.)). Diabetic rats were orally and daily administrated of ethanol extract from C. scolymus at two doses (200-400 mg/kg, b.w) or (12 mg/kg, b.w) with anti-diabetic reference drug, Acarbose for one month. Ethanol extract of C. scolymus effect was confirmed by biochemical analysis, antioxidant activity and histological study. RESULTS:The results indicated that the ethanol extract from leaves of C. scolymus showed the highest antioxidant activity by ABTS .+ (499.43g± 39.72 Trolox/g dry extract) and (128.75 ± 8.45 mg VC /g dry extract) for TAC and endowed the powerful inhibition in vitro of α-amylase activity with IC50=72,22 ug/uL. In vivo, the results showed that ethanol extract from the leaves of C. scolymus (200-400 mg/kg) decreased significantly (p < 0.001) the α-amylase levels in serum of diabetic rats, respectively associated with significant reduction (p < 0.001) in blood glucose rate of 42,84% and 37,91% compared to diabetic groups after 28 days of treatment, a significant lowered of plasma total cholesterol (T-Ch) by 18,11% and triglyceride (TG) by 60,47%, significantly and low-density lipoproteins (LDL-C) by 37,77%, compared to diabetic rats, moreover, the administration of ethanol extract appears to exert anti-oxidative activity demonstrated by the increase of CAT, SOD and GSH activities in liver, kidney and pancreas of diabetic rats. This positive effect of the ethanol extract from C. scolymus was confirmed by histological study. CONCLUSION:These observed strongly suggest that ethanol extract from the leaves of C. scolymus has anti-hyperglycemic properties, at least partly mediated by antioxidant and hypolipidemic effects.

背景与目标：

BACKGROUND & AIMS: Importance:Opioid use disorder (OUD) frequently begins in adolescence and young adulthood. Intervening early with pharmacotherapy is recommended by major professional organizations. No prior national studies have examined the extent to which adolescents and young adults (collectively termed youth) with OUD receive pharmacotherapy. Objective:To identify time trends and disparities in receipt of buprenorphine and naltrexone among youth with OUD in the United States. Design, Setting, and Participants:A retrospective cohort study was conducted using deidentified data from a national commercial insurance database. Enrollment and complete health insurance claims of 9.7 million youth, aged 13 to 25 years were analyzed, identifying individuals who received a diagnosis of OUD between January 1, 2001, and June 30, 2014, with final follow-up date December 31, 2014. Analysis was conducted from April 25 to December 31, 2016. Time trends were identified and multivariable logistic regression was used to determine sociodemographic factors associated with medication receipt. Exposures:Sex, age, race/ethnicity, neighborhood education and poverty levels, geographic region, census region, and year of diagnosis. Main Outcomes and Measures:Dispensing of a medication (buprenorphine or naltrexone) within 6 months of first receiving an OUD diagnosis. Results:Among 20 822 youth diagnosed with OUD (0.2% of the 9.7 million sample), 13 698 (65.8%) were male and 17 119 (82.2%) were non-Hispanic white. Mean (SD) age was 21.0 (2.5) years at the first observed diagnosis. The diagnosis rate of OUD increased nearly 6-fold from 2001 to 2014 (from 0.26 per 100 000 person-years to 1.51 per 100 000 person-years). Overall, 5580 (26.8%) youth were dispensed a medication within 6 months of diagnosis, with 4976 (89.2%) of medication-treated youth receiving buprenorphine and 604 (10.8%) receiving naltrexone. Medication receipt increased more than 10-fold, from 3.0% in 2002 (when buprenorphine was introduced) to 31.8% in 2009, but declined in subsequent years (27.5% in 2014). In multivariable analyses, younger individuals were less likely to receive medications, with adjusted probability for age 13 to 15 years, 1.4% (95% CI, 0.4%-2.3%); 16 to 17 years, 9.7% (95% CI, 8.4%-11.1%); 18 to 20 years, 22.0% (95% CI, 21.0%-23.0%); and 21 to 25 years, 30.5% (95% CI, 30.0%-31.5%) (P < .001 for difference). Females (7124 [20.3%]) were less likely than males (13 698 [24.4%]) to receive medications (P < .001), as were non-Hispanic black (105 [14.8%]) and Hispanic (1165 [20.0%]) youth compared with non-Hispanic white (17 119 [23.1%]) youth (P < .001). Conclusions and Relevance:In this first national study of buprenorphine and naltrexone receipt among youth, dispensing increased over time. Nonetheless, only 1 in 4 commercially insured youth with OUD received pharmacotherapy, and disparities based on sex, age, and race/ethnicity were observed.

背景与目标：

BACKGROUND & AIMS: OBJECTIVES:To evaluate temperament and character traits using the Junior Temperament and Character Inventory (JTCI) in children and adolescents with major depressive disorder (MDD) in comparison with healthy control subjects (HC), and to verify if comorbidity with disruptive behavioral disorders and being currently depressed influence JTCI scores. METHODS:A case-control study comprising 41 MDD children/adolescents matched to 40 HC by gender and age (8-17years). All participants were assessed diagnostically with the Kiddie Schedule for Affective Disorders and Schizophrenia - Present and Lifetime (K-SADS-PL). Temperament and character traits were measured with the parent and child versions of JTCI, and depression was evaluated with the Children's Depression Rating Scale (CDRS). RESULTS:According to child and parent data, MDD subjects had significantly higher scores on harm avoidance and novelty seeking, and lower scores on reward dependence, persistence, self-directedness and cooperativeness compared with HC. According to parent data only, MDD subjects significantly differed from HC on self-transcendence (lower spirituality scores and higher fantasy scores). Comorbidity with disruptive behavioral disorders exerted influence on almost all dimensions, in general increasing the mean differences between MDD and HC subjects. Also, being currently depressed did not influence the results, except for reward dependence according to parent data. LIMITATIONS:The cross-sectional nature of the study and its limited sample size. CONCLUSIONS:MDD children/adolescents have a different temperament and character profile compared to HC subjects. This study supports previous findings of trait-like characteristics of harm avoidance and self-directedness.

背景与目标：

BACKGROUND & AIMS: :Rooibos leaves and fine stems (Aspalathus linearis; Fabaceae) are increasingly enjoyed as herbal tea, largely in fermented (oxidised) red-brown form, but also in unfermented (unoxidised) green form. Rooibos is rich in antioxidant polyphenols, with the dihydrochalcone, aspalathin, as a major active ingredient. We used Caenorhabditis elegans as model organism to investigate the effect of rooibos extracts against oxidative stress in vivo. In a high glucose environment, C. elegans treated with rooibos extract exhibited an extended lifespan. Furthermore, green rooibos was a more potent antioxidant than red rooibos, probably due to its substantially higher aspalathin content. In addition, rooibos decreased acute oxidative damage caused by the superoxide anion radical generator, juglone, with aspalathin playing a major role in improving the survival rate of C. elegans. Quantitative real-time PCR results demonstrated that aspalathin targets stress and ageing related genes, reducing the endogenous intracellular level of ROS. These findings suggest that rooibos increases stress resistance and promotes longevity under stress, probably mediated via a regulation of the DAF-16/FOXO insulin-like signalling pathway, supporting some of the health claims put forward for rooibos tea.

背景与目标： : Rooibos的叶子和细茎 (Aspalathus linearis; Fabaceae) 作为凉茶越来越受到欢迎，主要以发酵 (氧化) 的红棕色形式，但也以未发酵 (未氧化) 的绿色形式。Rooibos富含抗氧化剂多酚，其中二氢查耳酮，aspalathin是主要的活性成分。我们使用秀丽隐杆线虫作为模型生物，研究了rooibos提取物对体内氧化应激的影响。在高葡萄糖环境中，用rooibos提取物处理的秀丽隐杆线虫的寿命延长。此外，绿色rooibos是比红色rooibos更有效的抗氧化剂，这可能是由于其aspalathin含量高得多。此外，rooibos降低了由超氧阴离子自由基发生器juglone引起的急性氧化损伤，而aspalathin在提高秀丽隐杆线虫的存活率中起着重要作用。实时定量PCR结果表明，aspalathin靶向应激和衰老相关基因，降低了细胞内ROS的内源性水平。这些发现表明，rooibos可能通过调节DAF-16/FOXO胰岛素样信号通路介导，可以提高应激抵抗力并促进应激状态下的寿命，从而支持rooibos茶提出的一些健康要求。

BACKGROUND & AIMS: :Mitochondrial dysfunction is the most prominent source of oxidative stress in acute and chronic kidney disease. NLRX1 is a receptor of the innate immune system that is ubiquitously expressed and localized in mitochondria. We investigated whether NLRX1 may act at the interface of metabolism and innate immunity in a model of oxidative stress. Using a chimeric mouse model for renal ischemia-reperfusion injury, we found that NLRX1 protects against mortality, mitochondrial damage, and epithelial cell apoptosis in an oxidative stress-dependent fashion. We found that NLRX1 regulates oxidative phosphorylation and cell integrity, whereas loss of NLRX1 results in increased oxygen consumption, oxidative stress, and subsequently apoptosis in epithelial cells during ischemia-reperfusion injury. In line, we found that NLRX1 expression in human kidneys decreased during acute renal ischemic injury and acute cellular rejection. Although first implicated in immune regulation, we propose that NLRX1 function extends to the control of mitochondrial activity and prevention of oxidative stress and apoptosis in tissue injury.

背景与目标： : 线粒体功能障碍是急性和慢性肾脏疾病中氧化应激的最突出来源。NLRX1是先天免疫系统的受体，广泛表达并定位在线粒体中。我们研究了NLRX1是否可能在氧化应激模型中作用于代谢和先天免疫的界面。使用嵌合小鼠肾缺血再灌注损伤模型，我们发现NLRX1以氧化应激依赖性方式保护死亡率，线粒体损伤和上皮细胞凋亡。我们发现NLRX1调节氧化磷酸化和细胞完整性，而NLRX1的丢失会导致缺血再灌注损伤期间的耗氧量增加，氧化应激以及上皮细胞的凋亡。我们发现，在急性肾缺血损伤和急性细胞排斥反应期间，人肾脏中NLRX1的表达降低。尽管首先涉及免疫调节，但我们建议NLRX1功能扩展到控制线粒体活性以及预防组织损伤中的氧化应激和凋亡。

BACKGROUND & AIMS: :The present study utilized longitudinal data from a high-risk community sample (N = 377; 166 trauma-exposed; 202 males; 175 females; 73% non-Hispanic Caucasian) to test pretrauma measures of adolescent internalizing and externalizing symptoms as unique prospective predictors of type of trauma exposure and PTSD over and above the influence of correlated family adversity (a composite of family conflict, stress, and parental psychopathology). Data were analyzed with logistic and multinomial logistic regressions. Results indicated that females, but not males, with higher levels of internalizing (OR = 2.91) and externalizing (OR = 2.37) symptoms during adolescence were significantly more likely to be exposed to assaultive violence (over and above family adversity). In fact, males with higher levels of internalizing symptoms were significantly less likely to be exposed to assaultive violence (OR = 0.54). Neither internalizing nor externalizing symptoms uniquely predicted exposure to traumatic events that did not involve assaultive violence. Among trauma-exposed participants, the unique association between internalizing symptoms and later PTSD yielded an odds ratio of 1.79 (p = .07) over and above the influences of family adversity, type of trauma exposure, and gender. Assaultive violence exposure fully mediated the association between females' externalizing symptoms and future PTSD. Findings may help inform the prevention of both assaultive violence exposure and PTSD.

背景与目标： : 本研究利用了来自高风险社区样本的纵向数据 (N = 377; 166创伤暴露; 202男性; 175女性; 73% 非西班牙裔高加索人) 测试青少年内在化和外在化症状的创伤前措施，作为创伤暴露类型和创伤后应激障碍的独特前瞻性预测因子，超越相关家庭逆境 (家庭冲突、压力和父母心理病理学的组合) 的影响。数据采用logistic和多项logistic回归分析。结果表明，女性而不是男性，在青春期具有较高水平的内在化 (或 = 2.91) 和外在化 (或 = 2.37) 症状的女性更容易遭受攻击性暴力 (超过家庭逆境)。事实上，具有较高水平内化症状的男性暴露于攻击性暴力的可能性显著降低 (OR = 0.54)。内部化或外部化症状都不能唯一地预测暴露于不涉及攻击性暴力的创伤事件。在创伤暴露的参与者中，内在化症状与后来的PTSD之间的独特关联产生了1.79的优势比 (p = .07)，超出了家庭逆境，创伤暴露类型和性别的影响。攻击性暴力暴露充分介导了女性外在症状与未来创伤后应激障碍之间的关联。研究结果可能有助于预防攻击性暴力暴露和PTSD。

BACKGROUND & AIMS: :Although skin picking has been documented in the medical literature since the 19th century, only now is it receiving serious consideration as a DSM psychiatric disorder in discussions for DSM-5. Recent community prevalence studies suggest that skin picking disorder appears to be as common as many other psychiatric disorders, with reported prevalences ranging from 1.4% to 5.4%. Clinical evaluation of patients with skin picking disorder entails a broad physical and psychiatric examination, encouraging an interdisciplinary approach to evaluation and treatment. Approaches to treatment should include cognitive-behavioral therapy (including habit reversal or acceptance-enhanced behavior therapy) and medication (serotonin reuptake inhibitors, N-acetylcysteine, or naltrexone). Based on clinical experience and research findings, the authors recommend several management approaches to skin picking disorder.

背景与目标： : 尽管自19世纪以来，医学文献中已经记录了皮肤采摘，但直到现在，在DSM-5讨论中，它才被视为DSM精神疾病。最近的社区患病率研究表明，皮肤采摘障碍似乎与许多其他精神疾病一样普遍，据报道患病率从1.4% 到5.4% 不等。对皮肤采摘障碍患者的临床评估需要进行广泛的身体和精神检查，从而鼓励采用跨学科的方法进行评估和治疗。治疗方法应包括认知行为疗法 (包括习惯逆转或接受增强行为疗法) 和药物 (5-羟色胺再摄取抑制剂，N-乙酰半胱氨酸或纳曲酮)。根据临床经验和研究结果，作者推荐了几种皮肤采摘障碍的管理方法。

BACKGROUND & AIMS: :Evidence for the stress-buffering effects of social support in intimate relationships raises important questions about whether partner support promotes recovery in physiological systems implicated in physical health. The present study examined (a) whether observed dyadic coping enhances cortisol stress recovery and (b) whether a stressed partner's self-reported attachment anxiety and avoidance moderate these effects. Stress was experimentally induced by asking either the man or woman in 123 heterosexual couples to participate in a standardized public speaking task. Stressed individuals recovered faster from stress the more positive dyadic coping they received from the partner, with women high in attachment anxiety benefiting less from these behaviors. Attachment avoidance did not moderate these associations. This study highlights the value of examining the interplay between partners' behaviors and attachment orientations in order to understand the impact of stress on close relationships and partners' health.

背景与目标： : 亲密关系中社会支持的压力缓冲作用的证据提出了有关伴侣支持是否促进生理系统恢复与身体健康有关的重要问题。本研究检查了 (a) 观察到的二元应对是否会增强皮质醇压力恢复，以及 (b) 压力伴侣的自我报告的依恋焦虑和回避是否会减轻这些影响。通过要求123异性恋夫妇中的男人或女人参加标准化的公开演讲任务，实验性地引发了压力。压力大的人从伴侣那里得到的积极的二元应对能力会更快地从压力中恢复过来，而依恋焦虑的女性从这些行为中受益较少。避免依恋并没有缓和这些关联。这项研究强调了检查伴侣行为与依恋取向之间相互作用的价值，以了解压力对亲密关系和伴侣健康的影响。

BACKGROUND & AIMS: :This corrects the article DOI: 10.1038/ncomms15111.

背景与目标： : 这更正了文章DOI: 10.1038/ncomms15111。

BACKGROUND & AIMS: BACKGROUND:In the first population-based study of psychopathology conducted in Haiti, we documented earthquake-related experiences associated with risk for posttraumatic stress disorder (PTSD) and major depressive disorder (MDD) 2-4 months following the 2010 Haiti earthquake. METHODS:A population-based survey was conducted of 1,323 survivors randomly selected from the general nondisplaced community, internally displaced persons camps, and a community clinic. Respondents were from the Nazon area of Port-au-Prince, ∼20 miles from the epicenter. RESULTS:Respondents (90.5%) reported at least one relative/close friend injured/killed, 93% saw dead bodies, and 20.9% lost their job post-earthquake. The prevalence of PTSD (24.6%) and MDD (28.3%) was high. History of violent trauma was associated with risk of PTSD and MDD (adjusted odds ratio [AOR] 1.4, 95% confidence interval [CI], 1.0-1.9; AOR, 1.7, 95% CI 1.3, 2.2, respectively). Low social support (AOR, 1.7, 95% CI 1.2, 2.3; AOR 1.4, 95% CI 1.0, 1.9, respectively) increased risk of PTSD and MDD among women. Suffering damage to the home increased risk of MDD in males (AOR 2.8, 95% CI 1.5, 5.5). Associations between being trapped in rubble, major damage to house, job loss, and PTSD; and participation in rescue/recovery, friends/family injured/killed, and MDD varied based on prior history of violent trauma. CONCLUSIONS:Addressing mental health in a post-earthquake setting such as Haiti will require focusing resources on screening and treatment of identified vulnerable groups while targeting improvement of post-earthquake living conditions. Investment in sources of social support for women may make help mitigate the vulnerability of women to PTSD and MDD.

背景与目标：

BACKGROUND & AIMS: :Sequestosome 1 (SQSTM1) also known as ubiquitin-binding protein p62 (p62) is a cargo protein involved in the degradation of misfolded proteins via selective autophagy. Disruption of autophagy and resulting accumulation of misfolded proteins in the endoplasmic reticulum (ER) leads to ER stress. ER stress is implicated in several neurodegenerative diseases and obesity. As knockout of p62 (p62KO) reportedly induces obesity in mice, we examined how p62 contributes to ER stress and the ensuing unfolded protein response (UPR) in hypothalamus using mouse organotypic cultures in the present study. Cultures from p62KO mice showed significantly reduced formation of LC3-GFP puncta, an index of autophagosome formation, in response to the chemical ER stressor thapsigargin compared to wild-type (WT) cultures. Hypothalamic cultures from p62KO mice exhibited higher basal expression of the UPR/ER stress markers CHOP mRNA and ATF4 mRNA than WT cultures. Thapsigargin enhanced CHOP, ATF4, and BiP mRNA as well as p-eIF2α protein expression in both WT and p62KO cultures, but all peak values were greater in p62KO cultures. A proteasome inhibitor increased p62 expression in WT cultures and upregulated the UPR/ER stress markers CHOP mRNA and ATF4 mRNA in both genotypes, but to a greater extent in p62KO cultures. Therefore, p62 deficiency disturbed autophagosome formation and enhanced both basal and chemically induced ER stress, suggesting that p62 serves to prevent ER stress in mouse hypothalamus by maintaining protein folding capacity.

背景与目标： : Sequestosome 1 (SQSTM1) 也称为泛素结合蛋白p62 (p62) 是一种通过选择性自噬参与错误折叠蛋白降解的货物蛋白。自噬的破坏和内质网 (ER) 中错误折叠的蛋白质的积累导致ER应激。ER应激与几种神经退行性疾病和肥胖症有关。据报道，由于p62 (p62KO) 的敲除会导致小鼠肥胖，因此我们在本研究中使用小鼠器官型培养物检查了p62如何促进下丘脑的内质网应激和随后的未折叠蛋白反应 (UPR)。与野生型 (WT) 培养物相比，来自p62KO小鼠的培养物显示出响应于化学ER应激源thapsigargin的LC3-GFP点形成显着减少，这是自噬体形成的指标。p62KO小鼠的下丘脑培养物显示出UPR/ER应激标记物CHOP mRNA和ATF4 mRNA的基础表达高于WT培养物。Thapsigargin在WT和p62KO培养物中均增强了CHOP，ATF4和BiP mRNA以及p-eIF2α 蛋白的表达，但在p62KO培养物中所有峰值均较大。蛋白酶体抑制剂在两种基因型中均增加了WT培养物中的p62表达，并上调了UPR/ER应激标记物CHOP mRNA和ATF4 mRNA，但在p62KO培养物中更大程度。因此，p62缺乏干扰了自噬体的形成，并增强了基础和化学诱导的ER应激，表明p62通过维持蛋白质折叠能力来预防小鼠下丘脑的ER应激。

BACKGROUND & AIMS: BACKGROUND:Epidemiological studies have shown significant ethnic differences in coronary heart disease death rates with South Asians showing significantly greater coronary heart disease mortality than other groups. PURPOSE:This research examined ethnic differences in cardiovascular reactivity (CVR) among Chinese, Malays and Indians in Singapore as well as a sample of Indians living in India. METHODS:Experiment 1 examined differences across 303 Chinese, Malay and Indian undergraduates in Singapore, while Experiment 2 looked at differences in CVR between Indian participants from Singapore, and 145 Indians living in India. Systolic and diastolic blood pressure (SBP, DBP), heart rate (HR), cardiac index (CI) and total peripheral resistance index (TPRI) were measured during baselines and five laboratory tasks. RESULTS:Ethnicity main effects for SBP and CI reactivity were obtained in Experiment 1, with Indians showing significantly lower BP and CI reactivity than the Chinese and Malays. Significant main effects for sex were found with females showing lower reactivity than males for TPRI, and greater reactivity than males for HR and CI. Experiment 2 found that participants from India showed higher reactivity for SBP, HR and CI, while Indian participants from Singapore showed higher TPRI reactivity. These differences, however, often varied by task. CONCLUSIONS:These results point to differences in CVR among ethnic groups in Singapore as well as between Indians living in India and those living in Singapore. These differences may reflect cultural differences and need to be explored further with respect to their relationship to different rates of coronary heart disease among these groups.

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