3-Chloro-N′-(3-eth­oxy-2-hy­droxy­benzyl­idene)benzohydrazide monohydrate

In the title compound, C16H15ClN2O3·H2O, the water mol­ecule is linked to the Schiff base mol­ecule via an O—H⋯O hydrogen bond. In the Schiff base mol­ecule, an intramolecular O—H⋯N hydrogen bond occurs and the dihedral angle between the two benzene rings is 20.5 (5)°. In the crystal, the Schiff base and water mol­ecules are linked by inter­molecular N—H⋯O and O—H⋯O hydrogen bonds, forming layers in the ab plane

No association between XRCC1 gene Arg194Trp polymorphism and risk of lung cancer: evidence based on an updated cumulative meta-analysis

X-ray repair cross-complementing group 1 (XRCC1) gene Arg194Trp polymorphism has been reported to be associated with risk of lung cancer in many published studies. Nevertheless, the research results were inconclusive and conflicting. To reach conclusive results, several meta-analysis studies were conducted by combining results from literature reports through pooling analysis. However, these previous meta-analysis studies were still not consistent. Hence, we used an updated and cumulative meta-analysis to get a more comprehensive and precise result from 25 case–control studies searching through the PubMed database up to September 1, 2013. The meta-analysis was carried out by the Comprehensive Meta-Analysis software and the odds ratio (OR) with 95 % confidence interval (CI) was used to estimate the pooled effect. The result involving 8,876 lung cancer patients and 11,210 controls revealed that XRCC1 Arg194Trp polymorphism was not associated with lung cancer risk [(OR = 0.97, 95 %CI = 0.92–1.03) for Trp vs. Arg; (OR = 0.92, 95 % CI = 0.85–0.98) for ArgTrp vs. ArgArg; (OR = 1.07, 95 % CI = 0.92–1.23) for TrpTrp vs. ArgArg; (OR = 0.93, 95 % CI = 0.87–1.00) for (TrpTrp + ArgTrp) vs. ArgArg; and (OR = 1.08, 95 % CI = 0.94–1.25) for TrpTrp vs. (ArgTrp + ArgArg)]. The cumulative meta-analysis showed that the results maintained the same, while the ORs with 95 % CI were more stable with the accumulation of case–control studies. The sensitivity and subgroups analyses showed that the results were robust and not affected by any single study with no publication bias. Relevant studies might not be needed for supporting these results

Life fingerprints of nuclear reactions in the body of animals

Nuclear reactions are a very important natural phenomenon in the universe. On the earth, cosmic rays constantly cause nuclear reactions. High energy beams created by medical devices also induce nuclear reactions in the human body. The biological role of these nuclear reactions is unknown. Here we show that the in vivo biological systems are exquisite and sophisticated by nature in influence on nuclear reactions and in resistance to radical damage in the body of live animals. In this study, photonuclear reactions in the body of live or dead animals were induced with 50-MeV irradiation. Tissue nuclear reactions were detected by positron emission tomography (PET) imaging of the induced beta+ activity. We found the unique tissue "fingerprints" of beta+ (the tremendous difference in beta+ activities and tissue distribution patterns among the individuals) are imprinted in all live animals. Within any individual, the tissue "fingerprints" of 15O and 11C are also very different. When the animal dies, the tissue "fingerprints" are lost. The biochemical, rather than physical, mechanisms could play a critical role in the phenomenon of tissue "fingerprints". Radiolytic radical attack caused millions-fold increases in 15O and 11C activities via different biochemical mechanisms, i.e. radical-mediated hydroxylation and peroxidation respectively, and more importantly the bio-molecular functions (such as the chemical reactivity and the solvent accessibility to radicals). In practice biologically for example, radical attack can therefore be imaged in vivo in live animals and humans using PET for life science research, disease prevention, and personalized radiation therapy based on an individual's bio-molecular response to ionizing radiation

FTO Knockout Causes Chromosome Instability and G2/M Arrest in Mouse GC-1 Cells

N6-methyladenosine (m6A) is the most abundant modification on eukaryotic mRNA. m6A plays important roles in the regulation of post-transcriptional RNA splicing, translation, and degradation. Increasing studies have uncovered the significance of m6A in various biological processes such as stem cell fate determination, carcinogenesis, adipogenesis, stress response, etc, which put forwards a novel conception called epitranscriptome. However, functions of the fat mass and obesity-associated protein (FTO), the first characterized m6A demethylase, in spermatogenesis remains obscure. Here we reported that depletion of FTO by CRISPR/Cas9 induces chromosome instability and G2/M arrest in mouse spermatogonia, which was partially rescued by expression of wild type FTO but not demethylase inactivated FTO. FTO depletion significantly decreased the expression of mitotic checkpoint complex and G2/M regulators. We further demonstrated that the m6A modification on Mad1, Mad2, Bub1b, Cdk1, and Ccnb2 were directly targeted by FTO. Therefore, FTO regulates cell cycle and mitosis checkpoint in spermatogonia because of its m6A demethylase activity. The findings give novel insights into the role of RNA methylation in spermatogenesis

Effect of Prunella vulgaris L extract on hyperprolactinemia in vitro and in vivo

Purpose: To investigate the anti-hyperprolactinemic activity of Prunella vulgaris L. extract (PVE) in vivo and in vitro.Methods: Rats were given intraperitoneal (i. p.) metoclopramide (MCP, 150 mg/kg daily) for 10 days to prepare hyperprolactinemia (hyperPRL) model. Bromocriptine was used as positive control drug. High (5.6 g/kg), medium (2.8 g/kg) and low (1.4 g/kg) doses of PVE were administered to hyperPRL rats. The effect of PVE on serum prolactin (PRL), estradiol (E2), progesterone (PGN), follicle stimulating hormone (FSH) and luteinizing hormone (LH) levels were investigated in the rats. MMQ cells derived from rat pituitary adenoma cells and GH3 cells from rat pituitary lactotropictumoral cells were used for in vitro experiments. The effect of PVE on PRL secretion were studied in MMQ cells and GH3 cells respectively.Results: Compared with the control group (446.21 ± 32.43 pg/mL), high (219.23 ± 10.62 pg/mL) and medium (245.47 ± 13.52 pg/mL) reduced PRL level of hyperPRL rats significantly (p 0.05). In MMQ cells, treatment with 5 mg/mL PVE or 10 mg/mL PVE) significantly suppressed PRL secretion and synthesis at 24h compared with controls (p < 0.01). Consistent with D2- action, PVE did not affect PRL in rat pituitary lactotropic tumor-derived GH3 cells that lack the D2 receptor expression, compared with controls.Conclusion: PVE showed anti-hyperPRL activity and can potentially be used for the treatment of hyperprolactinemi, but further studies are required to ascertain this.Keywords: Prunella vulgaris, Hyperprolactinemia, Prolactin, Bromocriptin