Resource utilization conditions as biochar of an invasive plant Spartina alterniflora in coastal wetlands of China

Converting feedstocks of invasive plants into biochar is a new and cost‐effective measure for their control, and benefits for the sustainable development of native ecosystems. Spartina alterniflora, an invasive plant widely distributed in coastal wetlands of China, was used to produce biochar. We aimed to analyze how S. alterniflora biochar properties changed with desalination of feedstocks, pyrolysis temperature, and residence time. Results showed that desalting feedstocks increased biochar pH, stability, porosity, and surface area, but diminished biochar yield and polarity. Pyrolysis temperature positively affected biochar pH, surface area, and pore volume, while it had negative effects on biochar yield, oxygen and hydrogen contents, hydrogen/carbon and oxygen/carbon ratios, pore size, and function groups. However, residence time of pyrolysis had slight effects on biochar properties. The results are valuable for optimizing pyrolysis temperature and pretreatment measure of feedstocks, to tune S. alterniflora biochar properties for specific environmental usage.     

IL-17Frs763780多态性和肿瘤易感性关联的Meta分析

目的评估IL-17Frs763780多态性与癌易感性的关联。方法通过检索Pubmed、Embase、OV-ID、CBM、WanfangData和CNKI,筛选出发表至2013年10月与IL-17基因多态性和癌易感性有关的病例对照研究。采用比值比（ORs）和95％可信区间（95％CIs）评价关联强度。结果最终纳入5篇病例对照研究,包括1407例肿瘤患者和2164例健康对照。然而,分析后发现IL-17Frs763780多态性和癌无统计学意义的关联（TT＋TC vs CC：OR=0．85,95％CI=0．46～1．57,P=0．60;TTVSTC＋CC：OR=1．00,95％CI=0．76-1．33,P=0．99;TC vs CC：OR=0．83,95％CI=0．44—1．55,P=0．55;TT vs CC：OR=0．85,95％CI=0．46-1．59,P=0．62）。按肿瘤类型亚组分析提示在胃癌和其他肿瘤存在相似的结果。结论IL-17Frs763780多态性可能并不增加肿瘤的易感性。     

Regulation of a Dynamic Interaction between Two Microtubule-binding Proteins,EB1 and TIP150, by the Mitotic p300/CBP-associated Factor (PCAF) Orchestrates Kinetochore Microtubule Plasticity and Chromosome Stability during Mitosis

The microtubule cytoskeleton network orchestrates cellular dynamics and chromosome stability in mitosis. Although tubulin acetylation is essential for cellular plasticity, it has remained elusive how kinetochore microtubule plus-end dynamics are regulated by p300/CBP-associated factor (PCAF) acetylation in mitosis. Here, we demonstrate that the plus-end tracking protein, TIP150, regulates dynamic kinetochore-microtubule attachments by promoting the stability of spindle microtubule plus-ends. Suppression of TIP150 by siRNA results in metaphase alignment delays and perturbations in chromosome biorientation. TIP150 is a tetramer that binds an end-binding protein (EB1) dimer through the C-terminal domains, and overexpression of the C-terminal TIP150 or disruption of the TIP150-EB1 interface by a membrane-permeable peptide perturbs chromosome segregation. Acetylation of EB1-PCAF regulates the TIP150 interaction, and persistent acetylation perturbs EB1-TIP150 interaction and accurate metaphase alignment, resulting in spindle checkpoint activation. Suppression of the mitotic checkpoint serine/threonine protein kinase, BubR1, overrides mitotic arrest induced by impaired EB1-TIP150 interaction, but cells exhibit whole chromosome aneuploidy. Thus, the results identify a mechanism by which the TIP150-EB1 interaction governs kinetochore microtubule plus-end plasticity and establish that the temporal control of the TIP150-EB1 interaction by PCAF acetylation ensures chromosome stability in mitosis.     

GSK-3β Polymorphism Discriminates Bipolar Disorder and Schizophrenia: A Systematic Meta-Analysis

Glycogen synthase kinase 3 (GSK-3) is a well-known conserved and ubiquitous protein kinase and playing a pivotal role in neurodevelopment, neurogenesis, learning/memory, and neuronal cell death. Dysfunction of GSK-3 had been seen in multiple neurodegenerative and psychiatric diseases. Bipolar disorder and schizophrenia are two common psychiatric diseases first occur in adolescence or young adulthood. They share similar risk genes as well as clinical symptoms, which make it is difficult to be discriminated from each other. Here, by using meta-analysis we reported that glycogen synthase kinase 3β promoter inactive mutant rs334558 may contribute to the development of schizophrenia not bipolar disorder. This might be used to distinguish these two diseases.     

Elevated 12-Month and Lifetime Prevalence and Comorbidity Rates of Mood,Anxiety, and Alcohol Use Disorders in Chinese Men Who Have Sex with Men

Background

This study aimed to assess whether Chinese men who have sex with men (MSM) had a significantly elevated prevalence of psychiatric disorders compared to urban males in China.

Methods

807 MSM were recruited using a respondent-driven sampling (RDS) method in urban area of northeast China. Psychiatric disorders were assessed employing the Composite International Diagnostic Interview (CIDI. Version 1.0) according to the criteria of the DSM-III-R.

Results

Chinese MSM had a significantly elevated standardized prevalence ratios (SPR) for lifetime prevalence of any disorder (SPR = 2.8; 95%CI: 2.5–3.2), mood disorder (SPR = 3.0; 95%CI: 2.3–3.7), anxiety disorder (SPR = 5.5; 95% CI: 4.6–6.5), alcohol use disorder (SPR = 2.4, 95%CI: 2.0–2.8), and combination of disorders (SPR = 4.2; 95%CI: 3.4–5.1).

Conclusions

Chinese MSM had significantly elevated prevalence and comorbidity of psychiatric disorders. RDS is a suitable sampling method for psychiatric epidemiological survey in MSM population.     

Berberine Targets AP-2/hTERT,NF-κB/COX-2, HIF-1α/VEGF and Cytochrome-c/Caspase Signaling to Suppress Human Cancer Cell Growth

Berberine (BBR), an isoquinoline derivative alkaloid isolated from Chinese herbs, has a long history of uses for the treatment of multiple diseases, including cancers. However, the precise mechanisms of actions of BBR in human lung cancer cells remain unclear. In this study, we investigated the molecular mechanisms by which BBR inhibits cell growth in human non-small-cell lung cancer (NSCLC) cells. Treatment with BBR promoted cell morphology change, inhibited cell migration, proliferation and colony formation, and induced cell apoptosis. Further molecular mechanism study showed that BBR simultaneously targeted multiple cell signaling pathways to inhibit NSCLC cell growth. Treatment with BBR inhibited AP-2α and AP-2β expression and abrogated their binding on hTERT promoters, thereby inhibiting hTERT expression. Knockdown of AP-2α and AP-2β by siRNA considerably augmented the BBR-mediated inhibition of cell growth. BBR also suppressed the nuclear translocation of p50/p65 NF-κB proteins and their binding to COX-2 promoter, causing inhibition of COX-2. BBR also downregulated HIF-1α and VEGF expression and inhibited Akt and ERK phosphorylation. Knockdown of HIF-1α by siRNA considerably augmented the BBR-mediated inhibition of cell growth. Moreover, BBR treatment triggered cytochrome-c release from mitochondrial inter-membrane space into cytosol, promoted cleavage of caspase and PARP, and affected expression of BAX and Bcl-2, thereby activating apoptotic pathway. Taken together, these results demonstrated that BBR inhibited NSCLC cell growth by simultaneously targeting AP-2/hTERT, NF-κB/COX-2, HIF-1α/VEGF, PI3K/AKT, Raf/MEK/ERK and cytochrome-c/caspase signaling pathways. Our findings provide new insights into understanding the anticancer mechanisms of BBR in human lung cancer therapy.