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Rhizosphere is a soil volume of high spatio-temporal heterogeneity and intensive plant-soil-microbial interactions, for which visualization and process quantification is of highest scientific and applied relevance, but still very challenging. A novel methodology for quick assessment of two-dimensional distribution of available phosphorus (P) in rhizosphere was suggested, tested, and development up to the application platform. Available P was firstly trapped by an in-situ diffusive gradients in thin-films (DGT) sampler with precipitated zirconia as the binding gel, and subsequently, the loaded gel was analyzed with an optimized colorimetric imaging densitometry (CID). The imaging platform was established linking: i) DGT, ii) planar optode, and iii) soil zymography techniques to simultaneously determine available P, oxygen, and acid phosphatase in rhizosphere at sub-millimeter spatial scales. The DGT identified available P level in rice rhizosphere were spatially overlapping to the localized redox hotspots and phosphatase activity. The spatial relationship between available P and acid phosphatase activity was dependent on root development. The root radial oxygen loss (ROL) remained active during the experimental observations (2–3 days), while a flux of available P of 10 pg cm−2 s−1 was visualized within 2–3 mm of roots, confirming the correlative response of rice roots to oxygen secretion and P uptake. Summarizing, the established imaging platform is suitable to capture spatial heterogeneity and temporal dynamics of root activities, nutrient bioavailability, ROL and enzyme activities in rhizosphere. [Display omitted] • Quick establishment of the two-dimensional distribution of available P was realized. • A versatile platform was established for imaging multiple analytes in rhizosphere. • Rhizosphere P dynamics were linked to localized redox conditions and root activity. • Relationship between P and acid phosphatase activities varied as root developed. [ABSTRACT FROM AUTHOR]

Unc-51 like autophagy activating kinase 1 (Ulk1) is a serine/threonine kinase that plays a key role in regulating autophagy processes. We attempted to investigate the effects of Ulk1 on traumatic brain injury (TBI) progression by using wild type (WT) mice and Ulk1-knockout (KO) mice suffered with or not TBI. The results were verified using LPS-treated primary astrocyte (AST). Here, Ulk1 was over-expressed in hippocampus of WT mice after TBI, as well as in lipopolysaccharide (LPS)-stimulated AST. Ulk1-deletion improved cognitive ability and hippocampus histological changes in TBI mice. Nissl and neuronal nuclei (NeuN) staining indicated that Ulk1-deletion increased the number of surviving neurons in hippocampus of TBI mice. Ulk1-ablation alleviated neuroinflammation, as evidenced by the reduced expression of hippocampus pro-inflammatory cytokines in TBI mice. TBI-induced apoptosis was also ameliorated by Ulk1-ablation, as proved by the reduced number of TUNEL-staining cells, and cleaved Caspase-3 and poly (ADP-ribose) polymerase (PARP) expressions. Moreover, Ulk1-knockout suppressed TBI-stimulated activation of astrocytes and microglia cells. Additionally, hippocampus autophagy induced by TBI was attenuated by Ulk1-knockout. Further, TBI-activated p38/c-Jun N-terminal Kinase (JNK) pathway was repressed by Ulk1-deletion in hippocampus of mice. The findings above were confirmed in LPS-stimulated AST with or without Ulk1 siRNA transfection. Intriguingly, pre-treatment of p38 or JNK activator markedly abolished the anti-inflammation, anti-apoptosis and anti-autophagy effects of Ulk1-knockdown on LPS-incubated AST. In conclusion, our results demonstrated that Ulk1 might be a potential target for developing therapeutic strategy against TBI in future. [ABSTRACT FROM AUTHOR]

This paper examines the impact of consumers’ creditworthiness, loan terms, loan amount, loan-to-value ratio, and loan purpose on mortgage pricing while controlling for market condition, macroeconomic performance, and loan sources. Applying quantile regression methods based on a lender-provided dataset covering the period of 2002–2007, this paper is able to differentiate these effects with respect to distribution of mortgage pricing. The regression results indicate that loan applicants with higher levels of creditworthiness in terms of credit score receive a lower mortgage premium above default and interest rate risk. For every 10 point increases in credit scores, the mortgage premium above default and interest rate risk declines consistently from by 1 basis point at the 10th quantile to 5 basis points at the 90th quantile. Loan applicants receive discounts ranging from 24 to 117 basis points, 22 to 115 basis points, 13 to 87 basis points for mortgage loans with LTV ratio below 60percent, between 60 and 70 percent, and between 70 percent and 80 percent, respectively. [ABSTRACT FROM AUTHOR]

Abstract: Aims: To explore whether reactive oxygen species (ROS) scavenger (tempol) in the hypothalamic paraventricular nucleus (PVN) attenuates renin–angiotensin system (RAS) and proinflammatory cytokines (PICs), and decreases the blood pressure and sympathetic activity in angiotensin II (ANG II)-induced hypertension. Methods and results: Male Sprague–Dawley rats were infused intravenously with ANG II (10ng/kg per min) or normal saline (NS) for 4weeks. These rats were treated with bilateral PVN infusion of oxygen free radical scavenger tempol (TEMP, 20μg/h) or vehicle (artificial cerebrospinal fluid, aCSF) for 4weeks. ANG II infusion resulted in increased mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). These ANG II-infused rats also had higher levels of gp91phox (a subunit of NAD(P)H oxidase), angiotensin-converting enzyme (ACE), and interleukin-1beta (IL-1β) in the PVN than the control animals. Treatment with PVN infusion of TEMP attenuated the overexpression of gp91phox, ACE and IL-1β within the PVN, and decreased sympathetic activity and MAP in ANG II-infused rats. Conclusion: These findings suggest that ANG II infusion induces elevated PICs and oxidative stress in the PVN, which contribute to the sympathoexcitation in hypertension. Inhibition of reactive oxygen species in hypothalamic paraventricular nucleus attenuates the renin–angiotensin system, proinflammatory cytokines and oxidative stress in ANG II-induced hypertension. [Copyright &y& Elsevier]

• An efficient Ti/TiO 2 -RNTs/Sb-SnO 2 /PbO 2 -ND electrode was synthesized for bentazone removal. • Nano-diamond doping rendered PbO 2 higher oxygen evolution potential and larger active area. • Reduced TiO 2 nanotubes interlayer enhanced service life of PbO 2 and the electron transmission. • The ACE for COD removal was sustained above 30% over the whole reaction time at 30 mA cm−2. • The formation of reactive chlorine species promoted COD removal by 20% in the presence of 10 mM Cl−. Anodic oxidation based on PbO 2 anode has been demonstrated as the feasible approach for the decontamination of organic pollutants; however, the performance of this process is hindered by its ordinary electrochemical activity and relatively low stability. In this study, we fabricated an efficient Ti/TiO 2 -RNTs/Sb-SnO 2 /PbO 2 -ND electrode with electrochemically reduced TiO 2 nanotubes as the interlayer and nano-diamond as the dopant. As compared with other electrodes, the constructed Ti/TiO 2 -RNTs/Sb-SnO 2 /PbO 2 -ND exhibited higher oxygen evolution overpotential, larger active area and less charge transfer resistance. Thus, the average current efficiency of 30% could be attained at 120 min with TiO 2 -NTs/Sb-SnO 2 /PbO 2 , which was 1.5 times higher in comparison with the typical Ti/Sb-SnO 2 /PbO 2 electrode. It was found that the removal efficiency of COD could be increased from 49% to 69% after 120 min treatment in the presence of 10 mM Cl−1 in the electrolyte. After 6 h of electrolysis, 74% of TOC was removed and 31% and 22% of initial N was transformed into NH 4 + and NO 3 − ions, respectively. And oxalic acid, glyoxylic acid, malonic acid and acetic acid were identified quantitatively as the intermediate products. Finally, it was estimated that the accelerated service life of Ti/TiO 2 -RNTs/Sb-SnO 2 /PbO 2 -ND electrode was approximately three times of Ti/Sb-SnO 2 /PbO 2 electrode. Generally, this study is of great interest for the engineering community to design an efficient electrode material for the wastewater treatment. [ABSTRACT FROM AUTHOR]

Abstract Background There is a strong correlation between liver fibrosis and postoperative morbidity after hepatectomy in hepatocellular carcinoma (HCC) patients. The aim of this study was to evaluate which noninvasive fibrosis index (gamma-glutamyl transpeptidase to platelet ratio [GPR], aspartate aminotransferase to platelet ratio index, fibrosis-4 index, or Forns index) was best able to predict complications in patients undergoing hepatectomy for HCC. Materials and methods This retrospective analysis included 275 patients who underwent hepatectomy for HCC from January 2008 to December 2012. Postoperative mortality was defined as death within 90 d after surgery. Complications were grouped into seven grades on the basis of the modified Clavien classification, and major postoperative complications were defined as grade 3 or above. The influence of noninvasive fibrosis indices on postoperative outcomes was assessed by receiver operating characteristic analysis. The primary outcomes were overall complications and major complications, estimated by univariate and multivariate analysis. Results Patients with HCC undergoing anatomical liver resection in the authors' department were evaluated for this study. Finally, 275 patients who underwent minor liver resection (≤2 liver segments) were included. Of these, 231 (84%) were male. The multivariate analysis indicated that the GPR index was not only independently associated with overall complications (hazard ratio, 2.692; 95% confidence interval [CI], 1.626-4.250; P < 0.001) but also independently predictive of major complications (hazard ratio, 1.143; 95% CI, 1.046-1.249; P = 0.03). The areas under the receiver operating characteristic curve for predicting overall complications and major complications for the GPR index were 0.704 (95% CI, 0.643-0.765; P < 0.001) and 0.752 (95% CI, 0.638-0.865; P < 0.001), respectively. Conclusions The data suggested that the GPR index could be a promising predictor of overall postoperative complications and major complications after minor hepatectomy for HCC. [ABSTRACT FROM AUTHOR]

The pathogenesis of attention-deficit/hyperactivity disorder (ADHD) has not been fully elucidated. Gestational hypertension could double the probability of ADHD in the offspring, while the initial bacterial communication between the mother and offspring has been associated with psychiatric disorders. Thus, we hypothesize that antihypertensive treatment during pregnancy may abate the impairments in neurodevelopment of the offspring. To test this hypothesis, we chose Captopril and Labetalol, to apply to pregnant spontaneously hypertensive rat (SHR) dams and examined the outcomes in the male offspring. Our data demonstrated that maternal treatment with Captopril and Labetalol had long-lasting changes in gut microbiota and behavioral alterations, including decreased hyperactivity and increased curiosity, spatial learning and memory in the male offspring. Increased diversity and composition were identified, and some ADHD related bacteria were found to have the same change in the gut microbiota of both the dam and offspring after the treatments. LC-MS/MS and immunohistochemistry assays suggested elevated expression of brain derived neurotrophic factor (BDNF) and dopamine in the prefrontal cortex and striatum of offspring exposed to Captopril/ Labetalol, which may account for the improvement of the offspring's psychiatric functions. Therefore, our results support the beneficial long-term effects of the intervention of gestational hypertension in the prevention of ADHD. [Display omitted] • Maternal Captopril/Labetalol treatment alleviated ADHD symptoms in SHR offspring. • Maternal Captopril/Labetalol treatment altered gut microbiota in SHR offspring. • Maternal Captopril/Labetalol treatment elevated brain dopamine in SHR offspring. [ABSTRACT FROM AUTHOR]

[Display omitted] In aqueous zinc-based batteries, the reaction by-product Zn 4 SO 4 (OH) 6 ·xH 2 O is commonly observed when cycling vanadium-based and manganese-based cathodes. This by-product obstructs ion transport paths, resulting in enhanced electrochemical impedance. In this work, we report a hybrid aqueous battery based on a Na 0.44 MnO 2 cathode and a metallic zinc foil anode. The surfactant sodium lauryl sulfate is added to the electrolyte as a modifier, and the performance before and after modification is compared. The results show that sodium lauryl sulfate can generate an artificial passivation film on the electrode surface. This passivation film reduces the generation of Zn 4 SO 4 (OH) 6 ·xH 2 O and inhibits the dissolution of Na 0.44 MnO 2 in the electrolyte. Therefore, the reaction kinetics and cycle stability of the battery are significantly enhanced. A battery with this electrolyte additive delivers an initial discharge capacity of 235 mA h g−1 at a current density of 0.1 A g -1. At the same time, the battery has excellent rate performance. Under the high-rate condition of 1 A g−1, the battery still maintains a capacity retention rate of 93% after 1500 cycles. Finally, the functional mechanism of by-product inhibition by the electrolyte additive is discussed. [ABSTRACT FROM AUTHOR]

Abstract: The Bi2O3/Bi2WO6 heterojunction photocatalysts were prepared by a two-step solvothermal process using Bi(NO3)3-ethylene glycol solution as Bi source. The catalysts were characterized by X-ray diffraction, scanning and transmission electron microscopy, X-ray photoelectron spectroscopy, and UV–vis diffuse reflection spectroscopy. The heterostructure catalysts are composed of Bi2O3 nanoparticles as modifier and 3D Bi2WO6 microspheres as substrate. Bi2O3 nanoparticles with diameters of about 10–15nm are tightly grown on the lateral surface of the Bi2WO6 microspheres. The hierarchical Bi2O3/Bi2WO6 microspheres exhibit higher photocatalytic activity than the single phase Bi2WO6 or Bi2O3 for the degradation of rhodamine B under visible light illumination (λ>420nm). The enhancement of the photocatalytic activity of the Bi2O3/Bi2WO6 heterojunction catalysts can be ascribed to their improved light absorption property and the reduced recombination of the photoexcited electrons and holes during the photocatalytic reaction. The effect of loading amount of Bi2O3 on the catalytic performance of the heterojunction catalysts was also investigated and the optimal content of Bi2O3 is 3wt%. The Bi2O3/Bi2WO6 heterojunction photocatalysts are essentially stable during the photocatalytic process. [Copyright &y& Elsevier]

Remifentanil is a potent, short-acting opioid analgesic drug that can protect tissues from ischemia and reperfusion injury though anti-inflammatory effects. However, the utility of remifentanil in liver regeneration after hepatectomy is not known. Using a 70% hepatectomy mouse model (PHx), we found that preconditioning animals with 4 μg/kg remifentanil enhanced liver regeneration through supporting hepatocyte proliferation but not through anti-inflammatory effects. These effects were also phenocopied in vitro where 40 mM remifentanil promoted the proliferation of primary mouse hepatocyte cultures. We further identified that remifentanil treatment increased the expression of β-arrestin 2 in vivo and in vitro. Demonstrating specificity, remifentanil preconditioning failed to promote liver regeneration in liver-specific β-arrestin 2 knockout (CKO) mice subjected to PHx. While remifentanil increased the expression of activated (phosphorylated)-ERK and cyclin D1 in PHx livers, their levels were not significantly changed in remifentanil-treated CKO mice nor in WT mice pretreated with the ERK inhibitor U0126. Our findings suggest that remifentanil promotes liver regeneration via upregulation of a β-arrestin 2/ERK/cyclin D1 axis, with implications for improving regeneration process after hepatectomy. [ABSTRACT FROM AUTHOR]

Cow mastitis, caused by Streptococcus infection of the mammary glands, is a common clinical disease that can lead to decreased milk quality and threaten animal welfare and performance. Esculetin (ESC) is a coumarin with anti-inflammatory and anti-asthmatic effects. However, whether ESC has therapeutic effects on mastitis remains unexplored. This study was conducted to investigate the protective effect of ESC against murine mastitis caused by Streptococcus isolated from bovine mammary glands and elucidate the underlying mechanisms. Streptococcus uberis was used to construct a mouse model of mastitis. The results showed that the mice exhibited edema and thickening of the acinar wall with inflammatory infiltration after S. uberis treatment. Intraperitoneal injection of ESC significantly reduced inflammatory cell infiltration, restored normal physiological function, and inhibited the production of the inflammatory cytokines interleukin-1β, interleukin-6, and tumor necrosis factor-α. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot analysis revealed that ESC reduced P38 phosphorylation, further inhibited the influence of mammary Streptococcus on cytoplasmic translocation of nuclear factor-κB (P65), and inhibited the transcriptional activation of P65, thus inhibiting the generation of inflammatory cells. Collectively, ESC may inhibit mitogen-activated protein kinase and nuclear factor-κB, thereby highlighting its potential for the treatment and prevention of mastitis. • Mastitis can lead to decreased milk quality, threatening animal welfare and performance, and affecting human health. • A mouse model of mastitis was constructed using Streptococcus mammary of bovine origin. • The natural herb esculetin protects against mastitis in mice caused by streptococcus isolated from bovine mammary glands. [ABSTRACT FROM AUTHOR]

Evaluating the health risks of the groundwater and surface water in landfill areas is of great significance to the health and safety of local residents. The current practice of health risk assessment is based only on the analysis results of groundwater and surface water samples, which reflect the current situation of water security in landfill areas. However, due to the neglect of risk causes analysis, thus a health risk assessment is insufficient to provide rigorous scientific countermeasures for risk prevention and control. The health risks caused by groundwater and surface water is mainly controlled by the water quality, which is comprehensively controlled by the conditions of its formation and evolution. When a landfill site is located in a hilly area, the environmental characteristics, causes, main controlling factors, and evolution processes of the surface water and groundwater in different parts of the catchment are significantly different. This study used a municipal solid waste landfill area in a hilly area as an example and defined the causes and main controlling factors of regional health risks caused by water based on an analysis of the characteristics of natural and anthropogenic factors affecting the groundwater and surface water. Then, prevention and control countermeasures were proposed for health risks caused by water in different parts of the landfill area. This study provides a method for the causes analysis and prevention and control countermeasures of health risks caused by water in municipal solid waste landfills in hilly areas. [Display omitted] • The health risks of water around landfills in hilly area are significantly different. • The controlling factors of water environmental health risk are different. • Natural and human factors affect the evolution of water around landfill. • Risk prevention and control measures based on causes of health risks are put forward. [ABSTRACT FROM AUTHOR]

β-cell dysfunction is one of the core pathogenetic mechanisms of type 2 diabetes mellitus (T2DM). However, there are currently no effective therapeutic strategies to preserve β-cell mass and function. The role of islet macrophage phenotype reprogramming in β-cell dysfunction has attracted great attention. Given that advanced glycation end products (AGEs) are major pathogenic factors in T2DM, we investigated the effect of AGEs on macrophage activation and their role in β-cell dysfunction. We examined cytokine secretion, M1 and M2 macrophage-associated marker expression and MAPK phosphorylation levels in AGEs-stimulated macrophages. MIN6 cells were cocultured with AGEs-pretreated macrophages to study the effect of AGEs-induced macrophage activation on β-cell dysfunction. We found that AGEs treatment significantly enhanced macrophage secretion of proinflammatory cytokines. The expression of M1 macrophage markers, such as iNOS and the surface marker CD11c, was significantly upregulated, whereas the expression of M2 macrophage markers, such as Arg1 and CD206, was reciprocally downregulated upon AGEs stimulation. AGEs treatment predominantly activated the MAPK pathway, and the inhibition of the MAPK pathway partially attenuated the AGEs-induced polarization of macrophages. In addition, coculture with AGEs-pretreated macrophages significantly inhibited the expression of molecules involved in β-cell function and was accompanied by the impairment of glucose-stimulated insulin secretion (GSIS) in MIN6 cells. AGEs enhance the expression of proinflammatory molecules by activating the MAPK pathway. Moreover, these data imply that AGEs induce macrophage M1 phenotype polarization but restrain M2 polarization, which might contribute to β-cell dysfunction in the pathogenesis of T2DM. • AGEs induce macrophage M1 phenotype polarization but restrain M2 polarization. • AGEs enhance M1 macrophage polarization by MAPK pathway. • AGEs play a role in the development of β-cell dysfunction by regulating macrophage phenotype reprogramming. [ABSTRACT FROM AUTHOR]

Previous findings from our laboratory and others indicate that the main therapeutic effect of angiotensin II type 1 receptor (AT1-R) antagonists is to decrease blood pressure and exert anti-inflammatory effects in the cardiovascular system. In this study, we determined whether AT1-R antagonist telmisartan within the hypothalamic paraventricular nucleus (PVN) attenuates hypertension and hypothalamic inflammation via both the TLR4/MyD88/NF-κB signaling pathway and peroxisome proliferator-activated receptor-γ (PPAR-γ) in the PVN in hypertensive rats. Spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) rats were treated for 4 weeks through bilateral PVN infusion with the AT1-R antagonist telmisartan (TEL, 10 μg/h), or losartan (LOS, 20 μg/h), or the PPAR-γ antagonist GW9662 (GW, 100 μg/h), or vehicle via osmotic minipump. Mean arterial pressure (MAP) was recorded by a tail-cuff occlusion method. PVN tissue and blood were collected for the measurement of AT1-R, PPAR-γ, pro-inflammatory cytokines (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6), inducible nitric oxide synthase (iNOS), TLR4, MyD88, nuclear factor-kappa B (NF-κB) activity and plasma norepinephrine (NE), respectively. Hypertensive rats exhibited significantly higher level of AT1-R and lower level of PPAR-γ in the PVN. PVN treatment with TEL attenuated MAP, improved cardiac hypertrophy, reduced TNF-α, IL-1β, IL-6, iNOS levels, and plasma NE in SHR but not in WKY rats. These results were associated with reduced TLR4, MyD88 and NF-κB levels and increased PPAR-γ level in the PVN of hypertensive rats. Our findings suggest that TLR4/MyD88/NF-κB signaling and PPAR-γ within the PVN are involved in the beneficial effects of telmisartan in hypertension. [ABSTRACT FROM AUTHOR]

Abstract: The renin–angiotensin system (RAS) in the brain is involved in the pathogenesis of hypertension. We hypothesized that inhibition of angiotensin-converting enzyme (ACE) in the hypothalamic paraventricular nucleus (PVN) attenuates angiotensin II (ANG II)-induced hypertension via restoring neurotransmitters and cytokines. Rats underwent subcutaneous infusions of ANG II or saline and bilateral PVN infusions of ACE inhibitor enalaprilat (ENL, 2.5μg/h) or vehicle for 4weeks. ANG II infusion resulted in higher mean arterial pressure and cardiac hypertrophy as indicated by increased whole heart weight/body weight ratio, whole heart weight/tibia length ratio, left ventricular weight/tibia length ratio, and mRNA expressions of cardiac atrial natriuretic peptide and beta-myosin heavy chain. These ANG II-infused rats had higher PVN levels of glutamate, norepinephrine, tyrosine hydroxylase, pro-inflammatory cytokines (PICs) and the chemokine monocyte chemoattractant protein-1, and lower PVN levels of gamma-aminobutyric acid, interleukin (IL)-10 and the 67-kDa isoform of glutamate decarboxylase (GAD67), and higher plasma levels of PICs, norepinephrine and aldosterone, and lower plasma IL-10, and higher renal sympathetic nerve activity. However, PVN treatment with ENL attenuated these changes. PVN microinjection of ANG II induced increases in IL-1β and IL-6, and a decrease in IL-10 in the PVN, and pretreatment with angiotensin II type 1 receptor (AT1-R) antagonist losartan attenuated these changes. These findings suggest that ANG II infusion induces an imbalance between excitatory and inhibitory neurotransmitters and an imbalance between pro- and anti-inflammatory cytokines in the PVN, and PVN inhibition of the RAS restores neurotransmitters and cytokines in the PVN, thereby attenuating ANG II-induced hypertension and cardiac hypertrophy. [Copyright &y& Elsevier]

Abstract: Three metal–organic complexes Cd(HBIDC)(phen)2·4H2O (1), [Cd(BIC)(phen)] n (2) and {[Eu(HBIDC)(H2BIDC)(H2O)]·H2O} n (3) (H3BIDC=benzimidazole-5,6-dicarboxylic acid, H2BIC=benzimidazole-6-carboxylic acid, phen=1,10-phenanthroline) have been synthesized under hydro(solvo)thermal conditions and structurally characterized by elemental analysis, IR spectrum, and single-crystal X-ray diffraction. With similar reaction conditions, reactions of the same ligand with different metal cations selected from different blocks (d-block and f-block) result in different coordination modes of carboxylate groups and final frameworks of complexes 1 and 3. The decarboxylation was observed in complex 2 and resulted in the formation of BIC2− ligand. Complexes 1–3 have intense fluorescent emissions at room temperature in dimethylsulfoxide (DMSO) solution and in the solid-state, which indicate they are potential fluorescence materials. The quantum yields and fluorescence lifetimes of these three complexes were systematically studied. [Copyright &y& Elsevier]

Gut dysbiosis and dysregulation of gut–brain communication have been identified in hypertensive patients and animal models. Previous studies have shown that probiotic or prebiotic treatments exert positive effects on the pathophysiology of hypertension. This study aimed to examine the hypothesis that the microbiota-gut-brain axis is involved in the antihypertensive effects of curcumin, a potential prebiotic obtained from Curcuma longa. Male 8- to 10-week-old spontaneously hypertensive rats (SHRs) and Wistar Kyoto (WKY) rats were divided into four groups: WKY rats and SHRs treated with vehicle and SHRs treated with curcumin in dosage of 100 or 300 mg/kg/day for 12 weeks. Our results show that the elevated blood pressure of SHRs was markedly decreased in both curcumin-treated groups. Curcumin treatment also altered the gut microbial composition and improved intestinal pathology and integrity. These factors were associated with reduced neuroinflammation and oxidative stress in the hypothalamus paraventricular nucleus (PVN). Moreover, curcumin treatment increased butyrate levels in the plasma, which may be the result of increased butyrate-producing gut microorganisms. In addition, curcumin treatment also activated G protein-coupled receptor 43 (GPR 43) in the PVN. These results indicate that curcumin reshapes the composition of the gut microbiota and ameliorates the dysregulation of the gut-brain communication to induce antihypertensive effects. [Display omitted] • Curcumin ameliorated hypertension and cardiac hypertrophy. • Curcumin altered composition of intestinal microbiota and reshaped gut microbiome. • Curcumin attenuated neuroinflammation and oxidative stress in the PVN. • Microbiota-gut-brain axis are involved in the antihypertensive effect of curcumin. [ABSTRACT FROM AUTHOR]

Whether meteorological factors influence COVID-19 transmission is an issue of major public health concern, but available evidence remains unclear and limited for several reasons, including the use of report date which can lag date of symptom onset by a considerable period. We aimed to generate reliable and robust evidence of this relationship based on date of onset of symptoms. We evaluated important meteorological factors associated with daily COVID-19 counts and effective reproduction number (R t) in China using a two-stage approach with overdispersed generalized additive models and random-effects meta-analysis. Spatial heterogeneity and stratified analyses by sex and age groups were quantified and potential effect modification was analyzed. Nationwide, there was no evidence that temperature and relative humidity affected COVID-19 incidence and R t. However, there were heterogeneous impacts on COVID-19 risk across different regions. Importantly, there was a negative association between relative humidity and COVID-19 incidence in Central China: a 1% increase in relative humidity was associated with a 3.92% (95% CI, 1.98%–5.82%) decrease in daily counts. Older population appeared to be more sensitive to meteorological conditions, but there was no obvious difference between sexes. Linear relationships were found between meteorological variables and COVID-19 incidence. Sensitivity analysis confirmed the robustness of the association and the results based on report date were biased. Meteorological factors play heterogenous roles on COVID-19 transmission, increasing the possibility of seasonality and suggesting the epidemic is far from over. Considering potential climatic associations, we should maintain, not ease, current control measures and surveillance. • Negative association between relative humidity and COVID-19 incidence in China. • Linear relationships found between meteorological variables and COVID-19 incidence. • Meteorological factors play heterogenous roles on COVID-19 transmission. [ABSTRACT FROM AUTHOR]

Exercise training is one of the major non-pharmacological treatments for hypertension. However, the central mechanism by which exercise training attenuates the hypertensive responses remains unclear. Irisin is a muscle-secreted cytokine derived from fibronectin type III domain containing 5 (FNDC5) that will be released into the circulation during exercise. We hypothesized that irisin may play a role in the blood pressure regulation by exercise. To examine the hypothesis, our study investigated the effect of irisin on hypertension and its central mechanism. The study was performed in spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto rats. We found that intravenous injection of irisin effectively reduced blood pressure, plasma norepinephrine, paraventricular nucleus (PVN) levels of neuronal activation, oxidative stress and inflammation in SHRs. Moreover, irisin activated nuclear factor E2-related factor-2 (Nrf2) and restored the imbalance of neurotransmitters in the PVN. Our study also found PVN knockdown of Nrf2 abolished the protective effects of irisin on hypertension. These findings demonstrate irisin can improve hypertension via Nrf2-mediated antioxidant in the PVN. [ABSTRACT FROM AUTHOR]

The hypothalamic paraventricular nucleus (PVN) plays crucial roles in central cardiovascular regulation. Increasing evidence in humans and rodents shows that vitamin D intake is important for achieving optimal cardiovascular function. The purpose of this study was to investigate whether calcitriol, an active form of vitamin D, improves autonomic and cardiovascular function in hypertensive rats and whether PVN oxidative stress and inflammation are involved in these beneficial effects. Male spontaneously hypertensive rats (SHR) and normotensive control Wistar Kyoto (WKY) rats were treated with either calcitriol (40 ng/day) or vehicle (0.11 μL/h) through chronic PVN infusion for 4 weeks. Blood pressure and heart rate were recorded continuously by radiotelemetry. PVN tissue, heart and plasma were collected for molecular and histological analysis. Compared to WKY rats, SHR exhibited increased systolic blood pressure, sympathetic drive, and cardiac hypertrophy and remodeling. These were associated with higher mRNA and protein expression levels of high mobility box 1 (HMGB1), receptor for advanced glycation end products (RAGE), toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-κB), proinflammatory cytokines, NADPH oxidase subunit in the PVN. In addition, increased norepinephrine in plasma, elevated reactive oxygen species levels and activation of microglia in the PVN were also observed in SHR. Chronic calcitriol treatment ameliorated these changes but not in WKY rats. Our results demonstrate that chronic infusion of calcitriol in the PVN ameliorates hypertensive responses, sympathoexcitation and retains cardiovascular function in SHR. Reduced inflammation and oxidative stress within the PVN are involved in these calcitriol-induced effects. • PVN infusion of calcitriol ameliorates autonomic dysfunction and hypertension. • Chronic calcitriol treatmen attenuates cardiac hypertrophy and remodeling. • Chronic calcitriol treatment reduces PVN neuroinflammation and oxidative stress. • HMGB1-RAGE/TLR4-NF-κB axis in PVN is associated with the effects of calcitriol. [ABSTRACT FROM AUTHOR]