高校女性日常能耗与肠道菌群的相关性研究

探讨高校女性日常能耗及肠道菌群结构特征,分析不同能耗指标与特征肠道菌群之间的相关性。

基于智能可穿戴设备人体运动能耗检测仪对广州两所大学的青年女性（Y组,n=30）、中年女性（M组,n=30）进行48 h能耗监测,统计分析日常能耗的组间差异。采集调查对象清晨粪便进行16S rRNA基因测序,运用多元统计学分析中青年女性肠道菌群结构特征。将目、属水平的特征菌群与能耗指标进行相关性检验及回归分析。

Y组人群的日均步数（t=4.250,P＜0.001）、每日能耗值（t=3.590,P＜0.001）、日均中高强度活动时长（t=4.357,P＜0.001）均显著高于M组;两组人群肠道菌群的目、属水平的丰度差异菌群主要为乳杆菌目（Lactobacillales）（t=2.537,P=0.014）、小杆菌属（Dialister）（t=2.904,P=0.005）、布劳特菌属（Blautia）（t=3.246,P=0.002）,其中Lactobacillales和Dialister与多项能耗指标呈正相关,Blautia与多项能耗指标呈负相关。

日均步数、每日能耗值、日均中高强度活动时长的能耗指标可用于预测更好的身体机能;一定条件下,增加低、中、高强度活动时长可能提高Lactobacillales和Dialister的丰度,进而延缓身体机能下降。

     

Molecular cloning and characterization of the glutathione reductase gene from Stipa purpurea

Reactive oxygen species (ROS) are a key factor in abiotic stresses; excess ROS is harmful to plants. Glutathione reductase (GR) plays an important role in scavenging ROS in plants. Here, a GR gene, named SpGR, was cloned from Stipa purpurea and characterized. The full-length open reading frame was 1497 bp, encoding 498 amino acids. Subcellular localization analysis indicated that SpGR was localized to both the plasma membrane and nucleus. The expression of SpGR was induced by cold, salt, and drought stresses. Functional analysis indicated that ectopic expression of SpGR in Arabidopsis thaliana resulted in greater tolerance to salt stress than that of wild-type plants, but no difference under cold or drought treatments. The results of GR activity and GSSG and GSH content analyses suggested that, under salt stress, transgenic plants produced more GR to reduce GSSG to GSH for scavenging ROS than wild-type plants. Therefore, SpGR may be a candidate gene for plants to resist abiotic stress.     

Population-attributable risks for ischemic stroke in a community in South Brazil: a case-control study

Background

Risk factors for ischemic stroke are mostly known, but it is still unclear in most countries, what are their combined population-attributable risk percent (PAR%). In a case-control study the individual odds ratios (ORs) and the individual and combined PAR%, including risk factors not addressed in previous studies were estimated.

Methods

Cases and controls were selected from patients attending to an emergency department. Cases were patients aged with 45 years or more with the first episode of ischemic stroke, characterized by a focal neurological deficit or change in the mental status occurring during the previous 24 hours. Controls, matched to cases by age and gender, were selected from patients without neurological complaints.

Results

133 cases and 272 controls were studied. Odds ratios for ischemic stroke were: atrial fibrillation (27.3; CI 95% 7.5–99.9), left ventricular hypertrophy (20.3; CI 95% 8.8–46.4), history of hypertension (11.2; CI 95% 5.4–23.3), physical inactivity (6.6; CI 95% 3.3–13.1), low levels of HDL-cholesterol (5.0; CI 95%2.8–8.9), heavy smoking (2.8; CI 95% 1.5–5.0), carotid bruit (2.5; CI 95% 1.3–4.6), diabetes (2.4; CI 95% 1.4–4.0) and alcohol abuse (2.1; CI 95% 1.1–4.0), The combination of these risk factors accounted for 98.9% (95% CI; 96.4%–99.7%) of the PAR% for all stroke.

Conclusions

Nine risk factors, easily identified, explain almost 100% of the population attributable risk for ischemic stroke.     

Luteolin promotes macrophage-mediated phagocytosis by inhibiting CD47 pyroglutamation

‘Don''t eat me’ signal of CD47 is activated via its interaction with SIRPα protein on myeloid cells, especially phagocytic cells, and prevents malignant cells from anti-tumor immunity in which pyroglutamate modification of CD47 by glutaminyl-peptide cyclotransferase-like protein (isoQC) takes an important part evidenced by our previous report that isoQC is an essential regulator for CD47-SIRPα axis with a strong inhibition on macrophage-mediated phagoctyosis. Therefore, we screened for potential isoQC inhibitors by fluorescence-activated cell sorting assay and identified luteolin as a potent compound that blocked the pyroglutamation of CD47 by isoQC. We further demonstrated that luteolin directly bound to isoQC using pull-down assay and isothermal calorimetric (ITC) assay. In consistency, we showed that luteolin markedly abrogated the cell-surface interaction between CD47 and SIRPα in multiple myeloma H929 cells and consequently promoted the macrophage-mediated phagocytosis. Collectively, our study discovered a promising lead compound targeting isoQC, luteolin, which functions distinctly from current CD47 antibody-based drugs and therefore may potentially overcome the clinical side effects associated with CD47 antibody treatment-induced anemia.Keyword: Luteolin, CD47-SIRPα, isoQC, Phagocytosis, Tumor immunotherapy     

Hypothermic oxygenated perfusion inhibits HECTD3-mediated TRAF3 polyubiquitination to alleviate DCD liver ischemia-reperfusion injury

Ischemia-reperfusion injury (IRI) is an inevitable and serious clinical problem in donations after heart death (DCD) liver transplantation. Excessive sterile inflammation plays a fateful role in liver IRI. Hypothermic oxygenated perfusion (HOPE), as an emerging organ preservation technology, has a better preservation effect than cold storage (CS) for reducing liver IRI, in which regulating inflammation is one of the main mechanisms. HECTD3, a new E3 ubiquitin ligase, and TRAF3 have an essential role in inflammation. However, little is known about HECTD3 and TRAF3 in HOPE-regulated liver IRI. Here, we aimed to investigate the effects of HOPE on liver IRI in a DCD rat model and explore the roles of HECTD3 and TRAF3 in its pathogenesis. We found that HOPE significantly improved liver damage, including hepatocyte and liver sinusoidal endothelial cell injury, and reduced DCD liver inflammation. Mechanistically, both the DOC and HECT domains of HECTD3 directly interacted with TRAF3, and the catalytic Cys (C832) in the HECT domain promoted the K63-linked polyubiquitination of TRAF3 at Lys138. Further, the ubiquitinated TRAF3 at Lys138 increased oxidative stress and activated the NF-κB inflammation pathway to induce liver IRI in BRL-3A cells under hypoxia/reoxygenation conditions. Finally, we confirmed that the expression of HECTD3 and TRAF3 was obviously increased in human DCD liver transplantation specimens. Overall, these findings demonstrated that HOPE can protect against DCD liver transplantation-induced-liver IRI by reducing inflammation via HECTD3-mediated TRAF3 K63-linked polyubiquitination. Therefore, HOPE regulating the HECTD3/TRAF3 pathway is a novel target for improving IRI in DCD liver transplantation.Subject terms: Molecular biology, Diseases     

Diuretics: again the first step in the treatment of most patients with hypertension

The results and interpretations of the most recent controlled clinical trials on antihypertensive drugs have fuelled the debate about the drug that should be used to begin treatment for hypertension. Every comparison of diuretics with other drugs has shown that the benefits of diuretics are equivalent to, or better than, other options. These findings, together with other practical reasons, such as left ventricular mass reducing effect, easy administration, few side effects and low cost, suggest that diuretics should regain their primacy as the first step in drug management of hypertension.     

High-valent intermediates of heme proteins and model compounds

Recent computational and experimental probes of high-valent intermediates in heme proteins and model compounds reveal a rich spectrum of chemical behavior that is dependent on the nature of the proximal ligand, metal center, distal- and proximal-binding site environment, porphyrin macrocycle architecture, and consequent electronic structure. The results of such studies reveal an underlying complexity, which is simply understood once one is cognizant of the 'chameleon'-like behavior of such intermediates is determined by the high-valent intermediate environment.