An analysis of risk factors of non-fatal drowning among children in rural areas of Guangdong Province, China: a case-control study

<p/> <p>Background</p> <p>Drowning is a major cause of morbidity and mortality for children, yet non-fatal drowning remains poorly understood. The aim of this study was to explore potential modifiable risk factors of non-fatal drowning among children in rural areas of China.</p> <p>Methods</p> <p>A cross-sectional survey was first conducted to obtain non-fatal drowning cases, and 7432 students in grades three to eight from 17 schools participated in the cross sectional survey. Of these, 805 students reported that they experienced non-fatal drowning in the previous year. Then 368 cases were selected randomly to participate in a 1:1 matched case-control study. Each drowning case was matched by one control with the same sex and similar age (the gap less than 2 years) who was selected randomly from the same class.</p> <p>Results</p> <p>Boys were more likely to be involved in non-fatal drowning. Non-fatal drowning most often happened in the afternoon (65.1%) and natural bodies of water were the most common sites of drowning (71.1%). Swimming, diving and playing in natural waters were the leading activities that preceded non-fatal drowning. The significant risk factors for non-fatal drowning were swimming in natural waters without adult supervision (OR = 3.40, 95% CI: 1.92-6.03), playing in or beside natural waters (OR = 2.08, 95% CI: 1.17-3.70) and poor swimming skills (OR = 2.74, 95% CI: 1.14-6.62). However, the following variables were protective factors: supervisor aged 30 years or over (OR = 0.20, 95% CI: 0.09-0.49) and no water activities (OR = 0.36, 95% CI: 0.18-0.70).</p> <p>Conclusions</p> <p>The reduction in dangerous water activities, swimming training and enhancement in supervision among children might decrease the risk of non-fatal drowning.</p

Cordyceps Sinensis: anti-fibrotic and inflammatory effects of a cultured polysaccharide extract

It has been suggested that the traditional Chinese herbal preparation Cordyceps Sinensis (CS) may have a beneficial effect in renal disease. To satisfy increasing demand, CS derivatives have been produced by aseptic mycelia cultivation. We have demonstrated antifibrotic activity of cultured CS previously. The aim of this study was to examine bioactivity of a polysaccharide isolated from cultured CS with a complicated monosaccharide composition, mainly consisting of Gal, Glc and Man. This polysaccharide antagonised the effect of TGF-b1 in stimulating the expression of collagen in the HK2 renal cell line. This was associated with down regulation of the TGF-b receptor Alk5. In addition the polysaccharide antagonised IL-1b stimulated sICAM-1 dependent adherence of monocytes to a monolayer of HK2 cell. This was associated with increased expression of the primary receptor for hyaluronan CD44, and was abrogated by removal of the cell surface hyaluronan pericellular coat. In summary we describe both anti-fibrotic and anti-inflammatory activity in a polysaccharide isolated from cultured CS

Introduction of Exogenous Glycolate Catabolic Pathway Can Strongly Enhances Photosynthesis and Biomass Yield of Cucumber Grown in a Low-CO2 Environment

Carbon dioxide (CO2) is very important for photosynthesis of green plants. CO2 concentration in the atmosphere is relatively stable, but it drops sharply after sunrise due to the tightness of the greenhouse and the absorption of CO2 by vegetable crops. Vegetables in greenhouses are chronically CO2 starved. To investigate the feasibility of using genetic engineering to improve the photosynthesis and yield of greenhouse cucumber in a low CO2 environment, five genes encoding glyoxylate carboligase (GCL), tartronic semialdehyde reductase (TSR), and glycolate dehydrogenase (GlcDH) in the glycolate catabolic pathway of Escherichia coli were partially or completely introduced into cucumber chloroplast. Both partial pathway by introducing GlcDH and full pathway expressing lines exhibited higher photosynthetic efficiency and biomass yield than wild-type (WT) controls in low CO2 environments. Expression of partial pathway by introducing GlcDH increased net photosynthesis by 14.9% and biomass yield by 44.9%, whereas the expression of the full pathway increased seed yield by 33.4% and biomass yield by 59.0%. Photosynthesis, fluorescence parameters, and enzymatic measurements confirmed that the introduction of glycolate catabolic pathway increased the activity of photosynthetic carbon assimilation-related enzymes and reduced the activity of photorespiration-related enzymes in cucumber, thereby promoting the operation of Calvin cycle and resulting in higher net photosynthetic rate even in low CO2 environments. This increase shows an improvement in the efficiency of the operation of the photosynthetic loop. However, the utilization of cucumber of low concentration CO2 was not alleviated. This study demonstrated the feasibility of introducing the pathway of exogenous glycolate catabolic pathway to improve the photosynthetic and bio-yield of cucumber in a low CO2 environment. These findings are of great significance for high photosynthetic efficiency breeding of greenhouse cucumber

Increased red cell distribution width in patients with slow coronary flow syndrome

OBJECTIVE: An elevated red cell distribution width has been recognized as a predictor of various cardiovascular diseases. Slow coronary flow syndrome is an important angiographic clinical entity with an unknown etiology. This study aimed to examine the relationship between red cell distribution width and the presence of slow coronary flow syndrome. METHODS: In total, 185 patients with slow coronary flow syndrome and 183 age- and gender-matched subjects with normal coronary flow (controls) were prospectively enrolled in this study. Red cell distribution width and C-reactive protein were measured upon admission, and the results were compared between the patients with slow coronary flow syndrome and normal controls. RESULTS: Red cell distribution width levels were significantly higher in the patients with slow coronary flow syndrome than the normal controls. Moreover, the data showed that the plasma C-reactive protein levels were also higher in the patients with slow coronary flow syndrome than in the normal controls. In addition, a multivariate analysis indicated that C-reactive protein and red cell distribution width were the independent variables most strongly associated with slow coronary flow syndrome. Finally, the red cell distribution width was positively correlated with C-reactive protein and mean thrombosis in the myocardial infarction frame counts of the patients with slow coronary flow syndrome. CONCLUSION: The data demonstrated that red cell distribution width levels are significantly higher and strongly positively correlated with both C-reactive protein and thrombosis in the myocardial infarction frame counts of patients with slow coronary flow syndrome. These findings suggest that red cell distribution width may be a useful marker for patients with slow coronary flow syndrome

Probiotic fermentation modifies the structures of pectic polysaccharides from carrot pulp

Previous studies have suggested that water-soluble polysaccharides from fermented carrot pulp (WSP-p) have stronger anti-diabetic effects than those from un-fermented carrot pulp (WSP-n). This study aimed to improve understanding of these functional differences by comparing their molecular structures. Weight-average molecular weights of WSP-p fractions were lower than those of the corresponding WSP-n fractions. While both WSPs had similar functional groups, more fragmented particles were observed on the surface of large particles of WSP-n than WSP-p. Monosaccharide composition and methylation analysis confirmed that both WSP-p and WSP-n were pectic polysaccharides, containing rhamnogalacturonan-I-type polysaccharides with 1,4-linked α-d-galacturonic acid residues and homogalacturonan regions with 1,4-GalpA linkages. 1H and 13C NMR showed that they had similar linkage patterns. These findings suggested that probiotic fermentation of WSP mainly cleaved the linkages between repeating units, and resulted in less polydisperse molecular size distributions

Interleukin-17A Contributes to Myocardial Ischemia/Reperfusion Injury by Regulating Cardiomyocyte Apoptosis and Neutrophil Infiltration

ObjectivesThis study tested whether interleukin (IL)-17A is involved in the pathogenesis of mouse myocardial ischemia/reperfusion (I/R) injury and investigated the mechanisms.BackgroundInflammatory processes play a major role in myocardial I/R injury. We recently identified IL-17A as an important cytokine in inflammatory cardiovascular diseases such as atherosclerosis and viral myocarditis. However, its role in myocardial I/R injury remains unknown.MethodsThe involvement of IL-17A was assessed in functional assays in mouse myocardial I/R injury by neutralization/repletion or genetic deficiency of IL-17A, and its mechanism on cardiomyocyte apoptosis and neutrophil infiltration were further studied in vivo and in vitro.ResultsInterleukin-17A was elevated after murine left coronary artery ligation and reperfusion. Intracellular cytokine staining revealed that γδT lymphocytes but not CD4+ helper T cells were a major source of IL-17A. Anti–IL-17A monoclonal antibody treatment or IL-17A knockout markedly ameliorated I/R injury, as demonstrated by reduced infarct size, reduced cardiac troponin T levels, and improved cardiac function. This improvement was associated with a reduction in cardiomyocyte apoptosis and neutrophil infiltration. In contrast, repletion of exogenous IL-17A induced the opposite effect. In vitro study showed that IL-17A mediated cardiomyocyte apoptosis through regulating the Bax/Bcl-2 ratio, induced CXC chemokine-mediated neutrophil migration and promoted neutrophil-endothelial cell adherence through induction of endothelial cell E-selectin and inter-cellular adhesion molecule-1 expression.ConclusionsIL-17A mainly produced by γδT cells plays a pathogenic role in myocardial I/R injury by inducing cardiomyocyte apoptosis and neutrophil infiltration

Cell Signaling of Caenorhabditis elegans in Response to Enterotoxigenic Escherichia coli Infection and Lactobacillus zeae Protection

Enterotoxigenic Escherichia coli (ETEC) infection causes the death of Caenorhabditis elegans, which can be prevented by certain Lactobacillus isolates. The host response of C. elegans to ETEC infection and its regulation by the isolates are, however, largely unclear. This study has revealed that, in agreement with the results of life-span assays, the expression of the genes encoding p38 mitogen-activated protein kinase (MAPK) pathway (nsy-1, sek-1, and pmk-1), insulin/insulin-like growth factor (DAF/IGF) pathway (daf-16), or antimicrobial peptides (lys-7, spp-1, and abf-3) and other defensing molecules (abf-2, clec-85) was upregulated significantly when the wild-type nematode (N2) was subjected to ETEC infection. This upregulation was further enhanced by the pretreatment with Lactobacillus zeae LB1, but not with L. casei CL11. Mutants defective in the cell signaling of C. elegans were either more susceptible (defective in NSY-1, SEK-1, PMK-1, or DAF16) or more resistant (defective in AGE-1, DBL-1, SKN-1, or SOD-3) to ETEC infection compared with the wild-type. Mutants defective in antimicrobial peptides (LYS-7, SPP1, or ABF-3) were also more susceptible. In addition, mutants that are defective in NSY-1, SEK-1, PMK-1, DAF16, ABF-3, LYS-7, or SPP1 showed no response to the protection from L. zeae LB1. The expression of the genes encoding antimicrobial peptides (lys-7, spp-1, and abf-3) and other defensing molecules (abf-2, clec-60, and clec-85) were almost all upregulated in AGE-1- or DBL-1-defective mutant compared with the wild-type, which was further enhanced by the pretreatment of L. zeae LB1. The expression of these genes was, however, mostly downregulated in NSY-1- or DAF-16-defective mutant. These results suggest that L. zeae LB1 regulates C. elegans signaling through the p38 MAPK and DAF/IGF pathways to control the production of antimicrobial peptides and defensing molecules to combat ETEC infection

Liver-heart crosstalk controls IL-22 activity in cardiac protection after myocardial infarction.

Interleukin (IL)-22 regulates tissue inflammation and repair. Here we report participation of the liver in IL-22-mediated cardiac repair after acute myocardial infarction (MI). Methods: We induced experimental MI in mice by ligation of the left ascending artery and evaluated the effect of IL-22 on post-MI cardiac function and ventricular remodeling. Results: Daily subcutaneous injection of 100 µg/kg mouse recombinant IL-22 for seven days attenuated adverse ventricular remodeling and improved cardiac function in mice at 28 days after left anterior descending coronary artery ligation-induced MI. Pharmacological inhibition of signal transducer and activator of transcription (STAT3) muted these IL-22 activities. While cardiomyocyte-selective depletion of STAT3 did not affect IL-22 activities in protecting post-MI cardiac injury, hepatocyte-specific depletion of STAT3 fully muted these IL-22 cardioprotective activities. Hepatocyte-derived fibroblast growth factor (FGF21) was markedly increased in a STAT3-dependent manner following IL-22 administration and accounted for the cardioprotective benefit of IL-22. Microarray analyses revealed that FGF21 controlled the expression of cardiomyocyte genes that are involved in cholesterol homeostasis, DNA repair, peroxisome, oxidative phosphorylation, glycolysis, apoptosis, and steroid responses, all of which are responsible for cardiomyocyte survival. Conclusions: Supplementation of IL-22 in the first week after acute MI effectively prevented left ventricular dysfunction and heart failure. This activity of IL-22 involved crosstalk between the liver and heart after demonstrating a role of the hepatic STAT3-FGF21 axis in IL-22-induced post-MI cardiac protection

The prevalence of metabolic syndrome and cardiovascular risk factors in adults in southern China

<p>Abstract</p> <p>Background</p> <p>The metabolic syndrome has been shown to increase the incidence of cardiovascular disease. Little information exists on the prevalence of the metabolic syndrome for southern Chinese. We therefore investigate the prevalence of the metabolic syndrome in a southern Chinese population with 85 million residents.</p> <p>Methods</p> <p>The Guangdong Nutrition and Health Survey 2002 is a cross-sectional survey designed to assess the health and nutritional status of 85 million residents in Guangdong province located in southern China. Stratified multistage random sampling method was applied in this survey and a provincial representative sample of 6,468 residents aged 20 years or above was obtained in the present study. The participants received a full medical check-up including measurement of blood pressure, obesity indices, fasting lipids and glucose levels. Data describing socioeconomic and lifestyle factors was also collected through interview. Metabolic syndrome was defined in accordance with the International Diabetes Federation criteria.</p> <p>Results</p> <p>The prevalence of metabolic syndrome was 7.30%, translating into a total of 4.0 million residents aged 20 years or above having the condition in this southern Chinese population. The urban population had higher prevalence of the syndrome than the rural population (10.57% vs 4.30%). Females had a higher prevalence of metabolic syndrome than males (8.99% vs 5.27%). More than 60% of the adults had at least one component of the metabolic syndrome.</p> <p>Conclusions</p> <p>Our results indicate that a large proportion of southern Chinese adults have the metabolic syndrome and associated risk factors. The metabolic syndrome has become an important public health problem in China. These findings emphasize the urgent need to develop population level strategies for the prevention, detection, and treatment of cardiovascular risk in China.</p