Cobalt-vanadium sulfide yolk-shell nanocages from surface etching and ion-exchange of ZIF-67 for ultra-high rate-capability sodium ion battery.

Development of high-performance metal sulfides anode materials is a great challenge for sodium-ion batteries (SIBs). In this work, a cobalt-based imidazolate framework (ZIF-67) were firstly synthesized and applied as precursor. After the successive surface etching, ion exchange and sulfidation processes, the final cobalt-vanadium sulfide yolk-shell nanocages were obtained (CoS2/VS4@NC) with VS4 shell and CoS2 yolk encapsulated into nitrogen doped carbon frameworks. This yolk-shell nanocage structure effectively increases the specific surface area and provides enough space for inhibiting the volume change during charge/discharge processes. Besides, the nitrogen doped carbon skeleton greatly improves the ionic conductivity and facilitates ion transport. When used as the anode materials for SIBs, the yolk-shell nanocages of CoS2/VS4@NC electrode exhibits excellent rate capability and stable cycle performance. Notably, it displays a long-term cycling stability with excellent capacity of 417.28 mA h g-1 after 700 cycles at a high current density of 5 A/g. This developed approach here provides a new route for the design and synthesis of various yolk-shell nanocages nanomaterials from enormous MOFs with multitudinous compositions and morphologies and can be extended to the application into other secondary batteries and energy storage fields.

Synergistic enhancement of chemisorption and catalytic conversion in lithium-sulfur batteries via Co3Fe7/Co5.47N separator mediator.

Lithium-sulfur batteries (LSBs) show considerable potential in next-generation high performance batteries, but the heavy shuttle effect and sluggish redox kinetics of polysulfide hinder their further applications. In this paper, to address these shortcomings of LSBs, Co3Fe7/Co5.47N heterostructure were prepared and constructed from their Fe-Co Prussian blue analogue precursors under the condition of high temperature pyrolysis. The obtained Co3Fe7/Co5.47N display excellent immobilization-diffusion-conversion performance for polysulfides by synergistic effect in successfully hindering the shuttle effect of polysulfides. When the Co3Fe7/Co5.47N heterostructure were applied to modify the commercial polypropylene (PP) separator, the batteries displayed fantastic rate capacity and cycling stability. Specifically, the Co3Fe7/Co5.47N-PP batteries exhibit an extremely satisfactory initial specific capacity of 1430 m Ah/g at 0.5C, wonderful rate capacity of around 780 m Ah/g at 3C and superior per cycle decaying rate of 0.08 % for 500 cycles at 0.5C. When the current density reaches to 2C, the batteries still exhibit 501 m Ah/g after 900 cycles with 0.015 % per cycle decay rate. Besides, even in the high loading of sulfur (3.0 mg cm-2) at 0.5C, the superior cycling stability (0.075 % per cycle decay rate after 200 cycles) and high specific capacity (741 mAh/g after 200 cycles) can still be performed. Thus, this work provides a facile method for high-powered and long-life Li-S batteries with eminent entrapping-conversion processes of polysulfides.

A Biodegradable Polyester-Based Polymer Electrolyte for Solid-State Lithium Batteries.

The low ionic conductivity, narrow electrochemical window, poor interfacial stability with lithium metal, and non-degradability of raw materials are the main problems of solid polymer electrolytes, restricting the development of lithium solid-state batteries. In this paper, a biodegradable poly (2,3-butanediol/1,3-propanediol/succinic acid/sebacic acid/itaconic acid) ester was designed and used as a substrate to prepare biodegradable polyester solid polymer electrolytes for solid-state lithium batteries using a simple solution-casting method. A large number of ester-based polar groups in the amorphous polymer become a high-speed channel for carrying lithium ions as a weak coordination site. The biodegradable polyester solid polymer electrolyte exhibits a wide electrochemical window of 5.08 V (vs. Li/Li+), high ionic conductivity of 1.03 mS cm-1 (25 °C), and a large Li+ transference number of 0.56. The electrolyte exhibits good interfacial stability with lithium, with stable Li plating/stripping behavior at room temperature over 2100 h. This design strategy for biodegradable polyester solid polymer electrolytes offers new possibilities for the development of matrix materials for environmentally friendly lithium metal solid-state batteries.

Impact of diabetes itself and glycemic control status on tuberculosis.

Objectives: To explore the impact of diabetes itself and glycemic control status on tuberculosis (TB). Methods: A total of 3393 patients with TB and diabetes mellitus (DM) who were hospitalized in the Public Health Clinical Center of Chengdu from January 1, 2019, to December 31, 2021, were retrospectively included and divided into three groups according to baseline glycemic control status: two groups according to glycemic status at discharge, two groups according to cavity occurrence, three groups according to sputum results, and three groups according to lesion location. The influencing factors and the differences in cavity occurrence, sputum positivity and lesion location among different glycemic control groups or between different glycemic status groups were analyzed. Results: In this TB with DM cohort, most of the subjects were male, with a male to female ratio of 4.54:1, most of them were 45-59 years old, with an average age of 57.44 ± 13.22 years old. Among them, 16.8% (569/3393) had cavities, 52.2% (1770/3393) were sputum positive, 30.4% (1030/3393) had simple intrapulmonary lesions, 68.1% (2311/3393) had both intra and extrapulmonary lesions, only 15.8% (537/3393) had good glycemic control,16.0% (542/3393) and 68.2% (2314/3393) had fair and poor glycemic control, respectively. Compared with the non-cavity group, the sputum-negative group and the extrapulmonary lesion group, the cavity group, sputum-positive group, intrapulmonary lesion group and the intra and extrapulmonary lesion group all had higher fasting plasma glucose (FPG) and glycosylated hemoglobin A 1c (HbA1c) and lower good glycemic control rates at admission (all P<0.001). Another aspect, compared with the good glycemic control group, the poor glycemic control group had a higher cavity occurrence rate, sputum positive rate, and greater proportion of intrapulmonary lesions. Moreover, FPG and HbA1c levels and poor glycemic control were significantly positively correlated with cavity occurrence, sputum positivity, and intrapulmonary lesions and were the main risk factors for TB disease progression. On the other hand, cavity occurrence, sputum positivity, and intrapulmonary lesions were also main risk factors for hyperglycemia and poor glycemic control. Conclusion: Diabetes itself and glycemic control status could impact TB disease. Good glycemic control throughout the whole process is necessary for patients with TB and DM to reduce cavity occurrence and promote sputum negative conversion and lesion absorption.

Diosgenin Targets CaMKK2 to Alleviate Type II Diabetic Nephropathy through Improving Autophagy, Mitophagy and Mitochondrial Dynamics.

Diabetic nephropathy (DN) is a worldwide health problem with increasing incidence. Diosgenin (DIO) is a natural active ingredient extracted from Chinese yams (Rhizoma dioscoreae) with potential antioxidant, anti-inflammatory, and antidiabetic effects. However, the protective effect of DIO on DN is still unclear. The present study explored the mitigating effects and underlying mechanisms of DIO on DN in vivo and in vitro. In the current study, the DN rats were induced by a high-fat diet and streptozotocin and then treated with DIO and metformin (Mef, a positive control) for 8 weeks. The high-glucose (HG)-induced HK-2 cells were treated with DIO for 24 h. The results showed that DIO decreased blood glucose, biomarkers of renal damage, and renal pathological changes with an effect comparable to that of Mef, indicating that DIO is potential active substance to relieve DN. Thus, the protective mechanism of DIO on DN was further explored. Mechanistically, DIO improved autophagy and mitophagy via the regulation of the AMPK-mTOR and PINK1-MFN2-Parkin pathways, respectively. Knockdown of CaMKK2 abolished AMPK-mTOR and PINK1-MFN2-Parkin pathways-mediated autophagy and mitophagy. Mitophagy and mitochondrial dynamics are closely linked physiological processes. DIO also improved mitochondrial dynamics through inhibiting fission-associated proteins (DRP1 and p-DRP1) and increasing fusion proteins (MFN1/2 and OPA1). The effects were abolished by CaMKK2 and PINK1 knockdown. In conclusion, DIO ameliorated DN by enhancing autophagy and mitophagy and by improving mitochondrial dynamics in a CaMKK2-dependent manner. PINK1 and MFN2 are proteins that concurrently regulated mitophagy and mitochondrial dynamics.

Diosgenin Inhibits ROS Generation by Modulating NOX4 and Mitochondrial Respiratory Chain and Suppresses Apoptosis in Diabetic Nephropathy.

Diosgenin (DIO) is a dietary steroid sapogenin possessing multiple biological functions, such as the amelioration of diabetes. However, the remission effect of DIO on diabetic nephropathy (DN) underlying oxidative stress and cell apoptosis remains unclear. Here, the effect of DIO on ROS generation and its induced cell apoptosis was studied in vitro and in vivo. Renal proximal tubular epithelial (HK-2) cells were treated with DIO (1, 2, 4 µM) under high glucose (HG, 30 mM) conditions. DN rats were induced by a high-fat diet combined with streptozotocin, followed by administration of DIO for 8 weeks. Our data suggested that DIO relieved the decline of HK-2 cell viability and renal pathological damage in DN rats. DIO also relieved ROS (O2- and H2O2) production. Mechanistically, DIO inhibited the expression of NOX4 and restored mitochondrial respiratory chain (MRC) complex I-V expressions. Further, DIO inhibited mitochondrial apoptosis by ameliorating mitochondrial membrane potential (MtMP) and down-regulating the expressions of CytC, Apaf-1, caspase 3, and caspase 9, while up-regulating Bcl2 expression. Moreover, the ER stress and its associated cell apoptosis were inhibited through decreasing PERK, p-PERK, ATF4, IRE1, p-CHOP, and caspase 12 expressions. Collectively, DIO inhibited ROS production by modulating NOX4 and MRC complexes, which then suppressed apoptosis regulated by mitochondria and ER stress, thereby attenuating DN.

Orbital Fulde-Ferrell-Larkin-Ovchinnikov state in an Ising superconductor.

In superconductors possessing both time and inversion symmetries, the Zeeman effect of an external magnetic field can break the time-reversal symmetry, forming a conventional Fulde-Ferrell-Larkin-Ovchinnikov (FFLO) state characterized by Cooper pairings with finite momentum1,2. In superconductors lacking (local) inversion symmetry, the Zeeman effect may still act as the underlying mechanism of FFLO states by interacting with spin-orbit coupling (SOC). Specifically, the interplay between the Zeeman effect and Rashba SOC can lead to the formation of more accessible Rashba FFLO states that cover broader regions in the phase diagram3-5. However, when the Zeeman effect is suppressed because of spin locking in the presence of Ising-type SOC, the conventional FFLO scenarios are no longer effective. Instead, an unconventional FFLO state is formed by coupling the orbital effect of magnetic fields with SOC, providing an alternative mechanism in superconductors with broken inversion symmetries6-8. Here we report the discovery of such an orbital FFLO state in the multilayer Ising superconductor 2H-NbSe2. Transport measurements show that the translational and rotational symmetries are broken in the orbital FFLO state, providing the hallmark signatures of finite-momentum Cooper pairings. We establish the entire orbital FFLO phase diagram, consisting of a normal metal, a uniform Ising superconducting phase and a six-fold orbital FFLO state. This study highlights an alternative route to achieving finite-momentum superconductivity and provides a universal mechanism to preparing orbital FFLO states in similar materials with broken inversion symmetries.

Self-Healing Binder for High-Voltage Batteries.

Lithium-ion batteries are core components of flexible electronic devices. However, deformation types, such as impinging, bending, stretching, folding, and twisting, can cause internal cracks and, eventually, damage these batteries. The cracks separate the active particles from the conductive particles and the binder, as well as the electrode from the collector. Self-healing binders can alleviate this mechanical damage and improve the stress response of active material particles during high rates of charging and discharging of these batteries and the operation at a high voltage, thereby enhancing their cycle performance. In the present study, a thermoplastic intrinsic self-healing polymer (TISP) binder is proposed. The TISP is obtained by polymerization of butanediol (2,3-BDO), propylene glycol (1,3-PDO), succinic acid (SuA), sebacic acid (SeA), and iconic acid (IA). The hydroxyl and ester groups in its structure can form diverse bonds including the hydrogen and ion-dipole with active particles and the current collector, thereby producing elevated adhesion. Its properties, including a low glass transition temperature (-60 °C), amorphous structure, and low cross-link density, improve the mobility of polymer chains at 40 °C, and this facilitates structural recovery and the maintenance of strong adhesions. Owing to its higher occupied molecular orbital (HOMO) level than the electrolyte solvent, the TISP is likely oxidized before the main component of the electrolyte during charging. This decomposition produces a chemical passivation interphase on the cathode which reduces side reactions of LiCoO2 and the electrolyte under high-voltage conditions. Tests reveal that a LiCoO2 electrode battery using the TISP as a binder retains 162.4 mAh g-1 after 349 cycles at 4.5 V, and this represents an 86.5% capacity retention. In addition, heating (40 °C, 1 h) of a scratch-damaged electrode can recover a specific capacity of 156.6 mAh g-1 after 349 cycles at 4.5 V. Relative to a battery without any mechanical scratch, this capacity recovery represents approximately 96%, and this demonstrates the importance of the TISP to the high-voltage damaged electrode.

Diosgenin Ameliorated Type II Diabetes-Associated Nonalcoholic Fatty Liver Disease through Inhibiting De Novo Lipogenesis and Improving Fatty Acid Oxidation and Mitochondrial Function in Rats.

Diosgenin (DIO) is a dietary and phytochemical steroidal saponin representing multiple activities. The present study investigated the protective effect of DIO on type II diabetes-associated nonalcoholic fatty liver disease (D-NAFLD). The rat model was established by high-fat diet and streptozotocin injection and then administered DIO for 8 weeks. The results showed that DIO reduced insulin resistance index, improved dyslipidemia, and relieved pancreatic damage. DIO decreased hepatic injury markers, including aspartate aminotransferase (AST) and alanine aminotransferase (ALT). H&E staining showed that DIO relieved hepatic lipid deposition. Mechanistically, DIO inhibited hepatic de novo lipogenesis (DNL) and increased fatty acid ß-oxidation (FAO) through regulation of the AMPK-ACC/SREBP1 pathway. Endoplasmic reticulum (ER) stress was inhibited by DIO through regulation of PERK and IRE1 arms, which may then inhibit DNL. DIO also decreased reactive oxygen species (ROS) and enhanced the antioxidant capacity via an increase in Superoxide dismutase (SOD), Catalase (CAT), and Glutathione peroxidase (GPx) activities. The mitochondria are the site for FAO, and ROS can damage mitochondrial function. DIO relieved mitochondrial fission and fusion disorder by inhibiting DRP1 and increasing MFN1/MFN2 expressions. Mitochondrial apoptosis was then inhibited by DIO. In conclusion, the present study suggests that DIO protects against D-NAFLD by inhibiting DNL and improving FAO and mitochondrial function.

Recent advances and potentiality of postbiotics in the food industry: Composition, inactivation methods, current applications in metabolic syndrome, and future trends.

Postbiotics are defined as "preparation of inanimate microorganisms and/or their components that confers a health benefit on the host". Postbiotics have unique advantages over probiotics, such as stability, safety, and wide application. Although postbiotics are research hotspots, the research on them is still very limited. This review provides comprehensive information on the scope of postbiotics, the preparation methods of inanimate microorganisms, and the application and mechanisms of postbiotics in metabolic syndrome (MetS). Furthermore, the application trends of postbiotics in the food industry are reviewed. It was found that postbiotics mainly include inactivated microorganisms, microbial lysates, cell components, and metabolites. Thermal treatments are the main methods to prepare inanimate microorganisms as postbiotics, while non-thermal treatments, such as ionizing radiation, ultraviolet light, ultrasound, and supercritical CO2, show great potential in postbiotic preparation. Postbiotics could ameliorate MetS through multiple pathways including the modulation of gut microbiota, the enhancement of intestinal barrier, the regulation of inflammation and immunity, and the modulation of hormone homeostasis. Additionally, postbiotics have great potential in the food industry as functional food supplements, food quality improvers, and food preservatives. In addition, the SWOT analyses showed that the development of postbiotics in the food industry exists both opportunities and challenges.

Linarin ameliorates dextran sulfate sodium-induced colitis in C57BL/6J mice via the improvement of intestinal barrier, suppression of inflammatory responses and modulation of gut microbiota.

Linarin is a natural flavonoid compound found in Chrysanthemum indicum, Mentha species and other plants with various biological activities. The study aimed to investigate the protective effect of linarin supplementation on dextran sulfate sodium (DSS)-induced colitis in C57BL/6J mice and its potential mechanisms. The results showed that doses of linarin at 25 and 50 mg kg-1 day-1 alleviated the DSS-induced histopathological damage, and improved the mucosal layer and intestinal barrier function. Importantly, Linarin significantly suppressed the levels of myeloperoxidase activity and pro-inflammatory cytokines (IL-6, TNF-α, IFN-γ and IL-1ß) in the colon, and enhanced the mRNA level of anti-inflammatory cytokine (IL-10). Moreover, 50 mg kg-1 day-1 linarin reversed the gut microbiota damaged by DSS, including Alistipes, Rikenella and Clostridia UCG-014_norank. Linarin also partly increased the relative abundance of short-chain fatty acids (SCFAs)-producing bacteria, including Lactobacillus, Roseburia, Parabacteroides and Blautia, and elevated the contents of SCFAs. Collectively, linarin attenuates DSS-induced colitis in mice, suggesting that linarin may be a promising nutritional strategy for reducing inflammatory bowel disease.

Effect of Delphinidin on Metabolomic Profile in Breast Carcinogenesis.

BACKGROUND: Breast cancer is a malignant tumor which threat to women's physical and mental health. Delphinidin, one of the main anthocyanidins, has potent anti-cancer properties. In previous study, we found that delphinidin has the preventive role in MNU-induced breast carcinogenesis of rats, but the molecular mechanism by which delphinidin combats breast cancer has not been completely elucidated.The aim of the present study was to identify metabolic profile that account for delphinidin on the preventive effect on 1-methyl-1-nitrosourea (MNU)-induced breast carcinogenesis of rats. METHODS: In the present study, liquid chromatography-mass spectrometry (LC-MS) was conducted to identify metabolic profiles of rat tissues collected from normal mammary glands (normal group), breast tumors derived from MNU-induced breast carcinogenesis models (control group) and delphinidin administration models (delphinidin group). Principal component analysis (PCA) and partial least squares-discriminate analysis (PLS-DA) were employed to identify biochemical patterns. The values of variable importance in the projection (VIP) in PLS-DA model combined with the P value of Student's t-test were used to determine important metabolites. An orthogonal partial least square discriminant analysis (OPLS-DA) was used to conduct the supervised analysis. The fitness and prediction capabilities of PCA modes were measured by R 2 and Q 2 value respectively. Potential biomarkers were subjected to pathway analysis with Metaboanalyst 3.0 based on the KEGG Pathway Database to identify related metabolic pathways. RESULTS: The PCA and PLS-DA analysis indicated that the proposed method were satisfactory for metabolomic analysis. Metabolites from the obtained features were further filtered by PLS-DA analysis with VIP>1.0 and P<0.05. The significant difference was appeared in 190 metabolites between normal group and control group (P<0.05). Eight most significant metabolic pathways were obtained on the basis of the results of P<0.05 data analysis between control and normal group, embodying in aminoacyl-tRNA biosynthesis, arginine biosynthesis, biosynthesis of unsaturated fatty acids, valine, leucine and isoleucine biosynthesis, purine metabolism, alanine, aspartate and glutamate metabolism, glycerophospholipid metabolism, histidine metabolism. A total of 48 metabolites were identified to be associated with protective effects of delphinidin on MNU-induced rats significantly(P<0.05). Compared with control group, a total of 5 metabolic pathways were significantly perturbed in response to delphinidin administration (p<0.05), including in taurine and hypotaurine metabolism, Glycerophospholipid metabolism, arachidonic acid metabolism, aminoacyl-tRNA biosynthesis and primary bile acid biosynthesis. CONCLUSION: Metabolites and metabolic pathways were identified to be associated with protective effects of delphinidin on MNU-induced rats. The findings provided new insights into the precise mechanism of delphinidin in preventing breast carcinogenesis.

Inactivation of Shigella flexneri by 405-nm Light-Emitting Diode Treatment and Possible Mechanism of Action.

Shigella flexneri, a common Gram-negative foodborne pathogen, is widely distributed in fresh-cut fruits and vegetables, unpasteurized milk, and food processing environments. The aims of this study were to evaluate the antibacterial effects of 405-nm light-emitting diode (LED) treatment on S. flexneri and to investigate the possible mechanism. The results showed that LED irradiation (360 min) reduced the number of S. flexneri in phosphate-buffered saline by 3.29 log colony-forming unit (CFU)/mL (initial bacterial count: 6.81 log CFU/mL). The cells in reconstituted infant formula, cells on fresh-cut carrot slices, and biofilm-associated cells on stainless steel surfaces were reduced by 1.83 log CFU/mL, 7.00 log CFU/cm2, and 4.35 log CFU/cm2 following LED treatment for 360, 120, and 120 min, respectively. LED treatment damaged both DNA and cell wall of S. flexneri and changed cell morphology and cell membrane permeability. In addition, LED treatment decreased total cell protein concentration of S. flexneri. These results indicated that 405-nm LED treatment effectively controlled S. flexneri contamination of foods and food contact surfaces and that the bacterial inactivation may be the result of damage to multiple cellular components. These findings highlight the potential of LED technology in controlling S. flexneri during food processing, storage, and preparation.

Correlated States in Strained Twisted Bilayer Graphenes Away from the Magic Angle.

Graphene moiré superlattice formed by rotating two graphene sheets can host strongly correlated and topological states when flat bands form at so-called magic angles. Here, we report that, for a twisting angle far away from the magic angle, the heterostrain induced during stacking heterostructures can also create flat bands. Combining a direct visualization of strain effect in twisted bilayer graphene moiré superlattices and transport measurements, features of correlated states appear at "non-magic" angles in twisted bilayer graphene under the heterostrain. Observing correlated states in these "non-standard" conditions can enrich the understanding of the possible origins of the correlated states and widen the freedom in tuning the moiré heterostructures and the scope of exploring the correlated physics in moiré superlattices.

Dioscin relieves diabetic nephropathy via suppressing oxidative stress and apoptosis, and improving mitochondrial quality and quantity control.

Dioscin is a steroidal saponin isolated from various kinds of vegetables and herbs and possesses various biological activities. In this study, the protective effect of dioscin on diabetic nephropathy (DN) was explored. Dioscin and metformin (positive control) were administered orally to diabetic rats daily for 8 weeks. The biochemistry parameters, pancreas and kidney histological changes, oxidative stress, inflammation, apoptosis, autophagy, and mitochondrial quality and quantity control (mitophagy and mitochondrial fission/fusion) were measured. Our results showed that dioscin effectively reduced blood glucose, pancreatic injury, renal function markers and renal pathological changes in DN rat kidneys. Dioscin reduced O2- and H2O2 levels, decreased MDA levels, enhanced antioxidant enzyme (SOD, CAT) activities, and reduced inflammatory factor expressions. Moreover, NOX4 expression and the disorder of the mitochondrial respiratory chain were reversed by dioscin. Furthermore, apoptosis mediated by the mitochondria and ER stress was inhibited by dioscin through downregulating the expressions of Bax, CytC, Apaf-1, caspase 9, p-PERK, p-EIF2α, IRE1, p-IRE1, XBP1s, ATF4, p-CHOP and caspase 12. In addition, autophagy was enhanced by dioscin via an AMPK-mTOR pathway. Mitophagy and mitochondrial fission/fusion belong to the mitochondrial quality and quantity control process, which was improved by dioscin via regulating Parkin, PINK1, DRP1, p-DRP1 and MFN2 expressions. Collectively, these results suggested that dioscin protected against DN through inhibiting oxidative stress, inflammation, and apoptosis mediated by the mitochondria and ER stress. Autophagy and mitochondrial quality and quantity control (mitophagy and mitochondrial fission/fusion) were also improved by dioscin.

Orally Administered Diosgenin Alleviates Colitis in Mice Induced by Dextran Sulfate Sodium through Gut Microbiota Modulation and Short-Chain Fatty Acid Generation.

Diosgenin (DIO) is a kind of steroid sapogenin derived from natural plants. It exerts strong anti-infection, antiallergy, antiviral, and antishock pharmacological properties. In this article, the protective effects of DIO against dextran sulfate sodium (DSS)-induced colitis in mice were researched. Compared with the 2.5% DSS treatment group, 15 mg/kg body weight of diosgenin alleviated colitis disease, evidenced by the increased body weight, the decrease in the disease activity index, and the histological scores. Furthermore, 16S rRNA high-throughput sequencing results demonstrated that DIO improved the colon homeostasis through modulating the gut microbiota, including increases in the relative abundance of several probiotic bacteria, such as Prevotellaceae (from 1.4% to 5.8%), Lactobacillus (from 12.3% to 29.7%), Mucispirillum (from 0.07% to 0.49%), and decreases in the pathogenic bacteria, such as Streptococcus (from 1.6% to 0.6%) and Pseudomonadaceae (from 0.004% to 0%). In addition, the concentration of gut microbial metabolites, total short-chain fatty acids (SCFAs), acetic acid, and propionic acid were significantly increased after DIO supplementation. In conclusion, our findings suggested that DIO attenuates DSS-induced colitis in mice by means of modulating imbalanced gut microbiota and increases in SCFA generation.

Detection performance of PCR for Legionella pneumophila in environmental samples: a systematic review and meta-analysis.

BACKGROUND: Legionellosis remains a public health problem. The most common diagnostic method to detect Legionella pneumophila (L. pneumophila) is culture. Polymerase chain reaction (PCR) is a fast and accurate method for this detection in environmental samples. METHODS: Four databases were searched for studies that evaluated the detection efficiency of PCR in L. pneumophila. The quality evaluation was conducted using Review Manager 5.3. We used Meta-DiSc 1.4 software and the Stata 15.0 software to create forest plots, a meta-regression, a bivariate boxplot and a Deeks' funnel plot. RESULTS: A total of 18 four-fold tables from 16 studies were analysed. The overall pooled sensitivity and specificity of PCR was 94% and 72%, respectively. The positive likelihood ratio (RLR) and negative likelihood ratio (NLR) was 2.73 and 0.12, respectively. The result of the diagnostic odds ratio (DOR) was 22.85 and the area under the curve (AUC) was 0.7884. CONCLUSION: Establishing a laboratory diagnostic tool for L. pneumophila detection is important for epidemiological studies. In this work, PCR demonstrated a promising diagnostic accuracy for L. pneumophila.

Autophagy and mitochondrial dynamics contribute to the protective effect of diosgenin against 3-MCPD induced kidney injury.

3-Chloro-1, 2-propanediol (3-MCPD) is a widespread food contaminant with kidney as the main target organ. The exploration of ingredients as intervention strategy towards 3-MCPD induced nephrotoxicity is needed. Diosgenin (DIO) is a steroidal saponin presented in several plants and foods. Here we assessed whether DIO attenuates nephrotoxicity induced by 3-MCPD using Human embryonic kidney 293 (HEK293) cells and Sprague-Dawley (SD) rats. The results showed that DIO (2, 6, 8 µM) increased cell viability and exerted inhibitory effect on caspase 3 and caspase 9 activities. Histological examination of rats showed that 15 mg/kg bw DIO ameliorated renal pathological changes caused by 3-MCPD (30 mg/kg bw). DIO also induced autophagy and the blockade of autophagy with 3-Methyladenine (3-MA) aggravated mitochondrial apoptosis induced by 3-MCPD in HEK293 cells. Moreover, treatment with DIO caused an increase in p-LKB1/LKB1 and p-AMPK/AMPK expressions and a decrease in p-mTOR/mTOR, p-ULK1(Ser757), p-P70S6K and p-4EBP1 expressions. Additionally, DIO improved mitochondrial dynamics mainly through inhibiting the relocation of DRP1 on mitochondria and enhancing MFN1 and MFN2 expressions. In conclusion, our study demonstrated for the first time that DIO protected against kidney injury induced by 3-MCPD through the induction of autophagy via LKB1-AMPK-mTOR pathway and the improvement of mitochondrial fission and fusion.

Association of occupational stress, period circadian regulator 3 (PER3) gene polymorphism and their interaction with poor sleep quality.

Occupational stress is associated with sleep quality among workers and the human variable number tandem repeat (VNTR) polymorphism of the period circadian regulator 3 (PER3) gene relates to sleep-wake regulation. The main aims of the present study were to examine the effects of PER3 VNTR genotypes, occupational stress, and their interactions on sleep quality. A cross-sectional study was conducted and 729 workers were recruited in Sichuan. Sleep quality were assessed using the Pittsburgh Sleep Quality Index. Occupational stress was measured using the Generic Job Stress Questionnaire. PER3 genotypes were determined with polymerase chain reaction. High and medium occupational stress were linked to a higher risk of poor sleep quality than low levels. Unconditional logistic regression indicated that PER3 genotype was significantly associated with sleep quality, and an increased risk of poor sleep of >1.5-times was observed in those with the allele 5 compared to allele 4. The 5/5 genotype was associated with both sleep latency and sleep duration. Crossover analysis showed an occupational stress × PER3 interaction. Compared to subjects with both low and medium occupational stress and 4/4 + 4/5 genotype, those with both high occupational stress and 5/5 genotype had a higher risk of poor sleep quality. Stratified logistic analyses found that compared with low and medium occupational stress, high occupational stress increased the risk of poor sleep by more than five-times in 5/5 genotype carriers. Occupational stress and PER3 genotype had both separate and combined effects on poor sleep quality of workers. The results suggest that occupational stress may increase the risk of poor sleep quality through interaction with the PER3 gene polymorphism.

Jujuboside A ameliorates high fat diet and streptozotocin induced diabetic nephropathy via suppressing oxidative stress, apoptosis, and enhancing autophagy.

Jujuboside A (JuA) is a triterpenoid saponins isolated from the seed of jujube (semen Ziziphi spinosae) with anti-oxidant, anti-inflammation and anti-apoptosis properties. The present study aimed to investigate the reno-protective effects of JuA on type II diabetes. JuA (20 mg/kg) and Metformin (Met, 300 mg/kg) were administrated to diabetic Sprague Dawley rat for 8 weeks daily. Our results showed that JuA reduced blood glucose and kidney function markers including 24 h urinary protein, urinary ß-NAG/urinary creatinine, serum urea nitrogen, serum uric acid and serum creatinine, and relieved renal pathological changes. In addition, JuA decreased O2- and H2O2 level, enhanced SOD, CAT and GPx activities, decreased NOX4 expression and improved mitochondrial respiratory chain function through regulating respiratory chain complex expression. Moreover, JuA downregulated the expressions of mitochondrial apoptosis proteins: Bax, CytC, Apaf-1 and caspase 9. Apoptosis mediated by ER stress also been inhibited by JuA via downregulating p-PERK, p-IRE1, XBP1s, ATF4, p-CHOP and caspase 12 expressions. JuA also enhanced autophagy and mitophagy via regulating CaMKK2-AMPK-p-mTOR and PINK1/Parkin pathways. Collectively, these results indicated that JuA protected against type II diabetic nephropathy through inhibiting oxidative stress and apoptosis mediated by mitochondria and ER stress. In addition, autophagy and mitophagy was enhanced by JuA.