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The purpose of this study is to assess the prevalence of overweight/obesity, abdominal obesity and obesity-related risk factors in southern China. A cross-sectional survey of 15,364 participants aged 15 years and older was conducted from November 2013 to August 2014 in Jiangxi Province, China, using questionnaire forms and physical measurements. The physical measurements included body height, weight, waist circumference (WC), body fat percentage (BFP) and visceral adipose index (VAI). Multivariate logistic regression analysis was performed to evaluate the risk factors for overweight/obesity and abdominal obesity. The prevalence of overweight was 25.8% (25.9% in males and 25.7% in females), while that of obesity was 7.9% (8.4% in males and 7.6% in females). The prevalence of abdominal obesity was 10.2% (8.6% in males and 11.3% in females). The prevalence of overweight/obesity was 37.1% in urban residents and 30.2% in rural residents, and this difference was significant (P < 0.001). Urban residents had a significantly higher prevalence of abdominal obesity than rural residents (11.6% vs 8.7%, P < 0.001). Among the participants with an underweight/normal body mass index (BMI), 1.3% still had abdominal obesity, 16.1% had a high BFP and 1.0% had a high VAI. Moreover, among obese participants, 9.7% had a low /normal WC, 0.8% had a normal BFP and 15.9% had a normal VAI. Meanwhile, the partial correlation analysis indicated that the correlation coefficients between VAI and BMI, VAI and WC, and BMI and WC were 0.700, 0.666, and 0.721, respectively. A multivariate logistic regression analysis indicated that being female and having a high BFP and a high VAI were significantly associated with an increased risk of overweight/obesity and abdominal obesity. In addition, living in an urban area and older age correlated with overweight/obesity. This study revealed that obesity and abdominal obesity, which differed by gender and age, are epidemic in southern China. Moreover, there was a very high, significant, positive correlation between WC, BMI and VAI. However, further studies are needed to explore which indicator of body fat could be used as the best marker to indirectly reflect cardiometabolic risk.

This study aimed to describe the prevalence and risk factors of prehypertension and hypertension in Jiangxi Province, China. Individuals with prehypertension frequently progress into hypertension and are at high risk of developing cardiovascular disease and stroke. A cross-sectional survey of 15,296 participants (15 years or older) was conducted in Jiangxi Province, China, in 2013, using questionnaire forms and physical measurements. The prevalence of prehypertension and hypertension was 32.3% (39.2% in men and 27.6% in women) and 29.0% (30.1% in men and 28.2% in women), respectively. The awareness, treatment, and control rates among all hypertensive participants were 64.8%, 27.1%, and 12.6%, respectively. The prevalence of prehypertension in males declined with age, but the prevalence of hypertension increased in different genders. The prevalence of prehypertension and hypertension increased with increasing body mass index (BMI). The prevalence of prehypertension decreased, in parallel to an increase in the prevalence of hypertension, with increasing waist circumference (WC). A combination of WC and BMI was superior to individual indices in identifying hypertension. A multivariate logistic regression analysis indicated that increasing age, high BMI, high visceral adipose index, and high heart rate were risk factors for prehypertension and hypertension. The high body fat percentage was significantly associated with prehypertension. Living in an urban area, male sex, abdominal obesity, and menopause were correlated with hypertension. Prehypertension and hypertension are epidemic in southern China. Further studies are needed to explore an indicator that can represent the visceral fat accurately and has a close relationship with cardiovascular disease.

The scope of atlas-level single-cell investigations reveals the pathogenesis and progression of various diseases. Accurate interpretation of phenotype-related single-cell data necessitates the pre-definition of single-cell subtypes and the identification of their abundance variations for downstream analysis. In this context, biases from batch correlation and the selection of clustering resolutions can significantly impact single-cell data analysis and result interpretation. To strengthen the associations across single cells in each sample and their clinical phenotype, and to enhance single-cell exploration by integrating cell and gene-level information. This study proposes a method to learn phenotype-related sample representations from single cells via the attention-based multiple instance learning (AMIL) mechanism. This approach incorporates gene expression profiles from each single cell for sample-level clinical phenotype prediction. By integrating deep learning interpretation methods and phenotype-specific single-cell attention weights across sample groups, this method highlights critical gene programs and cell subtypes that mostly contribute to the sample-level clinical phenotype, and facilitate mechanistic exploration. Using single-cell atlases from COVID-19 infected patients and age-related healthy human blood, we demonstrate that this method can accurately predict disease severity and age-related phenotypes. Additionally, variations in cellular attention reflect the underlying biological mechanisms associated with these phenotypes. This method proposes a supervised framework for single-cell data interpretation and can be further adapted for other atlas-level clinical phenotype analyses.

Mass spectrometry-based lipidomics is the primary tool for the structural analysis of lipids but the effective localization of carbon–carbon double bonds (C=C) in unsaturated lipids to distinguish C=C location isomers remains challenging. Here, we develop a large-scale lipid analysis platform by coupling online C=C derivatization through the Paternò-Büchi reaction with liquid chromatography-tandem mass spectrometry. This provides rich information on lipid C=C location isomers, revealing C=C locations for more than 200 unsaturated glycerophospholipids in bovine liver among which we identify 55 groups of C=C location isomers. By analyzing tissue samples of patients with breast cancer and type 2 diabetes plasma samples, we find that the ratios of C=C isomers are much less affected by interpersonal variations than their individual abundances, suggesting that isomer ratios may be used for the discovery of lipid biomarkers. Mass spectrometry is widely used for large-scale lipid profiling but distinguishing unsaturated lipid isomers is still challenging. Here, the authors present an analytical platform for high-throughput identification of lipid C=C location isomers in clinical samples, showing that isomer ratios may guide biomarker discovery.

Activation of RIPK1 controls TNF-mediated apoptosis, necroptosis and inflammatory pathways 1 . Cleavage of human and mouse RIPK1 after residues D324 and D325, respectively, by caspase-8 separates the RIPK1 kinase domain from the intermediate and death domains. The D325A mutation in mouse RIPK1 leads to embryonic lethality during mouse development 2 , 3 . However, the functional importance of blocking caspase-8-mediated cleavage of RIPK1 on RIPK1 activation in humans is unknown. Here we identify two families with variants in RIPK1 (D324V and D324H) that lead to distinct symptoms of recurrent fevers and lymphadenopathy in an autosomal-dominant manner. Impaired cleavage of RIPK1 D324 variants by caspase-8 sensitized patients’ peripheral blood mononuclear cells to RIPK1 activation, apoptosis and necroptosis induced by TNF. The patients showed strong RIPK1-dependent activation of inflammatory signalling pathways and overproduction of inflammatory cytokines and chemokines compared with unaffected controls. Furthermore, we show that expression of the RIPK1 mutants D325V or D325H in mouse embryonic fibroblasts confers not only increased sensitivity to RIPK1 activation-mediated apoptosis and necroptosis, but also induction of pro-inflammatory cytokines such as IL-6 and TNF. By contrast, patient-derived fibroblasts showed reduced expression of RIPK1 and downregulated production of reactive oxygen species, resulting in resistance to necroptosis and ferroptosis. Together, these data suggest that human non-cleavable RIPK1 variants promote activation of RIPK1, and lead to an autoinflammatory disease characterized by hypersensitivity to apoptosis and necroptosis and increased inflammatory response in peripheral blood mononuclear cells, as well as a compensatory mechanism to protect against several pro-death stimuli in fibroblasts. A dominantly inherited human autoinflammatory disease caused by mutations in RIPK1 is identified, and RIPK1 mutations that prevent caspase-8 cleavage sensitize cells to apoptosis, necroptosis and inflammation.

In terms of nutritional and metabolic indicators [Supplementary Table 3, http://links.lww.com/CM9/C113], the underweight group had the lowest levels of red blood cell, hemoglobin (HGB), glucose (GLU), albumin (ALB), creatinine (CR), uric acid (UA), triglyceride (TG), and low-density lipoprotein (LDL), and the highest level of NT-pro BNP (all P <0.05). Univariable Cox proportional hazards analysis showed that underweight increased the risk of death in CLD-PH (hazard ratio [HR], 1.66; 95% confidence interval [CI]: 1.13–2.46; P = 0.010) [Supplementary Table 4, http://links.lww.com/CM9/C113]. [...]malnutrition can also increase respiratory muscle atrophy and infection susceptibility, subsequently impairing lung function. [...]increased catabolic burden, cardiac cachexia, abnormal cytokine and neurohormonal secretion, impaired immune status, and lower socioeconomic status can also be considered the underlying mechanisms associated with being underweight and contribute to the high mortality in CLD-PH. [...]we only used a single method for measuring BMI to assess obesity, which would ignore the

Exosomal MicroRNA-21 (miRNA-21, miR-21) is significantly up-regulated in blood samples of patients with lung cancer. Exosomal-derived miR-21 can be used as a promising biomarker for the early diagnosis of lung cancer. This paper develops a fluorescent biosensor based on the combination of magnetic nanoparticles (MNPs), cascade strand displacement reaction (CSDR) and CRISPR/Cas12a to detect the exosomal miR-21 from lung cancer. The powerful separation performance of MNPs can eliminate the potential interference of matrix and reduce the background signal, which is very beneficial for the improvement of specificity and sensitivity. The CSDR can specifically transform one miR-21 into plenty of DNA which can specifically trigger the trans-cleavage nuclease activity of Cas12a, resulting in the cleavage of ssDNA bi-labeled with fluorescent and a quencher. Under the optimized experimental conditions, the developed fluorescence biosensor exhibited high sensitivity and specificity towards the determination of exosomal-derived miR-21 with a linear range from 10 to 1 × 105 fM and a low detection limit of about 0.89 fM. Most importantly, this method can be successfully applied to distinguish the exosomal miR-21 from the lung cancer patients and the healthy people.

Rutin, a flavonoid found in fruits and vegetables, is a potential anticancer compound with strong anticancer activity. Therefore, electrochemical sensor was developed for the detection of rutin. In this study, CoWO4 nanosheets were synthesized via a hydrothermal method, and porous carbon (PC) was prepared via high-temperature pyrolysis. Successful preparation of the materials was confirmed, and characterization was performed by transmission electron microscopy, scanning electron microscopy, and X-ray photoelectron spectroscopy. A mixture of PC and CoWO4 nanosheets was used as an electrode modifier to fabricate the electrochemical sensor for the electrochemical determination of rutin. The 3D CoWO4 nanosheets exhibited high electrocatalytic activity and good stability. PC has a high surface-to-volume ratio and superior conductivity. Moreover, the hydrophobicity of PC allows large amounts of rutin to be adsorbed, thereby increasing the concentration of rutin at the electrode surface. Owing to the synergistic effect of the 3D CoWO4 nanosheets and PC, the developed electrochemical sensor was employed to quantitively determine rutin with high stability and sensitivity. The sensor showed a good linear range (5–5000 ng/mL) with a detection limit of 0.45 ng/mL. The developed sensor was successfully applied to the determination of rutin in crushed tablets and human serum samples. [Display omitted] •Highly sensitive electrochemical sensor based on 3D porous carbon and CoWO4 nanosheets.•Electrochemical signal of rutin is mainly based on its concentration at the electrode surface.•The introduction of porous carbon improved the electrochemical performance of 3D CoWO4.•The sensor was successfully applied to determine rutin in human serum samples.