Maximally localized states and quantum corrections of black hole thermodynamics in the framework of a new generalized uncertainty principle

As a generalized uncertainty principle (GUP) leads to the effects of the minimal length of the order of the Planck scale and UV/IR mixing, some significant physical concepts and quantities are modified or corrected correspondingly. On the one hand, we derive the maximally localized states --- the physical states displaying the minimal length uncertainty associated with a new GUP proposed in our previous work. On the other hand, in the framework of this new GUP we calculate quantum corrections to the thermodynamic quantities of the Schwardzschild black hole, such as the Hawking temperature, the entropy, and the heat capacity, and give a remnant mass of the black hole at the end of the evaporation process. Moreover, we compare our results with that obtained in the frameworks of several other GUPs. In particular, we observe a significant difference between the situations with and without the consideration of the UV/IR mixing effect in the quantum corrections to the evaporation rate and the decay time. That is, the decay time can greatly be prolonged in the former case, which implies that the quantum correction from the UV/IR mixing effect may give rise to a radical rather than a tiny influence to the Hawking radiation.Comment: 27 pages, 10 figures, 4 tables; v2: 30 pages, sections 3-6 substantially revised but conclusions unchanged; v3: 27 pages, clarifications added; v4: 29 pages, clarifications and references added, final version to appear in Advances in High Energy Physic

Accumulation of the Mutations in Basal Core Promoter of Hepatitis B Virus Subgenotype C1 Increase the Risk of Hepatocellular Carcinoma in Southern China

Background: Hepatitis B virus (HBV) genotype C is associated with the development of hepatocellular carcinoma (HCC). In addition, HBV subgenotype C1 is the major subgenotype in Southern China. The aim of this study was to investigate whether there were the specific mutation patterns in HBV/C1 associated with Southern Chinese patients with HCC. Methods: Mutations in HBV basal core promoter (BCP) and their association with HCC were assessed in a matched cross-sectional control study of 102 HCC and 105 chronic hepatitis (CH) patients (from Guangdong, China) infected with HBV/C1. Functional analysis of HBx mutants was performed by the colony formation assay and the luciferase assays. Results: T1762/A1764 double mutations was frequently found in patients infected with HBV/C1, regardless of clinical status (64.7% in HCC and 51.4% in CH, P0.05). Unexpectedly, the adjacent V1753 or A1768 mutation significantly increased the risk of HCC (P0.05). Moreover, the prevalence of triple or quadruple mutations in BCP was significantly higher in patients with HCC than those with CH, particularly for HBeAg-positive-carriers (P0.05). Functional analysis revealed that T1762/A1764 mutation alone did not alter the transcriptional activity and the inhibitory effects on cell proliferation of HBx, but triple or quadruple mutations largely abrogated this effect.Conclusions: Accumulation of mutations involving V1753 or/and A1768 in addition to T1762/A1764 in BCP region were closely related to HCC among the patients infected with HBV/C1, particularly for HBeAg-positive-carriers. The increased risk of HCC caused by BCP variants may be attributable partially to modifying the biological functions of HBx

GABA, progesterone and zona pellucida activation of PLA2 and regulation by MEK-ERK1/2 during acrosomal exocytosis in guinea pig spermatozoa

AbstractWe investigated whether GABA activates phospholipase A2 (PLA2) during acrosomal exocytosis, and if the MEK-ERK1/2 pathway modulates PLA2 activation initiated by GABA, progesterone or zona pellucida (ZP). In guinea pig spermatozoa prelabelled with [14C]arachidonic acid or [14C]choline chloride, GABA stimulated a decrease in phosphatidylcholine (PC), and release of arachidonic acid and lysoPC, during exocytosis. These lipid changes are indicative of PLA2 activation and appear essential for exocytosis since inclusion of aristolochic acid (a PLA2 inhibitor) abrogated them, along with exocytosis. GABA activation of PLA2 seems to be mediated, at least in part, by diacylglycerol (DAG) and protein kinase C since inclusion of the DAG kinase inhibitor R59022 enhanced PLA2 activity and exocytosis stimulated by GABA, whereas exposure to staurosporine decreased both. GABA-, progesterone- and ZP-induced release of arachidonic acid and exocytosis were prevented by U0126 and PD98059 (MEK inhibitors). Taken together, our results suggest that PLA2 plays a fundamental role in agonist-stimulated exocytosis and that MEK-ERK1/2 are involved in PLA2 regulation during this process

DEFB1 rs11362 Polymorphism and Risk of Chronic Periodontitis: A Meta-Analysis of Unadjusted and Adjusted Data

Objective: Chronic periodontitis (CP) is a growing problem that affects the worldwide population, having significant impacts on people's daily lives and economic development. Genetics is an important component in the determination of individual susceptibility to periodontal diseases. Numerous studies have been performed to investigate the association between beta defensin 1 (DEFB1) rs11362 polymorphism and risk of CP, but the results are still inconclusive. Therefore, we conducted this meta-analysis to ascertain whether this variation in DEFB1 is associated with CP susceptibility.Methods: The relevant studies were searched in PubMed and Chinese National Knowledge Infrastructure (CNKI) databases up to January 9, 2018. Two independent authors selected citations and extracted the data from eligible studies. Odds ratios (ORs) with their 95% confidence intervals (95% CIs) were used to assess the strength of the association.Results: Seven case-control studies were included in this meta-analysis. Based on unadjusted data, there was no obvious association between DEFB1 rs11362 polymorphism and CP risk in all genetic models (A vs. G: OR = 0.86, 95%CI = 0.61–1.20; AA vs. GG: OR = 0.83, 95% CI = 00.50–1.39; AG vs. GG: OR = 1.01, 95%CI = 0.73–1.39; AG+AA vs. GG: OR = 0.91, 95% CI = 00.74–1.11; and AA vs. AG+GG: OR = 0.83, 95% CI = 00.57–1.21); the results of adjusted data also showed no significant relationship. Subgroup analyses based on ethnicity, participants' smoking status, HWE in controls and severity of CP all revealed similar results to that of the overall analysis. Sensitivity analysis indicated the results were robust and no evidence of publication bias was found.Conclusions: Our meta-analysis suggests that DEFB1 rs11362 polymorphism may not have an important effect on the risk of CP. Further large-scale and well-designed studies are necessary to validate our conclusion in the future

Barleriside A, an aryl hydrocarbon receptor antagonist, ameliorates podocyte injury through inhibiting oxidative stress and inflammation

IntroductionIncreasing evidence shows that hyperactive aryl hydrocarbon receptor (AHR) signalling is involved in renal disease. However, no currently available intervention strategy is effective in halting disease progression by targeting the AHR signalling. Our previous study showed that barleriside A (BSA), a major component of Plantaginis semen, exhibits renoprotective effects.MethodsIn this study, we determined the effects of BSA on AHR expression in 5/6 nephrectomized (NX) rats. We further determined the effect of BSA on AHR, nuclear factor kappa B (NF-ƙB), and the nuclear factor erythroid 2-related factor 2 (Nrf2) signalling cascade in zymosan-activated serum (ZAS)-stimulated MPC5 cells.ResultsBSA treatment improved renal function and inhibited intrarenal nuclear AHR protein expression in NX-treated rats. BSA mitigated podocyte lesions and suppressed AHR mRNA and protein expression in ZAS-stimulated MPC5 cells. BSA inhibited inflammation by improving the NF-ƙB and Nrf2 pathways in ZAS-stimulated MPC5 cells. However, BSA did not markedly upregulate the expression of podocyte-specific proteins in the ZAS-mediated MPC5 cells treated with CH223191 or AHR siRNA compared to untreated ZAS-induced MPC5 cells. Similarly, the inhibitory effects of BSA on nuclear NF-ƙB p65, Nrf2, and AHR, as well as cytoplasmic cyclooxygenase-2, heme oxygenase-1, and AHR, were partially abolished in ZAS-induced MPC5 cells treated with CH223191 or AHRsiRNA compared with untreated ZAS-induced MPC5 cells. These results indicated that BSA attenuated the inflammatory response, partly by inhibiting AHR signalling.DiscussionBoth pharmacological and siNRA findings suggested that BSA mitigated podocyte lesions by improving the NF-ƙB and Nrf2 pathways via inhibiting AHR signalling. Therefore, BSA is a high-affinity AHR antagonist that abolishes oxidative stress and inflammation

Reserarch on the Formulation Process of Malt Chewable Tablets and Its Digestion Promoting Function

Study on the formulation process of malt chewable tablets and its digestion promoting function.Using a method combining orthogonal experiment and fuzzy comprehensive evaluation to study the formulation process of malt chewable tablets; using small intestine ink advance rate of mice， pepsin excretion of rats， and animal weight change as indicators to study the digestion promoting function of malt chewable tablets. The best formulas are as follows: citric acid is 2%， stevioside is 1%， microcrystalline cellulose is 40%， and magnesium stearate is 1%. 2.67 g/kg BW (body weight) of malt chewable tablets can improve the ink advancing rate of the small bowel movement experiment in mice (P＜0.001)， and the chewable tablets had no adverse effects on rat weight gain， food intake， and food utilization. Malt chewable tablets preparation process is stable and reliable， and the animal function experiments show that it has the function of promoting digestion

Arachidonic acid metabolism as a therapeutic target in AKI-to-CKD transition

Arachidonic acid (AA) is a main component of cell membrane lipids. AA is mainly metabolized by three enzymes: cyclooxygenase (COX), lipoxygenase (LOX) and cytochrome P450 (CYP450). Esterified AA is hydrolysed by phospholipase A2 into a free form that is further metabolized by COX, LOX and CYP450 to a wide range of bioactive mediators, including prostaglandins, lipoxins, thromboxanes, leukotrienes, hydroxyeicosatetraenoic acids and epoxyeicosatrienoic acids. Increased mitochondrial oxidative stress is considered to be a central mechanism in the pathophysiology of the kidney. Along with increased oxidative stress, apoptosis, inflammation and tissue fibrosis drive the progressive loss of kidney function, affecting the glomerular filtration barrier and the tubulointerstitium. Recent studies have shown that AA and its active derivative eicosanoids play important roles in the regulation of physiological kidney function and the pathogenesis of kidney disease. These factors are potentially novel biomarkers, especially in the context of their involvement in inflammatory processes and oxidative stress. In this review, we introduce the three main metabolic pathways of AA and discuss the molecular mechanisms by which these pathways affect the progression of acute kidney injury (AKI), diabetic nephropathy (DN) and renal cell carcinoma (RCC). This review may provide new therapeutic targets for the identification of AKI to CKD continuum