Highly Drug-Resistant Salmonella enterica Serovar Indiana Clinical Isolates Recovered from Broilers and Poultry Workers with Diarrhea in China

Highly drug-resistant Salmonella enterica serovar Indiana became the most common serovar in broilers with diarrhea in China over the course of this study (15% in 2010 to 70% in 2014). While most S. Indiana isolates (87%, 384/440) were resistant to 13 to 16 of the 16 antibiotics tested, 89% of non-S. Indiana isolates (528/595) were resistant to 0 to 6 antibiotics. Class 1 integrons and IncHI2-type plasmids were detected in all S. Indiana isolates, but only in 39% and 1% of non-S. Indiana isolates.     

Regulation of pulmonary fibrosis by chemokine receptor CXCR3

CXC chemokine receptor 3 (CXCR3) is the receptor for the IFN-gamma-inducible C-X-C chemokines MIG/CXCL9, IP-10/CXCL10, and I-TAC/CXCL11. CXCR3 is expressed on activated immune cells and proliferating endothelial cells. The role of CXCR3 in fibroproliferation has not been investigated. We examined the role of CXCR3 in pulmonary injury and repair in vivo. CXCR3-deficient mice demonstrated increased mortality with progressive interstitial fibrosis relative to WT mice. Increased fibrosis occurred without increased inflammatory cell recruitment. CXCR3 deficiency resulted in both a reduced early burst of IFN-gamma production and decreased expression of CXCL10 after lung injury. We identified a relative deficiency in lung NK cells in the unchallenged CXCR3-deficient lung and demonstrated production of IFN-gamma by WT lung NK cells in vivo following lung injury. The fibrotic phenotype in the CXCR3-deficient mice was significantly reversed following administration of exogenous IFN-gamma or restoration of endogenous IFN-gamma production by adoptive transfer of WT lymph node and spleen cells. Finally, pretreatment of WT mice with IFN-gamma-neutralizing Ab's enhanced fibrosis following lung injury. These data demonstrate a nonredundant role for CXCR3 in limiting tissue fibroproliferation and suggest that this effect may be mediated, in part, by the innate production of IFN-gamma following lung injury.     

慕课在高职高专护理专业医学机能实验中的应用

慕课正逐步渗透进该校高职高专护理专业教学中,促进了该校护理专业教学的进步,尤其把慕课运用在医学机能实验技术课程时可充分发挥慕课的优势.高职高专护理专业普遍存在医学机能实验操作人数多、资源紧缺及仪器设备不足等问题,严重制约了高职高专护理专业的发展和学生的培养,慕课的介入为高职高专护理专业教学带来了便利,弥补了教学资源不足及设备紧缺的问题,逐步完善了高职高专护理专业医学机能实验技术的课程.     

急性病毒性肝炎患者胆囊排空功能研究

目的研究急性病毒性肝炎（ＡＶＨ）患者胆囊（ＧＢ）排空功能及其与病情程度和转归的关系．方法用实时超声研究了３２例ＡＶＨ患者及２６例健康对照者ＧＢ排空功能．结果空腹ＧＢ容量（ＦＧＶ）ＡＶＨ患者（１０２２±２３１）明显小于对照组（１９７９±１５１）（Ｐ＜０００１），随病程延长，ＦＧＶ渐增多．ＦＧＶ减少与病情程度呈显著负相关（Ｐ＜００５）．餐后ＧＢ排出量（ＧＥＦ）ＡＶＨ组显著少于对照组（Ｐ＜０００１），其减少与病情程度呈明显负相关（Ｐ＜００１），与血清胆红质、ＡＬＴ水平呈显著负相关（Ｐ＜００５～００１）．６０ｍｉｎ最大ＧＥＦ及ＧＢ排空速度明显减少、减慢（Ｐ＜０００１）．恢复期ＦＧＶ及餐后ＧＥＦ均恢复正常．结论ＡＶＨ患者存在ＦＧＶ和餐后ＧＥＦ异常．其机制与肝细胞损害，泌胆功能障碍及神经—激素调控失调有关．     

Antisense oligonucleotide reduction of DGAT2 expression improves hepatic steatosis and hyperlipidemia in obese mice

In this study, we investigated the role of acyl-coenzyme A:diacylglycerol acyltransferase 2 (DGAT2) in glucose and lipid metabolism in obese mice by reducing its expression in liver and fat with an optimized antisense oligonucleotide (ASO). High-fat diet-induced obese (DIO) C57BL/6J mice and ob/ob mice were treated with DGAT2 ASO, control ASO, or saline. DGAT2 ASO treatment reduced DGAT2 messenger RNA (mRNA) levels by more than 75% in both liver and fat but did not change DGAT1 mRNA levels in either of these tissues, which resulted in decreased DGAT activity in liver but not in fat. DGAT2 ASO treatment did not cause significant changes in body weight, adiposity, metabolic rate, insulin sensitivity, or skin microstructure. However, DGAT2 ASO treatment caused a marked reduction in hepatic triglyceride content and improved hepatic steatosis in both models, which was consistent with a dramatic decrease in triglyceride synthesis and an increase in fatty acid oxidation observed in primary mouse hepatocytes treated with DGAT2 ASO. In addition, the treatment lowered hepatic triglyceride secretion rate and plasma triglyceride levels, and improved plasma lipoprotein profile in DIO mice. The positive effects of the DGAT2 ASO were accompanied by a reduction in the mRNA levels of several hepatic lipogenic genes, including SCD1, FAS, ACC1, ACC2, ATP-citrate lyase, glycerol kinase, and HMG-CoA reductase. In conclusion, reduction of DGAT2 expression in obese animals can reduce hepatic lipogenesis and hepatic steatosis as well as attenuate hyperlipidemia, thereby leading to an improvement in metabolic syndrome.     

7个少数民族血清7种元素与血压关系的研究

采用原子吸收和火焰光谱分析法，检测我国7个少数民族脑中风病危人群血清微量元素Zn，Cu，Fe和常量元素K，Na，Ca，Mg的含量，并与血压的关系进行分析。结果发现高血压病高发区人群血清Na，Mg，Zn，Fe，Na／K，Zn／Cu明显高于低发区和对照组，而K，Ca，Cu，Ca／Mg则明显低于低发区和对照组。K，Ca，Cu，Ca／Mg与血压呈显著负相关，而Zn，Fe，Na／K与血压呈显著正相关。提示Fe，Na，Zn，Ca的含量变化与血压有密切的关系。     

Genome‐wide association study for femoral neck bone geometry

Poor femoral neck bone geometry at the femur is an important risk factor for hip fracture. We conducted a genome‐wide association study (GWAS) of femoral neck bone geometry, examining approximately 379,000 eligible single‐nucleotide polymorphisms (SNPs) in 1000 Caucasians. A common genetic variant, rs7430431 in the receptor transporting protein 3 (RTP3) gene, was identified in strong association with the buckling ratio (BR, P = 1.6 × 10^?7), an index of bone structural instability, and with femoral cortical thickness (CT, P = 1.9 × 10^?6). The RTP3 gene is located in 3p21.31, a region that we found to be linked with CT (LOD = 2.19, P = 6.0 × 10^?4) in 3998 individuals from 434 pedigrees. The replication analyses in 1488 independent Caucasians and 2118 Chinese confirmed the association of rs7430431 to BR and CT (combined P = 7.0 × 10^?3 for BR and P = 1.4 × 10^?2 for CT). In addition, 350 hip fracture patients and 350 healthy control individuals were genotyped to assess the association of the RTP3 gene with the risk of hip fracture. Significant association between a nearby common SNP, rs10514713 of the RTP3 gene, and hip fracture (P = 1.0 × 10^?3) was found. Our observations suggest that RTP3 may be a novel candidate gene for femoral neck bone geometry. © 2010 American Society for Bone and Mineral Research     

Neoadjuvant therapy induces loss of MSH6 expression in colorectal carcinoma

Immunohistochemical stains are routinely used to detect abnormal DNA mismatch repair (MMR) protein expression in colorectal carcinomas, particularly when Lynch syndrome is suspected. Complete loss of MMR protein expression is often associated with underlying microsatellite instability (MSI), and the combined results of mutL homolog 1 (MLH1), postmeiotic segregation increased 2 (PMS2), mutS homolog 2 (MSH2), or mutS homolog 6 (MSH6) immunostains may point to the defective MMR protein in tumors with MSI. We have noted that some neoadjuvantly treated colorectal carcinomas display loss of MMR protein immunoexpression, despite a lack of underlying MSI and preserved staining in pretreatment tumor samples. The purpose of this study was to determine the frequency of this finding. We identified 51 neoadjuvantly treated resected colorectal cancers. Posttreatment tumor samples were immunohistochemically stained with MLH1, PMS2, MSH2, and MSH6 antibodies. Loss of staining for any marker was followed by analysis for MSI and assessment of MMR protein expression in pretreatment tumor samples. All of the 51 posttreatment tumor samples showed preserved MLH1, PMS2, and MSH2, but 10 posttreatment tumor samples (20%) showed decreased MSH6 staining. Of these, 9 posttreatment tumor samples displayed loss of staining in less than 100% of tumor cells, but preserved MSH6 expression in pretreatment tumor samples. One case showed a complete absence of MSH6 staining in both pretreatment and posttreatment tumor samples. All 10 cases were microsatellite stable. We conclude that extensive loss of MSH6 immunoexpression is common among neoadjuvantly treated colorectal carcinomas, but generally does not reflect underlying MSI. Therefore, diminished MSH6 staining in treated tumors should prompt immunohistochemical evaluation of pretreatment biopsy samples before genetic testing for Lynch syndrome.