The mediating effect of math self-efficacy on the relationship between parenting style and math anxiety.

The present study aims to investigate the associations among math self-efficacy, parenting style, and math anxiety in primary school children. The sample comprised 400 participants, aged between 10 and 11 years old, from an elementary school in China. Participants completed three self-reported questionnaires on math anxiety, parenting styles and math self-efficacy. The results revealed that rejection was strongly and positively correlated with math anxiety, while emotional warmth was negatively related to math anxiety. Interestingly, math anxiety was found to be related to rejection, with math self-efficacy playing a mediating role in this relationship. Conversely, math self-efficacy played a mediating role in the relationship between parenting styles and math anxiety, while over protection exhibited no significant correlation with math anxiety. The study also showed that gender differences existed in the level of math anxiety and math self-efficacy, with boys exhibiting lower math anxiety and higher math self-efficacy than girls. These results provide important insights into the development and treatment of math anxiety in primary school children. Specifically, parents and educators should focus on enhancing children's math self-efficacy beliefs, while adopting a parenting style characterized by emotional warmth and low levels of rejection.

Characterization and Potential Applications of a Selenium Nanoparticle Producing and Nitrate Reducing Bacterium Bacillus oryziterrae sp. nov.

A novel nitrate- and selenite reducing bacterium strain ZYKT was isolated from a rice paddy soil in Dehong, Yunnan, China. Strain ZYKT is a facultative anaerobe and grows in up to 150, 000 ppm O2. The comparative genomics analysis of strain ZYKT implies that it shares more orthologues with B. subtilis subsp. subtilis NCIB 3610T (ANIm values, 85.4-86.7%) than with B. azotoformans NBRC 15712T (ANIm values, 84.4-84.7%), although B. azotoformans NBRC 15712T (96.3% 16S rRNA gene sequence similarity) is the closest Bacillus species according to 16S rRNA gene comparison. The major cellular fatty acids of strain ZYKT were iso-C14:0 (17.8%), iso-C15:0 (17.8%), and C16:0 (32.0%). The polar lipid profile consisted of phosphatidylethanolamine, diphosphatidylglycerol, phosphatidylglycerol and an unidentified aminophospholipid. Based on physiological, biochemical and genotypic properties, the strain was considered to represent a novel species of the genus Bacillus, for which the name Bacillus oryziterrae sp. nov. is proposed. The type strain is ZYKT (=DSM 26460T =CGMCC 1.5179T). Strain ZYKT can reduce nitrate to nitrite and ammonium and possesses metabolic genes for nitrate reduction including nar, nap and nrf. Biogenic selenium nanoparticles of strain ZYKT show a narrow size distribution and agree with the gaussian distribution. These selenium nanoparticles show significant dose-dependent inhibition of the lung cancer cell line H157, which suggests potential for application in cancer therapy.

Interleukin-1B 31 C>T polymorphism combined with Helicobacter pylori-modified gastric cancer susceptibility: evidence from 37 studies.

Gastric cancer is one of the most common malignancies worldwide. Interleukin-1-beta (IL-1ß) is a pro-inflammatory cytokine and potent inhibitor of gastric acid secretion. Some studies provided evidence of the association between IL-1B 31 polymorphism and gastric cancer risk while other studies did not. Therefore, we conducted a comprehensive meta-analysis to reassess the association. A systematic literature search of the PubMed and EMBASE databases identified 37 studies with 6108 cases and 8980 controls for this meta-analysis. The crude odd ratios (ORs) and the 95% confidence intervals (CIs) were calculated to evaluate the strength of the association. Meta-regression was used to determine the major source of heterogeneity across the studies. The pooled analysis did not suggest the significant association of IL-1B 31 C>T polymorphism with gastric cancer risk. Stratified analysis was performed by ethnicity, source of control, genotype method, and indicated a significantly increased gastric cancer risk associated with IL-1B 31T variant in the population-based subgroup (heterozygous model: OR = 1.22, 95% CI = 1.03-1.45). Moreover, stratified analysis by Helicobacter pylori infection status indicated that IL-1B 31 polymorphism increased gastric cancer risk in infection-positive subgroup (homozygous model: OR = 1.35, 95% CI = 1.02-1.78; heterozygous model: OR = 1.31, 95% CI = 1.04-1.66; recessive model: OR = 1.29, 95% CI = 1.04-1.61). The study suggested that IL-1B 31 polymorphism might confer susceptibility to gastric cancer in the presence of H. pylori infection, indicating a gene-environment interaction in gastric carcinogenesis.

In ovo exposure of a Fusarium mycotoxin butenolide induces hepatic and renal oxidative damage in chick embryos, and antioxidants provide protections.

Butenolide is a mycotoxin produced by several toxigenic Fusarium species. It frequently invades many important grains, and evokes a broad spectrum of toxic effects. For these reasons, butenolide poses a health risk to both humans and animals. However, many toxicology issues of butenolide including targets and mechanisms of toxicity remain to be elucidated so far. The present study therefore attempts to reveal the toxic profile of butenolide from a viewpoint of oxidative damage, using chick embryos as an in vitro model. A single in ovo injection of butenolide resulted in significant oxidative injuries in embryonic livers and kidneys, as manifested by a dose-dependent depletion of sulfhydryl groups, reduction of glutathione peroxidase activity, and increase of thiobarbituric acid reactive substances production, an indicator of lipid peroxidation. In contrast, co-injections of butenolide with antioxidants sodium selenite, vitamin C and a representative antioxidative enzyme superoxide dismutase markedly abated these oxidative toxicities. In conclusion, the present study suggests that oxidative damage may serve as a mediator in the toxicity of butenolide, and amelioration of antioxidant defense capacity by exogenous supplementation may play a role in the prevention and treatment of butenolide intoxication.

Repeated administration of a Fusarium mycotoxin butenolide to rats induces hepatic lipid peroxidation and antioxidant defense impairment.

Butenolide, a mycotoxin elaborated by several toxigenic Fusarium species, frequently contaminates important agricultural products, and has been considered a potential health risk to humans and animals. However, many toxicology issues including toxicity targets and mechanisms of butenolide remain unclear. Previous study indicated that acute butenolide exposure produced hepatic oxidative toxicity, but its chronic toxicity is still unknown. The present study therefore attempted to reveal the adverse effects of repeated butenolide exposure from a viewpoint of oxidative damage focusing on the liver. Intragastic administration of rats with butenolide for seven consecutive weeks resulted in hepatic injury as shown by obvious changes of serum biochemistry parameters indicating liver function. Repeated butenolide exposure also induced oxidative stress as manifested by impairment of antioxidant defenses including depletion of sulfhydryl groups and reduction of glutathione peroxidase activity, and enhancement of lipid peroxidation both in serum and liver. In conclusion, the present study indicated that repeated butenolide exposure induced a significant liver injury, and oxidative damage may serve as a mediator in the toxicity of butenolide. The current findings contribute to the understanding of the toxic profile of butenolide.

Lipid peroxidation and antioxidant defense impairment in the hearts of chick embryos induced by in ovo exposure to Fusarium mycotoxin butenolide.

Fusarium mycotoxin toxicosis has been implicated as an etiological factor for Keshan disease, an endemic cardiomyopathy prevailing in specific regions of China. Butenolide (4-acetamido-4-hydroxy-2-butenoic acid gamma-lactone) is one of the Fusarium mycotoxins frequently detected from the foodstuffs of endemic areas and has been shown to possess the potential to induce cardiotoxicity, implying this mycotoxin might play a role in the occurrence of Keshan disease. The present study was undertaken to further investigate the myocardial toxicity of butenolide from a viewpoint of oxidative damage. A single in ovo injection of butenolide to chick embryos, an excellent in vitro toxicology model resulted in significant oxidative injuries to the myocardium, manifested by a dose-dependent depletion of sulfhydryl groups, reduction of glutathione peroxidase (GPx) activity, and increase of thiobarbituric acid reactive substances production, a hallmark of lipid peroxidation. In contrast, co-injections of butenolide to chick embryos with sodium selenite or vitamin C, two potent antioxidants, markedly abated these oxidative injuries. In conclusion, the present study clearly indicated that butenolide could induce significant myocardial oxidative injuries. The current findings reinforce the hypothesis that toxicosis by Fusarium mycotoxins may be one of the etiological factors for Keshan disease, and oxidative damage is involved in the pathogenesis of myocardial toxicity.