Serum stromal cell-derived factor-1 concentrations are increased and associated with nonalcoholic fatty liver disease in children with obesity.

INTRODUCTION: Stromal cell-derived factor-1 (SDF-1) is a newly discovered small molecule adipocytokine, and research has shown that it is closely related to the occurrence and development of obesity. However, there are currently few research reports on SDF-1 in childhood obesity and nonalcoholic fatty liver disease (NAFLD), and this study aims to explore the relationship between SDF-1 and obesity related indicators in obese children. METHODS: Serum SDF-1 concentrations were measured using enzyme-linked immunosorbent assay (ELISA). Clinical and biochemical data were collected, such as body mass index (BMI), waist and hip circumference, blood pressure, liver enzymes, cholesterol, and fasting insulin. Children with NAFLD or not were evaluated through Color Doppler Ultrasound. RESULTS: Serum SDF-1 concentrations were significantly higher in obese subjects than in non-obese subjects (P < 0.05), and were elevated in the NAFLD obese subjects than in the non-NAFLD obese subjects (P < 0.05). SDF-1 was positively correlated with BMI, waist-to-hip ratio, systolic blood pressure, body fat percentage (BFP), basal metabolic rate (BMR), alanine transaminase (ALT), aspartate transaminase (AST), glutyltranspeptidase (GT), and homoeostasis model of HOMA-IR, independent of their uric acid (UA), total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), very-low-density lipoprotein (VLDL), gender and age. BFP and BMR were associated with the serum SDF-1 concentrations in multivariable linear regression analysis. CONCLUSION: These results suggest that SDF-1 levels are elevated in obese children and are associated with NAFLD, indicating that SDF-1 may play a role in the development of childhood obesity and metabolic disorders.

A Comprehensive Study on the Association between Plasma NOV/CCN3 Levels and Insulin Resistance in Childhood Obesity.

INTRODUCTION: Childhood obesity is a global health problem that is associated with various metabolic complications, such as insulin resistance, type 2 diabetes, dyslipidemia, and cardiovascular diseases. The mechanisms underlying the development of insulin resistance in childhood obesity are not fully understood. Nephroblastoma overexpressed gene (NOV), also known as CCN3, is a member of the CCN family of matricellular proteins that modulate cell proliferation, differentiation, adhesion, migration, and survival. Previous studies have shown that NOV/CCN3 is involved in glucose metabolism and insulin signaling in various tissues and cell types. However, the role of NOV/CCN3 in childhood obesity and insulin resistance remains unclear. METHODS: In this study, we aimed to investigate the association between plasma NOV/CCN3 levels and insulin resistance in 58 obese and 43 non-obese children aged 6-12 years. We measured plasma NOV/CCN3 levels by enzyme-linked immunosorbent assay (ELISA), and assessed insulin resistance by homeostasis model assessment of insulin resistance (HOMA-IR). We also collected clinical and biochemical data, such as body mass index (BMI), waist circumference (WC), blood pressure (BP), fasting glucose (FG), fasting insulin (FI), lipid profile, and inflammatory markers. RESULTS: We found that plasma NOV/CCN3 levels were significantly higher in obese children than in non-obese children (P<0.001), and positively correlated with BMI (r=0.42, P<0.001), WC (r=0.38, P<0.001), BP (r=0.35, P<0.001), FG (r=0.31, P<0.001), FI (r=0.45, P<0.001), HOMA-IR (r=0.48, P<0.001), triglycerides (r=0.28, P<0.001), low-density lipoprotein cholesterol (LDL-C) (r=0.26, P<0.001), and C-reactive protein (CRP) (r=0.32, P<0.001). Multiple linear regression analysis revealed that plasma NOV/CCN3 levels were independently associated with HOMA-IR after adjusting for age, sex, BMI, WC, BP, FG, FI, lipid profile, and CRP (ß=0.36, P<0.001). CONCLUSION: These results suggest that plasma NOV/CCN3 levels are elevated in childhood obesity and are associated with insulin resistance, indicating that NOV/CCN3 may play a role in the pathogenesis of metabolic disorders in obese children.

Study on network pharmacology of Ginkgo biloba extract against ischaemic stroke mechanism and establishment of UPLC-MS/MS methods for simultaneous determination of 19 main active components.

INTRODUCTION: Ginkgo biloba extract (GBE) is an effective substance from traditional Chinese medicine (TCM) G. biloba for treating ischaemic stroke (IS). However, its active ingredients and mechanism of action remain unclear. OBJECTIVES: This study aimed to reveal the potential active component group and possible anti-IS mechanism of GBE. MATERIALS AND METHODS: The network pharmacology method was used to reveal the possible anti-IS mechanism of these active ingredients in GBE. An ultra-high-performance liquid chromatography triple quadrupole electrospray tandem mass spectrometry (UPLC-MS/MS) method was established for the simultaneous detection of the active ingredients of GBE. RESULTS: The active components of GBE anti-IS were screened by literature integration. Network pharmacology results showed that the anti-IS effect of GBE is achieved through key active components such as protocatechuic acid, bilobalide, ginkgolide A, and so on. Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that the possible anti-IS mechanism of GBE is regulating the PI3K-Akt signalling pathway and other signal pathways closely related to inflammatory response and apoptosis regulation combined with AKT1, MAPK, TNF, ALB, CASP3, and other protein targets. Nineteen main constituents in seven batches of GBE were successfully analysed using the established UPLC-MS/MS method, and the results showed that the content of protocatechuic acid, gallic acid, ginkgolide A, and so forth was relatively high, which was consistent with network pharmacology results, indicating that these ingredients may be the key active anti-IS ingredients of GBE. CONCLUSION: This study revealed the key active components and the anti-IS mechanism of GBE. It also provided a simple and sensitive method for the quality control of related preparations.

Follistatin-Like 1 and Family with Sequence Similarity to 19 Member A5 Levels Are Decreased in Obese Children and Associated with Glucose Metabolism.

INTRODUCTION: Childhood obesity is a significant and growing problem worldwide. Recent evidence suggests Follistatin-like 1 (FSTL1) and family with sequence similarity to 19 member A5 (FAM19A5) to be novel adipokines. However, very few studies have examined the plasma levels of FSTL1 and FAM19A5 in children. Therefore, this cross-sectional study evaluated the association between serum FSTL1 and FAM19A5 levels and obesity in children and investigated the relationship between FSTL1 and FAM19A5 and glucose metabolism or endothelial injury. METHODS: Fifty-five obese children and 48 healthy controls were recruited. Plasma FSTL1 and FAM19A5 levels were detected using ELISA. In addition, the association between the clinical data and anthropometric parameters was analyzed. RESULTS: Serum FAM19A5 levels were significantly decreased in the obese children, at 189.39 ± 19.10 pg/mL, compared with those without obesity, at 211.08 ± 38.09 pg/mL. Serum concentrations of FSTL1 were also significantly lower in the obese children, at 0.64 (0.37-0.64) ng/mL, compared with those without obesity, at 1.35 (1.05-2.12) ng/mL. In addition, FAM19A5 (OR = 0.943; p = 0.003) was a predictor of insulin resistance in obese children compared with healthy controls. Lastly, serum FAM19A5 and FSTL1 played mediating roles in insulin resistance in children. CONCLUSION: The serum levels of FAM19A5 and FSTL1 were decreased in obese children; therefore, FAM19A5 and FSTL1 likely play important roles in glucose metabolism in obese children.

Inhibition of USP15 ameliorates high-glucose-induced oxidative stress and inflammatory injury in podocytes through regulation of the Keap1/Nrf2 signaling.

Ubiquitin-specific peptidase 15 (USP15) is implicated in the pathogenesis of numerous diseases. However, whether USP15 plays a role in diabetic nephropathy remains undetermined. This project was designed to determine the potential role of USP15 in mediating high glucose (HG)-induced podocyte injury, a key event in the pathogenesis of diabetic nephropathy. We found that USP15 levels were elevated in podocytes after HG stimulation. Inhibition of USP15 led to decreases in HG-evoked apoptosis, oxidative stress, and inflammation in podocytes. Further investigation showed that inhibition of USP15 enhanced the activation of NF-E2-related factor 2 (Nrf2) and expression of Nrf2 target genes in HG-simulated podocytes. Moreover, depletion of Kelch-like ECH-associated protein 1 (Keap1) diminished the regulatory effect of USP15 inhibition on Nrf2 activation. In addition, Nrf2 suppression reversed USP15-inhibition-induced protective effects in HG-injured podocytes. Taken together, these data indicate that USP15 inhibition protects podocytes from HG-induced injury by enhancing Nrf2 activation via Keap1.

Adropin and apelin-12 efficiently predict metabolic syndrome in obese children.

OBJECTIVE: Metabolic syndrome (MetS) is the most common condition associated with childhood and adolescent obesity and is a challenging public health issue. Very few studies have described the specificity and sensitivity of serum levels of adropin and apelin-12 as predictors of MetS. The aim of this study was to evaluate the association between serum levels of adropin and apelin-12 and MetS, and their sensitivity as predictors of MetS in obese children. METHODS: This study involved 138 children. The study group included obese subjects with MetS, and the two control groups included obese subjects without MetS and normal weight subjects. Anthropometric parameters and clinical data were collected. Plasma levels of apelin-12, adropin, leptin, adiponectin, and TNF-α were also measured. RESULTS: Obese children with MetS had significantly higher levels of apelin-12 and significantly lower levels of adropin when compared with those in children without MetS. In logistic regressions, we identified that apelin-12 was a risk factor for metabolic syndrome, and adropin was a protecting factor of having MetS after adjusting for age, sex, and puberty. Furthermore, ROC analysis revealed that adropin and apelin-12 are more sensitive predictors of metabolic syndrome than leptin and adiponectin. CONCLUSION: Serum adropin and apelin-12 levels can be useful biomarkers for predicting MetS in obese children. Our findings could provide a novel approach for the treatment and prevention of MetS.

Irisin as a mediator between obesity and vascular inflammation in Chinese children and adolescents.

BACKGROUND AND AIM: This study aims to characterize the role of Irisin in obesity and early onset metabolic and vascular sequelae in Chinese children. Furthermore, we aim to examine whether Irisin mediate endothelial cells dysfunction and vascular inflammation which eventually leads to obesity. METHODS AND RESULTS: We quantified plasma Irisin levels using enzyme-linked immunosorbent assay (ELISA) among 85 lean and 120 obese children, and assessed the association of Irisin levels with anthropometric, metabolic, cardiovascular and inflammatory parameters of obese children comparing with lean children. We further characterized the markers for endothelial cells and inflammation between obese and lean children to assess potential correlations. In addition, a potential direct effect of Irisin on the expression of endothelial adhesion molecules was assessed in human coronary artery endothelial cells. Irisin levels from obese children was significantly lower than lean children, and this reduced Irisin levels is correlated with certain physical parameters of studied children. Moreover, we identified significant inverse associations between inflammation markers of endothelial activation with Irisin levels in obese children. Multiple regression analyses confirm Irisin serves as a strong predictor of SDS-SBP, Ang-2, ICAM-1, E-selectin and hsCRP levels, independent of SDS-BMI. Lifestyle intervention results in a significant improvement of these cardiovascular and inflammatory parameters, and these were accompanied by a significant improvement of Irisin levels and weight loss. Finally, in the mediation effect model, our data showed that Irisin changes act as partial mediators of the relationship between SDS-BMI changes and changes in inflammatory and endothelial parameters for ICAM-1, E-selectin and hsCRP after controlling for covariates. Likewise, on the cellular level, Irisin inhibition hsCPR, ICAM-1 and E-selectin expression in endothelial cells, whereas Ang-2, VCAM-1 and eNOS expression were unaffected. CONCLUSIONS: Our study showed that Irisin levels change may indicate the early stages of cardiovascular disease in obese children.

Knockdown of CTRP6 inhibits high glucose-induced oxidative stress, inflammation and extracellular matrix accumulation in mesangial cells through regulating the Akt/NF-κB pathway.

C1qTNF-related protein 6 (CTRP6) is a member of the CTRP family and exerts a key role in the progression of diabetes mellitus. However, the role of CTRP6 in diabetic nephropathy remains unknown. The present study was designed to examine the roles of CTRP6 in diabetic nephropathy and explore the potential molecular mechanisms. Our results showed that the expression level of CTRP6 was significantly increased in high glucose (HG)-stimulated glomerular mesangial cells (MCs). The following loss/gain-of-function assays demonstrated that CTRP6 knockdown significantly inhibited HG-induced reactive oxygen species (ROS) production in MCs. CTRP6 knockdown caused significant decreases in tumour necrosis factor-α (TNF-α), interleukin (IL)-1ß and IL-6 production levels in HG-induced MCs. Moreover, knockdown of CTRP6 inhibited HG-stimulated extracellular matrix (ECM) accumulation in MCs characterized by decreased expression and production levels of fibronectin (FN) and collagen IV (Col IV). Furthermore, CTRP6 knockdown suppressed HG-induced the activation of Akt/NF-κB pathway in MCs, while overexpression of CTRP6 exhibited the opposite effects. Treatment with LY294002, an inhibitor of Akt, reversed the induction effects of CTRP6 overexpression on ROS production, inflammation and ECM accumulation in MCs. In conclusion, these findings demonstrated that CTRP6 knockdown inhibits HG-induced ROS production, inflammation and ECM accumulation in MCs, which were mediated by the inactivation of the Akt/NF-κB pathway. The roles of CTRP6 in diabetic nephropathy provided evidence for its therapeutic potential for the treatment of diabetic nephropathy.

Copeptin and Nesfatin-1 Are Interrelated Biomarkers with Roles in the Pathogenesis of Insulin Resistance in Chinese Children with Obesity.

BACKGROUND: Copeptin and nesfatin-1 have recently been identified as novel peptides that play a role in the pathogenesis of obesity-related insulin resistance in adults. However, the relationship between them has not yet been elucidated, and their circulating levels in children with obesity have not been adequately studied. Therefore, the current study aimed to investigate whether their levels are altered in Chinese children with obesity, as well as to determine the correlation of these 2 peptides with each other, with insulin resistance, and with other biochemical parameters. METHODS: A total of 156 children were enrolled in this study, including 101 children with obesity and 55 lean controls. Anthropometric parameters and clinical data of all subjects were collected, and circulating tumor necrosis factor-α, adiponectin, leptin, copeptin, and nesfatin-1 levels were measured using ELISA. RESULTS: Serum copeptin and nesfatin-1 levels were significantly elevated in children with obesity and children with insulin resistance compared to control subjects. In addition, nesfatin-1 and copeptin levels were found to be significantly positively correlated with one another by Pearson's correlation and partial correlation. In multiple regression analysis using nesfatin-1 or copeptin as the dependent parameter, a significant correlation was observed between nesfatin-1 and copeptin, and associations between each of them with homeostasis model assessment of insulin resistance (HOMA-IR) were detected. CONCLUSION: These novel findings shed light on the possible interplay role of these 2 molecules in obesity-related insulin resistance.

The role of the adipocytokines vaspin and visfatin in vascular endothelial function and insulin resistance in obese children.

BACKGROUND: We measured the concentrations of the adipocytokines vaspin and visfatin in obese Chinese children. Furthermore, we studied the correlation of these adipocytokines with early-onset metabolic and vascular sequelae among these children. METHODS: A total of 244 children (160 obese and 84 lean) were included in this study. Vaspin and visfatin were detected using enzyme-linked immunosorbent assays. We also assayed other metabolic and cardiovascular parameters. The associations of serum vaspin and visfatin concentrations with metabolic and cardiovascular parameters were determined. RESULTS: We found a significant elevation in the concentrations of vaspin and visfatin in obese children compared to the concentrations in lean children. Additionally, we found a significant positive correlation between visfatin and vaspin levels, as well as inflammatory cell infiltration and markers of endothelial activation, but these factors did not affect insulin resistance in obese children. Multiple regression analyses confirmed that vaspin is the strongest predictor of higher tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), angiotensin-2 (Ang-2), vascular cellular adhesion molecule-1 (VCAM-1), and E-selectin levels. We also found a significant association between visfatin and Ang-2, IL-6, VCAM-1, and E-selectin levels. CONCLUSION: The adipocytokines vaspin and visfatin are significantly interrelated, and both adipocytokines play a role in vascular endothelial function and inflammation.

Serum Asprosin Concentrations Are Increased and Associated with Insulin Resistance in Children with Obesity.

OBJECTIVE: Asprosin, a novel peptide that has recently discovered as an important regulatory adipokine, is relevant to obesity in animals and adult humans. Little is known about its roles in children. The aim of the current study was to determine the potential role of asprosin and explore its relationship to various obesity-related markers in children with obesity. METHODS: A cross-sectional study was conducted among 119 Chinese children, including 79 children with obesity and 40 lean controls. Anthropometric parameters, clinical data, and circulating tumor necrosis factor-α (TNF-α), adiponectin, leptin, and asprosin levels were measured. RESULTS: Serum asprosin concentrations were significantly elevated in children with obesity compared with lean controls. Children with insulin resistance (IR) had higher asprosin levels than non-IR group. Asprosin was positively correlated with waist-to-hip ratio (WHR), diastolic blood pressure, homoeostasis model of IR (HOMA-IR), leptin-to-adiponectin ratio, TNF-α independent of their body mass index, SDs score, and age. In multivariable linear regression analysis, WHR and HOMA-IR were associated with the circulating level of asprosin. CONCLUSIONS: Circulating asprosins are increased in children with obesity and associated with IR. It may be proposed as a novel marker to predict advanced disease.

HrpS Is a Global Regulator on Type III Secretion System (T3SS) and Non-T3SS Genes in Pseudomonas savastanoi pv. phaseolicola.

The type III secretion system (T3SS) is the main machinery for Pseudomonas savastanoi and other gram-negative bacteria to invade plant cells. HrpR and HrpS form a hetero-hexamer, which activates the expression of HrpL, which induces all T3SS genes by binding to a 'hrp box' in promoters. However, the individual molecular mechanism of HrpR or HrpS has not been fully understood. Through chromatin immunoprecipitation coupled to high-throughput DNA sequencing, we found that HrpR, HrpS, and HrpL had four, 47, and 31 targets on the genome, respectively. HrpS directly bound to the promoter regions of a group of T3SS genes and non-T3SS genes. HrpS independently regulated these genes in a hrpL deletion strain. Additionally, a HrpS-binding motif (GTGCCAAA) was identified, which was verified by electrophoretic mobility shift assay and lux-reporter assay. HrpS also regulated motility and biofilm formation in P. savastanoi. The present study strongly suggests that HrpS alone can work as a global regulator on both T3SS and non-T3SS genes in P. savastanoi. [Formula: see text] Copyright © 2018 The Author(s). This is an open-access article distributed under the CC BY-NC-ND 4.0 International license .

IL-10/STAT3 is reduced in childhood obesity with hypertriglyceridemia and is related to triglyceride level in diet-induced obese rats.

BACKGROUND: The prevalence of childhood obesity and obesity-related metabolic disorder such as dyslipidemia has sharply increased in the past few decades. Chronic low-grade inflammation is associated with the development of comorbidities and poor prognosis in obesity. This study aims to evaluate interleukin-10 (IL-10) in childhood obesity with hypertriglyceridemia. METHOD: We evaluated IL-10 and signal transducer and activator of transcription 3 (STAT3) mRNA expression in adipose tissue (AT) as well as serum IL-10 in 62 children of 3 groups and in high-fat diet (HFD) induced obese rat. Expression of IL-10 and STAT3 protein in AT of diet-induced obese rats were examined over feed period. RESULTS: Adipose IL-10 and STAT3 mRNA expression and serum IL-10 reduced in obese children with hypertriglyceridemia and in HFD obese rats. The protein expression of IL-10 and STAT3 decreased in AT of obese rats compared with the control rats at end time. Expression of IL-10 mRNA was negatively correlated to TG and LDL-C levels, and positively correlated to HDL-C, adiponectin and serum IL-10 levels. CONCLUSIONS: IL-10 expression and its downstream JAK-STAT pathway are down-regulated in obese children with hypertriglyceridemia and in HFD obese rats.

Serum complement factor 5a levels are associated with nonalcoholic fatty liver disease in obese children.

AIM: Nonalcoholic fatty liver disease (NAFLD) is a leading cause of progressive and chronic liver injury. Complement factor 5a (C5a) may be involved in many inflammation disorders. This study investigated levels of systemic C5a in patients with and without NAFLD and lean controls. METHODS: A cross-sectional study was conducted from July 2012 to June 2013 among 96 Chinese children, aged 6-17 years, recruited from the Pediatric Department of the Second Affiliated Hospital of Xi'an Jiao Tong University: 40 obese children with NAFLD, 31 obese children without NAFLD and 25 lean controls. Anthropometric parameters, clinical data and circulating C5a levels were measured. RESULTS: Obese children had higher serum concentrations of complement factor C5a compared with lean controls, especially in obese children with NAFLD. C5a was positively correlated with body mass index (BMI), waist circumference, diastolic blood pressure (BP), triglycerides and homoeostasis model of insulin resistance, independent of their body mass index standard deviations score and age. Of the well-known risk factors, C5a was a significant predictor of NAFLD in obese children. CONCLUSION: Serum C5a was elevated in obese children, especially in those with NAFLD and it may be proposed as a novel marker to predict advanced disease.

LncRNA Gm15290 sponges miR-27b to promote PPARγ-induced fat deposition and contribute to body weight gain in mice.

We found that Gm15290 was one of the most upregulated lncRNAs in the adipose of ob/ob mice through lncRNA microarray analysis. Then, manipulations of overexpression and silencing in mouse primary adipocytes showed that Gm15290 positively regulated adipogenesis, manifested by increasing lipid deposition and upregulating adipogenic genes including PPARγ, C/EBPα, and aP2. However, overexpression of mutant Gm15290 (at the binding site of miR-27c) did not have an promoting effect on adipogenesis. Additionally, Gm15290 was found to potentially interact with miR-27b that had been identified as a PPARγ targeting miRNA, and we verified their interaction by luciferase activity and RNA pull down assays. Furthermore, inhibition of Gm15290, by injection of the Gm15290 siRNA, decreased the body weight gain and mass of adipose tissues, including iWAT and eWAT, in mice fed with HFD. In conclusion, Gm15290 sponges miR-27b to increase fat deposition and body weight in HFD-fed mice.

Serum levels of omentin-1 are increased after weight loss and are particularly associated with increases in obese children with metabolic syndrome.

AIM: There have been very few paediatric studies on omentin-1, an anti-inflammatory adipokine that provides a link between adiposity, insulin resistance and metabolic syndrome. This Chinese study evaluated the association between omentin-1 and metabolic syndrome and analysed the effect of a six-month lifestyle intervention on the levels in obese children. METHODS: We recruited 119 obese outpatients (75% boys) aged 7-18 years from the Second Affiliated Hospital of Xi'an Jiaotong University, who underwent a six- month lifestyle intervention. Our controls were 55 matched children with normal weight. Anthropometric parameters, biochemical data and circulating omentin-1 levels were measured at baseline and after six months. RESULTS: Of the 119 obese children, 32 (27%) had metabolic syndrome. The obese children, particularly those with metabolic syndrome, had significantly lower serum omentin-1 levels at baseline than the controls. We also found that the omentin-1 levels were negatively associated with their body mass index, waist circumference and homoeostasis model assessment of insulin resistance. After the six-month lifestyle intervention, the obese children showed significant weight loss and their omentin-1 levels increased. CONCLUSION: Serum omentin-1 was regulated by weight and seemed to be associated with children's metabolic disorders. A six-month lifestyle intervention significantly increased serum omentin-1 levels.

Lon Protease Is Involved in RhpRS-Mediated Regulation of Type III Secretion in Pseudomonas syringae.

Pseudomonas syringae depends on the type III secretion system (T3SS) to directly translocate effectors into host cells. Previously, we reported a nonpathogenic rhpS mutant, suggesting that the two-component transduction system rhpRS is an important regulator of T3SS in P. syringae. rhpRS regulates itself and a variety of downstream genes under an inverted repeat element promoter in a phosphorylation-dependent manner. Here, we identify lon as a suppressor of the rhpS mutant through transposon screening. A lon/rhpS double mutant restored the phenotypes of the rhpS mutant. The expression level of lon was higher in rhpS and other T3SS-deficient mutants than the wild-type strain, suggesting a negative feedback mechanism between lon and T3SS genes. lon was also induced by a novel T3SS inhibitor, acetate, which substantially compromises the activation of T3SS genes in minimal medium and bacterial growth in host plants.

Enhanced butanol production in a microbial electrolysis cell by Clostridium beijerinckii IB4.

Reducing power such as NADH is an essential factor for acetone/butanol/ethanol (ABE) fermentation using Clostridium spp. The objective of this study was to increase available NADH in Clostridium beijerinckii IB4 by a microbial electrolysis cell (MEC) with an electron carrier to enhance butanol production. First of all, a MEC was performed without electron carrier to study the function of cathodic potential applying. Then, various electron carriers were tested, and neutral red (NR)-amended cultures showed an increase of butanol concentration. Optimal NR concentration (0.1 mM) was used to add in a MEC. Electricity stimulated the cell growth obviously and dramatically diminished the fermentation time from 40 to 28 h. NR and electrically reduced NR improved the final butanol concentration and inhibited the acetone generation. In the MEC with NR, the butanol concentration, yield, proportion and productivity were increased by 12.2, 17.4, 7.2 and 60.3 %, respectively. To further understand the mechanisms of NR, cathodic potential applying and electrically reduced NR, NADH and NAD(+) levels, ATP levels and hydrogen production were determined. NR and electrically reduced NR also improved ATP levels and the ratio of NADH/NAD(+), whereas they decreased hydrogen production. Thus, the MEC is an efficient method for enhancing the butanol production.

Shape of glucose curve can be used as a predictor for screening prediabetes in obese children.

AIM: We attempted to classify obese children with glucose abnormalities into different categories based on the plasma glucose (PG) at 0, 60, 120 and 180 min and extract the metabolic information from the shape of the PG curve. METHODS: We recruited 1205 obese children and 325 nonobese children. Their body weight, blood pressure, waist and hip circumferences were measured. An oral glucose tolerance test (OGTT) was carried out, and glucose, insulin and glucagon levels were tested. RESULTS: There were six forms of abnormal glucose tolerance (AGT) curves in obese children in addition to normal glucose tolerance (NGT). 58.3% of obese children had AGT. BMI, waist circumference, waist-to-hip ratio and systolic blood pressure of each obese group were much higher than in nonobese children (p < 0.05). HOMA-IR increased significantly in obese children with high fasting PG and obese children with high fasting and 3-h PG (p < 0.05), and HOMA-ß cell increased significantly in obese children with high 1- and 2-h but low 3-h PG (p < 0.05). CONCLUSION: Abnormal glucose tolerance was highly prevalent when concerning with glucose values at 60 and 180 min. The shape of PG which contains a net of metabolic information can be a predictor for screening prediabetes.

Possible non-linear relation between prostate specific antigen and vitamin D: a machine learning study based on cross-section data.

Objective: Due to inconsistent results in earlier investigations regarding the relationship between vitamin D and prostate-specific antigen (PSA), this study was conducted to gain a deeper understanding of the association between vitamin D and PSA. Methods: A total of 7174 male samples with 25(OH)D, PSA, and other variables were obtained from the National Health and Nutrition Examination Survey (NHANES) database. Three models, created through stepwise logistic regression, were employed to examine the dose-response association between PSA and 25(OH)D. Subsequently, restricted cubic spline analysis (RCS) was used to explore the nonlinear association between 25(OH)D and PSA. The study also compared the performance of four machine learning models in predicting PSA levels. Results: The dose-response relationship indicated a negative impact of high 25(OH)D levels on PSA (p for trend 0.05). The odds ratio (OR) of Q4 (7.73 with 95% CI (0.26, 15.76)) was significantly higher than Q1 (6.23 with 95% CI (0.24, 12.57)). OR values in Q2 and Q3 were less than 1 (Q2= 0.57 with 95% CI (-6.37, 8.04) and Q3= 0.26 with 95% CI (-5.94, 6.86)), suggesting a potential protective effect of 25(OH)D on PSA. RCS analysis revealed a U-shaped relationship between blood 25(OH)D levels and PSA, with serum 25(OH)D in the range of 20-134 ng/ml showing a potential decrease in PSA levels. Above this range, an increase in 25(OH)D might elevate PSA levels. Age (2.67 with 95% CI 2.24 to 3.1) and BMI (17.52 with 95% CI 7.65 to 26.32), along with the OR of obesity (10.36 with 95% CI 0.68 to 20.18), were identified as potential PSA risk factors. Among the machine learning models, the random forest algorithm performed the best in predicting PSA levels. Conclusion: This study revealed a U-shaped relationship between 25(OH)D and PSA, with PSA potentially declining when 25(OH)D is between 20 and 134 ng/mL and possibly rising above this range. The random forest method proved effective in both predicting PSA levels and guiding vitamin D dosage.