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Objective: This study aimed to evaluate the intervention effect of curcumin on hepatic fibrosis in rodent models through systematic review and meta-analysis, in order to provide meaningful guidance for clinical practice. Methods: A systematic retrieval of relevant studies on curcumin intervention in rats or mice hepatic fibrosis models was conducted, and the data were extracted. The outcome indicators included liver cell structure and function related indicators, such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), albumin (ALB), ratio of albumin to globulin (A/G), total bilirubin (TBIL), bax protein, bcl-2 protein and index of liver, as well as the relevant indicators for evaluating the degree of hepatic fibrosis, such as hyaluronic acid (HA), laminin (LN), type I collagen (Collagen I), type III collagen (Collagen III), type III procollagen (PCIII), type III procollagen amino terminal peptide (PIIINP), type IV collagen (IV-C), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), α-Smooth muscle actin (α-SMA), hydroxyproline (HYP), platelet derived factor-BB (PDGF-BB), connective tissue growth factor (CTGF) and transforming growth factor-β1 (TGF-β1), and oxidative stress-related indicators, such as superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px). These results were then analyzed by meta-analysis. Studies were evaluated for methodological quality using the syrcle's bias risk tool. Results: A total of 59 studies were included in the meta-analysis, and the results showed that curcumin can reduce the levels of ALT, AST, ALP, TBIL, bax protein, and index of liver in hepatic fibrosis models. It can also reduce HA, LN, Collagen I, Collagen III, PCIII, PIIINP, IV-C, TNF-α, α-SMA, HYP, PDGF-BB, CTGF, TGF-β1 and MDA, and increase the levels of ALB, A/G, SOD, and GSH-Px in the hepatic fibrosis models. However, the effects of curcumin on bcl-2 protein, IL-6 in hepatic fibrosis models and index of liver in mice were not statistically significant. Conclusion: The analysis results indicate that curcumin can reduce liver cell apoptosis by maintaining the stability of liver cell membrane, inhibit the activation and proliferation of hepatic stellate cells by reducing inflammatory response, and alleviate tissue peroxidation damage by clearing oxygen free radicals. [ABSTRACT FROM AUTHOR]

BACKGROUND: Chronic lower back pain (CLBP) is one of the most common disorders worldwide. Flash cupping has the ability to relieve CLBP; nevertheless, its impact on CLBP and the likely mechanism of action have not been studied. OBJECTIVE: The goal of this study was to assess the impact of a single, brief cupping session on CLBP and low back muscle activity using multichannel surface electromyography (sEMG). METHODS: In this randomized controlled trial, 24 patients with CLBP were enrolled and randomly assigned to the control group (treated by acupuncture) and cupping group (treated by acupuncture and flash cupping). Acupuncture was applied on the shen shu (BL23), dachang shu (BL25), and wei zhong (BL40) acupoints in both the groups. A brief cupping treatment was applied to the shen shu (BL23), qihai shu (BL24), dachang shu (BL25), guanyuan shu (BL26), and xiaochang shu (BL27) acupoints on both sides of the lower back in the cupping group. The numeric rating scale (NRS) was used to assess therapy efficacy for lower back pain (LBP) before and after treatment. Surface EMG data collected during symmetrical trunk flexion-extension movements were utilized to measure lower back muscle activity and the effectiveness of LBP therapy. RESULTS: There was no statistically significant difference (P = 0.63) in pain intensity between the two groups before and after treatment. There was a statistically significant difference (P = 0.04) between the control group and the cupping group in the sEMG topographic map parameter CoGx-To-Midline. CONCLUSION: This study established a connection between the action mechanism of flash cupping and enhanced horizontal synchronization of lower back muscular activity. [ABSTRACT FROM AUTHOR]

Pinus massoniana Lamb. is an important, common afforestation and timber tree species in China. Species of Pestalotiopsis are well-known pathogens of needle blight. In this study, the five representative strains were isolated from needle blight from needles of Pi. massoniana in Nanjing, Jiangsu, China. Based on multi-locus phylogenetic analyses of the three genomic loci (ITS, TEF1, and TUB2), in conjunction with morphological characteristics, a new species, namely Pestalotiopsis jiangsuensis sp. nov., was described and reported. Pathogenicity tests revealed that the five representative strains of the species described above were pathogenic to Pi. massoniana. The study revealed the diversity of pathogenic species of needle blight on Pi. massoniana. This is the first report of needle blight caused by P. jiangsuensis on Pi. massoniana in China and worldwide. This provides useful information for future research on management strategies of this disease. [ABSTRACT FROM AUTHOR]

The modern manufacturing industry faces increasing demands to customize products according to personal needs, thereby leading to the proliferation of complex designs. To cope with design complexity, manufacturing systems are increasingly equipped with advanced sensing and imaging capabilities. However, traditional statistical process control methods are not concerned with the stream of in-process imaging data. Also, very little has been done to investigate nonlinearity, irregularity, and inhomogeneity in the image stream collected from manufacturing processes. This paper presents the joint multifractal and lacunarity analysis to characterize irregular and inhomogeneous patterns of image profiles, as well as detect the hidden dynamics in the manufacturing process. Experimental studies show that the proposed method not only effectively characterizes surface finishes for quality control of ultraprecision machining but also provides an effective model to link process parameters with fractal characteristics of in-process images acquired from additive manufacturing. This, in turn, will allow a swift response to processes changes and consequently reduce the number of defective products. The proposed multifractal method shows strong potentials to be applied for process monitoring and control in a variety of domains such as ultraprecision machining and additive manufacturing. [ABSTRACT FROM AUTHOR]

The wick is the most crucial element of loop heat pipes (LHPs). At present, wick materials are limited to copper, stainless steel, nickel, and so on. Little research has been carried out on new wick materials. This paper reports the fabrication of aluminum wicks and performance tests of LHPs using aluminum wicks. Experimental data show that this LHP is capable of transferring a heating load of 130 W, while the thermal resistance is only approximately 0.04 K/W. Then, the experimental data were compared with those for LHPs using a polytetrafluoroethylene (PTFE) wick. Based on the SIMPLE algorithm, a 2-D unsteady-state heat transfer model and a 2-D steady-state flow model of the wicks are established to analyze the effects of wick material, pore size and porosity on the performance of the evaporator. The experimental data for LHPs with PTFE wicks are from the literature. The simulation results show that a PTFE wick can effectively reduce heat leakage, while an aluminum wick has better temperature uniformity and a lower casing temperature. However, wicks with large porosities have lower flow resistance. [ABSTRACT FROM AUTHOR]

By using the coupling method and the localization technique, we establish non-uniform gradient estimates for Markov semigroups of diffusions or stochastic differential equations driven by pure jump Lévy noises, where the coefficients only satisfy local monotonicity conditions. [ABSTRACT FROM AUTHOR]

Background: To investigate the construction situation, costs and charges associated with pharmacy intravenous admixture services (PIVAS) to provide references for the construction and development of PIVAS in mainland China.Methods: A multi-center cross-sectional survey was conducted via a WeChat Group targeting PIVAS leaders in hospitals to investigate the basic situation of PIVAS, including opening time, area, number of PIVAS, equipment, management mode, PIVAS costs and charges, as well as numbers of beds, open wards, and staff, and analyze differences in PIVAS construction at different provincial and hospital levels.Results: 137 questionnaires were collected from 29 provinces, representing a response rate of 99.3%. Most participants (88.4%) were from Level III Hospitals. The number of years of operations of PIVAS ranged from 1 to 22 (median: 6). PIVAS site area ranged between 100 and 1973 m2; daily average infusion volume was concentrated in the ranges 0-1000 bags (29.9%, 41/137) and 1001-2000 bags (26.3%, 36/137). In terms of PIVAS management mode, the vast majority used separate pharmacy management (65.0%, 89/137). Only 52.6% (72/137) of PIVAS have standardized charges, and 70.1% (96/137) operate at a loss. The median costs of mixed tumor chemotherapy drugs, total parenteral nutrition, general medicine, antibiotics were 20, 35, 4 and 5 RMB, respectively. With the exception of a few features, PIVAS construction does not obviously differ among different regions and hospital levels.Conclusions: In recent years, PIVAS in China has developed rapidly and become relatively large. The main problems are that most provinces lack standards for charges and PIVAS construction differs among hospitals. Therefore, standards for PIVAS construction and charges should be developed to provide a reference for the future development of PIVAS. [ABSTRACT FROM AUTHOR]

Quantitative measurement of the orbital soft tissue volume plays a very important role in the study of orbital diseases. The purpose of this study is to establish a computed tomography- (CT-) based three-dimensional (3D) reconstruction model and measure the orbital soft tissue volume in Chinese adults. We collected data from 103 Chinese adults (52 males and 51 females) who underwent orbital CT. The CT images of these adults were used to reconstruct a 3D model of the orbital bony cavity, orbital fat, extraocular muscle, and intraorbital optic nerve using Mimics software, and their respective volumes were measured. The mean (±SD) orbital bony cavity volume (OV), orbital fat volume (FV), extraocular muscle volume (MV), and intraorbital optic nerve volume (iONV) of the males were 22.2 ± 2.2 cm3, 8.9 ± 1.8 cm3, 1.9 ± 0.34 cm3, and 0.41 ± 0.08 cm3, respectively. The mean OV, FV, MV, and iONV of the females were 20.2 ± 1.5 cm3, 8.1 ± 1.7 cm3, 1.6 ± 0.3 cm3, and 0.36 ± 0.074 cm3, respectively, which were all significantly lower than those in males (all p<0.05). FV (r = 0.370; p<0.001) and MV (r = 0.283; p=0.007) were significantly correlated with body mass index (BMI), while iONV was not correlated with BMI (r = −0.070; p=0.480). This study shows that FV, MV, and iONV were higher in males than in females. With increasing BMI, FV and MV both increased, but iONV did not exhibit this trend. [ABSTRACT FROM AUTHOR]

Luminescent fluorinated chiral liquid crystalline oligomers containing Eu(III) complexes (Eu-LCOs) with good liquid crystalline properties and obvious luminescence properties were prepared using Poly(methylhydrogeno)siloxane (PMHS), chiral liquid crystalline monomer (M1), fluorinated liquid crystalline monomer (M2), fluorinated Eu(III) complex (M3). The chemical structures, liquid crystalline behaviours of Eu-LCOs were characterised by various experimental techniques. The introduction of small quantity of fluorinated Eu(III) complexes endowed the oligomers with excellent luminescence properties. The Eu(III) complexes did not change the liquid crystalline textures of the oligomers. Fourier transform infrared imaging showed that Eu(III) complexes were evenly distributed in oligomers. In order to express the mutual effect and distribution of the components, a structural representation of Eu-LCOs was established. The Eu-LCOs displayed wide mesophase temperature ranges and reversible mesomorphic phase transitions. The Eu-LCOs can emit soft red light when being excited. Luminescence intensities of Eu-LCOs gradually increased with an increase of Eu(III) complexes from 0 to 1.0 mol%. However, the luminescence intensities of Eu-LCOs decreased monotonically with the increase of temperature in liquid crystalline phase. [ABSTRACT FROM AUTHOR]

Introduction: Salivary adenoid cystic carcinoma (SACC) is a frequent type of salivary gland cancer which is characterized by slow growth but high incidence of distant metastasis. We aimed to identify therapeutic targets which are associated with metastasis of SACC.Material and Methods: Total RNA was isolated from a low metastatic SACC cell line (ACC-2) and a highly metastatic SACC cell line (ACC-M), which was screened from ACC-2 by combination of in vivo selection and cloning in vitro. Then the total RNA was subjected to microarray analysis. Differentially expressed genes (DEGs) were screened from ACC-M compared with ACC-2, followed by Gene Ontology function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Function annotation for DEGs also was performed. A protein-protein interaction network (PPI) was constructed for DEGs.Results: A total of 1128 DEGs were identified from ACC-M cells compared with ACC-2 cells. Both up- and down-regulated DEGs were enriched in different functions in biological process (BP), cellular component (CC) and molecular function (MF). Additionally, down-regulated DEGs were mainly enriched in "Apoptosis" and "Cytokine-cytokine receptor interaction" pathways which involved IFN-α1, NTRK1 and TGF-β1. In the PPI network, PIK3CA, PTPN11 and PIK3R1 had a number of nodes greater than 10.Conclusions: Transforming growth factor β1 might play a pivotal role during lung metastasis of SACC and be selected as a candidate target for treatment of metastatic SACC. IFNA1, NTRK1 and PIK3CA were also associated with tumor metastasis. [ABSTRACT FROM AUTHOR]

In this work, the η-Fe 2 O 3 nanospheres/diatomite composites (FNDCs) are prepared for the first time by a one-pot hydrothermal method, using the K 2 FeO 4 as iron source. Indeed, the η-Fe 2 O 3 can uniformly decorate the inner and outer surface of diatomite to form 3D porous structure. Such unique 3D structure and their high specific area are favorable to provide sufficient active sites for effective electrochemical reaction and enhance capacitive performances. In principle, these findings demonstrate that the low-cost η-Fe 2 O 3 modified diatomite structures are promising for energy storage and conversion application. [ABSTRACT FROM AUTHOR]

A previous study reported that Yi Guan Jian (YGJ) may increase the proliferation and differentiation of hepatic oval cells in a rat liver cirrhosis model. The aim of the present study was to investigate the effect and mechanism of action of YGJ on inducing hepatic differentiation in bone marrow‑derived mesenchymal stem cells (BM‑MSCs) via stromal‑cell derived factor‑1 (SDF‑1). Murine BM‑MSCs were isolated with whole bone marrow adherence, then identified by immunocytochemical staining and flow cytometry. Passage 2 cells were divided into 8 groups and their differentiation was induced by cell factors added to the medium, including hepatocyte growth factor (HGF), SDF‑1 and YGJ. Each of the cell factors was used alone and any two or three of them were combined to establish different cell microenvironments in the different treatment groups. Albumin (ALB) was selected as a hepatocellular marker and cytokeratin‑18 (CK‑18) as a cholangiocellular marker. The protein and mRNA expression levels of ALB and CK‑18 were used to determine the differentiation of BM‑MSCs using immunocytochemical staining, western blotting and reverse transcription‑quantitative polymerase chain reaction on days 7, 14, 21 and 28 during induction. The relative expression levels of ALB and CK‑18 resulted in time‑dependent increases in the groups supplemented only with HGF, SDF‑1 or YGJ. Combination treatment of any two HGF, SDF‑1 and YGJ led to a higher expression of ALB and CK‑18 compared with only one cell factor treatment. Additionally, when all three were used in a combined treatment the expression levels of ALB and CK‑18 occurred at an earlier time and was higher overall. Therefore, the present study suggested that YGJ had an effect on inducing hepatic differentiation in BM‑MSCs via SDF‑1 and may act in a synergistic manner with HGF and SDF‑1. [ABSTRACT FROM AUTHOR]

Yi Guan Jian decoction (YGD) may induce the differentiation of bone marrow mesenchymal stem cells (BMSCs) into hepatocyte-like cells (HLCs); however, the underlying mechanisms remain to be elucidated. The present study aimed to investigate this process. To do this, a dimethylnitrosamine (DMN)-induced liver cirrhosis mouse model was established. The mice from the model group were randomly divided into three subgroups: i) Negative control, ii) hepatocyte growth factor and iii) YGD. The overall health, liver function and histological alterations were monitored. The expression of a-smooth muscle actin (α-SMA), C-X-C chemokine receptor type 4 (CXCR4), extracellular signal-regulated kinase (ERK1/2), nuclear factor κB p65 subunit (NF-κB p65) and β-catenin were measured by immunohistochemistry, western blotting and reverse transcription-quantitative polymerase chain reaction. Following administration of DMN, the overall health of the mice significantly decreased, with an increase in pathological developments and liver damage resulting in a decrease in liver function. Immunohistochemistry revealed that the expression of α-SMA, CXCR4, ERK1/2, NF-κB p65 and β-catenin was upregulated. Following treatment with YGD, the overall health, liver function and pathology improved. The mRNA and protein expression levels of CXCR4 and ERK1/2 were upregulated, where as α-SMA, NF-κB p65 and β-catenin levels were downregulated. The results demonstrated that YGD may induce the differentiation of BMSCs into HLCs to reverse DMN-induced liver cirrhosis; this may be achieved via an upregulation of the SDF-1/CXCR4 axis to activate the mitogen activated protein kinase/ERK1/2 signaling pathway. [ABSTRACT FROM AUTHOR]

Diabetic nephropathy (DN) is characterized by increased macrophage infiltration, and proinflammatory M1 macrophages contribute to development of DN. Previous studies by us and others have reported that macrophage cyclooxygenase-2 (COX-2) plays a role in polarization and maintenance of a macrophage tissue-reparative M2 phenotype. We examined the effects of macrophage COX-2 on development of DN in type 1 diabetes. Cultured macrophages with COX-2 deletion exhibited an M1 phenotype, as demonstrated by higher inducible nitric oxide synthase and nuclear factor-κB levels but lower interleukin-4 receptor-α levels. Compared with corresponding wild-type diabetic mice, mice with COX-2 deletion in hematopoietic cells (COX-2 knockout bone marrow transplantation) or macrophages (CD11b-Cre COX2f/f) developed severe DN, as indicated by increased albuminuria, fibrosis, and renal infiltration of T cells, neutrophils, and macrophages. Although diabetic kidneys with macrophage COX-2 deletion had more macrophage infiltration, they had fewer renal M2 macrophages. Diabetic kidneys with macrophage COX-2 deletion also had increased endoplasmic reticulum stress and decreased number of podocytes. Similar results were found in diabetic mice with macrophage PGE2 receptor subtype 4 deletion. In summary, these studies have demonstrated an important but unexpected role for macrophage COX-2/prostaglandin E2/PGE2 receptor subtype 4 signaling to lessen progression of diabetic kidney disease, unlike the pathogenic effects of increased COX-2 expression in intrinsic renal cells. [ABSTRACT FROM AUTHOR]

Herpesviral hematopoietic necrosis caused by cyprinid herpesvirus-2 (CyHV-2) is highly prevalent in gibel carp (Carassius gibelio Bloch) and is associated with high mortality and great economic loss. Currently, no efficient methods of prevention and control of CyHV-2 infection are available. Increasing evidence suggests that antigen-specific egg yolk immunoglobulins (IgY) are highly effective against various pathogens in farmed fish. Therefore, the aim of this study was to develop a specific IgY against CyHV-2 infection in gibel carp. We first produced a recombinant D4ORFs protein that encodes four open reading frames of CyHV-2 and then generated specific IgY by immunizing laying hens with this protein. The eggs laid by immunized hens were processed into spray-dried egg powder containing D4ORFs IgY. The D4ORFs IgY showed high neutralizing activity in vitro against CyHV-2, as evidenced by a significant reduction in cytopathic effect in gibel carp brain cells cultured in the presence of the IgY antibodies. Whole-egg powder containing IgY specific to D4ORFs protein was incorporated into the basal diet at levels of 0, 0.1, 0.3, and 0.6% to prepare experimental diets for use in intervention studies in gibel carp. Another group received non-specific IgY. For preventive intervention, all fish were fed these experimental diets for 25 days before being immersion challenged with CyHV-2, after which the fish were switched to the basal diet for 21 days. For therapeutic intervention, fish were first challenged with CyHV-2 and then fed the diet with 0.6% D4ORFs IgY. Fish that received D4ORFs IgY prior to CyHV-2 challenge had significantly higher survival rates and significantly lower viral load in the trunk kidney compared to those that received non-specific IgY. Improved survival and reduced viral load were also observed in CyHV-2-challenged fish that received dietary supplementation of D4ORFs IgY. Hematological and serum biochemical analysis also showed improved health and enhanced antiviral defense in fish that received D4ORFs IgY. Overall, these findings demonstrated both preventive and therapeutic effects of anti-D4ORFs IgY against CyHV-2 infection. • D4ORFs encoded by four tandem ORFs of CyHV-2 showed high immunogenicity. • Anti-D4ORFs IgY can effectively neutralize CyHV-2 in vitro. • Dietary inclusion of anti-D4ORFs IgY improves survival in CyHV-2-infected gibel carp. • Anti-D4ORFs IgY is prophylactically and therapeutically effective against CyHV-2 infection. [ABSTRACT FROM AUTHOR]

Inhibition of prostaglandin (PG) production with either nonselective or selective inhibitors of cyclooxygenase-2 (COX-2) activity can induce or exacerbate salt-sensitive hypertension. This effect has been previously attributed to inhibition of intrinsic renal COX-2 activity and subsequent increase in sodium retention by the kidney. Here, we found that macrophages isolated from kidneys of high-salt-treated WT mice have increased levels of COX-2 and microsomal PGE synthase-1 (mPGES-1). Furthermore, BM transplantation (BMT) from either COX-2-deficient or mPGES-1-deficient mice into WT mice or macrophage-specific deletion of the PGE2 type 4 (EP4) receptor induced salt-sensitive hypertension and increased phosphorylation of the renal sodium chloride cotransporter (NCC). Kidneys from high-salt-treated WT mice transplanted with Cox2-/- BM had increased macrophage and T cell infiltration and increased M1- and Th1-associated markers and cytokines. Skin macrophages from high-salt-treated mice with either genetic or pharmacologic inhibition of the COX-2 pathway expressed decreased M2 markers and VEGF-C production and exhibited aberrant lymphangiogenesis. Together, these studies demonstrate that COX-2-derived PGE2 in hematopoietic cells plays an important role in both kidney and skin in maintaining homeostasis in response to chronically increased dietary salt. Moreover, these results indicate that inhibiting COX-2 expression or activity in hematopoietic cells can result in a predisposition to salt-sensitive hypertension. [ABSTRACT FROM AUTHOR]

Theisobaric vapor–liquid equilibrium data for binary systemsof 1,3,5-trichlorobenzene (1) + 3,5-dichloroaniline (2) and 3-chloroaniline(1) + 3,5-dichloroaniline (2) were measured experimentally under pressuresof 20.00, 60.00 and 101.20 kPa using an inclined ebulliometer. Thermodynamicconsistency of the vapor–liquid equilibrium data was testedby means of the Herington semiempirical method, and the isobaric vapor–liquidequilibrium data were correlated with three activity coefficient models,which were Wilson, NRTL and UNIQUAC. The energy interaction parameterswere acquired by a nonlinear least-squares regression method for thethree thermodynamic models. Results indicate that all the three activitycoefficient models can describe the measured isobaric vapor–liquiddata acceptably. The isobaric vapor–liquid equilibrium datadetermined in the present work are important in the design and operationfor purification of 3,5-dichloroaniline by distillation. [ABSTRACT FROM AUTHOR]

Normal intestinal microbiota play an essential role in host health, whereas intestinal dysbiosis is closely associated with a variety of inflammatory diseases. It has been confirmed that the use of antibiotics can induce intestinal dysbiosis in fish. However, it is not clear whether intestinal dysbiosis affects the susceptibility of farmed fish to bacterial infection. In this study, a grass carp model of antibiotic-induced intestinal dysbiosis (AID) was used in challenge experiments to determine the susceptibility to bacterial infection. AID fish were challenged by either immersion or anal intubation with a virulent strain of Aeromonas hydrophila. After immersion challenge, AID fish developed prominent inflammatory symptoms and showed high mortality compared with controls. In immersion-challenged AID fish, the bacterial load in blood and intestinal contents was significantly higher. The immersion challenge also resulted in a significant reduction in the spleen index of AID fish. Histological examination showed severe injury in the intestine, liver, and spleen occurred in immersion-challenged AID fish. Furthermore, AID fish had significantly higher mRNA levels of il1β , il6 and il17a/f1 , and lower levels of il17n , il23r and tnfα in intestinal tissue than control fish. Overall, our results indicate that the susceptibility of grass carp to A. hydrophila infection increased due to intestinal dysbiosis. Therefore, intestinal dysbiosis can be proposed as a risk factor for severe bacterial infection in cultured fish. • Susceptibility to A. hydrophila infection increased in grass carp with intestinal dysbiosis. • Immersion challenge caused high mortality in fish with intestinal dysbiosis. • Immersion and anal intubation evoked different inflammatory responses, regardless of microbiota status. [ABSTRACT FROM AUTHOR]

Normal intestinal microbiota play an essential role in host health, whereas intestinal dysbiosis is closely associated with a variety of inflammatory diseases. It has been confirmed that the use of antibiotics can induce intestinal dysbiosis in fish. However, it is not clear whether intestinal dysbiosis affects the susceptibility of farmed fish to bacterial infection. In this study, a grass carp model of antibiotic-induced intestinal dysbiosis (AID) was used in challenge experiments to determine the susceptibility to bacterial infection. AID fish were challenged by either immersion or anal intubation with a virulent strain of Aeromonas hydrophila. After immersion challenge, AID fish developed prominent inflammatory symptoms and showed high mortality compared with controls. In immersion-challenged AID fish, the bacterial load in blood and intestinal contents was significantly higher. The immersion challenge also resulted in a significant reduction in the spleen index of AID fish. Histological examination showed severe injury in the intestine, liver, and spleen occurred in immersion-challenged AID fish. Furthermore, AID fish had significantly higher mRNA levels of il1β , il6 and il17a/f1 , and lower levels of il17n , il23r and tnfα in intestinal tissue than control fish. Overall, our results indicate that the susceptibility of grass carp to A. hydrophila infection increased due to intestinal dysbiosis. Therefore, intestinal dysbiosis can be proposed as a risk factor for severe bacterial infection in cultured fish. • Susceptibility to A. hydrophila infection increased in grass carp with intestinal dysbiosis. • Immersion challenge caused high mortality in fish with intestinal dysbiosis. • Immersion and anal intubation evoked different inflammatory responses, regardless of microbiota status. [ABSTRACT FROM AUTHOR]

Renal tubule epithelia represent the primary site of damage in acute kidney injury (AKI), a process initiated and propagated by the infiltration of macrophages. Here we investigated the role of resident renal macrophages and dendritic cells in recovery from AKI after ischemia/reperfusion (I/R) injury or a novel diphtheria toxin-induced (DT-induced) model of selective proximal tubule injury in mice. DT-induced AKI was characterized by marked renal proximal tubular cell apoptosis. In both models, macrophage/dendritic cell depletion during the recovery phase increased functional and histologic injury and delayed regeneration. After I/R-induced AKI, there was an early increase in renal macrophages derived from circulating inflammatory (M1) monocytes, followed by accumulation of renal macrophages/dendritic cells with a wound-healing (M2) phenotype. In contrast, DT-induced AKI only generated an increase in M2 cells. In both models, increases in M2 cells resulted largely from in situ proliferation in the kidney. Genetic or pharmacologic inhibition of macrophage colony-stimulating factor (CSF-1) signaling blocked macrophage/dendritic cell proliferation, decreased M2 polarization, and inhibited recovery. These findings demonstrated that CSF-1-mediated expansion and polarization of resident renal macrophages/dendritic cells is an important mechanism mediating renal tubule epithelial regeneration after AKI. [ABSTRACT FROM AUTHOR]

The kidney has a local intrarenal dopaminergic system, and in the kidney, dopamine modulates renal hemodynamics, inhibits salt and fluid reabsorption, antagonizes the renin-angiotensin system, and inhibits oxidative stress. The current study examined the effects of alterations in the intrarenal dopaminergic system on kidney structure and function in models of type 1 diabetes. We studied catechol-O-methyl-transferase (COMT-/-) mice, which O have increased renal dopamine production due to decreased dopamine metabolism, and renal transplantation was used to determine whether the effects seen with COMT deficiency were kidney-specific. To determine the effects of selective inhibition of intrarenal dopamine production, we used mice with proximal tubule deletion of aromatic amino acid decarboxylase (ptAADC-/- ). Compared with wild-type diabetic mice, COMT-/- mice had decreased hyperfiltration, decreased macula densa cyclooxygenase-expression, decreased albuminuria, decreased glomerulopathy, and inhibition of expression of markers of in ammation, oxidative stress, and fibrosis. These differences were also seen in diabetic mice with a transplanted kidney from COMT-/- mice. In contrast, diabetic ptAADC-/- mice had increased nephropathy. Our study demonstrates an important role of the intrarenal dopaminergic system to modulate the development and progression of diabetic kidney injury and indicate that the decreased renal dopamine production may have important consequences in the underlying pathogenesis of diabetic nephropathy. [ABSTRACT FROM AUTHOR]

It is well-recognized that excessive angiotensin II (ANG II) can mediate progressive renal injury. Previous studies by us and others have indicated that dopamine may modulate actions of ANG II in the kidney. The current studies investigated whether altering intrarenal dopamine levels affected ANG II-mediated renal fibrosis. We utilized a model of increased intrarenal dopamine, catechol-O-methyl-transferase knockout (COMT KO) mice, which have increased kidney dopamine levels due to deletion of a major intrarenal dopaminemetabolizing enzyme. In wild-type mice, chronic ANG II infusion increased renal expression of both of the major dopamine-metabolizing enzymes, COMT and monoamine oxidase. After 8 wk of ANG II infusion, there were no significant differences in blood pressure between wild-type and COMT KO mice. Compared with wild-type, COMT KO mice had decreased albuminuria and tubulointerstitial injury. In response to ANG II infusion, there was decreased expression of both glomerular and tubulointerstitial injury markers (fibronectin, connective tissue growth factor, fibroblast-specific protein- 1, collagen I, podocyte vascular endothelial growth factor) in COMT KO mice. We recently reported that ANG II-mediated tubulointerstitial fibrosis is mediated by src-dependent epidermal growth factor receptor (EGFR) activation. In aromatic L-amino acid decarboxylase knockout (AADC KO) mice, a model of intrarenal dopamine deficiency due to selective proximal tubule AADC deletion, which inhibits intrarenal dopamine synthesis, ANG II infusion further increased expression of p-src and pTyr845-EGFR. In contrast, their expression was markedly attenuated in COMT KO mice. These results demonstrate a role for intrarenal dopamine to buffer the detrimental effects of ANG II upon the kidney. [ABSTRACT FROM AUTHOR]

Graceful labelling is studied on undirected graphs since graceful graphs can be used in some H-decomposition problems. In this note, we investigate the directed graceful problem for many orientations of undirected trees with short diameters, and provide some directed trees that deny any digraceful labelling. [ABSTRACT FROM AUTHOR]

Abstract: The first organic-templated Ba(II) perchlorate with open architecture, [(C6H8N)2Ba(ClO4)4] n (1), has been synthesized in the presence of 3-methylpyridine (3-MP) under hydrothermal conditions. The compound 1 was characterized by single crystal X-ray diffraction, elemental analysis, IR, powder XRD, 1H NMR, TGA and fluorescence spectra. The 12-coordinate Ba(II) ion was located in the center of the irregular icosahedral (BaO12) cage. Then the icosahedral BaO12 cages and the linkers joined together to form a (4, 4) topology. And the protonated amine molecules were residing in the interlamellar space of the inorganic macro-anionic topology layers in the aAa mode (a=amine, A=anionic layer). The N–H⋯O hydrogen bonds ensure the stability of the structure by mounted the organic molecules to the main body of the inorganic framework. The solid-state fluorescence spectrum of complex 1 exhibits broad emission at 381nm at room temperature, which is stronger than the free MPP (MPP=3-methylpyridinium perchlorate). In addition, the two different synthesis methods provide an effectual impetus about applying hydrothermal reaction chemistry to build novel structures. [Copyright &y& Elsevier]

In addition to its role as an essential neurotransmitter, dopamine serves important physiologic functions in organs such as the kidney. Although the kidney synthesizes dopamine through the actions of aromatic amino acid decarboxylase (AADC) in the proximal tubule, previous studies have not discriminated between the roles of extrarenal and intrarenal dopamine in the overall regulation of renal function. To address this issue, we generated mice with selective deletion of AADC in the kidney proximal tubules (referred to herein as ptAadc-/- mice), which led to selective decreases in kidney and urinary dopamine. The ptAadc-/- mice exhibited increased expression of nephron sodium transporters, decreased natriuresis and diuresis in response to l-dihydroxyphenylalanine, and decreased medullary COX-2 expression and urinary prostaglandin E2 excretion and developed salt-sensitive hypertension. They had increased renin expression and altered renal Ang II receptor (AT) expression, with increased AT1b and decreased AT2 and Mas expression, associated with increased renal injury in response to Ang II. They also exhibited a substantially shorter life span compared with that of wild-type mice. These results demonstrate the importance of the intrarenal dopaminergic system in salt and water homeostasis and blood pressure control. Decreasing intrarenal dopamine subjects the kidney to unbuffered responses to Ang II and results in the development of hypertension and a dramatic decrease in longevity. [ABSTRACT FROM AUTHOR]

Solubility data for the ternary p-nitrobenzoic acid + m-nitrobenzoic acid +ethanol system were measured at 273.1 K, 283.1 K, and 313.1 K, respectively. Three isothermal phase diagrams of the system were constructed on the basis of the measured solubilitities. Two solid phases, m-nitrobenzoic acid and p-nitrobenzoic acid, were formed and confirmed by Schreinemaker’s wet residue method. The crystallization regions of m-nitrobenzoic acid and p-nitrobenzoic acid increase as the temperature decreases. At different temperature, the crystallization region of p-nitrobenzoic acid is larger than that of m-nitrobenzoic acid. [ABSTRACT FROM AUTHOR]

Yao B, Xu J, Harris RC, Zhang M-Z. Renal localization and regulation of 15-hydroxyprostaglandin dehydrogenase. Am J Physiol Renal Physiol 294: F433-F439, 2008. First published December 5, 2007; doi: 10.1152/ajprenal.00436.2007.—Tissue prostaglandin levels are determined by both biosynthesis and catabolism. The current studies report the expression and localization of 15-hydroxyprostaglandin dehydrogenase (15-PGDH), a key enzyme in prostaglandin catabolism in the kidneys. We also investigated potential interactions between 15-PGDH and cyclooxygenase (COX), a key enzyme in prostaglandin biosynthesis. Both 15-PGDH mRNA and protein levels were significantly higher in kidney cortex than in papilla, which is opposite to the expression pattern of COX-2. In situ hybridization indicated that 15-PGDH mRNA was mainly localized to the tubular epithelial cells in kidney cortex and outer medulla but not in the glomerulus or papilla. Dual immunofluorescent staining indicated that 15-PGDH was expressed in the proximal tubule, cortical, and outer medullary thick ascending limb and collecting duct but not in the macula densa or papilla. 15-PGDH levels were significantly lower in a macula densa cell line (MMDD1) than in a proximal tubule cell line. Although a high-salt diet decreased COX-2 expression in macula densa, it increased macula densa 15-PGDH expression in both mouse and rat kidneys. In MMDDI cells, a COX-2 inhibitor increased 15-PGDH, whereas a COX-1 inhibitor had no effect. Furthermore, intense 15-PGDH immunofluorescent staining was found in both macula densa and glomerulus in COX-2 knockout mice. The intrare- nal distribution of 15-PGDH and its interactions with COX-2 suggest that differential regulation of COX-2 and 15-PGDH may play an important role in determining levels of prostaglandins involved in regulation of salt, volume, and blood pressure homeostasis. [ABSTRACT FROM AUTHOR]

Serotonin [5-hydroxytryptamine (5HT)] acts through multiple G protein-coupled 5-HT receptors, and its activity is also regulated by the 5-HT transporter. The current studies report the expression and localization of the 5-HT receptors and transporter in the kidney. In addition, the enzymatic pathway mediating 5-HT synthesis is present in renal cortex, especially in the proximal tubules and glomerular epithelial cells and mesangial cells. Expression of the 5-HT receptors and 5-HT transporter was detected by RT-PCR in cell lines of these cell types. In cultured proximal tubule cells and podocytes, 5-HT activated ERK1/2 and increased the expression of connective tissue growth factor and transforming growth factor-β, two key mediators of extra-cellular matrix accumulation. Immunohistochemistry and real-time RT-PCR studies also indicated that 5-HT stimulated expression of vascular endothelial growth factor in podocytes in vitro and in vivo. Therefore, these results indicate the presence of an integrated intrarenal serotonergic system and suggest a possible role for 5-HT as a mediator of renal fibrosis in the kidney. [ABSTRACT FROM AUTHOR]

The tidal bore at the estuary of the Qiantang River in China is one of the most spectacular bores in the world. Although it is a famous scenic spot, it may cause disasters due to its destructive power. In this paper, a new numerical model, based on a Godunov-type scheme with the water level–bottom topography formulation combined with the improved wet/dry techniques, is constructed to numerically simulate the tidal bore on the Qiantang River. The simulated results using the model agree well with observed data, which shows that the model can reproduce the formation, evolution, and dissipation of the tidal bore on the Qiantang River. [ABSTRACT FROM AUTHOR]

Macula densa cyclooxygenase 2 (COX-2)-derived prostaglandins serve as important modulators of the renin-angiotensin system, and cross-talk exists between these two systems. Cortical COX-2 induction by angiotensin-converting enzyme (ACE) inhibitors or AT1 receptor blockers (ARBs) suggests that angiotensin II may inhibit cortical COX-2 by stimulating the AT1 receptor pathway. In the present studies we determined that chronic infusion of either hypertensive or nonhypertensive concentrations of angiotensin II attenuated cortical COX-2. Angiotensin II infusion reversed cortical COX-2 elevation induced by ACE inhibitors. However, we found that angiotensin II infusion further stimulated cortical COX-2 elevation induced by ARBs, suggesting a potential role for an AT2 receptor-mediated pathway when the AT1 receptor was inhibited. Both WT and AT2 receptor knockout mice were treated for 7 days with either ACE inhibitors or ARBs. Cortical COX-2 increased to similar levels in response to ACE inhibition in both knockout and WT mice. In WT mice ARBs increased cortical COX-2 more than ACE inhibitors, and this stimulation was attenuated by the AT2 receptor antagonist PD123319. In the knockout mice ARBs led to significantly less cortical COX-2 elevation, which was not attenuated by PD123319. PCR confirmed AT1a and AT2 receptor expression in the cultured macula densa cell line MMDD1. Angiotensin II inhibited MMDD1 COX-2, and CGP42112A, an AT2 receptor agonist, stimulated MMDD1 COX-2. In summary, these results demonstrate that macula densa COX-2 expression is oppositely regulated by AT1 and AT2 receptors and suggest that AT2 receptor-mediated cortical COX-2 elevation may mediate physiologic effects that modulate AT1-mediated responses. [ABSTRACT FROM AUTHOR]

Renal cortical cyclooxygenase-2 (COX-2) is restricted to the macula densa and adjacent cortical thick ascending limbs (MD/cTALH). Renal cortical COX-2 increases in response to diabetes and renal ablation, both of which are characterized by hyperfiltration and reduced NaCI delivery to the MD due to increased proximal NaCI reabsorption. High-protein intake also induces hyperfiltration and decreases NaCI delivery to the MD due to increased NaCI reabsorption proximally. We investigated whether high protein induces cortical COX-2 and whether cortical COX-2 contributes to high protein-induced hyperfiltration and increased intrarenal renin biosynthesis. Cortical COX-2 increased after protein loading but decreased after protein restriction. COX-2 inhibition attenuated high protein-induced hyperfiltration but had no effect on high protein-induced intrarenal renin elevation. Therefore, induction of cortical COX-2 contributed to high protein-induced hyperfiltration but not intrarenal renin elevation. In the kidney cortex, neuronal nitric oxide synthase (nNOS) is also localized to the MD, and interactions between intrarenal nNOS and COX-2 systems have been proposed. Cortical COX-2 elevation seen in salt restriction was blocked by nNOS inhibiton. Cortical nNOS expression also increased after protein loading, and inhibition of nNOS activity completely reversed high protein-induced cortical COX-2 elevation and hyperfiltration. These results indicate that NO is a mediator of high protein-induced cortical COX-2 elevation and suggest that both intrarenal nNOS and COX-2 systems appear to regulate afferent arteriolar tone and subsequent hyperfiltration seen in high-protein intake. [ABSTRACT FROM AUTHOR]

To investigate the potential role of allelopathy in plant interference and in the successful invasion of alien species Solidago canadensis, aqueous and ethanolic extracts from rhizomes, stems and leaves of S. canadensis were prepared and used as treatment solutions to assess their effects on seed germination and seedling growth in four target species, mulberry (Morus alba); morning glory (Pharbitis nil), wheat (Triticum aestivum) and rape (Brassica campestris). Reduction and/or growth in germination and growth of the target plant species in the presence of both aqueous and ethanolic extracts at different concentrations indicated that the responses were species-specific and concentration-dependent. Generally, ethanolic extracts (especially from leaves) imposed stronger effects on both seed germination and seedling growth. Extracts with lower concentration at 0.001 g/ml dw could stimulate the seedling growth of rape and morning glory, whereas extracts at any given concentrations have inhibitory effects on wheat and mulberry. It is suggested that the aqueous and ethanolic extracts of all the three parts of S. canadensis have significant allelopathic effects. Although both inhibition and stimulation occurred in the germination and growth of the target species, extracts with higher concentrations definitely inhibit seed germination and seedling growth of all target plants. We suggest that allelopathy plays a more important role than other mechanisms do in the out-competition of S. canadensis over other plants, and make it invasive in new habitats. [ABSTRACT FROM AUTHOR]

Top-emitting organic light-emitting diodes (OLEDs) using aluminium (Al) and nickel (Ni) as the anode and Al as the semitransparent cathode were developed. Hole injection was largely improved by spin coating poly(ethylenedioxythiophene): poly(styrenesulfonate) (PEDOT) on the metal anode. For top-emitting OLEDs with a configuration of metal anode/PEDOT/NPB/Alq3/LiF/Al/Alq3, both devices using Al and Al/Ni anodes showed efficient green light emission with a narrow emission peak. Current efficiency was increased from 4.32 cd A-1 to 6.45 cd A-1 when replacing high work function Ni with low work function Al as the anode. A luminance of 20 000 cd m-2 can be achieved for these top-emitting OLEDs. The device made with the Al/Ni anode showed a low driving voltage and high power efficiency as compared to that made with the Al anode. The improvement on light-emitting efficiency was attributed to balanced charge carrier injection and utilization of the high reflective semitransparent Al cathode. [ABSTRACT FROM AUTHOR]

The syndrome of apparent mineralocorticoid excess (SAME) is an autosomal recessive form of salt-sensitive hypertension caused by deficiency of the kidney type 2 11β-hydroxy steroid dehydrogenase (11βHSD2). In this disorder, cortisol is not inactivated by 11βHSD2, occupies mineralocorticoid receptors (MRs), and causes excessive sodium retention and hypertension. In renal medulla, prostaglandins derived from cyclooxygenase-2 (COX-2) stimulate sodium and water excretion. and renal medullary COX-2 expression increases after mineralocorticoid administration. We investigated whether medullary COX-2 also increases in rats with 11βHSD2 inhibition and examined its possible role in the development of hypertension. 11βHSD2 inhibition increased medullary and decreased cortical COX-2 expression in adult rats and induced high blood pressure in high-salt-treated rats. COX-2 inhibition had no effect on blood pressure in control animals but further increased blood pressure in high-salt-treated rats with 11βHSD2 inhibition. COX-1 inhibition had no effect on blood pressure in either control or experimental animals. 11βHSD2 inhibition also led to medullary COX-2 increase and cortical COX-2 decrease in weaning rats, primarily through activation of MRs. In the suckling rats, medullary COX-2 expression was very low, consistent with a urinary concentrating defect. 11βHSD2 inhibition had no effect on either cortical or medullary COX-2 expression in the suckling rats, consistent with low levels of circulating corticosterone in these animals. These data indicate that COX-2 plays a modulating role in the development of hypertension due to 11βHSD2 deficiency and that 11βHSD2 regulates renal COX-2 expression by preventing glucocorticoid access to MRs during postnatal development. [ABSTRACT FROM AUTHOR]

In mammalian kidney, dopamine produced in the proximal tubule (PT) acts as an autocrine/paracrine natriuretic hormone that inhibits salt and fluid reabsorption in the PT. In high-salt-treated animals, PT dopamine activity increases and inhibits reabsorption, leading to increased salt and fluid delivery to the macula densa (MD) and subsequent natriuresis and diuresis. Regulated cyclooxygenase-2 (COX-2) in the MD represents another Intrinsic system mediating renal salt and water homeostasis. Renal cortical COX-2 is inversely related to salt intake, and decreased extracellular NaCl stimulates COX-2 expression in cultured MD/cortical thick ascending limb cells. The current study investigated interactions between renal dopamine and cortical COX-2 systems. In rats fed a control diet, the dopamine precursor L-dihydroxyphenylalanine (L-DOPA) or the DA1 receptor agonist SKF-81297 suppressed cortical COX-2 expression. High salt suppressed conical COX-2 expression, which was attenuated by inhibition of dopamine production with benserazide or the DA1 receptor antagonist, SCH-23390. In contrast, L-DOPA or the dopamine-metabolizing enzyme inhibitor entacapone suppressed low-salt-induced conical COX-2 expression. Inhibition of PT reabsorption with the carbonic anhydrase inhibitor acetazolamide suppressed cortical COX-2 expression. In contrast, treatment with distally acting diuretics led to elevation of cortical COX-2. These results indicate that dopamine modulates renal cortical COX-2 expression by modifying PT reabsorption. [ABSTRACT FROM AUTHOR]

Purpose: A major issue in analysis of experimental results after spinal cord injury is spontaneous functional recovery induced by remaining nerve fibers. The authors investigated the relationship between the degree of locomotor recovery and the percentage and location of the fibers that spared spinal cord transection.Methods: The spinal cords of 12 adult rats were transected at T9 with a razor blade, which often resulted in sparing of nerve fibers in the ventral spinal cord. The incompletely-transected animals were used to study the degree of spontaneous recovery of hindlimb locomotion, evaluated with the BBB rating scale, in correlation to the extent and location of the remaining fibers.Results: Incomplete transection was found in the ventral spinal cord in 42% of the animals. The degree of locomotor recovery was highly correlated with the percentage of the remaining fibers in the ventral and ventrolateral funiculi. In one of the rats, 4.82% of remaining fibers in unilateral ventrolateral funiculus were able to sustain a certain recovery of locomotion.Conclusions: Less than 5% of remaining ventrolateral white matter is sufficient for an unequivocal motor recovery after incomplete spinal cord injury. Therefore, for studies with spinal cord transection, the completeness of sectioning should be carefully checked before any conclusion can be reached. The fact that the degree of locomotor recovery is correlated with the percentage of remaining fibers in the ventrolateral spinal cord, exclusive of most of the descending motor tracts, may imply an essential role of propriospinal connections in the initiation of spontaneous locomotor recovery. [ABSTRACT FROM AUTHOR]

Examines the use of robust scene-change detection method for video segmentation. Consideration of intensity and motion information to detect scene changes; Development of novel intensity statistics model; Segmentation of video sequence into shots.

Intestinal microbiota has increasingly been recognized as a major determinant of host health due to its critical role in the maintenance of immune homeostasis. An experimental fish model with disrupted intestinal microbiota allows us to identify potential strategies for restoring or modulating microbiota composition. The aim of this study was to develop a reliable grass carp model with disrupted intestinal microbiota by treatment with an antibiotic cocktail consisting of vancomycin, enrofloxacin, florfenicol, and metronidazole at different concentrations. To identify the appropriate concentration and exposure time of antibiotic treatment required to disrupt intestinal microbiota, five antibiotic regimens were compared in terms of their effects on intestinal microbiota composition, growth and health status, and histological changes in the intestine, hepatopancreas, and spleen. Antibiotic-induced changes in the expression of inflammation- and apoptosis-related genes in grass carp intestines were also examined. The results revealed that the highest antibiotic concentration over a 28 day period was required to disrupt both luminal and mucosal microbiota through significant expansion of Proteobacteria and suppression of Fusobacteria. Treatment with this regimen induced significant down-regulation of caspase-8, MLCK, ZO-1, IL-17N, and IL-23R, and up-regulation of IL-1β and IL-6 in the intestine, suggesting possible effects on intestinal epithelial tight junction and inflammatory conditions. This treatment did not produce substantial histopathological changes, and was not directly detrimental to growth and health. Therefore, this antibiotic regimen may provide a suitable option to disrupt intestinal microbiota in grass carp. In addition, our study also implies that fish may serve as a promising model for investigating growth-promoting effects of antibiotics, when treated with antibiotics in low doses. • Antibiotic treatment did not affect alpha diversity of the luminal microbiota. • Antibiotic exposure duration matters more than concentration in disrupting microbiota. • The microbiota composition differed substantially between intestinal content and mucosa. • The growth-promoting effect of low-dose antibiotics was confirmed in grass carp. [ABSTRACT FROM AUTHOR]

[Display omitted] • 20E stimulates the expression of LdFoxO. • Silencing LdFoxO represses 20E signaling and reduces larval weight. • RNAi of LdFoxO impairs larva-pupa-adult transition. • 20E or JH consumption cannot restore defects in LdFoxO depleted animals. Forkhead box O (FoxO) protein, a major downstream transcription factor of insulin/insulin-like growth factor signaling/target of rapamycin pathway (IIS/TOR), is involved in the regulation of larval growth and the determination of organ size. FoxO also interacts with 20-hydroxyecdysone (20E) and juvenile hormone (JH) signal transduction pathways, and hence is critical for larval development in holometabolans. However, whether FoxO plays a critical role during larval metamorphosis needs to be further determined in Leptinotarsa decemlineata. We found that 20E stimulated the expression of LdFoxO. RNA interference (RNAi)-aided knockdown of LdFoxO at the third-instar stage repressed 20E signaling and reduced larval weight. Although the resultant larvae survived through the third-fourth instar ecdysis, around 70% of the LdFoxO depleted moribund beetles developmentally arrested at prepupae stage. These LdFoxO depleted beetles were completely wrapped in the larval exuviae, gradually darkened and finally died. Moreover, approximately 12% of the LdFoxO RNAi beetles died as pharate adults. Ingestion of either 20E or JH by the LdFoxO depletion beetles excessively rescued the corresponding hormonal signals, but could not alleviate larval performance and restore defective phenotypes. Therefore, FoxO plays an important role in regulation of larval-pupal-adult transformation in L. decemlineata , in addition to mediation of IIS/TOR pathway and stimulation of ecdysteroidogenesis. [ABSTRACT FROM AUTHOR]

Database machine architectures have been proposed as a promising alternative to improve database system performance, control, and flexibility. While many claims have been made for the database machine concept, few studies have been made to test the performance advantages and disadvantages of a database machine in an application environment. A comprehensive benchmark study comparing the performance of database systems on a conventional computer system and a database machine is reported in this paper. The results show the database machine architecture to have superior performance in most cases. The performance advantage is sensitive to the communication line speed between the host computer and the database machine. The effects of line speed are studied and displayed in the benchmark results. A summary of the similarities and differences between the architectures based upon our benchmark results completes the paper. [ABSTRACT FROM AUTHOR]

The genomic and coding sequences of four members of grass carp interleukin (IL)-17 cytokine family, IL-17A/F2, IL-17A/F3, IL-17C and IL-17N, were isolated using rapid amplification of cDNA ends and conventional PCR techniques. A phylogenetic analysis showed that grass carp IL-17 family genes, including previously identified IL-17A/F1 and IL-17D, clustered with their counterparts from other fish species. IL-17D had two exons and one intron, while all the other members were composed of three exons and two introns. A multiple sequence alignment revealed that grass carp IL-17 family cytokines shared a cystine-knot motif that was highly conserved in mammals. A quantitative real-time PCR analysis revealed that these genes were expressed in the different examined tissues at varying levels. Moreover, they displayed different tissue expression patterns in fish at 24 h after intraperitoneal injection (IP) or anal intubation (AI) of Aeromonas hydrophila , implying roles in inflammatory responses. Next, we compared disease activity status and histopathological changes in intestinal tissues over a 7 day period after IP or AI, and then examine the potential differential effects of different infection routes on the expression profiles of IL-17 family genes in inflamed intestinal tissues. The intraperitoneal route resulted in more pronounced pathological symptoms than the anal route in terms of the disease activity index (DAI). Changes in the DAI highly coincided with the severity of intestinal inflammation. The two infection routes resulted in differential IL-17 family gene expression patterns over time in grass carp intestine, which suggests that IL-17 family members may play differential roles in mucosal and systemic immune responses and that IL-17N and IL-17A/F1 might possibly function as pro-inflammatory cytokines that provide defense against bacterial infection in grass carp intestine. • Grass carp IL-17A/F2, IL-17A/F3, IL-17C and IL-17 N sequences were isolated. • Most grass carp IL-17 family genes exhibited an identical exon-intron structure. • Grass carp IL-17 family cytokines contained a cystine-knot motif found in mammals. • Tissue expression patterns of IL-17 family genes differed after bacterial infection. • IL-17 family members had unique roles in mucosal and systemic immune responses. [ABSTRACT FROM AUTHOR]

The long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) is involved in a variety of human cancers. Two overlapping NEAT1 isoforms, NEAT1_1 and NEAT1_2, are produced through mutually exclusive alternative 30 end formation. Previous studies extensively investigated NEAT1 dysregulation in tumors, but often failed to achieve distinct quantification of the two NEAT1 isoforms. Moreover, molecular mechanisms governing the biogenesis of NEAT1 isoforms and the functional impacts of their dysregulation in tumorigenesis remain poorly understood. In this study, we employed an isoform-specific quantification assay and found differential dysregulation of NEAT1 isoforms in patient-derived glioblastoma multiforme cells. We further showed usage of the NEAT1 proximal polyadenylation site (PAS) is a critical mechanism that controls glioma NEAT1 isoform production. CRISPRCas9–mediated PAS deletion reduced NEAT1_1 and reciprocally increased NEAT1_2, which enhanced nuclear paraspeckle formation in human glioma cells. Moreover, the utilization of the NEAT1 PAS is facilitated by the RNA-binding protein quaking (QKI), which binds to the proximal QKI recognition elements. Functionally, we identified transcriptomic changes and altered biological pathways caused by NEAT1 isoform imbalance in glioma cells, including the pathway for the regulation of cell migration. Finally, we demonstrated the forced increase of NEAT1_2 upon NEAT1 PAS deletion is responsible for driving glioma cell migration and promoting the expression of genes implicated in the regulation of cell migration. Together, our studies uncovered a novel mechanism that regulates NEAT1 isoforms and their functional impacts on the glioma transcriptome, which affects pathological pathways of glioma, represented by migration. [ABSTRACT FROM AUTHOR]

Background: During disc degeneration, inflammatory cytokine tumor necrosis factor (TNF)-α is correlated with nucleus pulposus (NP) cell apoptosis. Transforming growth factor (TGF)-β1 has the potential to regenerate degenerative disc. Objective: To investigate the protective role of TGF-β1 against TNF-α-mediated NP cell apoptosis and the underlying mechanism. Methods: Rat NP cells were treated with TNF-α (100 ng/ml) for 48 h. TGF-β1 was added into the culture medium to investigate its protective effects against TNF-α-induced NP cell apoptosis. Exogenous FasL was used to investigate the potential role of the Fas/FasL pathway in this process. Flow cytometry assay was used to analyze NP cell apoptosis. Real-time PCR andWestern blotting were used to analyze gene and protein expression of apoptosis-related molecules. Results: In TNF-α-treated NP cells, TGF-β1 significantly decreased NP cell apoptosis, declined caspase-3 and -8 activity, and decreased expression of Bax and caspase-3 (cleaved-caspase-3) but increased expression of Bcl-2. However, exogenous FasL partly reversed these effects of TGF-β1 in NP cells treated with TNF-α. Additionally, expression of Fas and FasL in TNF-α-treated NP cells partly decreased by TGF-β1, whereas exogenous FasL increased expression of Fas and FasL in NP cells treated with TGF-β1 and TNF-α. Conclusion: TGF-β1 helps to inhibit TNF-α-induced NP cell apoptosis and the Fas/FasL pathway may be involved in this process. The present study suggests that TGF-β1 may be effective to retard inflammation-mediated disc degeneration. [ABSTRACT FROM AUTHOR]

The RNA exosome is a ribonuclease complex that mediates both RNA processing and degradation. This complex is evolutionarily conserved, ubiquitously expressed, and required for fundamental cellular functions, including rRNA processing. The RNA exosome plays roles in regulating gene expression and protecting the genome, including modulating the accu-mulation of RNA-DNA hybrids (R-loops). The function of the RNA exosome is facilitated by cofactors, such as the RNA helicase MTR4, which binds/remodels RNAs. Recently, missense mutations in RNA exosome subunit genes have been linked to neurological diseases. One possibility to explain why missense mutations in genes encoding RNA exosome subunits lead to neurological diseases is that the complex may interact with cell- or tissue-specific cofactors that are impacted by these changes. To begin addressing this question, we performed immunoprecipitation of the RNA exosome subunit, EXOSC3, in a neuronal cell line (N2A), followed by proteomic analyses to identify novel interactors. We identified the putative RNA helicase, DDX1, as an interactor. DDX1 plays roles in doublestrand break repair, rRNA processing, and R-loop modulation. To explore the functional connections between EXOSC3 and DDX1, we examined the interaction following doublestrand breaks and analyzed changes in R-loops in N2A cells depleted for EXOSC3 or DDX1 by DNA/RNA immunoprecipitation followed by sequencing. We find that EXOSC3 interaction with DDX1 is decreased in the presence of DNA damage and that loss of EXOSC3 or DDX1 alters R-loops. These results suggest EXOSC3 and DDX1 interact during events of cellular homeostasis and potentially suppress unscrupulous expression of genes promoting neuronal projection. [ABSTRACT FROM AUTHOR]

Aerobic glycolysis, a phenomenon known historically as the Warburg effect, is one of the hallmarks of cancer cells. In this study, we characterized the role of BAG3 in aerobic glycolysis of pancreatic ductal adenocarcinoma (PDAC) and its molecular mechanisms. Our data show that aberrant expression of BAG3 significantly contributes to the reprogramming of glucose metabolism in PDAC cells. Mechanistically, BAG3 increased Hexokinase 2 (HK2) expression, the first key enzyme involved in glycolysis, at the posttranscriptional level. BAG3 interacted with HK2 mRNA, and the degree of BAG3 expression altered recruitment of the RNA-binding proteins Roquin and IMP3 to the HK2 mRNA. BAG3 knockdown destabilized HK2 mRNA via promotion of Roquin recruitment, whereas BAG3 overexpression stabilized HK2 mRNA via promotion of IMP3 recruitment. Collectively, our results show that BAG3 promotes reprogramming of glucose metabolism via interaction with HK2 mRNA in PDAC cells, suggesting that BAG3 may be a potential target in the aerobic glycolysis pathway for developing novel anticancer agents. [ABSTRACT FROM AUTHOR]

During embryonic and adult neurogenesis, neuronal stem cells follow a highly conserved path of differentiation to give rise to functional neurons at various developmental stages. Epigenetic regulation--including DNA modifications, histone modifications, and noncoding regulatory RNAs, such as microRNA (miRNA) and long noncoding RNA (lncRNA)--plays a pivotal role in embryonic and adult neurogenesis. Here we review the latest in our understanding of the epigenetic regulation in neurogenesis, with a particular focus on newly identified cytosine modifications and their dynamics, along with our perspective for future studies. [ABSTRACT FROM AUTHOR]

The regulation of cholesterol metabolism in fish is still unclear. Statins play important roles in promoting cholesterol metabolism development in mammals. However, studies on the role of statins in cholesterol metabolism in fish are currently limited. The present study evaluated the effects of statins on cholesterol metabolism in fish. Nile tilapia (Oreochromis niloticus) were fed on control diets supplemented with three atorvastatin levels (0, 12, and 24 mg/kg diet, ATV0, ATV12, and ATV24, respectively) for 4 wk. Intriguingly, the results showed that both atorvastatin treatments increased hepatic cholesterol and triglyceride contents mainly through inhibiting bile acid synthesis and efflux, and compensatorily enhancing cholesterol synthesis in fish liver (P < 0.05). Moreover, atorvastatin treatment significantly inhibited hepatic very-low-density lipoprotein (VLDL) assembly and thus decreased serum VLDL content (P < 0.05). However, fish treated with atorvastatin significantly reduced cholesterol and triglycerides contents in adipose tissue (P < 0.05). Further molecular analysis showed that atorvastatin treatment promoted cholesterol synthesis and lipogenesis pathways, but inhibited lipid catabolism and low-density lipoprotein (LDL) uptake in the adipose tissue of fish (P < 0.05). In general, atorvastatin induced the remodeling of lipid distribution between liver and adipose tissues through blocking VLDL efflux from the liver to adipose tissue of fish. Our results provide a novel regulatory pattern of cholesterol metabolism response caused by atorvastatin in fish, which is distinct from mammals: cholesterol inhibition by atorvastatin activates hepatic cholesterol synthesis and inhibits its efflux to maintain cholesterol homeostasis, consequently reduces cholesterol storage in fish adipose tissue. [ABSTRACT FROM AUTHOR]

Objectives To investigate the serum relationship of specific anti-auto antibodies and antiendometrium antibody. Methods The enzyme linked immune solid assay (ELISA) was used in both fifty patients with positive anti-endometrium antibody (test group) and fifty normal female (control group). Results In test group, the patients with positive anti-double stain DNA antibody are 6, and the total positive of ENA polypeptide antibodies are 24, among of them, the patients with anti-Sm, anti-RNP, anti-SSA and anti-SSB are 18, 15, 14 and 13, respectively. Contrast with control group, there are significant discrepancy. Conclusion There are anti-auto antibodies in patients with positive anti-endometrium antibody. [ABSTRACT FROM AUTHOR]