不同氮量全胃肠外营养支持对脓毒症病人蛋白质代谢的影响

如何提高脓毒症闰人营养支持的效果是当前的热点和难点之一。本实验前瞻性地对比观察了不同蛋白质供应负荷０．２５ｇ／Ｖ（ｋｇ．ｄ）ｖｓ０．３５ｇＮ／（ｋｇ．ｄ），在脓毒症病人全有肠外营养支持中对蛋白质代谢状况的影响。结果发现，与低氮量ＴＰＮ相比，高氮量ＴＰＮ支持可改善血浆蛋白水平，增加累积氮平衡，但尿中３－ＭＨ排出量也有相应增加。     

Identification of metabolites of the antitumor agentd-limonene capable of inhibiting protein isoprenylation and cell growth

Summary Limonene has been shown to be an effective, nontoxic chemopreventive and chemotherapeutic agent in chemically induced rat mammary-cancer models. The present study characterized circulating metabolites of limonene in female rats and determined their effects on cell growth. Metabolism of limonene was analyzed in plasma extracts by gas chromatography. Rapid conversion of limonene to two major metabolites was detected. These metabolites comprised more than 80% of the circulating limonene-derived material at 1 h after administration and thereafter, whereas limonene itself accounted for only 15%. The metabolites were characterized by mass spectroscopy and infrared spectroscopy. The probable structures were synthesized, and identities were confirmed by comparison of retention times and mass spectra. The two major circulating metabolites of limonene were found to be perillic acid and dihydroperillic acid. We have previously reported that limonene, perillic acid, and dihydroperillic acid inhibit the posttranslational isoprenylation of p21 ^ras and other 21- to 26-kDa cell-growth-associated proteins in NIH3T3 cells and in mammary epithelial cells. In the present study, perillic acid was found to inhibit cell growth in a dose-dependent manner. Thus, perillic acid and dihydroperillic acid, the two major circulating metabolites of limonene in the rat, are more potent inhibitors of protein isoprenylation than is limonene, and perillic acid is also a more potent inhibitor of cell growth. These data raise the possibility that the antitumor effects of limonene in vivo may be mediated via perillic acid and, perhaps, other metabolites.This work was supported by NIH, PHS grant CA 38 128 and in part by NIH training grant 5T32CA 09471 (to P. L. C.)     

Haemophilus aphrophilus bleb infection after a mitomycin trabeculectomy

Background: Haemophilus aphrophilus is a rare cause of ocular infection. It has been reported once as a cause of late-onset endophthalmitis in a patient with an inadvertent bleb after cataract surgery. We present a case of Haemophilus aphrophilus bleb infection after a mitomycin trabeculectomy.
Methods: A 56-year-old woman presented with a bleb infection 10 weeks after a mitomycin C augmented trabeculectomy at a University tertiary referral practice of one of the authors (GET). The causative organism was Haemophilus aphrophilus , identified by the Toronto Public Health Laboratory, Ontario, Canada.
Results: The bleb infection resolved following topical, subconjunctival and intravenous antibiotic therapy. A formal bleb revision was required to repair a persistent bleb leak.
Conclusion: Patients who have had trabeculectomies augmented with mitomycin C may be predisposed to bleb infection with unusual organisms. Prompt diagnosis and treatment is necessary to control the infection. Increased awareness and communication with laboratory personnel may increase the isolation of this fastidious organism.     

人亲环素A基因克隆及在大肠杆菌中表达

目的 :用基因重组技术表达人亲环素 A( Cy PA) ,以避免从人组织材料中提取纯化该蛋白的麻烦。　 方法 :应用反转录聚合酶链反应 ( RT- PCR)技术从人淋巴细胞系 ( MT4 )总 RNA中扩增得到 Cy PA基因片段 ,并用重组 DNA技术对该基因片段进行克隆 ,构建表达载体 ,转入大肠杆菌进行表达。　 结果 :DNA序列分析表明 ,得到的基因片段与设计编码 Cy PA的结构基因序列完全相同。所构建的表达载体 p ET11/Cy PA转入大肠杆菌获得表达 ,重组蛋白表达量占菌体可溶性蛋白的 4 1% ,经测定具有肽基脯氨酸顺 /反异构酶活性。　 结论 :利用基因重组技术使大肠杆菌高效表达出有生物活性的人 Cy PA。     

Targeting the AKT protein kinase for cancer chemoprevention

The AKT protein kinase transduces signals from growth factors and oncogenes to downstream targets that control crucial elements in tumor development. The AKT pathway is one of the most frequently hyperactivated signaling pathways in human cancers. Available data are reviewed herein to support targeting the AKT kinase for cancer prevention. This review will present data to show that AKT is up-regulated in preneoplastic lesions across a broad range of target tissues, briefly describe drug development efforts in this area, and present evidence that down-regulation of AKT signaling may be a viable strategy to prevent cancer.