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OBJECTIVE: We aimed at investigating the possible role and mechanism of NEAT1 in the pathogenesis of diabetic cataract. PATIENTS AND METHODS: YY1 and NEAT1 expressions in anterior lens capsule collected from diabetic cataract (DC) patients and normal controls were examined by quantitative real-time polymerase chain reaction (qRT-PCR) analysis, and their correlation was analyzed. The binding site between YY1 and NEAT1 sequences was predicted by JASPAR and detected by Dual-Luciferase reporter assay and chromatin immunoprecipitation (ChIP) assay. The proliferation and apoptosis of high-glucose-induced cells with NEAT1 knockdown were detected. Potential downstream targets of NEAT1 were predicted by bioinformatics and detected by Dual-Luciferase reporter assay. RESULTS: YY1 and NEAT1 expressions in the anterior capsule tissue of DC lens were remarkably reduced and positively correlated. Dual-Luciferase reporter assay and ChIP confirmed that YY1 could bind to locus 2 of NEAT1. Knockdown of NEAT1 inhibited proliferation while promoted apoptosis under high glucose conditions. Further mechanism studies revealed that knockdown of NEAT1 could upregulate microRNA-205-3p, and MMP16 was a potential target of miR-205. CONCLUSIONS: The low expression of YY1 induces NEAT1 downregulation, which regulates microRNA-205-3p/MMP16 axis and thus participates in the development of DC. [ABSTRACT FROM AUTHOR]

Investigates the effects of pump polarization on the performance of synchronously pumped mode-locked dye lasers. Energy level model used in the dye laser analysis; Temporal traces of the output pulses with pump polarization angles for the threshold parameters.

The replacement of SII CH4-C2H6-C3H8 hydrates in sandy sediments by CO2/N2 is studied to investigate the gas recovery from SII gas hydrate reservoirs. It was found that CH4 was the easiest one to be replaced in all experiments, and CO2/N2 played different roles during replacement in different CO2 concentrations. Particularly, the addition of N2 in replacement gas can cause the decrease in the replacement efficiency, which was related with the difference in swapping patterns. The increase of the N2 concentration may strengthen the structural stability of SII hydrates and lead to reducing the portion of SII hydrates transformed into SI hydrates. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Acute lung injury is a severe disease with a high rate of mortality, leading to more important illness. We aimed at exploring the protective role and potential mechanisms of lidocaine on lipopolysaccharide (LPS)-induced acute lung injury (ALI). MATERIALS AND METHODS: Sprague Dawley (SD) rats were randomly assigned to control group receiving 0.9% saline solution, LPS group treated with 4 mg/kg LPS i.p., LPS + lidocaine (treated with 4 mg/kg LPS i.p. followed by giving 1 mg/kg, 3 mg/kg, 5 mg/kg of lidocaine i.v.). Lung specimens and the bronchoalveolar lavage fluid (BALF) were collected for histopathological examination and biochemical analyze 12 h after LPS induction. The cytokines expression of TNF-α, IL-6 and MCP-1 was measured by ELISA. In addition, the malondialdehyde (MDA) content, the activities of total antioxidant capacity (T-AOC) and superoxide dismutase (SOD) in lung tissues were also detected using ELISA. The protein expressions of p38, p-p38, p65, p-p65 and IκB were analyzed by Western blot. RESULTS: The results indicated that after lidocaine treatment was able to decrease significantly wet-to-dry (W/D) ratio and ameliorate the histopathologic damage. Additionally, total protein content and the number of leukocytes in BALF significantly decreased. ELISA result indicated that the levels of TNF-α, IL-6 and MCP-1 in BALF were markedly suppressed. Meanwhile, the activities of T-AOC and SOD in lung tissues significantly increased, while the content of MDA significantly decreased after treatment with lidocaine. Moreover, Western blot suggested that lidocaine inhibited phosphorylation of NF-κB p65 and p38 MAPK. CONCLUSIONS: Therefore, lidocaine could ameliorate the LPS-induced lung injury via NF-κB/p38 MAPK signaling and excessive inflammatory responses, providing a potential for becoming the anti-inflammatory agent against lung injury. [ABSTRACT FROM AUTHOR]

The evolution routes and development stages in hydrological sciences are summarised from the following three dimensions: research object, discipline and methodology, by means of the descriptive-explanatory-humanistic ideology. Modern technical breakthroughs and socioeconomic developments have promoted hydrology from geographical hydrology, engineering or applied hydrology to water resources hydrology in terms of the focus of research objectives or problems. It has been observed from the point of view of methodology that hydrological sciences go through deterministic hydrology, stochastic hydrology, isotope hydrology, digital hydrology, etc. Hydrological sciences in the context of discipline dimensions can be divided into three main categories: physical hydrology, chemical/environmental hydrology, biological hydrology including eco-hydrology and socio-hydrology, although there are overlaps between these due to the complex and intertwined water-related challenges facing the hydrological community and other geosciences. Humans have played a significant role in changing land uses throughout the world and therefore, socio-hydrology is an increasingly significant branch of the hydrological sciences. It can be seen from analyses that biological hydrology is a new approach to cope with global change issues, and a new frontier direction in the field of hydrological sciences. It can also be seen from dialectical analysis of the different stages in the evolution of hydrology, that new frontiers or directions requiring investigation, scientific recognition and technical innovation will continue to be generated in the field of hydrology. The 3-dimensional diagram of evolution routes of hydrological sciences may provide some ideas for Panta Rhei, the new IAHS Science Initiative 2013-2022 for hydrological research under changing human and environmental systems in the real world. [ABSTRACT FROM AUTHOR]