Search

Mitochondrial aldehyde dehydrogenase 2 (ALDH2) is closely associated with organ injury. The aim of the present study was to investigate the change of ALDH2 expression in a rat model of sepsis-induced acute renal injury, and to observe the effect of ALDH2 inhibition on the kidney. A model of sepsis syndrome was established in Sprague-Dawley (SD) rats by cecal ligation and puncture (CLP). The rats were divided into sham, CLP and CLP + cyanamide (CYA, an ALDH2 inhibitor) groups. The hemodynamic parameters heart rate (HR) and mean arterial blood pressure (MABP) were measured. Plasma creatinine (CRE) and urea nitrogen (BUN) levels were measured using an automatic biochemical analyzer. Malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in the kidney tissue were measured. Histological changes of the kidney tissue were observed using hematoxylin and eosin staining and NF-κB p65 expression was observed by an immunohistochemical staining method. The expression of renal ALDH2 at the mRNA and protein levels was detected by reverse transcription-polymerase chain reaction and western blotting. In the CLP compared with the sham group after 24 h, the MABP was decreased, plasma CRE and BUN levels were elevated, the renal MDA level was increased and SOD activity was decreased. In addition, glomerular atrophy occurred, the renal protein expression of NF-κB p65 was increased, and the mRNA and protein expression levels of ALDH2 were decreased. In contrast with the CLP group, in the CLP + CYA group, the MABP and ALDH2 expression were further decreased while glomerular atrophy was aggravated. Furthermore, CRE, BUN, MDA levels and NF-κB p65 expression were further increased and SOD activity was further reduced. In this rat model of sepsis syndrome, the reduction of renal ALDH2 expression was accompanied by kidney injury. Inhibition of ALDH2 with CYA aggravated the renal injury, and was associated with the overproduction of reactive oxygen species and inflammatory reaction. [ABSTRACT FROM AUTHOR]

Background: Several studies on the association of tumor necrosis factor alpha (TNF-α) polymorphisms with recurrent pregnancy loss (RPL) risk have reported conflicting results. The present meta-analysis was conducted to provide a more precise estimation of these relationships and to investigate the real association between TNF-α polymorphisms and RPL. Methods: An extensive eligible literature search for relevant studies was conducted on PubMed, Embase, and The Cochrane Library from their inceptions to May 12, 2015. Specific inclusion criteria were used to evaluate articles. The odds ratio (OR) with 95% confidence intervals (CIs) were used to assess the strength of associations. Statistical analyses were performed by the STATA12.0 software. Results: 10 case-control studies including 1430 RPL patients and 1727 healthy controls were identified. Metaanalysis indicated that TNF-α-308G/A (rs1800629) polymorphism in the TNF-α gene correlated with elevated RPL risk whereas no significant association was observed between TNF-α-238G/A (rs361625) and RPL. Conclusions: The current meta-analysis demonstrates that TNF-α-308G/A polymorphism in the TNF-α gene is associated with susceptibility to RPL. [ABSTRACT FROM AUTHOR]

To study the roles of microRNA-223 (miR-223) in regulation of cell growth, we established a miR-223 over-expression model in HeLa cells infected with miR-223 by Lentivirus pLL3.7 system. We observed in this model that miR-223 significantly suppressed the proliferation, growth rate, colony formation of HeLa cells in vitro, and in vivo tumorigenicity or tumor formation in nude mice. To investigate the mechanisms involved, we scanned and examined the potential and putative target molecules of miR-223 by informatics, quantitative PCR and Western blot, and found that insulin-like growth factor-1 receptor (IGF-1R) was the functional target of miR-223 inhibition of cell proliferation. Targeting IGF-1R by miR-223 was not only seen in HeLa cells, but also in leukemia and hepatoma cells. The downstream pathway, Akt/mTOR/p70S6K, to which the signal was mediated by IGF-1R, was inhibited as well. The relative luciferase activity of the reporter containing wild-type 39UTR(39untranslated region) of IGF-1R was significantly suppressed, but the mutant not. Silence of IGF-1R expression by vector-based short hairpin RNA resulted in the similar inhibition with miR-223. Contrarily, rescued IGF-1R expression in the cells that over-expressed miR-223, reversed the inhibition caused by miR-223 via introducing IGF-1R cDNA that didn't contain the 39UTR. Meanwhile, we also noted that miR-223 targeted Rasa1, but the downstream molecules mediated by Rasa1 was neither targeted nor regulated. Therefore we believed that IGF-1R was the functional target for miR-223 suppression of cell proliferation and its downstream PI3K/Akt/mTOR/p70S6K pathway suppressed by miR-223 was by targeting IGF-1R. [ABSTRACT FROM AUTHOR]

Two new complexes [Zn(sal)(tpt)]·HO( 1), [Cd(sal)(tpt)(HO)]·HO( 2), have been obtained through ligands tpt and Hsal, where Hsal is salicylic acid and tpt is 2,4,6-tripyridyl-1,3,5-triazine, reacting with Zn(II) and Cd(II) salts. Their structures are fully characterized by IR spectroscopy, elemental analysis, single crystal X-ray diffraction. In complex 1, Zn(II) is coordinated by three N atoms and two O atom with a distorted square pyramidal coordination geometry. In 2, Each Cd(II) atom is seven-coordinated with a distorted pentagonal bipyramidal coordination geometry. The structural differences between two complexes show the influence of the coordinating orientation of metal ions. These two mononuclear complexes are further extended into three-dimensional structure via π-π, C-H···π and hydrogen bonding interactions. The solid state luminescent properties of complex 1, 2 are also reported. Graphical Abstract: Two complexes, [Zn(sal)(tpt)]·HO( 1), [Cd(sal)(tpt)(HO)]·HO( 2) have been prepared, and were characterized by elemental analysis, FT-IR and single-crystal X-ray diffraction. Structures indicate that exhibit that two complexes are single molecule structures. Two complexes are further extended into three-dimensional structure via π-π, C-H···π and hydrogen bonding interactions.[Figure not available: see fulltext.] [ABSTRACT FROM AUTHOR]

Uniform and water-soluble Ag@reduced graphene oxide (Ag@rGO) nanocomposites can be prepared by a facile approach in the absence of additional reductants, which display much better antibacterial properties than that of pure silver nanoparticles synthesized by microwave irradiation, and an equivalent antibacterial effect in comparison with that of the general antibacterial drug ampicillin. Their skin irritation tests with the use of rat models are taken in order to explore the toxicity of this nanocomposite, which confirm that no oedema or erythema appears on the injured rat skin after exposure to the as-prepared Ag@rGO nanocomposites. [ABSTRACT FROM AUTHOR]

Homogeneous diamond-like carbon (DLC) films were deposited on Si supports by a pulsed filtered cathodic vacuum arc deposition system. Using DLC films masked by Ni nanoparticles as precursors, highly aligned diamond-like carbon nanorod (DLCNR) arrays were fabricated by the etching of inductively coupled radio frequency oxygen plasma. The as-prepared DLCNR arrays exhibit excellent field emission properties with a low turn-on field of 2.005 V μm−1 and a threshold field of 4.312 V μm−1, respectively. Raman spectroscopy and x-ray photoelectron spectroscopy were employed to determine the chemical bonding structural change of DLC films before and after etching. It is confirmed that DLC films have good connection with Si supports via the formation of the SiC phase, and larger conductive sp2 domains are formed in the as-etched DLC films, which play essential roles in the enhanced field emission properties for DLCNR arrays. [ABSTRACT FROM AUTHOR]