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1.
J Phys Condens Matter ; 32(8): 085403, 2020 Feb 20.
Artigo em Inglês | MEDLINE | ID: mdl-31693999

RESUMO

Tungsten (W) oxides have shown broad applications such as photocatalyst and cathode of lithium ion batteries. It is well-known that pressure can induce structural phase transition, producing novel properties. On the other hand, the study of W oxides under high pressures is beneficial for the control of the oxygen fugacity. In this work, we built the high-pressure phase diagram of W-O binary compounds through first-principles swarm-intelligence structural search calculations. WO2 and WO3 are stable in the whole considered pressure range from 0 to 300 GPa. Besides reproducing the known structures, we identify two new phases of WO2 (e.g. C2/m and Cmca) and three ones for WO3 (e.g. Pnma, Cmcm, and Pm-3n), associating with the evolution of polyhedron (i.e. octahedron → distorted octahedron for WO2, and octahedron → hendecahedron → tetradecahedron → icosahedron for WO3). More interestingly, the Pm-3n-structured WO3 shows the highest coordination number of 12. Electron structure calculations indicate that pressure-induced nonmetal → metal transition occurs for WO2 and WO3. Our study provides an opportunity to understand the structures and electronic properties of W-O system under high pressure.

2.
J Nanosci Nanotechnol ; 20(2): 1098-1108, 2020 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-31383110

RESUMO

In this study, the 2D porous graphitic carbon nitride (g-C3N4) nanosheets were successfully fabricated via a facile thermal decomposition polymerization method without any help of templates, and then novel porous g-C3N4/CdS complex catalysts of different mass fractions were is situ synthesized by a simple solvothermal process. The results of photocatalytic experiments demonstrate that the coupling g-C3N4/CdS cocatalysts exhibit significant enhanced visible-light-driven photocatalytic activity for the decolorization of methyl orange (MO) compared with individual porous g-C3N4 and CdS. In particular, an optimal porous g-C3N4 content in the hybridized composite has been determined to be 70 wt.%, corresponding to pseudo-first-order rate constant of 0.046 min-1, which is 7 and 11 times faster than that of pure porous g-C3N4 and CdS, respectively. Photoluminescence (PL) spectroscopy measurements clearly confirmed that the recombination of photoproduced electrons and holes in g-C3N4/CdS composites was efficiently inhibited due to the formation of heterojunctions. Furthermore, the possible mechanism of enhanced photocatalytic activity and photostability of prous g-C3N4/CdS are also tentatively proposed.

3.
Fitoterapia ; : 104392, 2019 Oct 26.
Artigo em Inglês | MEDLINE | ID: mdl-31669961

RESUMO

Previous studies have shown that mitomycin C (MMC) can prevent scar adhesion after joint surgery, but the specific mechanism underlying this effect remains unclear. The purpose of this study was to explore the specific mechanism by which MMC promotes fibroblast apoptosis and prevents joint adhesion. The effect of MMC on fibroblasts was assessed using cell counting kit-8 (CCK-8) assays, western blotting, and TUNEL staining. We used qRT-PCR to measure the expression of miR-21 in fibroblasts treated with MMC. Luciferase activity assays were used to determine the relationships between miR-21 and Programmed cell death 4 (PDCD4). The effects of miR-21 and PDCD4 on fibroblast apoptosis were assessed using flow cytometry and western blotting. HE staining was used to determine the role of miR-21 in scar tissue formation in a model of joint adhesion. The results showed that MMC induced apoptosis of fibroblasts and decreased the expression of miR-21. Moreover, miR-21 down-regulation also induced apoptosis of fibroblasts. PDCD4 was confirmed to be a direct target of miR-21 by luciferase activity assay. The results from the animal model indicated that miR-21 attenuated the effect of MMC on reducing the number of fibroblasts. Our study shows that MMC can induce fibroblast apoptosis and prevent joint adhesion by regulating the expression of miR-21 and its target PDCD4.

4.
Environ Int ; 134: 105278, 2019 Nov 08.
Artigo em Inglês | MEDLINE | ID: mdl-31711021

RESUMO

Glucocorticoids (GCs) have been increasingly reported to have adverse effects on aquatic organisms, but the lack of comprehensive analytical methods for a broad number of GCs has limited the effective management of pollution by these molecules in surface and coastal waters. In this study, we developed an original analytical method for simultaneously monitoring 25 natural GCs, and 43 synthetic GCs (4 hydrocortisone types, 6 acetonide types, 8 betamethasone types, 14 halogenated esters, and 11 labile prodrug esters) in water samples. Of the river samples investigated, 15 natural and 25 synthetic compounds were detected with the concentrations ranging from 0.13 ng/L (11-epitetrahydrocortisol) to 433 ng/L (cortisone) and from 0.05 (clobetasol) to 94 ng/L (prednisolone), respectively. Thirteen natural metabolites of cortisol (CRL) were first detected, and their concentrations were up to 36 times higher than that of CRL. Hydrocortisone-type GCs were the dominant synthetic compounds (≤154 ng/L), followed by halogenated esters (≤81 ng/L), acetonide type GCs (≤57 ng/L), betamethasone type GCs (≤32 ng/L), and labile prodrug esters (≤22 ng/L). Considering the relative potencies for detected GCs compared to dexamethasone, halogenated esters predominantly contributed to the GC activities in the samples. Notably, this is the first report of the halogenated esters 11-oxo fluticasone propionate (OFP) and cloticasone propionate (CTP) in environmental waters. Untreated wastewater is the main source of GCs in the studied waters, and the concentration ratios between natural and synthetic GCs can be used as potential indicators of sewage input. Because of the high detected concentrations and bioactivity potency of halogenated GCs, they are the main contributors to GC activities in the studied waters, and deserved more study in the future.

5.
BMC Pregnancy Childbirth ; 19(1): 439, 2019 Nov 27.
Artigo em Inglês | MEDLINE | ID: mdl-31771540

RESUMO

BACKGROUND: Partner infection is a significant factor in preventing mother-to-child syphilis transmission. We compared pregnancy outcomes between syphilis discordant and syphilis concordant couples. METHODS: We conducted a retrospective study among 3076 syphilis-positive women who received syphilis screening together with their partners during pregnancy. Multivariate analysis was used to explore risks for abnormal outcomes in objects correcting for the major covariate factors. Adjusted odds ratios (OR) and 95% confidence intervals (CI) were estimated to compare pregnancy outcomes between syphilis concordant and syphilis discordant couples. RESULTS: Overall, 657 of the 3076 women were diagnosed with gestational syphilis and had a syphilis-positive partner, giving a partner concordance prevalence of 21.36%. Women in concordant couples were more likely to have higher parity, more children, late antenatal care and syphilis screening, a lower proportion of latent syphilis, and elevated serologic titers than women in discordant couples (P < 0.01 for all). Totally, 10.08% of women had adverse pregnancy outcomes. Multivariate analysis showed partners' syphilis infection (ORadj = 1.44, 95% CI: 1.10-1.89), untreated pregnancy syphilis (ORadj = 1.67, 95% CI: 1.15-2.43), and higher maternal serum titers (> 1:8) (ORadj = 1.53, 95% CI: 1.17-2.00) increased the risks of adverse pregnancy outcomes. Concordance was associated with increased risk for stillbirth (ORadj = 2.86, 95%CI:1.36-6.00), preterm birth (PTB) (ORadj = 1.38,95%CI:1.02-1.87) and low birth weight (LBW) (ORadj = 1.55, 95%CI:1.13-2.11) compared with discordance. Even among treated women, concordance was associated with increased risk for stillbirth (ORadj = 3.26, 95%CI:1.45-7.31) and LBW (ORadj = 1.52, 95%CI:1.08-2.14). Among women with one treatment course, the risks for PTB(ORadj = 1.81, 95%CI:1.14-2.88) and LBW(ORadj = 2.08, 95%CI:1.28-3.38)were also higher among concordant couples than discordant couples. Nevertheless, there were no significant differences between concordant and discordant couples in risks of stillbirth (ORadj = 2.64, 95% CI: 0.98-7.05),PTB (ORadj = 1.15, 95% CI: 0.76-1.74), and LBW(ORadj = 1.21, 95% CI: 0.78-2.02) among women with two treatment courses. CONCLUSION: Male partner coinfection increased the risks for stillbirth, PTB and LBW, particularly when gestational syphilis treatment was suboptimal. However, this risk could be reduced by adequate treatment.

6.
Adv Exp Med Biol ; 1182: 79-118, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31777015

RESUMO

The anticancer potential of Ganoderma (Lingzhi) and its extracts has been widely demonstrated, including antiproliferative and apoptosis inductive, antimetastatic, antiangiogenic, and multidrug resistance reversional activities, involving a variety of cellular and molecular mechanisms besides antitumor immunology. Intrinsic- and extrinsic-initiated apoptotic pathway in association with cell cycle arresting, telomerase inhibiting, autophagy, and oxidative stress is involved in the antiproliferative and apoptosis inductive activities of Ganoderma and its extracts. The inhibition of tumor cell adhesion, invasion, and migration by Ganoderma and its extracts involves molecular mechanisms such as AP-1, NF-κB, MMP, cadherin, ß-integrin, c-Met, FAK, EMT, and so on. Targeting the major pro-angiogenic stimulus, VEGF, and its receptor contributes to the inhibition of tumor angiogenesis by Ganoderma and its extracts. Inhibition against the ATP-dependent transmembrane drug transporter such as P-glycoprotein (P-gp) on the surface of resistant tumor cells to prevent reduction of the intracellular accumulation of anticancer drugs by pumping out the drugs plays an important role in the activities of Ganoderma and its extracts to reverse tumor cell multidrug resistance.

7.
Redox Biol ; 28: 101373, 2019 Nov 06.
Artigo em Inglês | MEDLINE | ID: mdl-31731100

RESUMO

It has been shown that anti-inflammatory cytokines interleukin-35 (IL-35) and IL-10 could inhibit acute endothelial cell (EC) activation, however, it remains unknown if and by what pathways IL-35 and IL-10 could block atherogenic lipid lysophosphatidylcholine (LPC)-induced sustained EC activation; and if mitochondrial reactive oxygen species (mtROS) can differentiate mediation of EC activation from trained immunity (innate immune memory). Using RNA sequencing analyses, biochemical assays, as well as database mining approaches, we compared the effects of IL-35 and IL-10 in LPC-treated human aortic ECs (HAECs). Principal component analysis revealed that both IL-35 and IL-10 could similarly and partially reverse global transcriptome changes induced by LPC. Gene set enrichment analyses showed that while IL-35 and IL-10 could both block acute EC activation, characterized by upregulation of cytokines/chemokines and adhesion molecules, IL-35 is more potent than IL-10 in suppressing innate immune signatures upregulated by LPC. Surprisingly, LPC did not induce the expression of trained tolerance itaconate pathway enzymes but induced trained immunity enzyme expressions; and neither IL-35 nor IL-10 was found to affect LPC-induced trained immunity gene signatures. Mechanistically, IL-35 and IL-10 could suppress mtROS, which partially mediate LPC-induced EC activation and innate immune response. Therefore, anti-inflammatory cytokines could reverse mtROS-mediated acute and innate immune trans-differentiation responses in HAECs, but it could spare metabolic reprogramming and trained immunity signatures, which may not fully depend on mtROS. Our characterizations of anti-inflammatory cytokines in blocking mtROS-mediated acute and prolonged EC activation, and sparing trained immunity are significant for designing novel strategies for treating cardiovascular diseases, other inflammatory diseases, and cancers.

8.
Redox Biol ; 28: 101364, 2019 Oct 29.
Artigo em Inglês | MEDLINE | ID: mdl-31731101

RESUMO

Inflammation is a self-defense response to protect individuals from infection and tissue damage, but excessive or persistent inflammation can have adverse effects on cell survival. Many individuals become especially susceptible to chronic-inflammation-induced sensorineural hearing loss as they age, but the intrinsic molecular mechanism behind aging individuals' increased risk of hearing loss remains unclear. FoxG1 (forkhead box transcription factor G1) is a key transcription factor that plays important roles in hair cell survival through the regulation of mitochondrial function, but how the function of FoxG1 changes during aging and under inflammatory conditions is unknown. In this study, we first found that FoxG1 expression and autophagy both increased gradually in the low concentration lipopolysaccharide (LPS)-induced inflammation model, while after high concentration of LPS treatment both FoxG1 expression and autophagy levels decreased as the concentration of LPS increased. We then used siRNA to downregulate Foxg1 expression in hair cell-like OC-1 cells and found that cell death and apoptosis were significantly increased after LPS injury. Furthermore, we used d-galactose (D-gal) to create an aging model with hair cell-like OC-1 cells and cochlear explant cultures in vitro and found that the expression of Foxg1 and the level of autophagy were both decreased after D-gal and LPS co-treatment. Lastly, we knocked down the expression of Foxg1 under aged inflammation conditions and found increased numbers of dead and apoptotic cells. Together these results suggest that FoxG1 affects the sensitivity of mimetic aging hair cells to inflammation by regulating autophagy pathways.

9.
Life Sci ; 239: 117083, 2019 Nov 20.
Artigo em Inglês | MEDLINE | ID: mdl-31759043

RESUMO

AIMS: The present study aims to evaluate the analgesic effect of ginsenoside Rg3 in different mouse pain models. MAIN METHODS: Formalin-, carrageenan- and S180 tumor cells induced mouse pain models were built in the study. The licking and biting time and PEG2 contents in the inflammatory sites were measured. The excitatory and inhibitory amino acids in the brains were determined by pre-column derivation FLD-HPLC method. KEY FINDING: We have found that ginsenoside Rg3 treated the pain phases and decreased the PGE2 in formalin and carrageenan induced models, respectively. It significantly increased the contents of EAAs (Asp and Glu) in the brains of S180 tumor inducing pain mice, meanwhile, the IAAs (Gly, Tau and GABA) decreased. SIGNIFICANCE: Our results revealed that ginsenoside Rg3 acted central and peripheral analgesic effect and regulated the inflammatory factors and pain-related amino acids. It could re-balance the abnormal EAAs/IAAs value when the pain occurred. The analgesic mechanism and the clinical application of ginsenoside Rg3 need be evaluated furtherly.

10.
Chemosphere ; 243: 125373, 2019 Nov 18.
Artigo em Inglês | MEDLINE | ID: mdl-31765895

RESUMO

The pyrethroid insecticide deltamethrin has been reported to have an effect on vertebrate development and cardiovascular disease. Sodium tanshinone IIA sulfonate (STS) is considered to have cardioprotective effects and melatonin is known to regulate sleep-waking cycles. In this experiment, we used transgenic zebrafish Tg (kdrl:mCherry) and Tg (myl7:GFP) to investigate whether STS and melatonin could reverse the cardiovascular toxicity and neurotoxicity induced by deltamethrin. Zebrafish embryos were exposed to 25 µg/L deltamethrin at 10 hpf and treated with 100 mmol/L STS and 1 µmol/L melatonin showed that deltamethrin treatment affected normal cardiovascular development. In situ hybridization and qRT-PCR results showed that deltamethrin could interfere with the normal expression of cardiovascular development-related genes vegfr2, shh, gata4, nkx2.5, causing functional defects in the cardiovascular system. In addition, deltamethrin could affect the sleep-waking behavior of larvae, increasing the activity of larvae, decreasing the rest behavior and the expression of hcrt, hcrtr, aanat2 were down-regulated. The addition of melatonin and STS can significantly alleviate cardiovascular toxicity and sleep-waking induced by deltamethrin, while restoring the expression of related genes to normal levels. Our study demonstrates the role of STS and melatonin in protecting cardiovascular and sleep-waking behavior caused by deltamethrin.

11.
J Viral Hepat ; 2019 Nov 21.
Artigo em Inglês | MEDLINE | ID: mdl-31755220

RESUMO

Antiviral therapy has been shown to improve the prognosis of hepatitis B virus (HBV) DNA-positive hepatocellular carcinoma (HCC) after radical treatment, but antiviral treatments require further optimization. This study aimed to evaluate the efficacies of different antiviral strategies with HCC patients after hepatectomy/ablation. This prospective, randomized, controlled, and multi-center trial enrolled HBV DNA-positive primary HCC patients after hepatectomy/ablation between January 2007 and January 2009. Patients were divided into four groups: early-combination (entecavir plus Peg-interferon [IFN]α-2a co-administration during year 1); late-combination (addition of Peg-IFNα-2a for 48 weeks after 1 year of entecavir); nucleos(t)ide analogue[NA] monotherapy; and non-antiviral treatment. Primary endpoints included recurrence-free survival and overall survival. A total of 447 patients were enrolled. The 2-year and 8-year recurrence free survival and 8-year overall survival rates were significantly higher in the early-combination group than in the other two antiviral groups (P<0.05). After 48 weeks treatment, more patients achieved an HBsAg reduction >1500 IU/ml and the mean HBsAg level was significantly lower in the early-combination group compared with the late-combination and NA monotherapy groups (P<0.05). Multivariate analysis showed that early-combination therapy and a reduction in HBsAg by >1500 IU/mL after 48 weeks of therapy correlated with reduced mortality and disease recurrence. Early introduction of combination antiviral treatment may represent a more effective therapeutic strategy for patients with HBV DNA-positive HCC after hepatectomy/ablation. A reduction in HBsAg by >1500 IU/mL after 48 weeks treatment is associated with reduced mortality and disease recurrence of HBV DNA-positive HCC patients after hepatectomy/ablation.

13.
J Crohns Colitis ; 2019 Nov 03.
Artigo em Inglês | MEDLINE | ID: mdl-31679013

RESUMO

BACKGROUND AND AIMS: Interleukin 6 (IL-6) or its receptor is currently a candidate for targeted biologic therapy of inflammatory bowel disease (IBD). Thus, a comprehensive understanding of the consequences of blocking IL-6 is imperative. We investigated these consequences by evaluating the effects of IL-6 deletion on the spontaneous colitis of IL-10 deficient mice (IL-10-/-). METHODS: IL-6/IL-10 double-deficient mice (IL-6-/-/IL-10-/-) were generated and analyzed for intestinal inflammation, general phenotypes, and molecular/biochemical changes in the colonic mucosa by comparing to those of WT and IL-10-/- mice. RESULTS: Unexpectedly, the IL-6-/-/IL-10-/- mice manifested more pronounced gut inflammation and earlier disease onset than IL-10-/- mice, both locally (colon and small bowel) and systemically (splenomegaly, ulcerative dermatitis, leukocytosis, neutrophilia, and monocytosis). IL-6-/-/IL-10-/- mice exhibited elevations of multiple cytokines (IL-1ß, IL-4, IL-12, TNFα) and chemokines (MCP-1 and MIG), but not IFN-γ (Th1), IL-17A and IL-17G (Th17), or IL-22 (Th22). FOXP3 and TGF-ß, two key factors for Regulatory T (Treg) cell differentiation, were significantly down-regulated in the colonic mucosa, but not in the thymus or mesenteric lymph nodes, of IL-6-/-/IL-10-/- mice. CTLA-4 was diminished while iNOS was upregulated in the colonic mucosa of IL-6-/-/IL-10-/- mice. CONCLUSION: In IL-10-/- mice, complete IL-6 blockade significantly aggravates gut inflammation, at least in part by suppressing Treg/CTLA-4 and promoting the IL-1ß/Th2 pathway. In addition, the double mutant exhibits signs of severe systemic inflammation. Our data define a new function of IL-6 and suggest that caution should be exercised when targeting IL-6 in IBD patients, particularly those with defects in IL-10 signaling.

14.
Theranostics ; 9(24): 7268-7281, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31695767

RESUMO

Rationale: An imbalance between protein synthesis and degradation is one of the mechanisms of cardiac hypertrophy. Increased transcription in cardiomyocytes can lead to excessive protein synthesis and cardiac hypertrophy. Maf1 is an RNA polymerase III (RNA pol III) inhibitor that plays a pivotal role in regulating transcription. However, whether Maf1 regulates of cardiac hypertrophy remains unclear. Methods: Cardiac hypertrophy was induced in vivo by thoracic aortic banding (AB) surgery. Both the in vivo and in vitro gain- and loss-of-function experiments by Maf1 knockout (KO) mice and adenoviral transfection were used to verify the role of Maf1 in cardiac hypertrophy. RNA pol III and ERK1/2 inhibitor were utilized to identify the effects of RNA pol III and ERK1/2. The possible interaction between Maf1 and ERK1/2 was clarified by immunoprecipitation (IP) analysis. Results: Four weeks after surgery, Maf1 KO mice exhibited significantly exacerbated AB-induced cardiac hypertrophy characterized by increased heart size, cardiomyocyte surface area, and atrial natriuretic peptide (ANP) expression and by exacerbated pulmonary edema. Also, the deficiency of Maf1 causes more severe cardiac dilation and dysfunction than wild type (WT) mice after pressure overload. In contrast, compared with adenoviral-GFP injected mice, mice injected with adenoviral-Maf1 showed significantly ameliorated AB-induced cardiac hypertrophy. In vitro study has demonstrated that Maf1 could significantly block phenylephrine (PE)-induced cardiomyocyte hypertrophy by inhibiting RNA pol III transcription. However, application of an RNA pol III inhibitor markedly improved Maf1 knockdown-promoted cardiac hypertrophy. Moreover, ERK1/2 was identified as a regulator of RNA pol III, and ERK1/2 inhibition by U0126 significantly repressed Maf1 knockdown-promoted cardiac hypertrophy accompanied by suppressed RNA pol III transcription. Additionally, IP analysis demonstrated that Maf1 could directly bind ERK1/2, suggesting Maf1 could interact with ERK1/2 and then inhibit RNA pol III transcription so as to attenuate the development of cardiac hypertrophy. Conclusions: Maf1 ameliorates PE- and AB-induced cardiac hypertrophy by inhibiting RNA pol III transcription via ERK1/2 signaling suppression.

15.
Am J Emerg Med ; 2019 Oct 24.
Artigo em Inglês | MEDLINE | ID: mdl-31704061

RESUMO

BACKGROUND: The purpose of this study was to evaluate the clinical symptoms, surgical management, and outcomes of pregnant women with adnexal torsion due to assisted reproductive technology. METHODS: It was a retrospective study that include 17 pregnant women with adnexal torsion, in which the maternal age, type of fertilization, gestational age, clinical symptoms, ultrasonic findings, side affected by the disease, surgical method, and pregnancy outcomes were evaluated. RESULTS: A total of 17 patients with adnexal torsion were included in this study, of which 8 patients conceived by in vitro fertilization-embryo transfer (IVF-ET), 1 by artificial insemination (AIH), and the other 8 conceived naturally after ovulation induction. About 14 were reported to have occurred in the first trimester of pregnancy, 1 case in the second trimester, and the other 2 in the third trimester. Clinical symptoms were abdominal pain with or without nausea and vomiting. 14 cases occurred in the right adnexa and the other 3 in the left. 5 of the patients underwent laparoscopy, and the other 12 underwent laparotomy. 8 cases were of full- term delivery, 6 twins gave birth prematurely, and 3 patients had inevitable abortion. CONCLUSIONS: Adnexal torsion is an acute onset of lower abdominal pain in women, which seldom occurs during pregnancy. However, because of the wide application of assisted reproductive technology (ART), its incidence has increased. Early diagnosis and treatment can lead to better results.

16.
J Dairy Res ; : 1-9, 2019 Nov 14.
Artigo em Inglês | MEDLINE | ID: mdl-31722754

RESUMO

Mastitis, a major infectious disease in dairy cows, is characterized by an inflammatory response to pathogens such as Escherichia coli and Staphylococcus aureus. To better understand the immune and inflammatory response of the mammary gland, we stimulated bovine mammary gland epithelial cells (BMECs) with E. coli-derived lipopolysaccharide (LPS). Using transcriptomic and proteomic analyses, we identified 1019 differentially expressed genes (DEGs, fold change ≥2 and P-value < 0.05) and 340 differentially expressed proteins (DEPs, fold change ≥1.3 and P-value < 0.05), of which 536 genes and 162 proteins were upregulated and 483 genes and 178 proteins were downregulated following exposure to LPS. These differentially expressed genes were associated with 172 biological processes; 15 Gene Ontology terms associated with response to stimulus, 4 associated with immune processes, and 3 associated with inflammatory processes. The DEPs were associated with 51 biological processes; 2 Gene Ontology terms associated with response to stimulus, 1 associated with immune processes, and 2 associated with inflammatory processes. Meanwhile, several pathways involved in mammary inflammation, such as Toll-like receptor, NF-κB, and NOD-like receptor signaling pathways were also represented. NLRP3 depletion significantly inhibited the expression of IL-1ß and PTGS2 by blocking caspase-1 activity in LPS-induced BMECs. These results suggest that NLR signaling pathways works in coordination with TLR4/NF-κB signaling pathways via NLRP3-inflammasome activation and pro-inflammatory cytokine secretion in LPS-induced mastitis. The study highlights the function of NLRP3 in an inflammatory microenvironment, making NLRP3 a promising therapeutic target in Escherichia coli mastitis.

17.
Plant Physiol ; 2019 Oct 30.
Artigo em Inglês | MEDLINE | ID: mdl-31666300

RESUMO

Histone H2B monoubiquitination (H2Bub1) plays critical roles in regulating growth and development as well as stress responses in Arabidopsis (Arabidopsis thaliana). In this study, we used wild-type and HUB1 and HUB2 loss-of-function Arabidopsis plants to elucidate the mechanisms involved in the regulation of the plant's defense responses to Verticillium dahliae toxins (Vd-toxins). We demonstrated that HUB-mediated H2Bub1 regulates the expression of NADPH oxidase RbohD by enhancing the enrichment of histone H3 tri-methylated on K4 in response to Vd-toxins. RbohD-dependent hydrogen peroxide (H2O2) signaling is a critical modulator in the defense response against Vd-toxins. Moreover, H2Bub1 also affects posttranscriptional mitogen-activated protein kinase (MAPK, or MPK) signaling. H2Bub1 was required for the activation of MPK3 and MPK6. MPK3 and MPK6 are involved in regulating RbohD-mediated H2O2 production. MPK3 and MPK6 are associated with protein Tyr phosphatases (PTPs), such as Tyr-specific phosphatase 1 and mitogen-activated protein kinases phosphatase 1, which negatively regulated H2O2 production. In addition, H2Bub1 is involved in regulating the expression of WRKY33. WRKY33 directly binds to RbohD and functions as a transcription factor to regulate the expression of RbohD. Collectively, our results indicate that H2Bub1 regulates NADPH oxidase RbohD-dependent H2O2 production, and the PTPs-MPK3/6-WRKY pathway plays an important role in the regulation of RbohD-dependent H2O2 signaling in defense responses to Vd-toxins in Arabidopsis.

18.
Langmuir ; 35(47): 15131-15136, 2019 Nov 26.
Artigo em Inglês | MEDLINE | ID: mdl-31682456

RESUMO

The synthesis of intermetallic antimonides usually depends on either the high-temperature alloying technique from high-purity metals or the flux method in highly poisonous Pb-melt. In this paper, we introduced a soft-chemical method to synthesize intermetallic antimonides from ternary chalcogenide precursors under an argon atmosphere below 200 °C. Powder X-ray diffraction and compositional analysis clearly indicate that a new phase of the Ag3Sb nanocrystal was synthesized from the Ag3SbS3 precursors. Three types of trialkylphosphines (TAPs) were applied as desulfurization agents, and the transformation mechanism was elucidated. The capability of the desulfurization agent follows the sequence of triphenylphosphine (TPP) > tributylphosphine (TBP) > trioctylphosphine (TOP). Besides, this TAP-driven desulfurization route to synthesize the intermetallic phase could also be possible for AgSbSe2 and Sb2S3. Therefore, this paper provides an efficient and mild technique for the fabrication of intermetallic nanocrystals.

19.
Vet Microbiol ; 239: 108483, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31699469

RESUMO

Colisepticemia caused by bloodstream infection of the extraintestinal pathogenic Escherichia coli (ExPEC) has become a serious public health problem. The recent emergence of the colistin-resistant Enterobacteriaceae, especially mcr-1-positive E. coli (MCRPEC) exerts great concern around the world. The molecular epidemiology and zoonosis risk of avian-origin MCRPEC are reported to be substantially lower. Here, we presented a system-wide analysis of emerging trends and zoonotic risk of MCRPEC recovered from avian colibacillosis in China. Our results showed the majority of avian-source MCRPEC isolates were classified as ExPECs. We also found that not only MCRPEC in phylogroups B2 and D, but also several E. coli populations in groups B1 and F possessed high virulence in the two models of avian colibacillosis and three rodent models for ExPEC-associated human infections. The high-virulent MCRPEC clones belong to ST131, as well as ST-types (such as ST48, ST117, ST162, ST501, ST648, and ST2085). Our data suggested the zoonotic risk of MCRPEC appeared to be a close association with ColV/ColBM type virulence plasmids. A comprehensive genomic analysis showed the overlapped of ColV/ColBM plasmids contents between MCRPEC isolates from humans and poultry. Identification of ColV/ColBM plasmids among human MCRPEC isolates revealed the potential transmission of avian-source mcr-1-positive ExPECs to humans. Moreover, the presence of ColV/ColBM plasmid-encoded virulence determinants, could be used as a predictive label for pathogenic MCRPEC. These findings highlighted avian-origin MCRPEC isolates could be recognized as a foodborne pathogen.

20.
Med Sci Monit ; 25: 8968-8974, 2019 Nov 25.
Artigo em Inglês | MEDLINE | ID: mdl-31766048

RESUMO

BACKGROUND Metrnl is a novel identified adipomyokine which might have therapeutic potential for metabolic and inflammatory diseases, including type 2 diabetes mellitus. We aimed to explore the associations of circulating Metrnl level with ß-cell function and insulin resistance (IR) and further explore the possible correlation between Metrnl and another adipomyokine named irisin in patients diagnosed type 2 diabetes. MATERIAL AND METHODS Our study recruited 59 participants with type 2 diabetes and 30 normal glucose tolerance (NGT) participants. We used enzyme-linked immunosorbent assay (ELISA) to measure serum levels of Metrnl and irisin. The associations of Metrnl level with indexes of ß-cell function and IR and irisin level were analyzed by multiple linear regression analysis or spearman correlation analysis. RESULTS Compared with NGT participants, serum Metrnl level was elevated in participants with type 2 diabetes: 210.30 pg/mL (range 105.94-323.91 pg/mL) versus 132.02 pg/mL (range 104.93-195.92 pg/mL). Metrnl level did not show significant correlation with ß-cell function-related indicators, but positively correlated with HOMA2-IR and negatively correlated with HOMA2-%S after controlling multiple covariates in participants with type 2 diabetes. Metrnl level was also not associated with obesity-related indicators (body mass index, waist circumference, body fat percentage, and visceral adipose tissue area) in the type 2 diabetes group. In addition, the correlation between Metrnl and irisin level was also not present (r=-0.159, P=0.229) in type 2 diabetes group. CONCLUSIONS Serum Metrnl level was associated with IR, but not with ß-cell function in participants with diagnosed type 2 diabetes.

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