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Ensuring stable water quality standards in drinking water source reservoirs plays a decisive role in ensuring water safety. In this study, a series of indicators such as secchi disk transparency (SD), permanganate index (CODMn), total phosphorus (TP), total nitrogen (TN), ammonia nitrogen (NH3-N) and Chlorophyll.a (Chl.a) were used to detect and characterize the water quality of Shanxi Reservoir in Wenzhou, China. And explore the water quality change points by combining the Water Pollution Index (WPI), Mann-Kendall test and rescaled extreme difference analysis. The results show that the overall water quality of Shanxi Reservoir is excellent and can safely perform its watershed function. The water quality pollution index value in the reservoir area showed an increasing trend, with an overall value range of 0.34-0.94. The water quality was monitored in the process of organic pollution, phosphorus and NH3-N with a significant trend of improvement. Future trends in water quality indicate that water quality in the reservoir will not deteriorate. Change points for SD, Chl.a, TN and CODMn occur in May 2019, December 2019, December 2018 and May 2021, NH3 -N and TP have no water quality change points throughout the monitoring process. It is recommended to avoid nitrogen pollution in water bodies to prevent harming water ecological safety. [ABSTRACT FROM AUTHOR]

The two-plasmon-decay instability (TPD) in the large-incidence-angle regime is studied via fluid and particle-in-cell (PIC) simulations. It is found that the TPD threshold in this regime within a narrow incidence angle range close to 60∘ can be orders of magnitude lower than the normal-incidence threshold. A threshold formula is proposed for this regime and is verified by fluid and PIC simulations. PIC simulations show significant laser absorption and energetic electron generation once TPD is excited. The incident angle and the laser spot size have a significant influence on the TPD in the large-incidence-angle regime. The low threshold and significant hot electron generation in this regime pose potentially unexpected preheating risks to inertial confinement fusion. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the protective effect of dexmedetomidine (Dex) against renal injury in diabetic nephropathy (DN) rats by inhibiting the nuclear factor-κB (NF-κB) pathway. MATERIALS AND METHODS: A total of 36 Sprague-Dawley rats were randomly divided into three groups, including: normal group (n=12), model group (n=12) and Dex group (n=12). The rats underwent no treatment in normal group. In model group, the diabetes model was successfully established, and normal saline was intraperitoneally injected after operation. In Dex group, the diabetes model was established as well, and Dex was intraperitoneally injected after operation. After intervention for 2 weeks, the samples were taken for use. Blood urea nitrogen (BUN) and serum creatinine (Cr) were detected using a full-automatic biochemical analyzer. The expression of Caspase-3 was detected via immunohistochemistry. Western blotting was conducted to detect the protein expression of NF-κB. The apoptosis was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. In addition, the levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were determined via enzyme-linked immunosorbent assay (ELISA). RESULTS: The levels of BUN and Cr were significantly higher in model group and Dex group than those in normal group (p<0.05). However, they were significantly lower in Dex group than those in the model group (p<0.05). Immunohistochemistry results showed that the mean optical density of Caspase-3 positive expression increase remarkably in model group and Dex group when compared with normal group (p<0.05). However, it significantly declined in Dex group when compared with the model group (p<0.05). The results of Western blotting revealed that model group and Dex group exhibited evidently higher relative protein expression of NF-κB than normal group (p<0.05). However, Dex group displayed notably lower relative protein expression of NF-κB than model group (p<0.05). TUNEL assay demonstrated that the apoptosis rate increased significantly in the model group and Dex group when compared with normal group (p<0.05). However, it remarkably declined in Dex group in comparison with the model group (p<0.05). Finally, ELISA assay indicated that model group and Dex group had markedly higher levels of IL-6 and TNF-α than normal group (p<0.05). However, the levels of IL-6 and TNF-α were significantly lower in Dex group than model group (p<0.05). CONCLUSIONS: Dex inhibits inflammation and apoptosis by suppressing the NF-κB signaling pathway, thereby exerting a protective effect against renal injury in DN rats. [ABSTRACT FROM AUTHOR]

Hepatitis B virus ( HBV) infection is one of the major causes of chronic liver inflammation. Tim-3 acts as a negative regulatory molecule and plays a critical role in immune tolerance. In the current study, we investigated Tim-3 expression on peripheral monocytes and CD3+ CD16/ CD56+ natural killer like T ( NKT-like) cells in chronic hepatitis B ( CHB) patients. Peripheral blood mononuclear cells (PBMCs) were isolated from 52 CHB patients and 60 healthy controls. Tim-3+ CD14+ cells and Tim-3+ CD3+ CD16/ CD56+ cells were analyzed by flow cytometry. Results showed that expression of Tim-3 was significantly increased on both the monocytes and NKT-like cells in CHB patients than in controls ( P = 0.002 and P < 0.001, respectively). Tim-3 levels on monocytes and NKT-like cells were further upregulated in patients with acute-on-chronic liver failure ( ACLF). In addition, we assessed the correlation of Tim-3 expression with levels of alanine aminotransferase ( ALT) and tumor necrosis factor alpha ( TNF-α). Data revealed that Tim-3 expression on both monocytes and NKT-like cells was positively correlated with level of ALT ( r = 0.59, P < 0.001, and r = 0.60, P < 0.001, respectively), whereas Tim-3 expression on NKT-like cells was negatively correlated with serum level of TNF-α ( r = −0.54, P < 0.001) in CHB patients. Our results suggest that Tim-3 may play important roles in the pathogenesis of CHB. [ABSTRACT FROM AUTHOR]

Objective: To investigate the risk factors for the short-term outcome of patients with hepatitis B virus (HBV)-related acute-on-chronic liver failure (ACLF), and to establish a risk model for predicting the short-term outcome of these patients., Methods: A total of 338 patients with HBV-related ACLF who were admitted to 30 Lod hospital of PLA hospital from January 2010 to January 2014 were enrolled, and a prospective clinical follow-up was performed for them. Multivariate logistic regression was used to determine the risk factors for short-term (12 weeks) outcome, the predictive model with logistic regression equation was established, and the predictive value of this model was evaluated., Results: The multivariate logistic regression analysis showed that age, a family history of hepatitis B, hepatic encephalopathy (HE), hepatorenal syndrome (HRS), white blood cell (WBC), platelet (PLT), international normalized ratio (INR), total bilirubin (TBil), total bile acid (TBA), creatinine, Na, HBV DNA, and HBeAg were the independent risk factors for the short-term outcome of these patients. Logistic(p) = -4.466 + 1.192 age + 1.631 family history of hepatitis B + 1.091 HE + 1.631 HRS + 1.208 WBC -1.487 PLT + 1.092 INR + 1.446 TBil + 1.608 TBA -1.101 CHE + 1.279 CRE -1.713 Na + 1.032 HBV DNA + 0.833 HBeAg. The area under the receiver operating characteristic curve of the model for the prediction of short-term outcome was 0.930, the cut-off value was 3.16, the sensitivity was 0.860, and the specificity was 0.871. With the increasing scores of the equation, the mortality of patients tended to increase gradually., Conclusion: Age, a family history of hepatitis B, HE, HRS, WBC, PLT, INR, TBil, TBA, CHE, CRE, Na, HBV DNA, and HBeAg are the independent risk factors for the short-term outcome of patients with HBV-related ACLF. The model for predicting short-term outcome established on the basis of independent risk factors has a better clinical value in guiding clinical therapy.

In order to study the role of afferent renal nerves in 2K2C Goldblatt hypertension, the renal afferent nerves were selectively lesioned by bilateral T9-L2 spinal dorsal rhizotomy before clipping (internal diameter, 0.3 mm) of birenal arteries. Systolic blood pressure of the rat was measured by tail-cuff method. Concentrations of catecholamines, Ang II, and aldosterone were determined respectively by HPLC-EC and RIA, and vascular structural changes were measured by blood vessel micro-image analysis system coupled with a computer. The results showed that the concentrations of NE and E in medulla oblongata, adrenal gland and plasma, and of plasma Ang II and aldosterone as well as body weight of the rat were all significantly increased. The heart coefficient (heart wt/body wt), the media thickness, and the media thickness/lumen diameter in superior mesenteric arteries were also increased in 2K2C hypertensive rats (clipping, 6 wk) as compared with those in control rats. Bilateral rhizotomy delayed development of 2K2C hypertension and prevented above-mentioned vascular structural changes, the NE and E concentrations of medulla oblongata, adrenal gland and plasma were all decreased, hypothalamic NE and E were increased, and plasma Ang II level was not significantly changed. These results suggest that afferent renal nerves may play a partial role in the development of hypertension in 2K2C rats by activating sympathetic nervous system as a result of affecting metabolic activities of brain catecholaminergic neurons, and that high-plasma Ang II and aldosterone as well as heart hypertrophy and proliferation of vascular smooth muscle cells may also participate in the pathogenesis of hypertension in 2K2C rats.