Virions of Heliothis armigera Entomopoxvirus contain a Homologue of the Vaccinia VP8 Major Core Protein

An antigenic 30 K virion protein of Heliothis armigera entomopoxvirus (HaEPV) has been identified as a homologue of the chordopoxvirus (ChPV) VP8 major virion core protein. Like its homologue in vaccinia virus, the mature HaEPV 30 K protein is derived by post-translational cleavage of a precursor at a conserved AGA motif. The HaEPV 30 K protein is the first EPV structural virion protein to be described, and elucidation of its characteristics provides evidence for the assumption that morphological similarities observed between virions of the sub-families Entomopoxvirinae and Chordopoxvirinae by microscopy reflect corresponding similarities at a molecular level. Sequencing of the HaEPV genome adjacent to the 30 K locus identified an ORF encoding a homologue of the regulatory sub-unit of the ChPV poly(A) polymerase enzyme; the conceptual product of this ORF showed 25–31% aa sequence identity to those of various ChPVs. The presence of this gene in the HaEPV genome supports the hypothesis that there is a substantial correspondence in basic metabolic processes of members of the two poxvirus sub-families, despite their utilization of divergent host groups. In contrast, the relative positions of the 30 K and poly(A) polymerase loci in the HaEPV genome provide further evidence of substantial genomic re-arrangement subsequent to divergence of these viral taxa.     

Impact of Early Salvage Radiation Therapy in Patients with Persistently Elevated or Rising Prostate-specific Antigen After Radical Prostatectomy

Background

Salvage radiation therapy (SRT) is a recommended treatment option for biochemical recurrence after radical prostatectomy (RP). However, its effectiveness may be limited to specific categories of patients.

External beam radiotherapy with or without androgen deprivation therapy in elderly patients with high metastatic risk prostate cancer

Objective

Several randomized controlled trials have documented significant overall survival benefit in high metastatic risk prostate cancer (PCa) patients treated with combination of androgen deprivation therapy (ADT) at radiotherapy (RT) relative to RT alone. Unfortunately, elderly patients are either not included or are underrepresented in these trials. In consequence, the survival benefit of combination of ADT at RT in the elderly warrants detailed reassessment, including its cost.

低血糖指数膳食改善超重老年糖尿病患者氧化应激水平

目的:观察低血糖指数的膳食对2型糖尿病患者氧化应激状态的影响。方法:2004-10/11在上海市静安区二个社区卫生服务中心招募受试者,经医生明确诊断为2型糖尿病、病程超过6个月,体质量指数≥24kg/m2的老年糖尿病志愿者43名,受试者对试验知情同意。采用随机交叉试验随机分配至低血糖指数饮食组和高血糖指数饮食组,每种膳食分别连续使用4周,间隔洗脱期4周,比较试验前后患者超氧化物歧化酶、脂质过氧化产物丙二醛和谷胱甘肽过氧化物酶含量的变化。结果:受试者依从性好,除1人因试验期间发现肿瘤而退出试验,42名志愿者按设计要求完成试验。膳食干预后低血糖指数饮食组和高血糖指数饮食组的超氧化物歧化酶活力分别升高了15.68%和21.33%,丙二醛水平分别下降23.94%和21.55%,谷胱甘肽过氧化物酶活力分别升高了15.74%和17.09%;干预后低血糖指数饮食组丙二醛下降水平与高血糖指数饮食组比较差异有显著性意义(P<0.05),而超氧化物歧化酶和谷胱甘肽过氧化物酶活性两组间差异无显著性意义(P>0.05)。结论:在控制总能量的基础上给予平衡膳食能够改善其氧化应激水平,采用低血糖指数食物有助于氧化应激水平的改善。     

Fibroblast growth factor 2 decreases bleomycin‐induced pulmonary fibrosis and inhibits fibroblast collagen production and myofibroblast differentiation

Fibroblast growth factor (FGF) signaling has been implicated in the pathogenesis of pulmonary fibrosis. Mice lacking FGF2 have increased mortality and impaired epithelial recovery after bleomycin exposure, supporting a protective or reparative function following lung injury. To determine whether FGF2 overexpression reduces bleomycin‐induced injury, we developed an inducible genetic system to express FGF2 in type II pneumocytes. Double‐transgenic (DTG) mice with doxycycline‐inducible overexpression of human FGF2 (SPC‐rtTA;TRE‐hFGF2) or single‐transgenic controls were administered intratracheal bleomycin and fed doxycycline chow, starting at either day 0 or day 7. In addition, wild‐type mice received intratracheal or intravenous recombinant FGF2, starting at the time of bleomycin treatment. Compared to controls, doxycycline‐induced DTG mice had decreased pulmonary fibrosis 21 days after bleomycin, as assessed by gene expression and histology. This beneficial effect was seen when FGF2 overexpression was induced at day 0 or day 7 after bleomycin. FGF2 overexpression did not alter epithelial gene expression, bronchoalveolar lavage cellularity or total protein. In vitro studies using primary mouse and human lung fibroblasts showed that FGF2 strongly inhibited baseline and TGFβ1‐induced expression of alpha smooth muscle actin (αSMA), collagen, and connective tissue growth factor. While FGF2 did not suppress phosphorylation of Smad2 or Smad‐dependent gene expression, FGF2 inhibited TGFβ1‐induced stress fiber formation and serum response factor‐dependent gene expression. FGF2 inhibition of stress fiber formation and αSMA requires FGF receptor 1 (FGFR1) and downstream MEK/ERK, but not AKT signaling. In summary, overexpression of FGF2 protects against bleomycin‐induced pulmonary fibrosis in vivo and reverses TGFβ1‐induced collagen and αSMA expression and stress fiber formation in lung fibroblasts in vitro, without affecting either inflammation or epithelial gene expression. Our results suggest that in the lung, FGF2 is antifibrotic in part through decreased collagen expression and fibroblast to myofibroblast differentiation. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.