β3—肾上腺素能受体兴奋剂BRL37344对非肥胖和肥胖小白鼠游离足底肌葡萄糖摄取糖原合成的作用

目的：研究β3－肾上腺素能受体兴奋剂BRL 37344对非肥胖和肥胖小白鼠游离足底肌葡萄糖摄取,糖原合成的作用,方法：纯种非肥胖（＋／＋）和肥胖（ob/ob）小白鼠,年龄范围17－22周;体重,非肥胖小白鼠75－100g/只,肥胖小白鼠150－180g/只。肥胖和非肥胖小白鼠各36只,用生理和生化以及放射标记的方法和技术,测定β2－肾上腺素能受体兴奋剂BRL37344刺激葡萄糖摄取及糖原合成的作用。结果：BRL37344刺激葡萄糖摄取和糖原合成在非肥胖和肥胖小白鼠所需的BRL37344浓度不同,在非肥胖小白鼠,BRL37344的浓度在10^-10M引起最大作用的葡萄糖摄取和10^-11M引起最大作用的糖原合成,对肥胖小白鼠BRL37344浓度在10^-7M,引起最大作用的葡萄糖摄取,以及BRL37344浓度为10^-6M引起最大作用的糖原合成,结论：研究提示一个不典型的β－肾上腺素能受体（称为β3－肾上腺素能受体）存在于小白鼠的游离足底肌,肥胖小白鼠β3－肾上腺素能受体的数目,可能较非肥胖小白鼠者少以及可能存在胰岛素抵抗,β3－肾上腺素能受 兴奋剂BRL37344在一定的浓度促进骨骼肌最大作用的葡萄糖摄取和糖原合成,使骨骼肌利用葡萄糖增加,因此,BRL37344作为开发治疗糖尿病的新药物,则具有实际意义。     

1998-2002年《中国防痨杂志》来稿与刊登情况分析

目的　分析中国防痨杂志来稿及刊登情况,进一步提高杂志质量,加快防痨学术交流。方法 以编辑部1998—2002年稿件登记本和1998—2003年出版的《中国防痨杂志》29册为样本,统计来稿和刊登稿件的数量以及出版时滞。结果 5年共来稿2592篇,年平均518.4篇,刊出759篇,平均刊登率为30.4%。但出版时滞稍长。结论 中国防痨杂志的稿源比较充足,但来稿质量仍需提高。出版时滞尚需改进。     

Report of the Task Force on Residency Training Information (2004-2005), American Board of Emergency Medicine

The American Board of Emergency Medicine gathers extensive background information on emergency medicine residency training programs and the residents training in those programs. We present the eighth annual report on the status of US emergency medicine residency programs.     

急性非静脉曲张性上消化道出血诊治指南(2009,杭州)

一、定义 急性非静脉曲张性上消化道出血(acute nonvariceal upper gastrointestinal bleeding,ANVUGIB)系指屈氏韧带以上消化道非静脉曲张性疾患引起的出血,包括胰管或胆管的出血和胃空肠吻合术后吻合口附近疾患引起的出血,年发病率为50/10万～150/10万,病死率为6%～10%~([1-2]).     

Comparative Analysis of Apoptosis and Inflammation Genes of Mice and Humans

Apoptosis (programmed cell death) plays important roles in many facets of normal mammalian physiology. Host-pathogen interactions have provided evolutionary pressure for apoptosis as a defense mechanism against viruses and microbes, sometimes linking apoptosis mechanisms with inflammatory responses through NFκB induction. Proteins involved in apoptosis and NFκB induction commonly contain evolutionarily conserved domains that can serve as signatures for identification by bioinformatics methods. Using a combination of public (NCBI) and private (RIKEN) databases, we compared the repertoire of apoptosis and NFκB-inducing genes in humans and mice from cDNA/EST/genomic data, focusing on the following domain families: (1) Caspase proteases; (2) Caspase recruitment domains (CARD); (3) Death Domains (DD); (4) Death Effector Domains (DED); (5) BIR domains of Inhibitor of Apoptosis Proteins (IAPs); (6) Bcl-2 homology (BH) domains of Bcl-2 family proteins; (7) Tumor Necrosis Factor (TNF)-family ligands; (8) TNF receptors (TNFR); (9) TIR domains; (10) PAAD (PYRIN; PYD, DAPIN); (11) nucleotide-binding NACHT domains; (12) TRAFs; (13) Hsp70-binding BAG domains; (14) endonuclease-associated CIDE domains; and (15) miscellaneous additional proteins. After excluding redundancy due to alternative splice forms, sequencing errors, and other considerations, we identified cDNAs derived from a total of 227 human genes among these domain families. Orthologous murine genes were found for 219 (96%); in addition, several unique murine genes were found, which appear not to have human orthologs. This mismatch may be due to the still fragmentary information about the mouse genome or genuine differences between mouse and human repertoires of apoptotic genes. With this caveat, we discuss similarities and differences in human and murine genes from these domain families.