Analyzing river disruption factors and ecological flow in China's Liu River Basin amid environmental changes.

Water resources variability and availability in a basin affect river flows and sustain river ecosystems. Climate change and human activities disrupt runoff sequences, causing water environmental issues like river channel interruptions. Therefore, determining ecological flow in changing environments is challenging in hydrological research.

Quantifying the impact of climate variability and human activities on streamflow variation in Taoer River Basin, China.

Climate variability and human activity are the two driving forces that alter the hydrological cycle and spatiotemporal distribution of water resources. Using the Taoer River Basin (TRB) as an example, this study analyzed the impacts of climate variability and human activities on streamflow discharge in various periods and the resulting hydrological alterations. First, historical streamflow data were divided into four periods (baseline period and altered periods 1, 2, and 3).

[Distribution Characteristics and Influencing Factors of Nitrate Pollution in Shallow Groundwater of Liujiang Basin].

Taking the nitrate in shallow groundwater of Liujiang basin as the research object, a total of 215 groups of shallow groundwater samples were collected during the wet period in July 2014 and the drought period in April 2015 on the basis of groundwater pollution investigation. The characteristics of spatial and temporal variability and the account of nitrate pollution were analyzed based on the model of semivariogram, the geostatistics of ArcGIS and factor analysis, respectively. The results showed that the study region in the southeast was the main nitrate-polluted area, with concentrations of up to 30-120 mg · L⁻¹, in both wet and drought periods, while the nitrate-contaminated area in drought period was about 1.

IL-33 accelerates cutaneous wound healing involved in upregulation of alternatively activated macrophages.

IL-33 is a recently recognized member of the IL-1 family and has been best identified as a potent inducer of Th2-type immune responses. Increasing evidence, however, indicates that IL-33 also represents an important mediator of mucosal healing and epithelial restoration and repair. In this study, we further explore the potential effect of IL-33 in cutaneous wound healing.

IL-33 promotes Staphylococcus aureus-infected wound healing in mice.

Interleukin (IL)-33, a newly identified member of IL-1 family of cytokines, plays a crucial role in polarizing Th2-associated immune responses. Recently growing evidence indicates that IL-33 also represents an important mediator of mucosal healing and epithelial restoration. In this study, we investigated the effect of IL-33 on antimicrobial infection and wound healing using a Staphylococcus aureus-infected incision model in mice.

Sirolimus ameliorates inflammatory responses by switching the regulatory T/T helper type 17 profile in murine colitis.

Inflammatory bowel disease is characterized by dysregulated immune responses in inflamed intestine, with dominance of interleukin-17 (IL-17)--producing cells and deficiency of regulatory T (Treg) cells. The aim of this study was to investigate the effect and mechanisms of sirolimus, an inhibitor of the mammalian target of rapamycin, on immune responses in a murine model of Crohn's disease. Murine colitis was induced by intrarectal administration of 2,4,6-trinitrobenzene sulphonic acid at day 0.

Heme oxygenase-1 ameliorates LPS-induced acute lung injury correlated with downregulation of interleukin-33.

Although studies have shown that heme oxygenase-1 (HO-1) can abrogate leukocyte recruitment and tissue injury after LPS stimulation, the underlying mechanisms remain incompletely understood. Interleukin (IL)-33, a new member of the IL-1 family, is found to play a crucial immunoregulatory effect on the MD2/TLR4 complex expression. Moreover, TLR4 further promotes the activation of NF-κB and the production of proinflammatory mediators, which exacerbate neutrophil infiltration and organ damage.

Association of -27T>C and its haplotype at the putative promoter for IgA-specific receptor gene with IgA nephropathy among the Chinese Han population.

Background: One-third to half of IgA nephropathy (IgAN) patients have raised serum IgA levels. Decreased clearance of IgA/IgA complex has been observed in IgAN patients. FCAR codes for IgA-specific receptor and plays an important role in IgA metabolism.

[Effect of sodium phenylbutyrate on the apoptosis of human tongue squamous cancer cell line and expression of p21 and survivin genes].

Objective: To examine the effects of sodium phenylbutyrate on the apoptosis of human tongue squamous cancer cell line and expression of p21 and survivin genes.

Methods: The inhibition effects of sodium phenylbutyrate on Tca8113 and human tongue squamous cell carcinoma (TCSSA) cell lines were detected by methyl thiazoly terazolium (MTT) and the apoptosis of the cancer cells after being induced by sodium phenylbutyrate examined by flow cytometry (FCM). The expression of p21 and survivin genes were observed with Western blotting and RT-PCR.

Heme oxygenase-1 upregulation improves lipopolysaccharide-induced acute lung injury involving suppression of macrophage migration inhibitory factor.

Although studies have demonstrated that heme oxygenase-1 (HO-1) prevents leukocyte infiltration and organ damage following LPS challenge, the mechanisms involved in this protection are incompletely understood. Macrophage migration inhibitory factor (MIF) is thought to play a pivotal role in modulation of inflammatory and immune response through upregulation of TLR4 expression. Activation of TLR4 results in the production of proinflammatory mediators including MIF, which induce neutrophils recruitment and subsequent tissue insults.

[Radiosensitivity of nasopharyngeal carcinoma in relation to cell cycle synchronization effect of tumor necrosis factor alpha].

Objective: To investigate the effect of tumor necrosis factor alpha (TNFalpha) on radiosensitivity of nasopharyngeal carcinoma (NPC) in relation to TNFalpha-induced cell cycle synchronization.

Methods: The radio-resistance of a NPC cell line subclone CNE-2Z-S1 was verified by in vivo experiments and flow cytometry was performed to evaluate cell cycle synchronization in TNFalpha-treated CNE-2Z-S1 cells. The radiosensitivity of the cell synchronized CNE-2Z-S1 cells was determined by clone formation in vitro and in vivo experiment in nude mice.