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Objective: One mechanism of hypothyroidism involves the disruption of thyroid hormone synthesis and secretion by thyrocytes. Hydrogen sulfide (H2S), as a gas signaling molecule, participates in many physiopathologic processes by upregulating sirtuin-1 (SIRT1). The aim of the current study was to explore whether H2S promotes the synthesis and secretion of thyroid hormones by upregulating SIRT1.Methods: Real-time PCR and immunohistochemistry were used to detect the mRNA and protein expression of H2S-generating enzymes in normal human thyroid tissues. Serum H2S concentrations from hypothyroid patients (n = 32) and euthyroid participants (n = 41) were detected by H2S-selective sensors. Thirty-one Sprague–Dawley rats were divided into control group (n = 10), hypothyroid group (induced by MMI, n = 10) and hypothyroid + NaHS group (n = 11), and the FT4, TT4 and TSH levels were assayed. Human primary thyrocytes were incubated with H2S donor sodium hydrosulfide (NaHS) or NaHS plus SIRT1 inhibitor (EX527) in vitro. Thyroid hormone synthesis- and secretion-related proteins [thyroid peroxidase (TPO), sodium iodide transporter (NIS), Pendrin, monocarboxylic acid transporter 8 (MCT8)] were analyzed by real-time PCR and Western blot.Results: H2S levels in serum from hypothyroid patients were decreased compared to those from euthyroid participants (p < .05), and serum H2S levels were positively correlated with FT3, FT4, TT3, and TT4 levels in all subjects (all p < .0001). In vivo, NaHS promoted thyroid function in hypothyroid rats (p < .05). In vitro, H2S was detected in supernatant, and CBS mRNA was higher than CSE and 3-MPST in human primary thyrocytes (p < .05). The protein levels of TPO, NIS, Pendrin and MCT8 were upregulated in a concentration-dependent manner for NaHS in thyrocytes. After blocking SIRT1 with EX527, we found that the increasing levels of TPO, NIS, Pendrin, and MCT8 and TPO activity were downregulated in thyrocytes incubated with NaHS, and FT4 levels in the cell supernatant were also decreased significantly (all p < .05).Conclusion: H2S is mainly generated in thyrocytes by CBS. Serum H2S levels are decreased with hypothyroidism. H2S promotes the synthesis and secretion of thyroid hormones and the expression of related molecules by upregulating SIRT1.

Abstract Background Reversible splenial lesion syndrome (RESLES) is known to cause severe psychiatric symptoms but is also a very rare clinical disease in which the specific aetiology is unknown. According to current reports, there are major causes of the disease, including viral or bacterial infection, epilepsy, anti-epileptic drug withdrawal, high-altitude cerebral oedema, and metabolic disorders such as hypoglycaemia and hypernatraemia. In this article, we report a patient with thrombotic thrombocytopenic purpura (TTP) who presented with RESLES. Case presentation A 34-year-old female patient who presented with fever and progression of disorder of consciousness was eventually diagnosed with RESLES based on brain imaging. Moreover, clinical features and peripheral smears demonstrating schistocytes and thrombocytopenia confirmed a diagnosis of TTP. RESLES can be improved by plasma exchange therapy. Conclusion This rare case highlights the occurrence of RESLES as a presenting feature of the expanding list of unusual neurological manifestations of TTP.

Abstract Background Insulin resistance (IR) in obesity is associated with the occurrence of metabolic and cardiovascular diseases. Dipepidyl peptidase 4 (DPP4) plays a pivotal role during the development of IR, and was found to be a target gene of microRNA-214 (miR-214) in our study. This study sought to assess the expression and clinical value of miR-214 in obese patients with IR, and investigate its therapeutic potential in obese rats and adipocytes with IR. Methods Serum expression of miR-214 in obese patients with or without IR was estimated by quantitative real-time-PCR. A receiver operating characteristic curve was plotted to evaluate the diagnostic value of miR-214 in the patients. Obesity-induced IR animal and cell models were constructed, and the therapeutic ability of miR-214 was explored. Results Serum expression of miR-214 was decreased in obese patients compared with the healthy controls, and the lowest expression was observed in the cases with IR. Downregulation of miR-214 was significantly correlated with the serum DPP4 levels and HOMA-IR of the patients upon IR conditions, and was demonstrated to perform diagnostic accuracy for distinguishing obese patients with IR from those without IR. In obesity-associated IR animal and cell models, the downregulation of miR-214 was also been detected. According to the measurement of glucose and insulin tolerance and glucose uptake abilities, we found that the overexpression of miR-214 could be used to alleviate IR in the IR models, especially when collaboratively used with DPP4 inhibitor vildagliptin. Conclusion All data revealed that miR-214, as a regulator of DPP4, is decreased in obese patients with IR and may serve as a diagnostic biomarker. The upregulation of miR-214 could improve IR in obese rats and adipocytes, indicating that miR-214 has the therapeutic potential for obesity and IR.

Aims. To explore the associations between polymorphisms in SIRT1 and coronary heart disease (CHD) risk in Chinese Han patients with type 2 diabetes (T2D). Methods. This case-controlled study enrolled 492 patients with T2D: 297 with CHD and 195 without CHD. Five SIRT1 haplotype-tagging single-nucleotide polymorphisms (rs3818291, rs12242965, rs3818292, rs4746720, and rs16924934) were selected from Chinese Han data in the GRCh37.p13 phase 3 database and genotyped by polymerase chain reaction-restriction fraction length polymorphism or sequencing. Results. The rs16924934 G allele was associated with a higher risk of CHD than the A allele (odds ratio OR=1.429; 95% confidence interval CI=1.003–2.037; P=0.048). Using an additive inheritance model, the rs3818291 G/A genotype was associated with a higher CHD risk than the G/G genotype (OR’=1.683; 95%CI=1.033–2.743; P’=0.037 after adjustment for CHD risk factors). Smokers carrying G/A or A/A rs3818291 genotypes had a 3-fold higher CHD risk than those carrying GG (adjusted OR’=3.035; P’=0.011) and a 2.6-fold higher CHD risk than nonsmokers carrying GG (adjusted OR’=2.604; P’=0.033). Conclusions. Genetic polymorphisms of SIRT1 are associated with the risk of CHD in a Chinese Han population with T2D.

(R)-5-hydroxy-1,7-diphenyl-3-heptanone (DPHC) from the natural plant Alpinia officinarum has been reported to have antioxidation and antidiabetic effects. In this study, the therapeutic effect and molecular mechanism of DPHC on type 2 diabetes mellitus (T2DM) were investigated based on the regulation of oxidative stress and insulin resistance (IR) in vivo and in vitro. In vivo, the fasting blood glucose (FBG) level of db/db mice was significantly reduced with improved glucose tolerance and insulin sensitivity after 8 weeks of treatment with DPHC. In vitro, DPHC ameliorated IR because of its increasing glucose consumption and glucose uptake of IR-HepG2 cells induced by high glucose. In addition, in vitro and in vivo experiments showed that DPHC could regulate the antioxidant enzyme levels including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), thereby reducing the occurrence of oxidative stress and improving insulin resistance. Western blotting and polymerase chain reaction results showed that DPHC could promote the expressions of nuclear factor erythroid 2-related factor 2 (Nrf2), the heme oxygenase-1 (HO-1), protein kinase B (AKT), and glucose transporter type 4 (GLUT4), and reduced the phosphorylation levels of c-Jun N-terminal kinase (JNK) and insulin receptor substrate-1 (IRS-1) on Ser307 both in vivo and in vitro. These findings verified that DPHC has the potential to relieve oxidative stress and IR to cure T2DM by activating Nrf2/ARE signaling pathway in db/db mice and IR-HepG2 cells.

BackgroundChanges in IgG glycosylation, as a novel pathological feature, are observed in various autoimmune diseases (AIDs). The glycosylation patterns of IgG play a critical role in regulating the biological function and stability of IgG involved in the pathophysiology of many AIDs. However, the intracellular regulatory mechanisms underlying the effects of disturbances in various cytokines on IgG glycosylation are poorly understood. Thus, we investigated the regulatory effects of elevated cytokines in AIDs on intracellular IgG glycosylation within B cells.MethodsFirst, we established a controlled primary culture system in vitro to differentiate human CD19+ B cells into antibody-secreting cells (ASCs). Then, the IgG concentrations in the supernatants were measured by enzyme-linked immunoassay (ELISA) under IFN-γ, TNF-α, IL-21, IL-17A, BAFF, or APRIL stimulation. Next, the glycosylation levels of IgG under different stimuli were compared via a lectin microarray. The fine carbohydrate structures of IgG were confirmed by matrix-assisted laser desorption/ionization-quadrupole ion trap-time of flight-mass spectrometry (MALDI-TOF-MS). Finally, the expression of glycosyltransferases and glycosidases in B cells under stimulation with several cytokines was detected by real-time PCR and western blotting.ResultsWe found that cytokines significantly promoted IgG production in vitro and led to considerably different IgG glycan patterns. Specifically, the results of lectin microarray showed the galactose level of IgG was increased by IFN-γ stimulation (p

Introduction. The interactions of central obesity and body composition with thyroid hormones and the hypothalamus-pituitary-adrenal (HPA) axis are unclear; both central obesity and body composition have an impact on energy homeostasis. Our study aimed to investigate the association between body composition and pituitary hormones, including the HPA axis and pituitary-thyroid axis, in a Chinese population of euthyroid overweight and obese individuals. Methods. This was a cross-sectional study. Overweight and obese patients who regularly visited the multidisciplinary team (MDT) for obesity at Peking University First Hospital were enrolled in the study. Thyroid function, morning serum ACTH and cortisol levels, thyroid peroxidase antibody (TPOAb), thyroglobulin antibody (TgAb), body composition, and metabolic indicators, including liver function and the lipid profile, were measured at the first visit. Statistical analysis was performed using SPSS version 21.0 (IBM, USA). Results. In total, 441 patients with overweight or obesity were enrolled (male/female, 123/318). Patients were assigned to four groups according to the thyroid-stimulating hormone (TSH) level stratified by quartiles, and increased body mass index (BMI) was revealed in the highest TSH quartile group (p=0.002). Hip circumference (HC) of patients in the highest TSH quartile group was significantly increased (p=0.021). Morning ACTH levels and fasting insulin levels were significantly elevated in patients in the highest TSH quartile group (p=0.027 for fasting insulin, p

Introduction. Autoimmune thyroid diseases (AITDs) and antiphospholipid syndrome (APS) are commonly seen in childbearing-age women and can lead to recurrent miscarriages. Studies with a relatively small sample size were conducted and concluded inconsistent results on the relationship between AITDs and APS or the presence of antiphospholipid (aPL) antibodies. This meta-analysis aimed to provide evidence on the possible association between AITDs and APL using primary data from all relevant studies. Methods. Literature databases including PubMed, Embase, and Cochrane were searched from the time when the databases were established to March 2022. A total of 7 studies that met all inclusion criteria were selected in this meta-analysis, with 475 AITD patients and 764 healthy controls. After data extraction, the pooled odds ratio (OR) and the 95% confidence interval (95% CI) were calculated. Results. The risk of positive APL in AITD patients was approximately 3 folds higher in AITD patients compared with those in healthy controls (OR 3.41, 95% CI 2.29–5.08, p

A method based on capacitively coupled contactless conductivity detection (C4D), which has been proven effective for the rapid detection of available soil potassium content, was firstly proposed to apply to soil nutrient detection. By combining a detection signal spectrum analysis, geographic information system (GIS) data, and a cluster analysis, a soil nutrient management system to match the detection device was developed. This system included six modules: soil sample information management, electrophoresis analysis, quantitative calculation, nutrient result viewing, cluster analysis, and nutrient distribution map generation. The soil samples, which were collected from an experimental field in Xuchang City of Henan Province, were analyzed using the C4D and flame photometer methods. The results showed that the detection results for the soil samples obtained via the two methods were in good agreement. C4D technology was feasible for the detection of the soil available nutrients and had the advantages of a high timeliness, low sample volume, and low pollution. The soil nutrient management system adopted the hierarchical clustering method to classify the grid cells of the experimental field according to the nutrient detection results. A soil nutrient distribution map displayed the spatial difference in nutrients. This paper provides a systematic solution for soil nutrient zone management that includes nutrient detection, signal analysis, data management for the nutrient zone, and field nutrient distribution map generation to support decision making in variable fertilization.

Although cities only account for 3% of the global land area, they have disproportionately contributed 70% of total anthropogenic CO2 emissions; the main issue in estimating urban anthropogenic CO2 emissions is their large uncertainty. Tower-based atmospheric CO2 observations and simulations in urban areas have been frequently used as an independent approach to constrain and evaluate greenhouse gas emissions from city to regional scales, where only daytime CO2 observations and simulations are used considering the consensus that the large bias in simulating nighttime planetary boundary layer heights (PBLH) and atmospheric CO2 concentration will cause overestimation/underestimation in CO2 emission inversions. The above strategy of only using daytime observations makes the numbers of available concentration observations largely decrease even with the fact that tower-based atmospheric CO2 observations are sparsely distributed and conducted. Here, to solve the issue of large bias in nighttime CO2 simulations, we conducted four months of atmospheric CO2 observations from January to April in 2019, and raised an approach by coupling emission heights with dynamic PBLH variations in a WRF-STILT model. We found (1) the overestimation of simulated nighttime CO2 concentration decreased by 5–10 ppm, especially between 0:00 and 7:00. (2) The statistics for nighttime simulations were largely improved by using a revised model and posteriori emissions. The regression slopes of daily averages were 0.93 and 0.81 for the default model using a priori emissions and the revised model using the same a priori emissions, and the slope largely improved to 0.97 for the revised model using posteriori emissions. Moreover, the correlation coefficient also increased from 0.29 and 0.37 to 0.53; these results indicate our revised model obviously calibrated the bias in both nighttime and daily CO2 concentration simulations. In general, it is strongly recommended to use the revised WRF-STILT model in future inversion studies, which can effectively reduce the overestimation of nighttime spikes and make full use of nighttime observations.

The optical response of inorganic two-dimensional semiconductors is dominated by Wannier-Mott excitons, but molecular systems can host localised Frenkel excitons. Here, the authors report strong optical response in a class of monolayer molecular J-aggregates due to the coherent Coulomb interaction between localised Frenkel excitons.

Autoimmune thyroid diseases (AITDs), which include Hashimoto’s thyroiditis (HT) and Graves’ disease (GD), have a higher prevalence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in the literature. The effects of AITD-associated cytokines on SARS-CoV-2 infection-mediating molecule levels might be involved in the pathogenesis of susceptibility. We speculated that hydrogen sulfide (H2S) might attenuate this process since H2S has antiviral effects. Using immunohistochemistry, we found that angiotensin-converting enzyme-II (ACE2) expression was higher in the HT group and neuropilin 1 (NRP1) expression was higher in HT and GD groups than in the normal group, while transmembrane protease serine type 2 (TMPRSS2) expression was lower in HT and GD groups. When culturing primary thyrocytes with cytokines or sodium hydrosulfide (NaHS) plus cytokines, we found that ACE2 and NRP1 mRNA levels were upregulated while TMPRSS2 levels were downregulated by interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α). After pretreatment with NaHS in thyrocytes, ACE2 and NRP1 expression were downregulated compared to IFN-γ or TNF-α treatment, and NaHS had no effect on TMPRSS2 expression. Our findings suggested that IFN-γ and TNF-α, which are elevated in AITDs, promoted ACE2 and NRP1 expression and inhibited TMPRSS2 expression. H2S might protect against SARS-CoV-2 infection by downregulating ACE2 and NRP1 levels.

Substantial evidence indicated that maternal malnutrition could increase the susceptibility to obesity, insulin resistance, and type 2 diabetes in adulthood. It is increasingly apparent that the brain, especially the hypothalamus, plays a critical role in glucose homeostasis. However, little information is known about the mechanisms linking maternal protein restriction combined with post-weaning high-fat (HF) feeding with altered expression of brain neurotransmitters, and investigations into the epigenetic modifications of hypothalamus in offspring have not been fully elucidated. Our objective was to explore the effects of maternal protein restriction combined with post-weaning HF feeding on glucose metabolism and hypothalamic POMC methylation in male offspring mice. C57/BL6 mice were fed on either low-protein (LP) or normal chow (NC) diet throughout gestation and lactation. Then, the male offspring were randomly weaned to either NC or high-fat (HF) diet until 32 weeks of age. Gene expressions and DNA methylation of hypothalamic proopiomelanocortin (POMC) and melanocortin receptor 4 (MC4R) were determined in male offspring. The results showed that birth weights and body weights at weaning were both significantly lower in male offspring mice of the dams fed with a LP diet. Maternal protein restriction combined with post-weaning high-fat feeding, predisposes higher body weight, persistent glucose intolerance (from weaning to 32 weeks of age), hyperinsulinemia, and hyperleptinemia in male offspring mice. POMC and MC4R expressions were significantly increased in offspring mice fed with maternal LP and postnatal high-fat diet (P < 0.05). Furthermore, maternal protein restriction combined with post-weaning high-fat feeding induced hypomethylation of POMC promoter in the hypothalamus (P < 0.05) and POMC-specific methylation (%) was negatively correlated with the glucose response to a glucose load in male offspring mice (r = −0.42, P = 0.039). In conclusion, maternal LP diet combined with post-weaning high-fat feeding predisposed the male offspring to impaired glucose metabolism and hypothalamic POMC hypomethylation. These findings can advance our thinking about hypothalamic POMC gene methylation between maternal LP diet combined with post-weaning high-fat feeding and metabolic health in offspring.

Context: Hashimoto thyroiditis (HT) is related to intestinal microbiota alteration, but the causal relationship remains unclear. Hydrogen sulfide (H2S) is a microbiota-derived metabolite. We speculated that abnormal intestinal microbiota might limit H2S production capacity, promoting HT pathogenesis. Objective: This work aimed to illustrate that the intestinal microbiota plays important roles in HT pathogenesis via microbiota-derived H2S levels. Methods: We collected feces from HT patients and healthy donors for fecal microbiota transplantation (FMT). Thirty-six female CBA/J mice were randomly assigned to 4 groups: experimental autoimmune thyroiditis (EAT) group, EAT + Healthy group, EAT + HT group, and EAT + HT + H2S group. 16S ribosomal RNA sequencing was performed to examine gut microbiota alterations and the H2S production pathway. Serum TgAb and H2S levels were assayed by enzyme-linked immunosorbent assay and H2S-selective sensors, respectively. T-cell subpopulations in the spleen were detected by flow cytometry. Results: The gut microbiota was different after FMT among the EAT, EAT + Healthy, and EAT + HT groups. The thyroiditis score assessed by hematoxylin and eosin staining was higher in the EAT + HT group than that in the EAT and EAT + HT + H2S groups. Helper T (Th1) and Th17 cell differentiation ratios were increased in the EAT + HT group compared to the other 3 groups. Serum H2S levels were decreased and the dissimilatory sulfate reduction (DSR) pathway was attenuated in the EAT + HT group compared to the EAT + Healthy group. Conclusion: H2S alleviated thyroiditis severity and related immune disorders, which were aggravated by the FMT from HT patients. The attenuated DSR pathway in the gut microbiota from HT patients might be involved in thyroiditis pathogenesis. [ABSTRACT FROM AUTHOR]

Abstract Aims/Introduction We have previously reported that glycine suppresses the advanced glycation end‐products signaling pathway and mitigates subsequent oxidative stress in the kidneys of diabetic rats. In the present study, we investigated whether this beneficial effect was associated with upregulation of glyoxalase‐1 (Glo1) and activation of the nuclear factor erythroid 2‐related factor 2 (Nrf2). Materials and Methods Both healthy rats and streptozotocin‐induced diabetic rats were administrated with glycine (1% added to the drinking water) for 12 weeks. The function of Glo1, messenger ribonucleic acid (mRNA) and protein expressions of Nrf2, and markers of oxidative status were measured in the kidneys. The mRNA expressions of other downstream signaling molecules of the Nrf2 pathway were also determined. Results The mRNA and protein expressions, as well as the activity of Glo1, were decreased in the kidneys of diabetic rats, accompanied by diminished glutathione levels. After glycine treatment, these parameters of Glo1 function were markedly increased. Compared with the control group, the levels of Nrf2 mRNA and protein in the total kidney lysis were both markedly elevated in the diabetic group and glycine‐treated group. However, the nuclear translocation of Nrf2 was significantly increased in the glycine‐treated group than in the diabetic group. In addition, the anti‐oxidant capacity and the expressions of other downstream molecules of the Nrf2 signaling pathway were significantly increased after glycine treatment. Conclusions The present study shows that glycine might enhance the function of Glo1 and restore anti‐oxidant defense by promoting the nuclear translocation of Nrf2, thus inhibiting advanced glycation end‐products formation and protecting against renal oxidative stress.

Ixeris chinensis (Thunb.) Nakai (IC) is a folk medicinal herb used in Mongolian medical clinics for the treatment of hepatitis and fatty liver diseases even though its pharmacological mechanism has not been well characterized. This study investigated the hepatoprotective mechanism of IC on mice with nonalcoholic fatty liver disease (NAFLD) by integrating gut microbiota and metabolomic analysis. A high-fat diet (HFD) was used to develop nonalcoholic fatty liver disease, after which the mice were treated with oral IC (0.5, 1.5 and 3.0 g/kg) for 10 weeks. HFD induced NAFLD and the therapeutic effects were characterized by pathological and histological evaluations, and the serum indicators were analyzed by ELISA. The gut microbial and metabolite profiles were studied by 16S rRNA sequencing and untargeted metabolomic analysis, respectively. The results showed that the administration of IC resulted in significant decreases in body weight; liver index; serum biomarkers such as ALT, TG, and LDL-C; and the liver inflammatory factors IL-1β, IL-6, and TNF-α. The 16S rRNA sequencing results showed that administration of IC extract altered both the composition and abundance of the gut microbiota. Untargeted metabolomic analysis of liver samples detected a total of 212 metabolites, of which 128 were differentially expressed between the HFD and IC group. IC was found to significantly alter the levels of metabolites such as L-glutamic acid, pyridoxal, ornithine, L-aspartic acid, D-proline, and N4-acetylaminobutanal, which are involved in the regulation of glutamine and glutamate, Vitamin B6 metabolism, and arginine and proline metabolic pathways. Correlation analysis indicated that the effects of the IC extract on metabolites were associated with alterations in the abundance of Akkermansiaceae, Lachnospiraceae, and Muribaculaceae. Our study revealed that IC has a potential hepatoprotective effect in NAFLD and that its function might be linked to improvements in the composition of gut microbiota and their metabolites.

Background. This study evaluated the effectiveness of the multidisciplinary team (including a specialist, a dietitian, a physical exercise trainer, a surgeon for bariatric surgery, an acupuncturist, and several health educators) for obesity management and the body composition change and improvements in metabolic biomarkers during a 2-year follow-up. Materials and Methods. A total of 119 patients participated in the multidisciplinary team for obesity. Patients were followed up at 3 months, 6 months, 1 year, 18 months, and 2 years after their first visit. Individuals were divided into the high-protein diet (HPD) and standard-protein diet (SPD) group according to their results on a diet questionnaire that they filled out during follow-up. Results. After 1.2 years, the mean body weight of the participants dropped from 89.7 kg to 80.9 kg (p

Background: The coronavirus disease 2019 (covid-19) has brought physical risks as well as psychological challenges to the whole world. High school students are a special group suffering from both the academic pressure and the threat of the epidemic. The present study aims to conduct an online survey to investigate the psychological status of high school students in Shandong Province.Methods: Using a web-based cross-sectional survey, data was collected from 1,018 voluntary high school students assessed with demographic information, the Patient Health Questionnaire-9 (PHQ-9), the Generalized Anxiety Disorder-7 (GAD-7) and a self-designed online-study effect survey. Correlation analysis was performed to explore the relationships between depression symptoms, anxiety symptoms, and study effect.Result: The prevalence of depressive symptoms, anxiety symptoms, and a combination of depressive and anxiety symptoms was 52.4, 31.4, and 26.8%, respectively, among high school students in Shandong Province during the COVID-19 epidemic. And from moderate to severe severity level, the rates of depressive symptoms and anxious symptoms were 17.6 and 4.6%. Female students exhibited a higher rate and severity of mental symptoms than male, and grade one senior high school students got a higher rate and severity of mental symptoms than the other two grades. Nearly half of the students were not satisfied with their online-study effect. The PHQ-9 score had a strong positive correlation with the GAD-7 score. Both the PHQ-9 score the GAD-7 score had a negative correlation with the study-effect survey score.Conclusion: Quite a number of high school students suffered from depression and anxiety symptoms during the COVID-19 epidemic. Sufficient attentions should be paid, and necessary supports should be provided, to protect the mental health of this special group.

The acquisition of nutrient data on a precise scale has played a vital role in nutrient management processes for soils. However, the lack of rapid precise and multi-index detection techniques for soil macronutrient contents hinders both rational fertilization and cost reduction. In this paper, a rapid detection method and device were devised, combining capillary electrophoresis (CE) and capacitively coupled contactless conductivity detection (C4D), and presented to detect macronutrient contents of soil. The device consisted of a capillary channel, C4D detector, high-voltage system, etc. It separated macronutrient ions using capillary electrophoresis and then measured the ion concentration based on the C4D principle. Lime concretion black soil samples from a complete field were collected and detected. NO3−, NH4+, H2PO4− and K+ in sample solutions could be detected in 5 min with relative standard deviations (RSDs) from 1.0 to 7.51%. The injection voltage was set to 10 kV for 5 s, and the separation voltage was set to 14 kV. This demonstrated the excellent performance of the C4D device on the detection of soil macronutrients, which could help to guide fertilization operations more effectively.

Background Maternal malnutrition is a critical factor in determining the risk of obesity and glucose intolerance in offspring. However, little is known about the effects of a maternal high-fat diet (HFD) on the β cell phenotype in offspring, which is a major factor in glucose homeostasis, especially during the early life of offspring. Methods Dams were randomly fed a HFD (60% kcal from fat) or a chow diet before pregnancy and during gestation and lactation. Glucose metabolism and the β cell phenotype were assessed in male offspring at weaning. Results Dams fed a HFD showed impaired glucose tolerance. A HFD predisposed the offspring to increased impairment of metabolic health, including obesity, glucose intolerance and insulin resistance, compared with offspring from chow diet-fed dams. Furthermore, increased islet sizes and islet densities were observed in male offspring from HFD-fed dams at weaning. There were increases in the insulin-positive area, β cell mass and β cell proliferation in male offspring from HFD-fed dams at weaning age. Next, we further determined whether a maternal HFD could affect β cell apoptosis in mouse offspring and found that there was no significant change in β cell apoptosis between the HFD and control groups. Conclusion Our study is novel in showing that a maternal HFD predisposes offspring to impaired glucose metabolism and has a profound effect on β cell mass and proliferation in offspring mice, which is observed in mice as early as at weaning age. However, further study to clarify the underlying mechanisms is warranted.

Aims. The objective of the present study was to explore the long-term postpartum glucose metabolism in women with previous GDM, and study the mechanism of hyperglycemia from gestation to postpartum by investigating the postpartum insulin resistance and insulin secretion. Methods. A total of 321 females with previous GDM were followed up once during 1- to 6-years postpartum. Characteristics during pregnancy, perinatal period, and postpartum were compared between postpartum NGT and hyperglycemic women. HOMA-IR and HOMA-β were used to assess insulin resistance and insulin secretion levels with different glucose statuses. Results. The prevalence of postpartum hyperglycemia had a fluctuant increase from 25.9% at 1 year, to 53.7% at 5 year. 75 g OGTT 2 hPG during pregnancy was an independent predictor of postpartum hyperglycemia with an OR of 2.15 (95% CI 1.245, 3.722) (P=0.006). After ROC analysis, the best equilibrium between sensitivity (70.3%) and specificity (60.4%) for 2 hPG was 9.03 mmol/L. HOMA-IR was increased in postpartum normal glucose tolerance (NGT), prediabetes, and T2DM (1.64 vs. 2.14 vs. 4.27, P

Glycine exerts renoprotective effects, but the mechanism remains unclear. Glycine is increasingly recognized as a factor that attenuates oxidative stress, a key mechanism underlying diabetic nephropathy. In this study, we investigated the effects of glycine on diabetic renal injury and oxidative stress by adding 1% glycine in the drinking water of rats with streptozotocin-induced diabetes for 20 weeks. Glycine levels decreased in the plasma and kidney homogenates of diabetic rats but were restored by oral glycine administration. In these diabetic rats, glycine attenuated renal damage, as evidenced by the decreased mesangial expansion, tubular interstitial fibrosis, and neutrophil gelatinase-associated lipocalin (NGAL) expression. Glycine also ameliorated the raise in urinary malondialdehyde (MDA) levels and partially restored renal glutathione levels in diabetic rats. Renal levels of the Nox4 mRNA and protein, a major source of renal oxidative stress, were suppressed by the treatment with glycine. Immunohistological analysis revealed that glycine had protective effects on the tubular area rather than the glomerular area. Our results strongly suggest that the protective effect of glycine on renal oxidative stress and structural damage may be linked to enhancement of GSH synthesis and suppression of renal Nox4 expression in diabetic rats. Keywords: Glycine, Diabetic nephropathy, Oxidative stress, Glutathione, Nox4

Context: Alpinia officinarum Hance (Zingiberoside) has a long history in treating gastrointestinal diseases, but its mechanisms of action are not yet known. Objective: To investigate the effects and underlying mechanisms of the ethanol extract of A. officinarum rhizomes in an indomethacin-induced gastric injury rat model. Material and methods: Indomethacin (0.3 g/kg) was orally administered to Sprague-Dawley rats to induce gastric damage; after 7 h, the rats were treated with 0.03, 0.09, or 0.18 g/kg of the plant extract, galangin (0.2 g/kg), or bismuth potassium citrate (0.08 g/kg), once a day for 6 days. Rats in the control group received an equivalent volume of vehicle solution for 6 days. Gastric damage was evaluated by gross ulcer and histological indexes. Cyclooxygenase and non-cyclooxygenase pathway proteins were quantified by western blotting and ELISA. Results: Alpinia officinarum extract ameliorated gastric injury in a dose-dependent manner, and 0.18 g/kg dose exhibited the best performance by reducing the gross ulcer (from 20.23 ± 1.38 to 1.66 ± 0.37) and histological (from 4.67 ± 1.03 to 0.33 ± 0.51) indexes, decreasing serum TNF-α level (14.17%), increasing serum VEGF level (1.58 times), increasing cyclooxygenase-1 level (1.25 times, p