农田林网化地区近地面层廓线特征研究

大面积林网化地区近地面层大气的系留气球观测发现,近地面层大气的风、温、湿分为两层,即下边界层和扰动边界层,其厚度和廓线分布与理查逊数有关,在中性天气条件下均满足对数分布规律,边界层（特别是扰动边界层）内的摩擦速度Ｕ．＂与旷野对比点的摩擦速度Ｕ０增大１个数量级,而粗糙度Ｚ＂０增大２个数量级,甚至更大。     

多糖抗病毒作用研究进展Ⅰ-多糖抗病毒作用

近年来,多糖的抗病毒作用已引起极大关注。本文综述了多糖的抗病毒作用,概述了多糖构效关系、抗病毒机理、分子修饰及其与其他抗病毒药物的协同作用。多糖抗病毒药物研究前景广阔。     

Who Are the High-Cost Users? A Method for Person-Centred Attribution of Health Care Spending

Objective

To develop person-centered episodes of care (PCE) for community-dwelling individuals in the top fifth percentile of Ontario health care expenditures in order to: (1) describe the main clinical groupings for spending; and (2) identify patterns of spending by health sector (e.g. acute care, home care, physician billings) within and across PCE.

Data sources

Data were drawn from population-based administrative databases for all publicly funded health care in Ontario, Canada in 2010/11.

Study design

This study is a retrospective cohort study.

Data collection/extraction methods

A total of 587,982 community-dwelling individuals were identified among those accounting for the top 5% of provincial health care expenditures between April 1, 2010 and March 31, 2011. PCE were defined as starting with an acute care admission and persisting through subsequent care settings and providers until individuals were without health system contact for 30 days. PCE were classified according to the clinical grouping for the initial admission. PCE and non-PCE costs were calculated and compared to provide a comprehensive measurement of total health system costs for the year.

Principal findings

Among this community cohort, 697,059 PCE accounted for nearly 70% ($11,815.3 million (CAD)) of total annual publicly-funded expenditures on high-cost community-dwelling individuals. The most common clinical groupings to start a PCE were Acute Planned Surgical (35.2%), Acute Unplanned Medical (21.0%) and Post-Admission Events (10.8%). Median PCE costs ranged from $3,865 (IQR = $1,712-$10,919) for Acute Planned Surgical to $20,687 ($12,207-$39,579) for Post-Admission Events. Inpatient acute ($8,194.5 million) and inpatient rehabilitation ($434.6 million) health sectors accounted for the largest proportions of allocated PCE spending over the year.

Conclusions

Our study provides a novel methodological approach to categorize high-cost health system users into meaningful person-centered episodes. This approach helps to explain how costs are attributable within individuals across sectors and has applications in episode-based payment formulas and quality monitoring.     

Silencing of Long Noncoding RNA AK139328 Attenuates Ischemia/Reperfusion Injury in Mouse Livers

Recently, increasing evidences had suggested that long noncoding RNAs (LncRNAs) are involved in a wide range of physiological and pathophysiological processes. Here we determined the LncRNA expression profile using microarray technology in mouse livers after ischemia/reperfusion treatment. Seventy one LncRNAs were upregulated, and 27 LncRNAs were downregulated in ischemia/reperfusion-treated mouse livers. Eleven of the most significantly deregulated LncRNAs were further validated by quantitative PCR assays. Among the upregulated LncRNAs confirmed by quantitative PCR assays, AK139328 exhibited the highest expression level in normal mouse livers. siRNA-mediated knockdown of hepatic AK139328 decreased plasma aminotransferase activities, and reduced necrosis area in the livers with a decrease in caspase-3 activation after ischemia/reperfusion treatment. In ischemia/reperfusion liver, knockdown of AK139328 increased survival signaling proteins including phosphorylated Akt (pAkt), glycogen synthase kinase 3 (pGSK3) and endothelial nitric oxide synthase (peNOS). Furthermore, knockdown of AK139328 also reduced macrophage infitration and inhibited NF-κB activity and inflammatory cytokines expression. In conclusion, these findings revealed that deregulated LncRNAs are involved in liver ischemia/reperfusion injury. Silencing of AK139328 ameliorated ischemia/reperfusion injury in the liver with the activation of Akt signaling pathway and inhibition of NF-κB activity. LncRNA AK139328 might be a novel target for diagnosis and treatment of liver surgery or transplantation.     

The inhibitory effect of BSP-A1/-A2 on protein kinase C and tyrosine protein kinase

Bovine seminal plasma contains a group of similar proteins, namely BSP-A1, BSP-A2, BSP-A3, and BSP-30-kDa (collectively called BSP proteins), and they are secreted by the seminal vesicles. In our study, we purified the BSP-A1/-A2 through affinity chromatography and found for the first time that BSP-A1/-A2 can inhibit the activity of protein kinase C (PKC) and tyrosine protein kinase (TPK). The inhibition was dose dependent. When the PKC and TPK activities are expressed as the logarithm of percentage activity taking the activity in the absence of the BSP-A1/-A2 as 100%, there is a linear relationship between the their activities and the dose of BSP-A1/-A2.     

亚临床甲亢和甲减发病的实验室调查

目的　探讨本地区亚临床甲状腺疾病的发病情况。　方法　随机抽样 2 550例健康体检者作甲状腺功能检测 ,以促甲状腺素 ( TSH)水平异常的检出率来判断亚临床甲状腺疾病的发病率。　结果　亚临床甲亢的检出率为5.4 5% ,亚临床甲减的检出率为 6 .98% ;两种疾病 T3、T4、FT3、 FT4 和 TSH的均数比较具有非常显著性差异 ( P <0 .0 1)。　结论　本地区具有亚临床甲状腺疾病的发病现象 ,亚临床甲减的发病率比亚临床甲亢稍高     

Ubiquitination of a novel deubiquitinating enzyme requires direct binding to von Hippel-Lindau tumor suppressor protein.

von Hippel-Lindau (VHL) disease is a hereditary cancer syndrome caused by germline mutations of the VHL gene. Recent studies suggest that VHL protein (pVHL) is a component of an E3 ubiquitin ligase, but the detailed biological function of pVHL remains to be determined. To further elucidate the biological functions of pVHL, we searched pVHL-interacting proteins using yeast two-hybrid screening. A novel protein named VHL-interacting deubiquitinating enzyme 1 (VDU1) was identified as being able to directly interact with pVHL in vitro and in vivo. We have determined the full-length cDNA of this enzyme, which includes two putative subtypes. Type I consists of 942 amino acids, and type II consists of 911 amino acids with predicted molecular masses of 107 and 103 kDa, respectively. We have also cloned a mouse homologue of this enzyme. Sequence analysis reveals that this protein is conserved between human and mouse and contains the signature motifs of the ubiquitin-specific processing protease family. Enzymatic function studies demonstrate its deubiquitinating activity. We have determined that the VDU1-interacting region in pVHL is located in its beta-domain, and several naturally occurring mutations located in this domain disrupt the interaction between pVHL and VDU1 protein. Co-immunoprecipitation demonstrates that VDU1 can be recruited into the pVHL-elongin C-elongin B complex. Finally, we demonstrate that VDU1 is able to be ubiquitinated via a pVHL-dependent pathway for proteasomal degradation, and VHL mutations that disrupt the interaction between VDU1 and pVHL abrogate the ubiquitination of VDU1. Our findings indicate that VDU1, a novel ubiquitin-specific processing protease, is a downstream target for ubiquitination and degradation by pVHL E3 ligase. Targeted degradation of VDU1 by pVHL could be crucial for regulating the ubiquitin-proteasome degradation pathway.     

1,2‐Diacylglycerol choline phosphotransferase catalyzes the final step in the unique Treponema denticola phosphatidylcholine biosynthesis pathway

Treponema denticola synthesizes phosphatidylcholine through a licCA‐dependent CDP‐choline pathway identified only in the genus Treponema. However, the mechanism of conversion of CDP‐choline to phosphatidylcholine remained unclear. We report here characterization of TDE0021 (herein designated cpt) encoding a 1,2‐diacylglycerol choline phosphotransferase homologous to choline phosphotransferases that catalyze the final step of the highly conserved Kennedy pathway for phosphatidylcholine synthesis in eukaryotes. T. denticola Cpt catalyzed in vitro phosphatidylcholine formation from CDP‐choline and diacylglycerol, and full activity required divalent manganese. Allelic replacement mutagenesis of cpt in T. denticola resulted in abrogation of phosphatidylcholine synthesis. T. denticola Cpt complemented a Saccharomyces cerevisiae CPT1 mutant, and expression of the entire T. denticola LicCA‐Cpt pathway in E. coli resulted in phosphatidylcholine biosynthesis. Our findings show that T. denticola possesses a unique phosphatidylcholine synthesis pathway combining conserved prokaryotic choline kinase and CTP:phosphocholine cytidylyltransferase activities with a 1,2‐diacylglycerol choline phosphotransferase that is common in eukaryotes. Other than in a subset of mammalian host‐associated Treponema that includes T. pallidum, this pathway is found in neither bacteria nor Archaea. Molecular dating analysis of the Cpt gene family suggests that a horizontal gene transfer event introduced this gene into an ancestral Treponema well after its divergence from other spirochetes.     

Differential antibacterial activity of nitric oxide from the immunological isozyme of nitric oxide synthase transduced into endothelial cells.

Primary cultures of endothelial cells, grown on the three-dimensional matrix Gelfoam where they take on the morphology of these cells in vivo, were found to phagocytose Staphylococcus aureus and two strains of Escherichia coli. The phagocytosis was independent of opsonization, although once opsonized, these bacteria were phagocytosed by endothelial cells. As cytochalsin D inhibited the internationalization of S. aureus and E. coli, the phagocytosis by endothelial cells appears to be actin-dependent. Transducing the gene for nitric oxide synthase (NOS) II into endothelial cells allowed us to determine the importance of NO(*) in host immunity against these bacteria. While the growth of S. aureus was impeded by NOS II endothelial cells, two strains of E. coli were killed by an NO(*)-dependent pathway. We conclude that endothelial cells have microbicidal mechanisms that are selective for the type of pathogen encountered.