[Analysis of the Urban Water Eco-environment Protection Strategy in the Beijing-Tianjin-Hebei Region from "Three Waters" Overall Planning].

Clarifying the direction and strategy of water eco-environment protection in the Beijing-Tianjin-Hebei region is of great significance for realizing the water eco-environment protection and high-quality, coordinated development of the Beijing-Tianjin-Hebei area, as well as the goal of building a beautiful China by 2035. From the perspective of "Three Waters" overall planning, based on the urban scale of the Beijing-Tianjin-Hebei region, this study constructed six dimensions of water resources, water environment, water ecology (Three Waters), socio-economic development level, pollutant emissions, and environmental governance efforts. The water eco-environment protection strategy analysis system provided a logical framework for quantifying the current status of the water eco-environment. The ideal value was compared in each city, the PROMETHEE method was used to quantify the gap between each city and the ideal value of water eco-environment protection, and the current situation of the water eco-environment in Beijing-Tianjin-Hebei cities was evaluated. Additionally, water eco-environment protection strategies were formulated according to local conditions. The ranking of the comprehensive level of water eco-environment protection from high to low was Beijing>Tianjin>Qinhuangdao>Hengshui>Zhangjiakou>Langfang>the mean value of net flow value (Phi)>Handan>Chengde>Cangzhou>Baoding>Tangshan>Shijiazhuang>Xingtai; a large gap remained between the level and the ideal value. The hierarchical analysis showed that the advantages and disadvantages of each city's water eco-environment protection were different from dimensions to indicators, and they had the characteristics of local water eco-environment protection. Future efforts should determine the water ecological, environmental protection indicator level of each city in the Beijing-Tianjin-Hebei region, conduct a separate analysis for each city, and propose protection strategies for future development, as well as continue to help the water eco-environmental protection in the Beijing-Tianjin-Hebei region.

Association between serum soluble membrane type matrix metalloproteinase-1 (MT1-MMP) levels and bone mineral density, and biochemical markers in postmenopausal women.

BACKGROUND: Recently, membrane type matrix metalloproteinase-1 (MT1-MMP) was found to participate in bone metabolism. We investigated the relationship between serum MT1-MMP and bone mineral density (BMD) as well as bone metabolic markers in 206 Chinese postmenopausal women aged 43-80 years. METHODS: Western analysis and ELISA were performed to detect serum soluble MT1-MMP levels. BMD was measured by dual energy X-ray absorptiometry (DXA). Serum alkaline phosphatase (BAP) and N-telopeptides of type I collagen (NTX) were assayed using ELISA. RESULTS: We found that soluble MT1-MMP abundantly existed in human serum as protein lack of transmembrane domain. Serum MT1-MMP levels were detectable in all participants and the range of value was 221.2-863.0 ng/ml (435.6+/-98.2 ng/ml). We found a significant negative weaker correlation between MT1-MMP and BMD at lumbar spine, total hip (Thip), and femoral neck (FN) (all P<0.05). After adjustment for age and BMI, the correlation with BMD at FN and Thip disappeared (all P>0.05). Multiple linear stepwise regression analysis showed that MT1-MMP was not a determinant factor for BMD. The significant positive correlations between MT1-MMP and BAP, NTX were found, and remained significant after adjustment for age and BMI (all P<0.05). Moreover, serum MT1-MMP, BAP, and NTX decreased in response to alendronate therapy. CONCLUSION: Circulating MT1-MMP and bone turnover markers are correlated, and serum MT1-MMP levels may rise with increase in bone turnover.

Apelin and its receptor are expressed in human osteoblasts.

OBJECTIVES: Apelin is a recently discovered peptide that is the endogenous ligand for the orphan G-protein-coupled receptor APJ. Adipocytes can express and secrete apelin. The aim of this study was to characterize apelin and APJ expression in human osteoblasts and to investigate the effects of apelin on osteoblasts. RESULTS: Apelin and APJ were expressed in human osteoblasts. Apelin stimulated proliferation of human osteoblasts, but had no effect on alkaline phosphatase (ALP) activity, osteocalcin and type I collagen production in human osteoblasts. Suppression of APJ with small-interfering RNA (siRNA) abolished the apelin-induced cell proliferation. Apelin induced activation of Akt (Phosphatidylinositol-3 kinase downstream effector), but not MAPKs, such as c-jun N-terminal Kinase (JNK), p38 and ERK1/2 in human osteoblasts. This effect was blocked by suppression of APJ with siRNA. Furthermore, LY294002 (PI3 kinase inhibitor) blocked the activation of Akt by apelin and abolished the apelin-induced cell proliferation. CONCLUSIONS: Human osteoblasts express apelin and APJ and apelin enhances human osteoblast proliferation, but has no effect on osteoblast differentiation, and APJ/PI3 kinase/Akt pathway is involved in the proliferation response. These findings suggest that apelin may function as a mitogenic agent for osteoblasts.

Rhein lysinate decreases inflammation and adipose infiltration in KK/HlJ diabetic mice with non-alcoholic fatty liver disease.

The objective of this study was to investigate the protective effects of rhein lysinate (RHL) on the liver. Mice were divided into four groups: C57BL/J control, the KK/HlJ diabetic model, and 25 and 50 mg/kg/day RHL-treated KK/HlJ groups. The KK/HlJ diabetic mouse model was made by injecting STZ and feeding mice diabetic food. At 16 weeks, mice were sacrificed and their livers were harvested. The results indicated that compared with the C57BL/J control group, the body weights, liver weights and liver weight-to-body weight ratio were increased in KK/HlJ diabetic mice; however, these values were decreased following treatment with RHL. Compared with the C57BL/J control, KK/HlJ diabetic mice had a significantly lower level of SOD and GSH-px in their livers, but had a significantly higher level of MDA. However, these effects were ameliorated by RHL. Hepatic adipose infiltration was observed in KK/HlJ mice, but not in C57BL/J mice. RHL decreased the incidence of hepatic adipose infiltration and significantly decreased the expression of TNF-α, IL-6, NF-κB, SREBP-1c, and Fas, as well as the phosphorylation of NF-κB in the liver. In conclusion, RHL can improve hepatic function by decreasing hepatic adipose infiltration and the expression of inflammatory factors.

[Effect of nutrient support on severe infant pneumonia].

OBJECTIVE: To explore the effect of nutrient support on severe infant pneumonia. METHODS: Prospective study was conducted on the outcome of 567 inpatients suffering from severe pneumonia in 13 hospitals randomly selected in Hunan. Twelve factors were surveyed and data analyzed by multiple logistic regression. RESULTS: Malnnutrition, anemia and rickets were risk factors in severe pneumonia, and nutrient support had protective effect on severe pneumonia. CONCLUSION: Nutrient support contributes to the positive outcome of severe infant pneumonia.

Vasoactive intestinal peptide induces vascular endothelial growth factor production in human HaCaT keratinocytes via MAPK pathway.

Psoriasis is a chronic skin disease characterized by abnormal keratinocyte proliferation and differentiation, inflammation, and angiogenesis. Although dysfunction of the immune system is known to be an important factor in the pathogenesis of psoriasis, there is also strong evidence that psychological stresses are involved. Neuropeptides are thought to be main mediators of neurogenic inflammation, presumably involved in the pathogenesis of psoriasis. Vasoactive intestinal peptide (VIP) is one of the major neuropeptides in human and rodent skin. In the present study, we examined the effect and mechanism of VIP on vascular endothelial growth factor (VEGF) production by HaCaT cells which is a spontaneous, immortalized, human keratinocyte cell line. Our data indicate the mRNA and protein levels of VEGF by VIP were increased in a concentration-dependent manner. However, this increase was abrogated by pretreatment with an extracellular signal-regulated kinase (ERK) inhibitor PD98059 or p38MAPK inhibitor SB203580; pretreatment with c-Jun N-terminal kinase (JNK) inhibitor SP600125 did not attenuate the effects of VIP on the expression of VEGF. In addition, VIP treatment induced rapid phosphorylation of ERK1/2 and p38MAPK, and PD98059 and SB203580 were able to inhibit VIP-induced phosphorylation of ERK1/2 and p38MAPK, respectively. These results suggest that VIP increases the expression of VEGF through the ERK1/2 and p38MAPK signaling pathway in human HaCaT cells.