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Much evidence has shown that ambient particulate matter (PM) exposure is associated with abnormal glucose metabolism, but the underlying mechanism has not yet been fully characterized. Circadian disruption has adverse effects on glucose metabolism. In this study, we investigated the effects of long-term ambient PM exposure on the hepatic circadian clock and the expression rhythm of genes associated with hepatic glucose metabolism in mice. C57BL/6 mice were exposed to filtered air (FA), ambient PM, or ambient PM plus resveratrol (RES). After 15 weeks (12 h per day, 7 days per week) of exposure, glucose homeostasis, the rhythmic expression of clock genes, and genes associated with hepatic glucose metabolism were determined. Our results found that PM exposure induced glucose metabolism disorder and perturbed the rhythmic mRNA expression of core clock genes and their target genes involved in hepatic glucose metabolism. Mechanistic investigations demonstrated that ambient PM exposure markedly altered the expression patterns of BMAL1, clock, and SIRT1 in vivo. Simultaneously, we demonstrated that RES (an activator of SIRT1) changed the expression pattern of SIRT1, thereby reversing the rhythm misalignment of BMAL1 and clock and hepatic glucose metabolism disorder induced by ambient PM exposure. In addition, PM

Aims Type 2 diabetes (T2D) is a chronic disease that manifests as endocrine and metabolic disorders that seriously threatening public health. This study aimed to investigate the effects of Bacillus sp. DU-106 on anti-diabetic effects and gut microbiota in C57BL/6J mice fed a high-fat diet and streptozotocin-induced T2D. Methods and Results Bacillus sp. DU-106 was administered to model mice for eight consecutive weeks. Oral administration of Bacillus sp. DU-106 decreased food and water intake and alleviated body weight loss. Moreover, Bacillus sp. DU-106 imparted several health benefits to mice, including balanced blood glucose, alleviation of insulin resistance in T2D mice and an improvement in lipid metabolism. Furthermore, Bacillus sp. DU-106 protected against liver and pancreatic impairment. Additionally, Bacillus sp. DU-106 treatment reshaped intestinal flora by enhancing gut microbial diversity and enriching the abundance of certain functional bacteria. Conclusion Collectively, these findings suggest that Bacillus sp. DU-106 can ameliorate T2D by regulating the gut microbiota. Significance and Impact of Study Therefore, a novel probiotic, Bacillus sp. DU-106 may be a promising therapeutic agent for improving and alleviating T2D in mice.

Background Anthocyanins are metabolites of phenylpropanoid pathway, and involves in diverse processes of plant development and adaptation, which are regulated by the MYB-bHLH-WD40 (MBW) protein complexes. Many R2R3-MYB activators have been well characterized, but the MYB repressors in anthocyanin biosynthesis were recognized recently, which are also important in modulating phenylpropanoid metabolism in plants. The regulatory mechanism of anthocyanin biosynthesis in oil crop Brassica napus remains to be revealed. Results In this study, we identified an anthocyanin repressor BnCPC in B. napus. BnCPC encoded a typical R3-MYB protein containing a conserved [D/E]Lx2[R/K]x3Lx6Lx3R motif for interaction with bHLH proteins. Overexpression of BnCPC in B. napus inhibited anthocyanin accumulation, especially under anthocyanin inducible conditions. Protein–protein interaction and dual-luciferase assays confirmed that BnCPC could compete with BnPAP1 to interact with bHLHs (BnTT8 and BnEGL3), and repress the expression of anthocyanin biosynthetic genes (e.g., BnDFR) that activated by MBW complexes. Moreover, we found BnCPC inhibited the MBW complex-induced BnCPC activity. Conclusions Overall, this research demonstrated that BnCPC repressed anthocyanin biosynthesis by affecting the formation of MBW complex, and formed a feedback loop to regulate anthocyanin accumulation in B. napus.

The circadian clock is closely associated with inflammatory reactions. Increased inflammatory cytokine levels have been detected in the airways of nocturnal asthma. However, the mechanisms that contribute to the nocturnal increase in inflammatory responses and the relationship with circadian clock remain unknown.MethodsInflammatory cytokine levels were measured in asthma patients with and without nocturnal symptoms. Allergic airway disease was induced in mice by ovalbumin (OVA), and different periods of light/dark cycles were used to induce circadian rhythm disorders. Serum shock was used to stimulate the rhythmic expression in human bronchial epidermal cells (16HBE). The expression and oscillation of circadian clock genes and inflammatory cytokines in 16HBE cells subjected to brain and muscle ARNT-like protein-1 (BMAL1) and Forkhead Box A2 (FOXA2) knockdown and treatment with a FOXA2 overexpression plasmid were assessed.ResultsSerum IL-6 was found to be significantly higher in asthmatic patients with nocturnal symptoms than those without nocturnal symptoms. The OVA-induced asthma model with a circadian rhythm disorder and 16HBE cells treated with serum shock showed an increase in IL-6 levels and a negative correlation with BMAL1 and FOXA2. The knockdown of BMAL1 resulted in a lower correlation between IL-6 and other rhythm clock genes. Furthermore, knockdown of the BMAL1 and FOXA2 in 16HBE cells reduced the expression and rhythmic fluctuations of IL-6.ConclusionsOur findings suggest that there are increased IL-6 levels in nocturnal asthma resulting from inhibition of the BMAL1/FOXA2 signalling pathway in airway epithelial cells.

MicroRNAs (miRNAs), a class of endogenous small RNAs, are broadly involved in plant development, morphogenesis and responses to various environmental stresses, through manipulating the cleavage, translational expression, or DNA methylation of target mRNAs. miR393 is a conserved miRNA family present in many plants, which mainly targets genes encoding the transport inhibitor response1 (TIR1)/auxin signaling F-box (AFB) auxin receptors, and thus greatly affects the auxin signal perception, Aux/IAA degradation, and related gene expression. This review introduces the advances made on the miR393/target module regulating plant development and the plant’s responses to biotic and abiotic stresses. This module is valuable for genetic manipulation of optimized conditions for crop growth and development and would also be helpful in improving crop yield through molecular breeding.

Multi-walled carbon nanotubes (MWNTs) were prepared by pyrolysis of cheap natural gas over Ni/La2O3-MgO catalyst at 740 °C. The purified MWNTs were easily dispersed by ball milling method and aqueo...

Brassica napus is one of the important oil crops grown worldwide, and oil quality improvement is a major goal in rapeseed breeding. Yellow seed is an excellent trait, which has great potential in improving seed quality and economic value. In this study, we created stable yellow seed mutants using a CRISPR/Cas9 system and obtained the yellow seed phenotype only when the four alleles of two BnTT2 homologues were knocked out, indicating that the two BnTT2 homologues had conserved but redundant functions in regulating seed color. Histochemical staining and flavonoid metabolic analysis proved that the BnTT2 mutation hindered the synthesis and accumulation of proanthocyanidins. Transcriptome analysis also showed that the BnTT2 mutation inhibited the expression of genes in the phenylpropanoid and flavonoid biosynthetic pathway, which might be regulated by the complex of BnTT2, BnTT8 and BnTTG1. In addition, the homozygous mutants of BnTT2 homologues increased oil content and improved fatty acid composition with higher linoleic acid (C18:2) and linolenic acid (C18:3), which could be used for the genetic improvement of rapeseed. Overall, this research showed that the BnTT2 mutation can be used for yellow seed breeding and oil improvement, which is of great significance in improving the economic value of rapeseeds.

Age-related macular degeneration (AMD) and glaucoma are global ocular diseases with high blindness rate. RNA interference (RNAi) is being increasingly used in the treatment of these disorders with siRNA drugs, bevasiranib, AGN211745 and PF-04523655 for AMD, and SYL040012 and QPI-1007 for glaucoma. Administration routes and vectors of gene drugs affect their therapeutic effect. Compared with the non-viral vectors, viral vectors have limited payload capacity and potential immunogenicity. This review summarizes the progress of the ocular siRNA gene-silencing therapy by focusing on siRNA drugs for AMD and glaucoma already used in clinical research, the main routes of drug delivery and the non-viral vectors for siRNA drugs.

Although labor pain is treated clinically by the administration of local anesthetics alone or with opioids in the epidural or spinal spaces, however, the mechanisms of labor pain mechanisms have not been fully elucidated during to the lack of animal models, and the side effects of drugs still existed. Spinal microglia can be activated or mobilized under several pain states, and we want to explore the activation of spinal microglia is involved in the acute uterine cervical distension rats or not.(I) The electromyographic (EMG) response to uterine cervical distension (UCD) was observed. Twenty-four Sprague-Dawley rats were randomly divided into three groups: standard group, sham group, and UCD group (n=8). EMG response to UCD was recorded at 30, 60 and 120 min after distension, respectively. The activation of microglia in the spinal cord at UCD 60 min was seen. Grouping following the first part (n=4), four rats were executed perfusion after distension of 60 min, the T12 to L2 spinal cord segments were removed for immunohistochemical analysis. (II) After successfully implantation of the intrathecal catheter, 36 Sprague-Dawley rats were randomly divided into the PBS group, minocycline group and UCD group (n=12). EMG response to UCD was recorded before distension and after 30, 60, and 120 min after distension (n=8). Four rats of each group were executed perfusion at 60 min after distension, the T12 to L2 spinal cord segments were removed for immunohistochemical analysis. (III) Thirty-six Sprague-Dawley rats were randomly divided into an electrical acupuncture group, non-acupuncture group, and UCD group (n=12). EMG response to UCD was recorded at 30, 60, and 120 min after distension. Four rats of each group were executed at 60 min after distension, and the T12 to L2 spinal cord segments were removed for immunohistochemical analysis to observe the effect of Hegu and Sanyinjiao acupuncture electric stimulation in the activation of spinal microglia.(I) EMG based value of sham group, standard group, and the UCD group were no statistical significance (P0.05). After UCD, the EMG of the UCD group were increased at 30, 60, 120 min. Compared with fundamental values (P0.05), which the most apparent EMG change at 60 min after UCD (P0.05). Sixty min after UCD, compared with the sham group and the standard group, the EMG of the UCD group was higher (P0.05), but no difference was observed between standard group and sham group (P0.05). Compared with the sham group, the number of Iba1 (microglia markers)positive cells in thoracic, lumbar spinal cord (T12 to L2) was higher at 60 min after UCD (P0.05), the most Iba1 labeled cells expressed in IV-V layer and X layer of lumbar spinal cord dorsal horn. (II) EMG based value of UCD group, PBS group, and minocycline group had no significant difference (P0.05). Sixty min after UCD, compared with the PBS and UCD group, the EMG of the minocycline group was decreased significantly (P0.05), but there was no difference between the PBS group and UCD group (P0.05). At 30 and 120 min after UCD, the difference of EMG among the UCD group, PBS group, and minocycline group was no statistical significance (P0.05). Compared with the PBS and UCD group, the number of Iba1 positive cells at the thoracic, lumbar spinal cord in the minocycline group decreased significantly (P0.05). But no difference was observed between the PBS group and minocycline group (P0.05). (III) In the fourth part of the study: EMG based value of electrical acupuncture group, non-acupuncture group, and UCD group were no different (P0.05). Sixty min after UCD, compared with non-acupuncture and UCD group, the EMG of the acupuncture group was decreased significantly (P0.05), but no difference was observed between the UCD group and non-acupuncture group (P0.05).The activation of spinal microglia is involved in the formation of acute visceral pain induced by uterine cervical distension, Electrical acupuncturing Hegu, and Sanyinjiao alleviate pain, and the possible mechanism is inhibiting the activation of spinal microglia in the acute uterine cervical distension rats.

Multi-walled carbon nanotubes (MWNTs) with high-yield were prepared by pyrolysis of mixture of natural gas (NG) and propylene (C3H6) over Fe-Ni/Al2O3-MgO catalyst. For C3H6/NG flow rate ratio rangi...

Type 2 diabetes (T2D) is a chronic disease that manifests with endocrine and metabolic disorders, seriously threatening public health. This study aims to investigate the effects of Bacillus sp. DU-106 on anti-diabetic and gut microbiota in C57BL/6J mice on a high-fat diet (HFD) and streptozotocin (STZ)-induced T2D. Bacillus sp. DU-106 was administered to model mice for 8 consecutive weeks. Oral administration of Bacillus sp. DU-106 led to decreased food and water intake and alleviated body weight loss. And Bacillus sp. DU-106 imparted several health benefits to the mice, including balanced blood glucose, alleviation of insulin resistance in the T2D mice, and an improvement in lipid metabolism. Furthermore, Bacillus sp. DU-106 protected against liver and pancreas impairment to some extent. Additionally, Bacillus sp. DU-106 treatment reshaped the intestinal flora by enhancing gut microbial diversity and enriching the abundance of certain functional bacteria. Collectively, these findings suggested that Bacillus sp. DU-106 has the potential to ameliorate T2D by regulation of the gut microbiota. Therefore, a novel probiotic proposed here, Bacillus sp. DU-106 might be a promising therapeutic agent to prevent and alleviate T2D in mice.

Recent investigations have demonstrated that the chronic stress-induced behavioral disorders can be ameliorated by probiotics including Clostridium butyricum (C. butyricum) via the gut-brain-axis. However, the molecular mechanisms underlying the beneficial effects of C. butyricum on brain remain largely unknown. Here, we investigated whether chronic foot shock stress (CFSS) paradigm used for a hypertensive animal model could induce mood disorders such as anxiety, depression and cognitive impairments. Then, we assessed the impact of C. butyricum RH2 on the behavior disorders and neurobiological alterations in the hippocampus. Male Sprague-Dawley (SD) rats received intermittent electric shocks for consecutive 14 days and were treated with C. butyricum RH2 for 17 days. Anxiety- or depression-like behaviors were evaluated by open field test (OFT), and elevated plus maze (EPM). The Morris water maze test (MWM) was used to evaluate the cognitive functions. CFSS intervention led to mild anxiety- or depression-like behavior or cognitive impairment and C. butyricum RH2 treatment reversed the CFSS-induced symptoms. The serum ACTH or CORT was increased following CFSS but was completely reversed by C. butyricum RH2 treatment. In the hippocampus of CFSS rats, the expressions of BDNF and TrkB were downregulated but proBDNF and P75NTR were upregulated. These expression changes were partially reversed by C. butyricum RH2, suggesting a mode of action on BDNF and proBDNF balance. CFSS exposure resulted in downregulation of tissue-type plasminogen activator (tPA) but upregulation of plasminogen activator inhibitor 1(PAI-1), which could contribute to the decrease in BDNF by reduced conversion from proBDNF to BDNF in the hippocampus. C. butyricum RH2 treatment reversed the upregulated PAI-1 but not the downregulated tPA, which was in parallel with the amelioration of behavioral abnormalities, suggesting a novel tPA independent mechanism for PAI-1 action. Our results demonstrate for the first time that C. butyricum RH2 attenuates stress-induced behavior disorders via inhibiting the expression of brain PAI-1.

The

Chronic kidney disease (CKD) is a public health problem of which the prevalence is increasing worldwide. Several studies have reported that ambient particulate matter (PM) causes kidney injury, which may be related to the risk of CKD. However, the underlying molecular mechanisms have not been fully clarified. In addition, whether a high-fat diet (HFD) could exacerbate ambient PM-induced nephrotoxicity has not been evaluated. This study aimed to investigate the combined effect of ambient PM and a HFD on renal injury.Male C57BL/6 J mice were fed either a normal diet or a HFD and exposed to filtered air (FA) or particulate matter (PM) for 18 weeks. In the present study, we observed that renal function changed (serum blood urea nitrogen and serum creatinine), and exposure to PM and a HFD caused a synergistic effect on renal injury. Histopathological analysis showed that PM exposure induced renal fibrosis in mice, and combined exposure to PM and a HFD exacerbated these adverse effects. Moreover, ambient PM exposure activated the nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome and increased the inflammatory response, as indicated by the increases in interleukin-1β, interleukin-6 and tumor necrosis factor-α in the serum and kidney, as well as the upregulation of specific renal fibrosis-related markers (transforming growth factor-β1 and p-Smad2) in the kidney tissues of mice. Furthermore, combined exposure to PM and a HFD augmented these changes in the kidney. In vitro, inhibition of the NLRP3 inflammasome by MCC950 (an inhibitor of NLRP3) reduced the levels of proinflammatory cytokines and the expression of transforming growth factor-β1 and p-Smad2 in HK-2 cells.Taken together, our data indicated that PM exposure caused renal inflammation and induced profibrotic effects on the kidney, and combined exposure to ambient PM and a HFD exacerbated renal injury, which may involve activation of the NLRP3 inflammasome and the TGF-β1/Smad2 signaling pathway.

Objective Primary mediastinal B-cell lymphoma (PMBCL) lacks standard treatment regimens. This study aimed to identify the disease’s clinical features and prognostic factors. Methods This retrospective study included 56 patients with PMBCL. Patient demographic details and clinicopathological characteristics were summarized, and their effects on progression-free survival (PFS) and overall survival (OS) were analyzed. Results The median patient age was 29 years (range, 14–56). Twenty-two patients received DA-EPOCH-R (dose-adjusted etoposide, vincristine, and doxorubicin for 96 hours with bolus doses of cyclophosphamide and oral prednisone, as well as rituximab), and 34 patients received R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone). Clinical/laboratory parameters, overall response rates, and 5-year PFS and OS rates did not differ between the treatment groups. Kaplan–Meier analysis indicated that late-stage disease and a higher International Prognostic Index (IPI) were associated with shorter PFS and OS. Furthermore, patients with B symptoms and first-line treatment non-responders exhibited worse OS. 18Fluorodeoxyglucose-positron emission tomography/computed tomography quantitative parameters, such as higher metabolic tumor volume (MTV) and total lesion glycolysis (TLG), were corrected with shorter PFS. Conclusions This study revealed that stage IV disease, higher IPI, and B symptoms were poor prognostic factors in patients with PMBCL. Significantly, higher MTV and TLG portended worse PFS.

Growing body of research indicates that Traditional Chinese Medicine (TCM) interact with gut microbiota (GM) after oral administration.

Phosphorus stress is one of the important factors restricting plant growth and development, and the microRNA (miRNA) family is involved in the regulation of the response to plant nutrient stress by repressing the expression of target genes at the post-transcriptional or translational level. miR399 is involved in the transportation of phosphate in multiple plants by improving tolerance to low Pi conditions. However, the effect of miR399 on the response of low Pi stress in rapeseed (Brassica napus L.) is unclear. The present study showed a significant increase in taproot length and lateral root number of plants overexpressing Bna-miR399c, while the biomass and Pi accumulation in shoots and roots increased, and the anthocyanin content decreased and chlorophyll content improved under low Pi stress. The results illustrate that Bna-miR399c could enhance the uptake and transportation of Pi in soil, thus making B. napus more tolerant to low Pi stress. Furthermore, we confirmed that BnPHO2 is one of the targets of Bna-miR399c, and the rejection of Pi in rapeseed seedlings increased due to the overexpression of BnPHO2. Hence, we suggest that miR399c-PHO2 module can effectively regulate the homeostasis of Pi in B. napus. Our study can also provide the theoretical basis for germplasm innovation and the design of intelligent crops with low nutrient input and high yield to achieve the dual objectives of income and yield increase and environmental protection in B. napus.

In this study, A Acinetobacter pittii sp. was isolated with high efficiency for heterotrophic nitrification and aerobic denitrification (HN-AD). The boundary conditions for total nitrogen (TN) removal were as follows: C/N ratios 8-14, temperature 25-35 °C, initial pH 7-9, and shaker speed 100-120 rpm. Addition of mixed carbon resources achieved 97.38 % ammonia-N and 91.50 % TN removal, which was higher than that of the group with sole carbon resources. The ammonia-N and TN removal profiles matched well with first-order kinetics in the rapid response period and zero-order kinetics in the slow reaction period. Meanwhile, enzyme activity related to nitrogen conversion would remarkably increase with mixed carbon resources. Furthermore, proposed a possible relationship between the solid carbon source, hydrolysis, soluble small molecule organic matter, microbial activity, and heterotrophic nitrification and aerobic denitrification (HN-AD). This study provides a new strategy for improving nitrogen removal in wastewater with low-carbon resources.

Esophageal cancer has a high incidence and one of the highest mortality rates worldwide. There are few studies on the effects of sevoflurane on postoperative metastasis and recurrence of esophageal cancer. This study aimed to investigate the effect of sevoflurane on the progression of esophageal cancer and the underlying mechanism of the sensitivity to cisplatin.We used the esophageal squamous cell carcinoma (ESCC) line EC109 and esophageal adenocarcinoma (EADC) line SKGT-4. Cell proliferation and stemness potential were determined by MTT assay and sphere-forming assays, respectively. The protein expression of (sex determining region Y)-box 2 (SOX2) and octamer-binding transcription factor 4 (OCT4) was determined by western blot. Cell migration and invasion ability were separately determined by scratch assay and transwell assays, respectively. The distribution of cell cycle and apoptosis were detected by flow cytometry, and the levels of lactate dehydrogenase (LDH) were measured by the enzyme-linked immunosorbent assay (ELISA).In the SKGT-4 cells, exposure to sevoflurane inhibited proliferation, increased the migration and invasion potential, increased the number of cells in S phase, promoted self-renewal ability, and up-regulated the expression of SOX2 and OCT4 compared with control cells. Compared with the cisplatin treated group, treatment with sevoflurane plus cisplatin reduced the level of LDH and inhibited apoptosis in the SKGT-4 cells. However, sevoflurane did not affect EC109 cells.Long-term exposure to sevoflurane inhibited the proliferation, increased migration and invasion capacity, and decreased the sensitivity to cisplatin in EADC by promoting stemness. However, sevoflurane had no effect on the behavior of ESCC.

Electroless nickel–phosphorus films were produced on silicon substrates in alkaline bath solutions, with the addition of thiourea in a concentration range of 1.0–5.0 mg L−1. The influence of thiourea on the chemical composition, morphology and corrosion resistance of the films was studied. The results revealed thiourea had a major influence on plating rate, phosphorus-content and aggregate size. The optimal content of thiourea was 1 mg L−1. Thiourea accelerated the deposition rate at low concentration of 1 mg L−1, but deceased the deposition rate and the phosphorus content at high concentration. The surface of the film without thiourea was smooth and dense. Also, with increasing thiourea content, the surface evolved into coarse nodular morphology with clear intercolonial boundaries. With the addition of 1 mg L−1 thiourea, the film had better corrosion resistance compared to film without thiourea.

Objectives To study whether Vitamin D levels are causally associated with ankylosing spondylitis (AS). Methods Two-sample Mendelian randomization (TSMR) analysis was performed by employing MR-Egger regression, weighted median (WM1), inverse-variance weighted (IVW), and weight mode (WM2) methods. The odds ratio (OR) with 95% confidence intervals (CIs) was used to evaluate this association. Results The results of IVW show that no causal association between vitamin D and AS (OR = 0.999, 95%CI = 0.997, 1.002, P = 0.724). The MR-Egger regression results show that genetic pleiotropy does not bias the results (intercept = −4.474E-05, SE = 2.830E-05, P = 0.255). The MR-Egger method no supported causal association between vitamin D and AS (OR = 1.000, 95%CI = 0.996, 1.005, P = 0.879). WM1 (OR = 1.002, 95%CI = 0.999, 1.005, P = 0.837) and WM2 (OR = 0.998, 95%CI = 0.996, 1.002, P = 0.910) approach also not found a causal relationship between vitamin D levels and AS. The significant heterogeneity was not observed by Cochran's Q test. The “leave-one-out” analysis also proved lack of a single SNP affected the robustness of our results. Conclusion Based on our analysis, there is lack of a strong evidence to support a causal inverse association between vitamin D levels and ankylosing spondylitis.

Action accuracy of train drivers is closely related to the train safety. However, at present, the video of cabs of train drivers is difficult to be monitored in real time, along with poor alarm accuracy, long response time and difficulties in analysis of video data. Therefore, action recognition in video of the train driver is studied in this paper. First, based on the clips of collected video, the emergence of key actions in the whole video can be distinguished, and image enhancement and segmentation technology can be used to extract the images of key actions. Second, three improved convolutional neural networks (C3D, R(2+1)D and R3D) are compared to realize accurate recognition of actions. Third, a comparative experiment based on pre-training models and non-pre-training models is designed to analyze the application effects of different algorithms in this problem. The results show that the method proposed can improve the accuracy of action recognition, which effectively reduce the accidents of train driving.

Numerous epidemiological data and experimental studies support a strong link between fine particulate matter (less than 2.5 mm in aerodynamic diameter, PM2.5) exposure and the development of insulin resistance/type 2 diabetes mellitus (T2DM). Quercetin (Que), a flavonoid compound with anti-inflammatory effects, has been confirmed to improve glucose metabolic disorders in rodents and humans. In this study, we investigated the underlying mechanisms of particulate matter (PM)-induced glucose metabolic disorder and subsequently examined the protective effect and mechanism of quercetin supplementation. Male C57BL/6 mice in the control group and PM group were exposed to ambient filtered air (FA) or PM (6 h/day, 7 days/week) for 18 weeks. Mice in the Que group were exposed to PM for 18 weeks and administered Que (50 or 100 mg/kg bw). Glucose tolerance, insulin sensitivity, and systemic and visceral white adipose tissue (vWAT) inflammatory responses were measured. The expression of proteins involved in insulin signal transduction in vWAT was assessed. Chronic PM exposure caused systemic and vWAT inflammation characterized by an increase in serum IL-6 and TNF-α levels and increased vWAT macrophage filtration, triggering NLRP3 inflammasome activation, impairing the classic glucose metabolism signal in vWAT, and inducing whole-body insulin resistance. Moreover, Que administration significantly alleviated systemic and vWAT inflammation, abolished NLRP3 inflammasome activation, and improved signaling abnormalities characteristic of insulin resistance in vWAT and adipocytes. Based on these findings, chronic PM exposure activated the NLRP3 inflammasome and subsequently caused systemic and WAT inflammation and impaired insulin signaling in vWAT and adipocytes. Most importantly, Que administration inhibited NLRP3 inflammasome-mediated inflammation and insulin signaling in vWAT to improve these adverse effects.

Background Several studies have shown that resveratrol (RES), a naturally occurring polyphenol found in many plants, is beneficial for preventing cardiovascular diseases. However, the mechanism underlying the RES-mediated protection against myocardial infarction has not yet been revealed entirely. In this study, we investigated the protective effects of RES on cardiac function in a rat model of acute myocardial infarction (AMI) and the related underlying mechanisms. Methods Male Sprague-Dawley rats were randomly divided into four groups: Sham (sham operation), Sham-RES, AMI (AMI induction), and AMI-RES. The rat AMI model was established by the permanent ligation of left anterior descending coronary artery method. The rats in the RES-treated groups were gavaged with RES (50 mg/kg/day) daily for 45 days after the Sham operation or AMI induction; rats in the Sham and AMI groups were gavaged with deionized water. Cardiac function was evaluated by echocardiography. Atrial interstitial fibrosis was assessed by hematoxylin-eosin or Masson’s trichrome staining. Real-time PCR and western blotting analyses were performed to examine the levels of signaling pathway components. Results RES supplementation decreased the inflammatory cytokine levels, improved the cardiac function, and ameliorated atrial interstitial fibrosis in the rats with AMI. Furthermore, RES supplementation inhibited NLRP3 inflammasome activity, decreased the TGF-β1 production, and downregulated the p-SMAD2/SMAD2 expression in the heart. Conclusion RES shows notable cardioprotective effects in a rat model of AMI; the possible mechanisms underlying these effects may involve the improvement of cardiac function and atrial interstitial fibrosis via the RES-mediated suppression of NLRP3 inflammasome activity and inhibition of the TGF-β1/SMAD2 signaling pathway in the heart.

Hyperlipidemia is associated with lipid metabolic disorders, chronic inflammation, and intestinal dysbiosis. Previous studies have shown that the metabolic improvement of high-fat diet (HFD)-induced mice by buckwheat is correlated with gut microbiota; however, the anti-hyperlipidemia effects and potential mechanism of probiotics-fermented rice buckwheat (FRB) are not well understood. Here, we aimed to investigate the lipid-lowering and gut microbiota regulation of FRB in HFD-induced hyperlipidemic mice. We observed that probiotic fermentation markedly increased the contents of γ-aminobutyric acid, rutin, total polyphenols, and total flavonoids in rice buckwheat. FRB supplementation over eight weeks significantly reduced body weight gain and visceral obesity, as well as alleviating dyslipidemia in HFD-fed mice. Moreover, FRB treatment effectively ameliorated oxidative stress and chronic inflammation. We further demonstrated that FRB intervention significantly inhibited hepatic cholesterol synthesis and lipogenesis, and promoted lipolysis. More important, FRB treatment reversed HFD-induced gut dysbiosis by decreasing the ratio of Firmicutes to Bacteroidetes and increasing the abundance of SCFA-producing bacteria such as Bacteroides, Lactobacillus, and Blautia, along with increasing the total SCFAs contents. Overall, these results show that FRB is a beneficial nutraceutical for hyperlipidemia amelioration.

Fine particulate matter (PM2.5 ) exposure is correlated with the risk of developing cardiac fibrosis. Melatonin is a major secretory product of the pineal gland that has been reported to prevent fibrosis. However, whether melatonin affects the adverse health effects of PM2.5 exposure has not been investigated. Thus, this study was aimed to investigate the protective effect of melatonin against PM2.5 -accelerated cardiac fibrosis. The echocardiography revealed that PM2.5 had impaired both systolic and diastolic cardiac function in ApoE-/- mice. Histopathological analysis demonstrated that PM2.5 induced cardiomyocyte hypertrophy and fibrosis, particularly perivascular fibrosis, while the melatonin administration was effective in alleviating PM2.5 -induced cardiac dysfunction and fibrosis in mice. Results of electron microscopy and confocal scanning laser microscope confirmed that melatonin had restorative effects against impaired mitochondrial ultrastructure and augmented mitochondrial ROS generation in PM2.5 -treated group. Further investigation revealed melatonin administration could significantly reverse the PM2.5 -induced phenotypic modulation of cardiac fibroblasts into myofibroblasts. For the first time, our study found that melatonin effectively alleviates PM2.5 -induced cardiac dysfunction and fibrosis via inhibiting mitochondrial oxidative injury and regulating SIRT3-mediated SOD2 deacetylation. Our findings indicate that melatonin could be a therapy medicine for prevention and treatment of air pollution-associated cardiac diseases.

The relationship between 18F-FDG uptake and HER2 expression in colorectal cancer has not been investigated yet. This study aimed to investigate the predictive efficiency of preoperative 18F-FDG PET/CT for HER2 expression and prognosis in colorectal cancer. We retrospectively analyzed 131 colorectal cancer patients who underwent 18F-FDG PET/CT scans in our center before surgery. HER2 positivity was defined as a score of 2+ or 3+, and HER2 negativity was defined as a score of 0 or 1+ in immunohistochemistry of HER2 expression. The relationships between 18F-FDG PET/CT metabolic parameters and HER2 expression and the prognosis of colorectal patients were systematically studied. From 131 colorectal cancer patients, there were 27 (20.6%) HER2-positive patients. SUVmax of the primary tumor (mean ± SD) in the HER2-positive and the HER2-negative group was 18.238±8.912 and 14.455±6.531, respectively. SUVmax in the HER2-positive group was higher than in the negative group (p=0.034). When the cutoff was based on 5 cm, tumor size demonstrated significant positive correlations with SUVmax (p=0.012) and HER2 expression (p=0.014). Multivariate analysis showed that both SUVmax and tumor size had a significant correlation with HER2 expression (p=0.049 vs. p=0.043, respectively). There was no statistical difference in PFS between the HER2-positive and the HER2-negative group (p=0.28). 18F-FDG metabolic parameters had a significant correlation with HER2 expression in colorectal cancer. SUVmax combined with primary tumor size were better for predicting the HER2 status of colorectal cancer. 18F-FDG metabolic parameters had a significant correlation with HER2 expression in colorectal cancer. SUVmax combined with primary tumor size were better for predicting the HER2 status of colorectal cancer.

Fine particulate matter (PM2.5) exposure is correlated with the risk of developing cardiac fibrosis. Melatonin is a major secretory product of the pineal gland that has been reported to prevent fibrosis. However, whether melatonin affects the adverse health effects of PM2.5 exposure has not been investigated. Thus, this study was aimed to investigate the protective effect of melatonin against PM2.5‐accelerated cardiac fibrosis. The echocardiography revealed that PM2.5 had impaired both systolic and diastolic cardiac function in ApoE−/− mice. Histopathological analysis demonstrated that PM2.5 induced cardiomyocyte hypertrophy and fibrosis, particularly perivascular fibrosis, while the melatonin administration was effective in alleviating PM2.5‐induced cardiac dysfunction and fibrosis in mice. Results of electron microscopy and confocal scanning laser microscope confirmed that melatonin had restorative effects against impaired mitochondrial ultrastructure and augmented mitochondrial ROS generation in PM2.5‐treated group. Further investigation revealed melatonin administration could significantly reverse the PM2.5‐induced phenotypic modulation of cardiac fibroblasts into myofibroblasts. For the first time, our study found that melatonin effectively alleviates PM2.5‐induced cardiac dysfunction and fibrosis via inhibiting mitochondrial oxidative injury and regulating SIRT3‐mediated SOD2 deacetylation. Our findings indicate that melatonin could be a therapy medicine for prevention and treatment of air pollution‐associated cardiac diseases.

Abnormal tapetum degradation and anther development in cytoplasmic male sterility SaNa-1A are the main reasons for the anther abortion. SaNa-1A is a novel cytoplasmic male sterility (CMS) line of Brassica napus derived from somatic hybrids of B. napus-Sinapis alba, and SaNa-1B is the corresponding maintainer line. Ultrastructural comparison between developing anthers of sterile and maintainer lines revealed abnormal subcellular structure of pollen mother cells (PMCs) in the CMS line. The PMC volume and size of nucleus and nucleolus in the CMS line were smaller than those in the maintainer line. The abnormal tapetum cell development and delayed tapetum degradation inhibited microspore development. Finally, anther abortion in the CMS line occurred. Physiological and biochemical analyses of developing anthers and mitochondria revealed that over-accumulation of reactive oxygen species (ROS) in the SaNa-1A and deficiency in antioxidant enzyme system aggravated the oxidization of membrane lipids, resulting in malondialdehyde (MDA) accumulation in anthers. High MDA content in the CMS line was toxic to the cells. ROS accumulation in SaNa-1A also affected anther development. Abnormal structure and function of terminal oxidase, which participates in the electron transport chain of mitochondrial membrane, were observed and affected the activity of cytochrome c oxidase and F1F0-ATPase, which inhibited ATP biosynthesis. Proline deficiency in SaNa-1A also affected anther development. Few hybridization signals of programmed cell death (PCD) in tetrads of SaNa-1A were identified using TdT-mediated dUTP Nick-End Labeling assay. PCD was not obvious in tapetum cells of SaNa-1A until the unicellular stage. These results validated the cytological differences mentioned above, and proved that abnormal tapetum degradation and anther development in SaNa-1A were the main reasons for the anther abortion.

Nowadays, the great majority of toxicological studies have focused on immediate cardiovascular effects of simultaneous exposure to long-term or short-term PM

The Cation Diffusion Facilitator (CDF) family, also named Metal Tolerance Protein (MTP), is one of the gene families involved in heavy metal transport in plants. However, a comprehensive study of MTPs in Brassica napus has not been reported yet. In the present study, we identified 33 BnMTP genes from the rapeseed genome using bioinformatic analyses. Subsequently, we analyzed the phylogenetic relationship, gene structure, chromosome distribution, conserved domains, and motifs of the BnMTP gene family. The 33 BnMTPs were phylogenetically divided into three major clusters (Zn-CDFs, Fe/Zn-CDFs, and Mn-CDFs) and seven groups (group 1, 5, 6, 7, 8, 9, and 12). The structural characteristics of the BnMTP members were similar in the same group, but different among groups. Evolutionary analysis indicated that the BnMTP gene family mainly expanded through whole-genome duplication (WGD) and segmental duplication events. Moreover, the prediction of cis-acting elements and microRNA target sites suggested that BnMTPs might be involved in plant growth, development, and stress responses. In addition, we found the expression of 24 BnMTPs in rapeseed leaves or roots could respond to heavy metal ion treatments. These results provided an important basis for clarifying the biological functions of BnMTPs, especially in heavy metal detoxification, and will be helpful in the phytoremediation of heavy metal pollution in soil.

Electroless nickel–phosphorus (Ni–P) films were produced on the surface of p-type monocrystalline silicon in the alkaline citrate solutions. The influences of bath chemistry and plating variables on the chemical composition, deposition rate, morphology, and thermal stability of electroless Ni–P films on silicon wafers were studied. The as-deposited Ni–P films were almost all medium- and high-P deposits. The concentrations of Ni2+ and citric ions influenced the deposition rate of the films but did not affect P content in the deposits. With increasing H2PO2− content, the P content and deposition rate were steadily increased. The pH and plating temperature had a significant effect on the chemical composition and the deposition rate of the films. The thermal stability of the medium-P film was better than that of the high-P deposit. At the same time, the proposed mechanism of Ni–P films on monocrystalline silicon substrates in the alkaline bath solution was discussed and addressed.

Nickel–iridium (Ni-Ir) alloy films were electrodeposited from aqueous solutions on copper substrates under galvanostatic conditions. The effects of bath composition and deposition time on the faradaic efficiency (FE), partial current densities, chemical composition, morphology and crystallographic structure of the films were studied. The results show that the Ni–Ir alloys with Ir content as high as 37 at% and FE as high as 44% were obtained. Increase in concentration of citric acid had little or no effect on the composition of the alloys, but resulted in a significant decrease in FE and partial current densities of Ni and Ir. The FE and the partial current density of Ni slightly decreased with increasing Ir3+ concentration, however, Ir content increased while partial current density of Ir remained stable. The increase of Ni2+ concentration could result in the increase of the FE and the rate of Ni–Ir deposition, and even no cracks formed on the surface. The surface average roughness and root mean square roughness of the film were 6.8 ± 0.3 nm and 5.4 ± 0.3 nm, respectively. The mixture phases contained significant amounts of Ni oxides and a small amount of metallic Ni, Ir and Ir oxides on the surface. After argon ion sputter cleaning, the film was mainly composed of metallic Ni and Ir. The film consisted of the amorphous and nanocrystalline phases. The Ni content in the deposits was higher than that in the electrolyte, the co-deposition of Ni–Ir alloy was a normal deposition.

Three dimensional (3D) nano-LiMn0.6Fe0.4PO4@C/CNT composite was successfully synthesized by an oleylamine-assisted solvothermal method. The prepared composite showed excellent electrochemical performance, especially superior high rate capability. It could deliver a specific discharge capacity of 103.1 mAh/g, even at 80 C. The superior high rate performance of the as-prepared LiMn0.6Fe0.4PO4@C/CNT electrode is attributed to its unique 3D conducting network: (1) the prepared LiMn0.6Fe0.4PO4@C active particles were in nano-scale with a size of 30–50 nm; (2) LiMn0.6Fe0.4PO4 nanoparticles were uniformly coated by amorphous carbon with a thickness of 3 nm; (3) the graphitized conductive CNTs were dispersed homogenously among the LiMn0.6Fe0.4PO4@C active particles. The synergistic effect of the nanoscale amorphous carbon coated LiMn0.6Fe0.4PO4@C active particles and the graphitized CNTs reduces the diffusion path of the lithium ions and benefits the transference ability of electron.

Objective Primary mediastinal B-cell lymphoma (PMBCL) lacks standard treatment regimens. This study aimed to identify the disease’s clinical features and prognostic factors. Methods This retrospective study included 56 patients with PMBCL. Patient demographic details and clinicopathological characteristics were summarized, and their effects on progression-free survival (PFS) and overall survival (OS) were analyzed. Results The median patient age was 29 years (range, 14–56). Twenty-two patients received DA-EPOCH-R (dose-adjusted etoposide, vincristine, and doxorubicin for 96 hours with bolus doses of cyclophosphamide and oral prednisone, as well as rituximab), and 34 patients received R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone). Clinical/laboratory parameters, overall response rates, and 5-year PFS and OS rates did not differ between the treatment groups. Kaplan–Meier analysis indicated that late-stage disease and a higher International Prognostic Index (IPI) were associated with shorter PFS and OS. Furthermore, patients with B symptoms and first-line treatment non-responders exhibited worse OS. 18Fluorodeoxyglucose-positron emission tomography/computed tomography quantitative parameters, such as higher metabolic tumor volume (MTV) and total lesion glycolysis (TLG), were corrected with shorter PFS. Conclusions This study revealed that stage IV disease, higher IPI, and B symptoms were poor prognostic factors in patients with PMBCL. Significantly, higher MTV and TLG portended worse PFS.

Silicon (Si) is regarded as a great promising anode material for lithium-ion batteries (LIBs) due to its high theoretical capacity and low lithium storage potential. However, the practical application of pure silicon is greatly limited by its low electrical conductivity and large volume expansion. It is well known that the modification ofsilicon negative materials with carbon tubes is a good strategy to overcome the low conductivity and poor cycling stability of silicon anode. In this work, the APOCs@Si composite is successfully synthesized by 1-aminopyrene (AP) modified oxidized carbon nanotubes (OCs) compounded silicon nanoparticles under ultrasonication-stirring condition. The APOCs@Si electrode presents a considerable reversible capacity of 913.7 mAh·g−1 with a stable structure after 610 cycles at a current density of 0.5A g−1, and the first reversible capacity is 3543.0 mAh g−1 at 0.1A g−1. The physico-chemical properties indicate that the incorporation of AP and OCs builds the interwoven CNTs networks, which serve as a matrix to buffer the volume expansion of silicon and boost the electronic conductivity of the electrode, to achieve remarkable capacity and cycle performance of APOCs@Si electrode. These remarkable results have further showed AP modified OCs as a buffer matrix significantly improve the cycle performance of silicon anode materials.

Multilayer iridium coating was manufactured on tungsten carbide substrates by a double glow plasma process. As comparison, monolayer was also produced. The microstructure and morphology were observed using scanning electron microscopy. Grain orientation and phase were determined using X-ray diffraction. The residual stress of the coating was studied by glancing incidence X-ray diffraction. The adhesive force of the coating was measured by a scratch tester. The results showed that both monolayer and multilayer had a polycrystalline phase with a strong (110) reflection. The coating had an excellent adhesion with no evidence of delamination. The adhesive force of the monolayer and multilayer was about 50 and 43 N, respectively. The interfacial reaction between the substrate and the layer occurred and a new WIr phase was found due to the high-temperature deposition process. The residual stress in the monolayer and multilayer was -1.6 and -1.1 GPa, respectively.

Accumulating evidences support that exposure to fine particulate matter (PM

Cardiac fibrosis is associated with fine particulate matter (PM2.5) exposure. In addition, whether high-fat diet (HFD) could exacerbate the PM2.5-induced cardiac injury was unevaluated. Thus, this study was aimed to investigate the combined effects of PM2.5 and HFD on cardiac fibrosis. The echocardiography and histopathological analysis showed that co-exposure of PM2.5 and HFD had a significant deleterious effect on both cardiac systolic and diastolic function accompanied the myofibril disorder and myocardial fibrosis in C57BL/6 J mice than exposed to PM2.5 or HFD alone. The augmented oxidative damage and increased α-SMA area percentage were detected in heart tissue of mice exposed to PM2.5 and HFD together. PM2.5 upregulated the expressions of cardiac fibrosis-related special markers, including collagen-I, collagen-III, TGF-β1, p-Smad3 and total Smad3, which had more pronounced activations in co-exposure group. Meanwhile, the factorial analysis exhibited the synergistic interaction regarded to the combined exposure of PM2.5 and HFD. Simultaneously, PM2.5 and palmitic acid increased intracellular ROS generation and activated the TGF-β1/Smad3 signaling pathway in cardiomyocytes. While the ROS scavenger NAC had effectively attenuated the ROS level and suppressed the TGF-β1/Smad3 signaling pathway. Taken together, our results demonstrated combined exposure to PM2.5 and HFD could aggravate cardiac fibrosis via activating the ROS/TGF-β1/Smad3 signaling pathway.

Epidemiological studies have confirmed that PM

Up to now, while some toxicological studies have identified pulmonary fibrosis immediately induced by long-term PM

ObjectiveTo summarize the clinical features and laboratory examination of ANK1 gene in 12 children with hereditary spherocytosis in China, and to determine the genetic mutations in those children.MethodsThe clinical data of children and their parents were collected and analyzed. The sequence of related genes was analyzed by second-generation sequencing technology. The suspected pathogenic mutations were detected by Sanger sequencingResultsNew mutations in the coding region of ANK1 was detected in 12 patients, which caused amino acid changes in the gene encoding, causing structural changes or loss of function.ConclusionANK1 (c.1914_c.1918delTTTG), ANK1 (c.399T>G), ANK1 (c.1564delC), ANK1 (c.4439dupA), ANK1 (c.4510_4513del), ANK1 (c.2961delC), ANK1 (c.2142dupT), ANK1 (c.2858+1G>C), ANK1 (c.3235delG), ANK1 (c.4739A>G), ANK1 (c.2638-2 A>G), ANK1 (c. 4739A>G) mutations in the coding region of the gene are the cause of suspicious disease in these 12 Chinese children. At the same time, second-generation gene sequencing technology is an effective means of confirming HS. Different types of mutations (P=0.388)and different mutation areas (P=0.660)had no significant effect on the severity of anemia. The 12 gene mutation sites in this study have not been included in the human genome database, dbSNP (v138) and ExAC databases. The new ANK1 gene mutations found in HS children can provide further exploration of the genetic etiology of HS in Chinese population.