Eustress and Distress: Neither Good Nor Bad,but Rather the Same?

The terms “eustress” and “distress” are widely used throughout the scientific literature. As of February 2020, 203 items in the Web of Science show up in a search for “eustress,” however, there are almost 16 400 items found in a search for the term “distress.” Based on the reasoning in this article, however, it is believed there is no such thing as eustress or distress. The adaptation reaction of an organism under stress is not intrinsically good or bad, and its effect on health or performance depends on a plethora of other interactions of the body with the environment as well as on the history of such interactions. The vagueness of the terms “eustress/distress” has historically led to vast differences in the perception and application of the terms across disciplines. While psychology or sociology perceive eustress as something inextricably linked to positive perception and enhanced cognition, biomedicine perceives eustress as generally associated with better survival, health, or increased longevity, no matter how the event is perceived. In this paper, the authors review the current understanding of the term “eustress” in different fields, discuss possible implications of its misleading use, and suggest that the term may be replaced by “stress” only.     

Behavioural ecology at the spatial–social interface

Spatial and social behaviour are fundamental aspects of an animal's biology, and their social and spatial environments are indelibly linked through mutual causes and shared consequences. We define the ‘spatial–social interface’ as intersection of social and spatial aspects of individuals' phenotypes and environments. Behavioural variation at the spatial–social interface has implications for ecological and evolutionary processes including pathogen transmission, population dynamics, and the evolution of social systems. We link spatial and social processes through a foundation of shared theory, vocabulary, and methods. We provide examples and future directions for the integration of spatial and social behaviour and environments. We introduce key concepts and approaches that either implicitly or explicitly integrate social and spatial processes, for example, graph theory, density-dependent habitat selection, and niche specialization. Finally, we discuss how movement ecology helps link the spatial–social interface. Our review integrates social and spatial behavioural ecology and identifies testable hypotheses at the spatial–social interface.     

Dieting,Exercise, or Disordered Eating Does Not Account for Extremes of Body Weight within Families

Objective : Families having both members with obesity and thin members should contain substantial information for genetics studies, provided measured phenotype is an accurate indicator of genetic predisposition. We assessed the impact of potentially complicating behavioral factors on obesity phenotypes of family members selected for a long-term project to identify genes for human obesity. Research Methods and Procedures : Ninety-nine Caucasian families were selected for study because they contained both extremely obese and average-weight family members. Family members (n = 492) were queried about their diet and exercise habits, their psychiatric histories as they pertained to eating disorders, and for a subset of subjects (n = 329), a lifetime dieting history and a lifetime maximum weight were recorded. Results : Subjects with average body weights in these families did not appear to be maintaining their weight by dieting and <4% of the average-weight subjects had ever been obese in the past. Discussion : Although dieting and other weight loss practices potentially could either mask or complicate the genotype-phenotype relationship, we found little evidence for this possibility in the families studied.     

Activation of mitochondrial ATP-sensitive potassium channels increases cell viability against rotenone-induced cell death

We recently showed that activation of ATP-sensitive potassium (KATP) channels in PC12 cells induces protection against the neurotoxic effect of rotenone, a mitochondrial complex I inhibitor. In this study, we sought to determine the locus of the KATP channels that mediate this protection in PC12 cells. We found that pretreatment of PC12 cells with diazoxide, a mitochondrial KATP channel selective opener, dose-dependently increases cell viability against rotenone-induced cell death as indicated in trypan blue exclusion assays. The protective effect of this preconditioning is attenuated by 5-hydroxydecanoic acid (5-HD), a selective mitochondrial KATP channel antagonist but not in the presence of HMR-1098, a selective plasma membrane KATP potassium channel antagonist. In contrast, P-1075, a selective plasma membrane KATP channel opener, does not induce protection. Using specific antibodies against SUR1 and Kir6.1, we detected immunoreactive proteins of apparent molecular masses 155 and 50 kDa, corresponding to those previously reported for SUR1 and Kir6.1, respectively, in the mitochondria-enriched fraction of PC12 cells. In addition, whole cell patch-clamp studies revealed that inward currents in PC12 cells are insensitive to P-1075, HMR-1098, glibenclamide and diazoxide, indicating that functional plasma membrane KATP channels are negligible. Taken together, our results demonstrate for the first time that activation of mitochondrial KATP channels elicits protection against rotenone-induced cell death.     

中国人群(京津地区)载脂蛋白E基因多态性和表型分布的研究

本文利用作者建立的密度梯度超速离心分离VLDL的新方法和分析等电聚焦电泳,测定了95例中国人Apo-E基因多态性和其表型分布以及血脂水平。所得表型分布趋势与国外报告一致:E_3/E_3频率最高,E_3/E_2和E_3/E_4次之,E_4/E_4,E_4/E_2和E_2/E_2最低。同对发现中国人群的E_3/E_3表型百分分布明显高于西方人群,但未发现有E_2/E_2表型。我国人群Apo-E表型分布的这种特征可能与中国人群冠心病的患病率较西方人群为低有关。血清脂质测定和分析表明,具有不同表型人群的血脂水平无显著的统计学差异。     

Long-term effects of birth weight and breastfeeding duration on inflammation in early adulthood

Chronic inflammation is a potentially important physiological mechanism linking early life environments and health in adulthood. Elevated concentrations of C-reactive protein (CRP)—a key biomarker of inflammation—predict increased cardiovascular and metabolic disease risk in adulthood, but the developmental factors that shape the regulation of inflammation are not known. We investigated birth weight and breastfeeding duration in infancy as predictors of CRP in young adulthood in a large representative cohort study (n = 6951). Birth weight was significantly associated with CRP in young adulthood, with a negative association for birth weights 2.8 kg and higher. Compared with individuals not breastfed, CRP concentrations were 20.1%, 26.7%, 29.6% and 29.8% lower among individuals breastfed for less than three months, three to six months, 6–12 months and greater than 12 months, respectively. In sibling comparison models, higher birth weight was associated with lower CRP for birth weights above 2.5 kg, and breastfeeding greater than or equal to three months was significantly associated with lower CRP. Efforts to promote breastfeeding and improve birth outcomes may have clinically relevant effects on reducing chronic inflammation and lowering risk for cardiovascular and metabolic diseases in adulthood.     

Cellular prion proteins in human platelets show a phenotype different to those in brain tissues

Prion diseases are characterized by high accumulation of infectious prion proteins (PrP(Sc)) in brains. PrP(Sc) are propagated by the conversion of host-encoded cellular prion proteins (PrP(C)) which are essential for developing the disease but are heterogeneously expressed in brains. The disease can be transmitted to humans and animals through blood and blood products, however, little attention has been given to molecular characterization of PrP(C) in blood cells. In this presented study, we characterized phenotypically PrP(C) of platelets (plt) and characterized the proteins regarding their glycobanding profiles by quantitative immunoblotting using a panel of monoclonal antibodies. The glycosylation patterns of plt and brain PrP(C) were compared using the ratios of di-, mono-, and non-glycosylated prions. The detergent solubility of plt and brain PrP(C) was also analyzed. The distinct banding patterns and detergent solubility of plt PrP(C) differed clearly from the glycosylation profiles and solubility characteristics of brain PrP(C). Plt PrP(C) exhibited single or only few prion protein types, whereas brain PrP(C) showed more extensive banding patterns and lower detergent solubility. Plt PrP(C) are post-translational modified differently from PrP(C) in brain. These findings suggest other or less physiological functions of plt PrP(C) than in brain.     

稳定期慢性阻塞性肺病患者血嗜酸性粒细胞水平与炎症表型相关性研究

摘要 目的：探究稳定期慢性阻塞性肺病患者血嗜酸性粒细胞水平与炎症表型相关性研究。方法：选择淮安市第一人民医院（我院）2017年5月至2020年3月诊治的稳定期慢性阻塞性肺病患者280例,按照外周血嗜酸性粒细胞计数分为3组,嗜酸性粒细胞＜100为A组86例,嗜酸性粒细胞100~300为B组102例,嗜酸性粒细胞＞300为C组92例。同时纳入同期进行体检的健康者100例为对照组。结果：A组、B组和C组的FeNO显著高于对照组,且C组>B组>A组（P<0.05）;FEV₁占预测值和FEV₁/FVC 显著低于对照组（P<0.05）;A组、B组和C组的FEV₁占预测值和FEV1/FVC对比无差异（P>0.05）。A组、B组和C组的CRP、IL-6、IL-8和TNF-α显著高于对照组（P<0.05）,且C组>B组>A组（P>0.05）。经相关性分析发现,A组和B组患者的嗜酸性粒细胞计数与FeNO、CRP、IL-6、IL-8和TNF-α、FEV₁占预测值和FEV₁/FVC无明显相关性（P>0.05）。C组的嗜酸性粒细胞计数与FeNO、CRP、IL-6、IL-8和TNF-α呈正相关（P<0.05）,与FEV₁/FVC%呈负相关（P<0.05）;与FEV₁占预测值无显著相关性（P>0.05）。结论：稳定期慢性阻塞性肺病患者外周血嗜酸性粒细胞计数与FeNO水平呈正相关,二者能够反映稳定期慢性阻塞性肺病患者气道的炎症反应,对于稳定期慢性阻塞性肺病患者炎症的评估、病情的程度及后期的治疗具有一定的临床指导意义。     

脂肪细胞衰老通过衰老相关分泌表型诱导微血管内皮细胞早衰和功能紊乱

摘要 目的：探讨衰老脂肪细胞对微循环内皮细胞（ECs）功能状态的影响,以及异常早衰在糖尿病肾病（DKD）中的潜在作用。方法：3T3-L1细胞被诱导分化为年轻和衰老的脂肪细胞。HMEC-1细胞分别培养在年轻、衰老脂肪细胞制成的条件培养基和对照培养基中。通过免疫荧光检测γH2AX和SA-β-半乳糖苷酶活性鉴定细胞衰老状态。通过qPCR、Western blot检测衰老相关分泌表型（SASP）、胰岛素受体底物1（IRS1）、Jun原癌基因（JUN）、组蛋白H3第4位赖氨酸二甲基化、三甲基化（H3K4me2、H3K4me3）等指标的表达水平。利用GEO数据库对衰老肾脏和早期糖尿病肾病的差异表达基因（DGE）进行生物信息学分析。结果：衰老脂肪细胞的SASP表达显著升高,其条件培养基成功诱导HMEC-1细胞衰老。与年轻HMEC-1细胞相比,诱导衰老的HMEC-1细胞中斯钙素1（STC1）表达上调,前炎症因子、JUN和H3K4me3均表达下调。与对照组相比,IRS1在年轻HMEC-1细胞中显著下调,在诱导衰老的HMEC-1细胞中无显著变化。生物信息学结果显示差异基因的交集仅存在于衰老肾脏的上调基因和早期糖尿病肾病的下调基因之间。PPI网络分析、GO及KEGG富集分析表明IL6-SOCS3-IRS1是异常早衰机制参与早期DKD发生的核心信号通路。结论：脂肪细胞衰老导致微循环内皮细胞早衰并损害其正常功能状态,异常早衰机制参与了DKD的发生发展。