Effects of storm runoff on the spatial-temporal variation and stratified water quality in Biliuhe Reservoir, a drinking water reservoir.

Stormflow runoff is an important non-point source of pollution in drinking water reservoirs. Storm runoff is usually very turbid and contains a high concentration of organic matter, therefore affecting water quality when it enters reservoirs. In order to investigate the impact of storm runoff on spatial-temporal variation and stratification of water quality during this rainstorm event, the inflow process of the storm runoff was studied through a combination of field investigation and simulation using the Delft3D-Flow model. Water samples were collected from Biliuhe Reservoir at four different periods: before storm runoff, storm runoff flood peak period, 1 week after storm runoff, and 5 weeks after storm runoff. The results showed that the input of storm runoff resulted in a significant increase in the nitrogen (N) and phosphorus (P) in the reservoir water, especially in the reservoir entrance. The concentrations of total nitrogen (TN) and total phosphorus (TP) gradually decreased after the flood peak period; however, the average concentrations of TN and TP in the entire reservoir remained higher than those before the storm runoff levels for an extended duration. The storm runoff will greatly contribute to the contamination of water quality in a reservoir, and the water quality cannot be quickly restored by self-purification in the short term. During the flood peak period, under the influence of density current, the electrical conductivity (EC) and turbidity increased significantly in the water depth of 10-15 m, so that the reservoir water had obvious stratification between 10 and 15 m. The form of pollutants in storm runoff was mostly in particle phosphorus. Total particulate phosphorus (TPP) concentration was 0.015 ± 0.011 mg/L, accounting for 44.12% of total phosphorus (TP) concentration in storm runoff flood peak period. The process of a rainstorm caused runoff, which carried high levels of turbidity, particulate phosphorus, and organic matter. The storm runoff disrupts the stratification of the reservoir water. In terms of vertical distribution, the turbidity in the reservoir area increased to 73.75 NTU. Therefore, the occurrence of significant turbidity density flow in the reservoir is frequently accompanied by intense rainfall events. Gaining insights into the impact of storm runoff on the vertical distribution of reservoir turbidity can help managers in selecting an appropriate inlet height to mitigate high turbidity outflow.

[Protective effect and mechanism of ß-CM7 on renin angiotensin system & diabetic cardiomyopathy].

This article aimed at exploring the effects and protective mechanism of ß-CM7 on renin angiotensin system (RAS) in diabetic rats myocardial tissue. We divided 32 male SD rats into 4 groups: control group, diabetic model control group, insulin (3.7x10(-8) mol/d) treatment group and ß-CM7 (7.5x10(-8) mol/d) treatment group. After 30 days, all rats were decapitated and myocardical tissues were collected immediately. After injection, ß-CM7 could decrease the content of Ang II, increase the content of Angl-7. And ß-CM7 could improve the mRNA of AT1 receptor and Mas receptor. ß-CM7 also could improve the mRNA of ACE and ACE2, enhance the activity of ACE and ACE2. These data confirmed tli ß-CM7 could activate ACE2-Angl-7-Mas axis, negative passage in RAS, to inhibit the expression ACE mnRiJA and protein in rat myocardium, alleviate the myocardial tissue damage induced by Ang II. The effect of ß-CM7 on inhibiting myocardium damage might be related to ACE/ACE2 passageway.

Protective effect of ß-casomorphin-7 on cardiomyopathy of streptozotocin-induced diabetic rats via inhibition of hyperglycemia and oxidative stress.

ß-Casomorphin-7 (ß-CM-7) is regarded as the most representative milk-derived bioactive peptide. The present work studies the efficacy of ß-CM-7 against myocardial injury in streptozotocin-induced diabetic rats, focusing on the following assays: (1) the level of blood glucose and advanced glycosylation end product (AGE), the activity of lactate dehydrogenase (LDH) in serum; (2) the level of hydrogen peroxide (H2O2), the activity of Na(+)K(+)-ATPase, Ca(2+)Mg(2+)-ATPase and enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) in myocardial tissue; (3) the protein expression of glucose transporter-4 (GLUT-4) in myocardial tissue. It showed that with the influence of ß-CM-7, the levels of blood glucose of ß-CM-7 treatment group decreased markedly compared with model group (P<0.01) accompanied with their alleviated symptoms of diabetes. In the antioxidant and oxidant levels, ß-CM-7 treatment group signified a remarkable increase in the activity of GSH-Px, SOD and CAT of the anti-oxidation system and meanwhile demonstrated a considerable reduction in H2O2 content (all P<0.05) in comparison with model group. We also found both the content of AGE and the activity of LDH of ß-CM-7 treated group considerably reduced while the content of GLUT-4 and the activity of Na(+)K(+)-ATPase and Ca(2+)Mg(2+)-ATPase of ß-CM-7 treated group increased obviously (P<0.05). Meanwhile the cardiac indexes were significantly lessened. Thus our assay validates that the remedy employing ß-CM-7 may treat diabetic cardiomyopathy with high efficacy predominantly associated with the mechanism that ß-CM-7 ameliorates myocardial energy metabolism and abates free-radical-mediated oxidative stress in blood and myocardium.

ß-Casomorphin-7 attenuates the development of nephropathy in type I diabetes via inhibition of epithelial-mesenchymal transition of renal tubular epithelial cells.

This study was designed to investigate the putative protective effect of ß-casomorphin-7 on diabetic nephropathy in a rat model, and to explore the possible mechanism of this effect. SD rats were randomly divided into the following three groups: control group, diabetes group and ß-casomorphin-7-treatment group. All rats were euthanized after 30 days with or without ß-casomorphin-7 treatment. Biochemical parameters including blood glucose and renal function were quantified. The concentration of plasma TGF-ß1 was measured by ELISA. Histopathological changes to the kidney were studied by Masson and Sirius red staining. Expressions of α-smooth muscle actin (α-SMA), E-cadherin, vimentin, cytokeratin19 and TGF-ß1 mRNA in rat renal cortices were analyzed by real-time PCR. Changes in α-SMA and E-cadherin protein expression in rat renal cortices were quantified by Western blot. ß-Casomorphin-7 treatment of diabetic rats reduced urinary glucose, urinary protein, serum creatinine, blood urinary nitrogen, plasma TGF-ß1 and the ratio of kidney: body weight. Masson and Sirius red staining showed that ß-casomorphin-7 treatment attenuated renal interstitial fibrosis in diabetic rats. Compared to the control rats, diabetic rats had elevated expressions of α-SMA, vimentin and TGF-ß1 mRNA and α -SMA protein and decreased expression of E-cadherin and cytokeratin19 mRNA, and E-cadherin protein. ß-Casomorphin-7 treatment of diabetic rats partially normalized these changes. Our results suggest that administration of ß-casomorphin-7 attenuates renal interstitial fibrosis caused by diabetes. This protective effect may be associated, in part, with down regulation of epithelial-mesenchymal transition of renal tubular epithelial cells.