Association of dexmedetomidine and intraoperative thermal insulation with postoperative outcomes in colorectal cancer resection.

OBJECTIVE: To investigate the effects of dexmedetomidine combined with intraoperative thermal insulation on postoperative cognitive function, cellular immune status and inflammatory markers in patients undergoing radical resection for colorectal cancer. METHODS: Fifty patients who underwent radical resection of colorectal cancer in our hospital from March 2020 to September 2021 were selected and divided into observation group (26 cases with dexmedetomidine combined with intraoperative thermal insulation intervention) and control group (24 cases with conventional anesthesia management). The evaluation measures included the mini-mental state scale (MMSE) score, CD4+ T cell, CD8+ T cell ratio and CD4+/CD8+ ratio, the level of inflammatory markers (IL-6, TNF-α, CRP), and the incidence of postoperative complications. RESULTS: The MMSE score of the observation group was significantly higher than that of the control group on the 3rd day after operation (p < 0.001). After treatment, the proportion of CD4+ T cells, the proportion of CD8+ T cells and the ratio of CD4+/CD8+ in observation group were higher than those in control group (p < 0.01), while the inflammatory markers IL-6, TNF-α and CRP were lower than those in control group (p < 0.01). The incidence of postoperative cognitive dysfunction (POCD) in the observation group (7.69%) was significantly lower than that in the control group (33.33%) (p = 0.010), and the postoperative infection rate was also significantly decreased (p = 0.042). CONCLUSION: Dexmedetomidine combined with intraoperative insulation can significantly improve postoperative cognitive function, maintain immune balance, reduce inflammatory response, and reduce the incidence of POCD and other postoperative complications in patients with radical resection of colorectal cancer.

Effects of dietary tryptophan on the antioxidant capacity and immune response associated with TOR and TLRs/MyD88/NF-κB signaling pathways in northern snakehead, Channa argus (Cantor, 1842).

Introduction: Dietary tryptophan (Trp) has been shown to influence fish feed intake, growth, immunity and inflammatory responses. The purpose of this study was to investigate the effect and mechanism of Trp on immune system of juvenile northern snakehead (Channa argus Cantor, 1842). Methods: A total of 540 fish (10.21 ± 0.11 g) were fed six experimental diets containing graded levels of Trp at 1.9, 3.0, 3.9, 4.8, 5.9 and 6.8 g/kg diet for 70 days, respectively. Results and Discussion: The results showed that supplementation of 1.9-4.8 g/kg Trp in diets had no effect on the hepatosomatic index (HSI) and renal index (RI), while dietary 3.9 and 4.8 g/kg Trp significantly increased spleen index (SI) of fish. Dietary 3.9, 4.8, 5.9 and 6.8 g/kg Trp enhanced the total hemocyte count (THC), the activities of total antioxidant capacity (T-AOC) and superoxide dismutase (SOD). Malondinaldehyde (MDA) levels in the blood were significantly decreased by consuming 3.9 and 4.8 g/kg Trp. Fish fed with 3.0 and 3.9 g/kg Trp diets up-regulated interleukin 6 (il-6) and interleukin 8 (il-8) mRNA levels. The expression of tumor necrosis factor α (tnf-α) was highest in fish fed with 3.0 g/kg Trp diet, and the expression of interleukin 1ß (il-1ß) was highest in fish fed with 3.9 g/kg Trp diet. Dietary 4.8, 5.9 and 6.8 g/kg Trp significantly decreased il-6 and tnf-α mRNA levels in the intestine. Moreover, Trp supplementation was also beneficial to the mRNA expression of interleukin 22 (il-22). Additionally, the mRNA expression levels of target of rapamycin (tor), toll-like receptor-2 (tlr2), toll-like receptor-4 (tlr4), toll-like receptor-5 (tlr5) and myeloid differentiation primary response 88 (myd88) of intestine were significantly up-regulated in fish fed 1.9, 3.0 and 3.9 g/kg Trp diets, and down-regulated in fish fed 4.8, 5.9 and 6.8 g/kg Trp diets. Dietary 4.8 and 5.9 g/kg Trp significantly increased the expression of inhibitor of nuclear factor kappa B kinase beta subunit (ikkß) and decreased the expression of inhibitor of kappa B (iκbα), but inhibited nuclear transcription factor kappa B (nf-κb) mRNA level. Collectively, these results indicated that dietary 4.8 g/kg Trp could improve antioxidant capacity and alleviate intestinal inflammation associated with TOR and TLRs/MyD88/NF-κB signaling pathways.

Associations of personal exposure to domestic heating and cooking fuel emissions and epidemiological effects on rural residents in the Fenwei Plain, China.

Solid fuel combustion for domestic heating in northern China in the wintertime is of great environmental and health concern. This study assesses personal exposure to particulate matter with different aerodynamic diameters and multiple gaseous pollutants from 123 rural residents in Yuncheng, the Fenwei Plain. The subjects are divided into groups based on the unique energy source applied, including biomass, coal, and electricity/no heating activities. The health effects of the exposures are expressed with four urinary biomarkers. The personal exposure levels to three different aerodynamic particle sizes (i.e., PM10, PM2.5, and PM1) of the electricity/no heating group are 5.1 % -12 % lower than those of the coal group. In addition, the exposure levels are 25 %-40 % lower for carbon monoxide (CO) and 10.8 %-20.3 % lower for ozone (O3) in the electricity/no heating group than the other two fuel groups. C-reactive protein (CRP) in the urine of the participants in biomass and coal groups is significantly higher than that in the electricity/no heating group, consistent with the observations on other biomarkers. Increases in 8-hydroxy-2 deoxyguanosine (8-OHdG), interleukin-8 (IL-8), and vascular endothelial growth factor (VEGF) are observed for the exposures to higher concentrations of air pollutants. For instance, PMs and nitrogen dioxide (NO2) show significant impacts on positive correlations with 8-OHdG and IL-8, while O3 positively correlates with CRP. PM1 exhibits higher effects on the biomarkers than the gaseous pollutants, especially on VEGF and IL-8. The study indicates that excessive use of traditional domestic solid fuels could pose severe health effects on rural residents. The promotion of using clean energy is urgently needed in the rural areas of northern China.

Preparation, characteristic and anti-inflammatory effect of selenium nanoparticle-enriched probiotic strain Enterococcus durans A8-1.

BACKGROUND: Elemental selenium, a new type of selenium supplement, can be biosynthesized via microorganisms. This study is to characterize a patent probiotic bacteria Enterococcus durans A8-1, capable of reducing selenite (Se6+ or Se4+) to elemental selenium (Se0) with the formation of Se nanoparticles (SeNPs). METHODS: The selenium nanoparticles synthesized from A8-1 were characterized using scanning electron microscopy (SEM), transmission electron microscopy (TEM), energy dispersive spectroscopy (EDS), and X-ray photoelectron energy (XPS). The Caco2 cells were used to investigate the effects of Se-enriched A8-1 on the viability, membrane integrity, and the regulation of cellular inflammation through MTT and ELISA assays. The selenium-enriched metabolic function of A8-1 was analyzed by transcriptome sequencing. RESULTS: E. durans A8-1 has the ability to synthesize intracellular SeNPs that are incubated with 60 mg/L sodium selenite for 18 h at 37 °C with 7 % inoculum under aerobic conditions. The selenium-enriched transformation rate increased to 43.46 %. After selenium enrichment, there were no significant morphological changes in E. durans A8-1 cells. The cells also exhibited no cytotoxicity when incubated with Caco-2 cells, and increased cellular proliferation. Furthermore, Se-enriched A8-1 cells antagonize the adhesion of S. typhimurium ATCC14028 onto the surface of Caco-2 cells protecting cell membrane integrity and was assessed by measuring LDH and AKP activities (P <0.001, P <0.001). Moreover, Se-enriched A8-1 could protect Caco-2 cells from inflammation induced by lipopolysaccharide and help the cells alleviate the inflammation through the reduced expression of cytokine IL-8 (P = 0.0012, P <0.001) and TNF-α (P <0.001, P <0.001). Based on transcriptome sequencing in Se-enriched E. durans A8-1 cells, there were 485 up-regulated genes and 322 down-regulated genes (Padj < 0.05). There were 19 predicted up-regulated genes that are highly related to the potential selenium metabolism pathway, which focuses on the transportation of Na2SeO3 by membrane proteins, and gradually reduces Na2SeO3 to elemental selenium aggregates that are deposited onto the membrane surface via the intracellular redox response. CONCLUSION: E. durans A8-1 could convert extracellular selenite into intracellular biological SeNPs via redox pathway with strong selenium-rich metabolism, and its biological SeNPs have anti-inflammatory properties, which have the potential for the development of composite selenium nanomaterials and can be further studied for the function of SeNPs with potential applications.

Transcriptome and metabolome profiling of interspecific CSSLs reveals general and specific mechanisms of drought resistance in cotton.

In order to understand the molecular mechanism of cotton's response to drought during the flowering and boll stage, transcriptomics and metabolomics were carried out for two introgression lines (drought-tolerant line: T307; drought-sensitive line: S48) which were screened from Gossypium hirsutum cv. 'Emian22' with some gene fragments imported from Gossypium barbadense acc. 3-79, under drought stress by withdrawing water at flowering and boll stage. Results showed that the basic drought response in cotton included a series of broad-spectrum responses, such as amino acid synthesis, hormone (abscisic acid, ABA) signal transduction, and mitogen-activated protein kinases signal transduction pathway, which activated in both drought-tolerant and drought-sensitive lines. However, the difference of their imported fragments and diminished sequences triggers endoplasmic reticulum (ER) protein processing, photosynthetic-related pathways (in leaves), and membrane solute transport (in roots) in drought-tolerant line T307, while these are missed or not activated in drought-sensitive line S48, reflecting the different drought tolerance of the two genotypes. Virus-induced gene silencing assay of drought-tolerant differentially expressed heat shock protein (HSP) genes (mainly in leaf) and ATP-binding cassette (ABC) transporter genes (mainly in roots) indicated that those genes play important role in cotton drought tolerant. Combined analysis of transcriptomics and metabolomics highlighted the important roles of ER-stress-related HSP genes and root-specific ABC transporter genes in plants drought tolerance. These results provide new insights into the molecular mechanisms underlying the drought stress adaptation in cotton.

Effects of domestic solid fuel combustion emissions on the biomarkers of homemakers in rural areas of the Fenwei Plain, China.

BACKGROUND: The health effects of heavy solid fuel use in winter in rural China are of concern. The effects of air pollution resulting from domestic solid fuel combustion in rural households on rural homemakers' biomarkers were revealed in this study. METHODS: In total, 75 female homemakers from rural areas of Guanzhong Basin, the Fenwei Plain, People's Republic of China, were randomly selected and divided into three groups (biomass users, coal users, and nonusers of solid fuel user [control group]). The differences in biological indicators, including 8-hydrox-2'-deoxyguanosine (8-OHdG), interlukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) in urine samples as well as blood pressure (BP, including systolic BP [SBP] and diastolic BP [DBP]) and heart rate (HR) among the groups in winter and summer were investigated using statistical analysis. RESULTS: IL-6, 8-OHdG, HR, SBP, and DBP were significantly higher in winter than in summer (P < 0.05) owing to the poor air quality resulted from the excessive use of solid fuels in winter. Significant seasonal differences in 8-OHdG were observed for both coal and biomass users. After the influence of confounders was removed, only IL-6 levels in the urine of solid fuel users were significantly higher than that of the control group. CONCLUSIONS: IL-6 is a sensitive biomarker representing inflammatory responses to particulate matter emitted through household solid fuel combustion. Locally, excessive use of solid fuels in winter posed serious PM2.5 pollution in this area and adverse effects on inflammatory biomarkers in these rural homemakers and induced DNA damage related to oxidative stress.

A novel STING agonist for cancer immunotherapy and a SARS-CoV-2 vaccine adjuvant.

A novel STING agonist, CDGSF, ipsilaterally modified with phosphorothioate and fluorine, was synthesized. The phosphorothioate in CDGSF might be a site for covalent conjugation. Injection of CDGSF generated an immunogenic ("hot") tumor microenvironment to suppress melanoma, more efficiently than dithio CDG. In particular, immunization with SARS-CoV-2 spike protein using CDGSF as an adjuvant elicited an exceptionally high antibody titer and a robust T cell response, overcoming the drawbacks of aluminum hydroxide. These results highlighted the therapeutic potential of CDGSF for cancer immunotherapy and the adjuvant potential of the STING agonist in the SARS-CoV-2 vaccine for the first time.

A host-guest ATP responsive strategy for intracellular delivery of phosphopeptides.

We developed a host-guest ATP responsive strategy for efficient intracellular delivery of phosphopeptides, employing a pegylated arginine clustered calix[5]arene nanocarrier system that has great capability of recognizing the phosphate moieties on peptides and penetrating the cell membrane.

Effects of dietary Pediococcus acidilactici GY2 single or combined with Saccharomyces cerevisiae or/and ß-glucan on the growth, innate immunity response and disease resistance of Macrobrachium rosenbergii.

One Pediococcus acidilactici strain, named PA-GY2 was isolated from the gut of cultured Macrobrachium rosenbergii. In order to better examine the potential scope and applicability of this strain in M. rosenbergii culture, based on the control diet, four experimental diets containing single or combined immunostimulants were produced by supplementing with yeast (Saccharomyces cerevisiae, SC) or/and ß-glucan (G), then fed to the prawns (6.70 g ± 0.74) in five groups, which were named as group C (control group), P (PA-GY2), PS (PA-GY2 + SC, 1:1), PG (PA-GY2 + G) and PGS (PA-GY2 + SC + G), respectively. After a 60-day feeding trial, growth performance, feed utilization, immune response and disease resistance of prawns were evaluated in the present study. Results indicated that (1) The growth performance of the prawns in group PS and PGS were significantly improved. The prawns in group PGS presented the lowest feed coefficiency (FC), while prawns in group C presented the highest FC. (2) The protease activity was significantly improved by dietary immunostimulants supplementation, meanwhile, prawns in the group PS presented the highest lipase activity. (3) The highest total hemocyte count and respiratory burst activity were found in the group P and PG, respectively. The phagocytic index of the prawns in the group C was significantly lower than those in group P and PGS. (4) Dietary PA-GY2 single or combined with SC or/and ß-glucan increased the immune related genes expression, including some antibacterial and antioxidant enzymes, while decreased the tumor necrosis factor-α gene expression, which led to the decreased cumulative mortality rate of prawns during the Aeromonas hydrophila challenge test. Based on the results of growth performance, digestive enzymes activity and immune response of M. rosenbergii, PA-GY2 supplementation, single or combined with SC or/and ß-glucan could be suggested as promising immunostimulants in prawns farming.

A site-specific branching poly-glutamate tag mediates intracellular protein delivery by cationic lipids.

Intracellular protein delivery is of significance for cellular protein analysis and therapeutic development, but remains challenging technically. Herein, we report a general and highly potent strategy for intracellular protein delivery based on commercially available cationic lipids. In this strategy, a designed double branching poly-glutamate tag is site-specifically attached onto the C-terminal of protein cargos via expressed protein ligation (EPL), which mediates the entrapment of proteins into cationic liposomes driven by electrostatic interaction. The resultant protein-lipid complexes can enter into cytosol with a high efficiency even at the low protein concentration while maintaining protein's biological activity.

Bacterial Outer Membrane Vesicles from Dextran Sulfate Sodium-Induced Colitis Differentially Regulate Intestinal UDP-Glucuronosyltransferase 1A1 Partially Through Toll-Like Receptor 4/Mitogen-Activated Protein Kinase/Phosphatidylinositol 3-Kinase Pathway.

UDP-glucuronosyltransferase 1A1 (UGT1A1) constitutes an important part of intestinal epithelial barrier and catalyzes glucuronidation of many endogenous compounds and drugs. Downregulation of UGT1A1 in inflammation has been reported, whereas the association with gut dysbiosis is poorly defined. This study verified the involvement of gut microbiota in intestinal UGT1A1 regulation using dextran sulfate sodium (DSS)-induced rat colitis model plus fecal microbiota transplantation (FMT). Generally, both DSS induction and colitis-to-normal FMT suppressed mRNA and protein expressions of UGT1A1 and nuclear xenobiotic receptors (NRs) in colon, but enhanced mRNA and decreased protein of rat UGT1A1/rat NRs in small intestine. Normal-to-colitis FMT alleviated DSS-induced changes. Bacterial outer membrane vesicles (OMVs) from colitis rats and rats receiving colitis feces reduced both mRNA and protein of human UGT1A1 (hUGT1A1)/human NRs (hNRs) in Caco-2 cells. Interestingly, using deoxycholate to reduce lipopolysaccharide, normal OMVs upregulated hUGT1A1/hNRs, whereas colitis OMVs decreased, indicating the involvement of other OMVs components in UGT1A1 regulation. The 10- to 50-kDa fractions from both normal and colitis OMVs downregulated hUGT1A1, human PXR, and human PPAR-γ, whereas >50-kDa fractions from normal rats upregulated hUGT1A1 and human CAR. Additionally, the conditioned medium from OMVs-stimulated rat primary macrophages also reduced hUGT1A1/hNRs expression. Both Toll-like receptor (TLR)2 and TLR4 were activated by DSS, colitis-to-normal FMT, and the opposite, whereas only TLR4 was increased in OMVs-treated cells. TLR4 small interfering RNA blocked hUGT1A1/hNRs downregulation and phosphatidylinositol 3-kinase/Akt, extracellular signal-regulated kinase, and nuclear factor κB phosphorylation evoked by bacterial OMVs. Taken together, this study demonstrated that gut microbiota regulate intestinal UGT1A1 partially through secreting OMVs, which interact with intestinal epithelial cells directly or via activating macrophage.

Cathepsin L deficiency results in reactive oxygen species (ROS) accumulation and vascular cells activation.

Recent evidence suggests a link between cathepsin L (CTSL) and vascular diseases. However, its contribution to reactive oxygen species (ROS) homeostasis in the vasculature remains unknown. p66shc is a redox enzyme implicated in mitochondrial ROS generation and translation of oxidative signals. In this study, we explored the relationship between CTSL and oxidative damage in vasculature and whether the oxidative damage is mediated by p66shc.Carotid arteries from aged mice (24 months old) showed a reduction in CTSL expression compared with young wild-type mice (4 months old). Local knockdown of CTSL in carotid arteries of young mice by adenoviral vector encoding the short hairpin RNA targeting CTSL leading to premature vascular aging, as shown by mitochondrial disruption, increased ß-galactosidase-positive cells, reduced telomerase activity, and up-regulation of p66shc. Knockdown of CTSL decreased the expression of mitochondrial oxidative phosphorylation (OXPHOS) complexes I, III, and IV, leading to increased mitochondrial ROS and hyperpolarization of the mitochondrial membrane in vitro. Furthermore, knockdown of CTSL also stimulated ROS production and senescence in vascular cells, accompanied by the up-regulation of p66shc.However, p66shc knockdown blunted the alteration in ROS production, and senescence in CTSL knockdown vascular cells. This study suggests that CTSL knockdown partially induces vascular cells damage via increased ROS production and up-regulation of p66shc.

Effect of high-fat diet and growth stage on the diversity and composition of intestinal microbiota in healthy bovine livestock.

BACKGROUND: This study aimed to investigate the composition of bacteria in the bovine rectum and their functions during growth, in relation to different diets. Fecal samples were collected from 6-, 12-, 18- and 24-month cattle fed high-fat diet, and healthy female parents fed regular diet. Total DNA was amplified (V3-V4 of 16S rRNA) and submitted to barcode-DNA pyrosequencing. Intestinal microbiota profiles and functions were then analyzed. RESULTS: A total of 114 512 operational taxonomic units were detected from the 1 802 243 sequences obtained. In 6-month-old and female parent groups, the top three abundant phyla were Bacteroidetes (37.6%, 32.2%), Firmicutes (34.4%, 48.2%) and Proteobacteria (9.1%, 6.3%); in the 12-, 18- and 24-month groups, they were Proteobacteria (45.5%, 47.1%, 38.8%), Firmicutes (27.4%, 22.2%, 20.1%) and Bacteroidetes (14.9%, 19.4%, 17.7%), respectively. Paludibacter and Desulfopila in abundance showed negative (P < 0.001) and positive (P < 0.05) correlation, respectively, to cattle weight gain through metagenomic functional prediction of methane, cysteine and methionine metabolism. Meanwhile, cofactor/vitamin and amino acid metabolic processes were significantly higher in bacteria from the regular diet group than high-fat diet groups, with markedly lower cellular processes and signaling, and reduced glycan biosynthesis and metabolism (P < 0.01). CONCLUSIONS: The 6-month cattle and female parents shared similar intestinal bacteria; the community structure of fecal microbiota was significantly affected by high-fat diet in older cattle. © 2017 Society of Chemical Industry.

Sesamin ameliorates hepatic steatosis and inflammation in rats on a high-fat diet via LXRα and PPARα.

Nonalcoholic fatty liver disease (NAFLD) is defined by a nonalcohol relevant pathological accumulation of fat in the liver. Previous studies have shown that sesamin exerts antioxidant effects and improves lipid metabolism of the fatty liver. In this study, we hypothesized that sesamin improves lipid homeostasis of Sprague-Dawley rats fed a high-fat diet (HFD) by regulating the expression of genes related to de novo lipogenesis and ß-oxidation. We induced NAFLD in rats with HFD and examined the effect of sesamin in vivo. The results showed that HFD rats accumulated total cholesterol and triacylglycerols in the liver and developed inflammation, as evidenced by the elevation of interleukin-6 and tumor necrosis factor-α in the liver and serum. Sesamin attenuated the disease progression by improving the blood lipid profile in a dose-dependent manner. Sesamin reduced the serum levels of total cholesterol, triacylglycerols, low-density lipoprotein cholesterol, and free fatty acid, whereas it increased the level of high-density lipoprotein cholesterol. Meanwhile, sesamin increased the activities of hepatic glutathione peroxidase and superoxide dismutase while reducing the level of malonaldehyde and cytochrome P450 2E1. Furthermore, higher doses of sesamin reduced the expression of liver X receptor α and its downstream target genes, whereas it upregulated the peroxisome proliferator-activated receptor α-mediated signaling. These findings suggest that sesamin attenuates diet-induced dyslipidemia and inflammation of NAFLD in rats via mechanisms regulated by liver X receptor α and peroxisome proliferator-activated receptor α.

High Glucose Induces Down-Regulated GRIM-19 Expression to Activate STAT3 Signaling and Promote Cell Proliferation in Cell Culture.

Recent studies indicated that Gene Associated with Retinoid-IFN-Induced Mortality 19 (GRIM-19), a newly discovered mitochondria-related protein, can regulate mitochondrial function and modulate cell viability possibly via interacting with STAT3 signal. In the present study we sought to test: 1) whether GRIM-19 is involved in high glucose (HG) induced altered cell metabolism in both cancer and cardiac cells, 2) whether GRIM-19/STAT3 signaling pathway plays a role in HG induced biological effects, especially whether AMPK activity could be involved. Our data showed that HG enhanced cell proliferation of both HeLa and H9C2 cells, which was closely associated with down-regulated GRIM-19 expression and increased phosphorylated STAT3 level. We showed that GRIM-19 knock-down alone in normal glucose cultured cells can also result in an increase in phosphorylated STAT3 level and enhanced proliferation capability, whereas GRIM-19 over-expression can abolished HG induced STAT3 activation and enhanced cell proliferation. Importantly, both down-regulated or over-expression of GRIM-19 increased lactate production in both HeLa and H9C2 cells. The activated STAT3 was responsible for increased cell proliferation as either AG-490, an inhibitor of JAK2, or siRNA targeting STAT3 can attenuate cell proliferation increased by HG. In addition, HG increased lactate acid levels in HeLa cells, which was also observed when GRIM-19 was genetically manipulated. However, HG did not affect the lactate levels in H9C2 cells. Of note, over-expression of GRIM-19 and silencing of STAT3 both increased lactate production in H9C2 cells. As expected, HG resulted in significant decreases in phosphorylated AMPKα levels in H9C2 cells, but not in HeLa cells. Interestingy, activation of AMPKα by metformin was associated with a reversal of the suppressed GRIM-19 expression in H9C2 cells, the fold of changes in GRIM-19 expression by metformin were much less in HeLa cells. Metformin did not affect the phosphorylated STAT3 lelvels, however, decreased its levels in H9C2, especially in the setting of HG culture. Not like HG alone which resulted in no changes in lactate acid in H9C2 cells, metformin can increase lactate acid levels in H9C2 cells. Increased lactate induced by metformin was also observed in HeLa cells.

[Analysis the epidemiological features of 3,258 patients with allergic rhinitis in Yichang City].

OBJECTIVE: To investigate the epidemiological features in patients with allergic rhinitis (AR) in Yichang city, and put forward effective prevention and control measures. METHOD: Collecting the data of allergic rhinitis in city proper from 2010 to 2013, input the data into the database and used statistical analysis. RESULT: In recent years, the AR patients in this area increased year by year. The spring and the winter were the peak season of onset. The patients was constituted by young men. There was statistically significant difference between the age, the area,and the gender (P < 0.01). The history of allergy and the diseases related to the gender composition had statistical significance difference (P < 0.05). The allergens and the positive degree in gender, age structure had statistically significant difference (P < 0.01). CONCLUSION: Need to conduct the healthy propaganda and education, optimizing the environment, change the bad habits, timely medical treatment, standard treatment.

Two novel exopolysaccharides from Bacillus amyloliquefaciens C-1: antioxidation and effect on oxidative stress.

Two odorless, water-soluble exopolysaccharide (EPS) fractions, EPS-1 and EPS-2, were isolated from a newly isolated Bacillus amyloliquefaciens strain C-1 and purified by ion exchange and gel chromatography. The purified EPS-1 contained glucose/mannose/galactose/arabinose in a relative proportion of 15:4:2:1, and possessed a molecular weight of 79.6 kDa, while EPS-2 contained only glucose and mannose in a 3:1 ratio, with the molecular weights of 19.8 kDa. The antioxidant activity results showed that EPS-1 exhibited strong reducing power, superoxide radicals (O(2-)·), and hydroxyl free radicals (OH·) scavenging activities. For the H2O2-induced injury in HepG2 cells, EPS-1 significantly decreased the formation of reactive oxygen species, intracellular malondialdehyde levels, and restored intracellular superoxide dismutase activity. For EPS-2, there had no detectable antioxidant activities. And all these results collectively showed that as a natural antioxidant, only EPS-1 produced by C-1 had considerable potential to be used as medical compounds or functional additives.

Vasohibin­2 promotes proliferation in human breast cancer cells via upregulation of fibroblast growth factor­2 and growth/differentiation factor­15 expression.

Vasohibin­2 (VASH2) is an angiogenic factor, and has been previously reported to be a cancer­related gene, with cytoplasmic and karyotypic forms. In the current study VASH2 expression in human breast cancer tissue and adjacent non­cancerous tissue was investigated with immunohistochemistry. MCF­7 and BT474 human breast cancer cells were transfected with lentiviral constructs to generate in vitro VASH2 overexpression and knockdown models. In addition, BALB/cA nude mice were inoculated subcutaneously with transfected cells to generate in vivo models of VASH2 overexpression and knockdown. The effect of VASH2 on cell proliferation was investigated using a bromodeoxyuridine assay in vitro and immunohistochemistry of Ki67 in xenograft tumors. Growth factors were investigated using a human growth factor array, and certain factors were further confirmed by an immunoblot. The results indicated that the expression level of cytoplasmic VASH2 was higher in breast cancer tissues with a Ki67 (a proliferation marker) level of ≥14%, compared with tissues with a Ki67 level of <14%. VASH2 induced proliferation in vitro and in vivo. Four growth factors activated by VASH2 were identified as follows: Fibroblast growth factor 2 (FGF2), growth/differentiation factor­15 (GDF15), insulin­like growth factor­binding protein (IGFBP)3 and IGFBP6. FGF2 and GDF15 may contribute to VASH2­induced proliferation. The current study identified a novel role for VASH2 in human breast cancer, and this knowledge suggests that VASH2 may be a novel target in breast cancer treatment.

[Skin prick test of inhalative allergens for patients with allergic rhinitis in Yichang].

OBJECTIVE: To investigate the allergens in patients with allergic rhinitis in Yichang, so that to find common allergens of Yichang and to provide statistic basis for a reasonable prevention and treatment to allergic rhinitis. METHOD: 1,979 patients with allergic rhinitis in Yichang were detected for allergens by skin prick test and the distribution of positive rates to inhaled allergens was compared between different genders and ages. RESULT: 1,545 (78.1%) of 1,979 suspected allergic rhinitis patients presented positive reaction. The positive rate in male was significantly higher than in female, and that in juvenile group was significantly higher than in adults. Among positive cases in inhalation group, the most common allergen was flour mite (80.4%), followed by house dust mite (64.9%), cockroach (13.3%) and artemisia pollen (8.2%). CONCLUSION: The study shows that the flour mite and house dust mite are the most common inhaled allergens causing allergic rhinitis in Yichang. We should pay more attention to the prevention and treatment for the juvenile patients.

Anticancer activity of binary toxins from Lysinibacillus sphaericus IAB872 against human lung cancer cell line A549.

The inhibitory effect of binary toxic (Bin) protein produced by Lysinibacillus sphaericus IAB872 on cell proliferation of human lung, liver, stomach and cervical tumor cell lines was assessed using MTT assay. The effect of Bin protein on A549 cell proliferation, apoptosis, cell cycle, migration and invasion were examined by MTT assay, Western blotting, Immunocytochemical staining, flow cytometry assay and wound-healing assay. Results showed that Bin protein inhibits proliferation of a range of human cancer cells in vitro. The anti-proliferative effect of Bin is associated with cell apoptosis as a result of an increased ratio of cellular Bax/bcl-2, up-regulated CyclinB1 and down-regulated Cdc25c expression, and its anti-proliferative action was associated with cell cycle arrest in the G2/M-phase. Bin protein could promote apoptosis and inhibit motility and invasion of A549 cancer cells. The anti-proliferative effect of Bin protein was associated with the induction of apoptotic cell death and cell cycle disruption. These results show that Bin protein has the potential to be developed as a chemotherapeutic agent by induction of human tumor cell apoptosis.