2型糖尿病肺癌患者生存期影响因素分析

目的探讨2型糖尿病肺癌患者生存期及其影响因素。方法选取2014年至2016年在我院诊断的T2DM合并肺癌的患者43为观察组,同期诊断单纯肺癌不合并T2DM的患者40为对照组,查阅患者的一般资料,调查所有可能影响患者预后的危险因素,如年龄、性别、肺癌TNM分期、病理分型、远处转移、合并症、吸烟、治疗情况、血糖及控制血糖的方法等,随访患者的生存情况。结果观察组PFS时间为7.8±5.1月,对照组PFS时间为11.1±6.1月,观察组PFS时间明显短于对照组;观察组OS时间为15.0±7.5月,对照组OS时间为18.5±8.8月,观察组OS时间明显短于对照组。Cox回归分析发现,患者生存时间与是否合并糖尿病、远处转移、病理分期有关,差异具有统计学意义(P<0.05),而年龄、性别、是否吸烟、病理分型等对总生存期的影响较差,差异无统计学意义((P>0.05),Kaplan-Meier分析结果显示:合并T2DM的肺癌患者PFS明显低于单纯未合并T2DM的肺癌患者,远处转移的的肺癌患者PFS明显低于无远处转移的肺癌患者,IV期的肺癌患者低于II期的肺癌患者,II期肺癌患者低于I期的肺癌患者。结论T2DM合并肺癌无论是无进展生存期还是总生存期均低于单纯肺癌不合并T2DM的患者,T2DM合并肺癌患者除了传统的因素如远处转移、肿瘤TNM分期等影响肺癌患者的预后外,T2DM也是影响肺癌患者预后的独立危险因素。     

Graphene oxide regulates cox2 in human embryonic kidney 293T cells via epigenetic mechanisms: dynamic chromosomal interactions

To extend the applications of engineered nanomaterials, such as graphene oxide (GO), it is necessary to minimize cytotoxicity. However, the mechanisms underlying this cytotoxicity are unclear. Dynamic chromosomal interactions have been used to illustrate the molecular bases of gene expression, which offers a more sensitive and cutting-edge technology to elucidate complex biological processes associated with epigenetic regulations. In this study, the role of GO-triggered chromatin interactions in the activation of cox2, a hallmark of inflammation, was investigated in normal human cells. Using chromosome conformation capture technology, we showed that GO triggers physical interactions between the downstream enhancer and the cox2 promoter in human embryonic kidney 293T (293T) via p65 and p300 complex-mediated dynamic chromatin looping, which was required for high cox2 expression. Moreover, tumor necrosis factor-α (TNF-α), located upstream of the p65 signaling pathway, contributed to the regulation of cox2 activation through dynamic chromatin architecture. Compared with pristine GO and aminated GO (GO-NH₂), poly (acrylic acid)-functionalized GO (GO-PAA) induced a weaker inflammatory response and a weaker effect on chromatin architecture. Our results mechanistically link GO-mediated chromatin interactions with the regulation of cox2 and suggest that GO derivatives may minimize toxicity in practical applications.     

南京市城区居民家庭人均收入与自我报告2型糖尿病关系

目的了解江苏省南京市城区居民以家庭人均收入为指标的社会经济状况与自我报告2型糖尿病之间的关系。方法采用横断面研究方法,于2011年8—9月对南京市4个城区的年满35岁并在当地居住满5年的9 446名常住居民进行调查。结局变量为调查对象自我报告的2型糖尿病,解释性变量为家庭人均收入(三等分)。结果南京市城区居民中自我报告2型糖尿病的患病率为8.2%(95%CI=7.59%~8.80%),存在明显的年龄分布差异,但性别间的分布差异无统计学意义。经多因素调整后,家庭人均收入与自我报告2型糖尿病的患病风险之间存在正向的剂量–反应关系,与低收入相比,中、高收入者患2型糖尿病的风险分别增加35%(OR=1.35,95%CI=1.06~1.74)和58%(OR=1.58,95%CI=1.23~2.02);年龄越大、高收入者患2型糖尿病的风险越大。结论家庭人均收入与南京市城区居民自我报告2型糖尿病存在密切的流行病学联系。     

柚皮苷对H_2O_2诱导H9c2心肌细胞损伤保护作用

目的探讨柚皮苷对H_2O_2诱导的H9c2心肌细胞凋亡的保护作用及机制。方法体外培养H9c2心肌细胞,用H_2O_2诱导建立细胞凋亡模型。实验设对照组、模型组、柚皮苷低、中、高剂量组(10、20、40μmol/L),噻唑蓝法检测细胞活力并用显微镜观察各组细胞形态;原位末端标记法检测H9c2心肌细胞凋亡情况;RT-PCR及Western blot法检测凋亡相关因子Bcl-2、Bax、caspase-3 m RNA及蛋白表达。结果与对照组比较,模型组细胞凋亡率[(17.2±2.1)%]明显升高(P<0.01);与模型组比较,10、20、40μmol/L柚皮苷组细胞凋亡率[分别为(10.7±1.9)%、(5.7±1.2)%、(6.4±1.5)%]均下降(均P<0.05)。与对照组比较,模型组H9c2心肌细胞Bcl-2蛋白表达水平(0.76±0.16)明显下调,Bax、caspase-3蛋白表达水平[分别为(5.42±0.52)、(1.09±0.11)]均上调(均P<0.01);与模型组比较,10、20、40μmol/L柚皮苷组H9c2心肌细胞Bcl-2蛋白表达水平[分别为(1.37±0.11)、(1.65±0.09)、(1.65±0.15)]均上调,Bax、caspase-3蛋白表达水平[分别为(2.78±0.55)、(3.43±0.15)、(2.69±0.26)和(0.59±0.08)、(0.77±0.06)、(0.82±0.05)]均下调(均P<0.05)。结论柚皮苷对H_2O_2诱导的H9c2心肌细胞损伤具有一定保护作用,其机制可能与其对凋亡信号途径的抑制作用有关。     

五味消毒饮治疗CO_2激光术后复发性尖锐湿疣临床研究

目的:观察五味消毒饮治疗CO_2激光术后复发性尖锐湿疣的临床疗效。方法:将126患者随机分为观察组和对照1组、对照2组,每组各42例。对照1组在CO_2激光术除去尖锐湿疣后仅给予肌肉注射卡介菌多糖核酸注射液,对照2组在CO_2激光术除去尖锐湿疣后待伤口愈合后给予咪喹莫特外用,观察组在上述两组综合治疗的基础上口服中药五味消毒饮。观察三组患者的临床疗效及复发情况。结果:观察组有效率为85.71%,对照1组有效率为64.25%,对照2组有效率为59.52%,观察组与对照1组和对照2组比较,差异具有统计学意义(P0.05),观察组复发率显著低于对照1组、对照2组,差异具有统计学意义(P0.05)。结论:五味消毒饮治疗CO_2激光术后复发性尖锐湿疣疗效显著,复发率低,安全性高。     

岷当归有效成分对高同型半胱氨酸血症兔TXB_2的影响

目的:探讨岷当归有效成分(当归挥发油、当归多糖、阿魏酸)对高同型半胱氨酸血症(HHcy)兔致动脉粥样硬化(AS)的影响。方法:将48只日本大耳白兔随机分为正常组、模型组、当归挥发油组、当归多糖组、阿魏酸组和叶酸对照组,每组8只。采用L-蛋氨酸皮下注射法建立HHcy家兔模型。造模8周后,当归挥发油组、当归多糖组、阿魏酸组分别给予岷当归有效成分灌胃治疗,叶酸组给予叶酸+维生素B_6+维生素B_(12)灌胃治疗。12周后检测各组血清同型半胱氨酸(Hcy)、血浆血栓素B_2(TXB_2)水平。结果:模型组血清Hcy水平高于正常组,差异有统计学意义(P0.05),HHcy模型形成;与模型组比较,当归挥发油组、阿魏酸组、叶酸组血清Hcy水平明显降低,差异有统计学意义(P0.05);与模型组比较,叶酸组、当归挥发油组、当归多糖组、阿魏酸组血浆TXB2水平降低,差异有统计学意义(P0.05)。阿魏酸组血浆TXB_2水平比叶酸组、当归挥发油组、当归多糖组较低,差异有统计学意义(P0.05)。结论:岷当归有效成分阿魏酸能够降低血清Hcy与血浆TXB2水平,减少Hcy对血管内皮的损伤及毒性作用。     

Nicotine effects on PGE2 and IL-1β release by LPS-treated human monocytes

Cigarette smoking is a major risk factor in the development and further progression of periodontitis. However, little is known regarding the pathogenesis of smoking-related periodontal diseases. The purpose of this study was to examine the effects of nicotine, alone and in combination with lipopolysaccharide (LPS), on monocyte secretion of bone-resorbing factors, PGE₂ and IL-1β. Peripheral blood monocytes (PBM) were isolated by counterflow centrifugal elutriation from 15 healthy, non-smoking donors. PBM were incubated for 24 h in RPMI 1640 containing nicotine (0, 50 μg/ml, I μg/ml, 10 μg/ml and 100 μg/ml) with or without 10 μg/ml Porphyromonas gingivalis LPS or Escherichia coli LPS. Culture supernatants were assayed for PGE₂ and IL-1β by ELISA. None of the nicotine preparations resulted in significant PBM secretion of PGE₂ and IL-1β above that of unstimulated cultures. However, PGE₂ release was potentiated 1.7-fold by the combination of P. gingivalis LPS and 10 μg/ml nicotine relative to P. gingivalis LPS alone (p<0.05, one-way ANOVA). Prostaglandin E₃ release also was potentiated 3.5-fold by P. gingivalis LPS and 100 μg/ml nicotine relative to P. gingivalis LPS alone (p<0.00001, one-way ANOVA) and 3.1-fold by E. coli LPS and 100 μg/ml nicotine relative to E. coli LPS alone (p<0.00001, I. one-way ANOVA). IL-1β secretion was lower for either LPS plus 100 μg/ml nicotine relative to LPS alone, although not significantly. These data demonstrate upregulation of LPS-mediated monocyte secretion of PGE₂ by nicotine and suggest a potential role for nicotine in periodontal disease pathogenesis.     

Genomic variation in Streptococcus mutans: deletions affecting the multiple pathways of β‐glucoside metabolism

The genome of Streptococcus mutans UA159 contains two phospho‐β‐glucosidase genes, bglA and celA, which occur in operon‐like arrangements along with genes for components of phosphotransferase transport systems and a third phospho‐β‐glucosidase encoded by the arb gene, which does not have its own associated transport system but relies on uptake by the bgl or cel systems. Targeted inactivation of each of the phospho‐β‐glucosidase genes revealed that bglA is involved in aesculin hydrolysis, celA is essential for utilisation of cellobiose, amygdalin, gentobiose and salicin, and arb is required for utilisation of arbutin. Inactivation of genes for the phosphotransferase systems revealed an overlap of specificity for transport of β‐glucosides and also indicated that further, unidentified transport systems exist. The cel and arb genes are subject to catabolite repression by glucose, but the regM gene is not essential for catabolite repression. Screening a collection of isolates of S. mutans revealed strains with deletions affecting the msm, bgl and/or cel operons. The phenotypes of these strains could largely be explained on the basis of the results obtained from the knockout mutants of S. mutans UA159 but also indicated the existence of other pathways apparently absent from UA159. The extensive genetic and phenotypic variation found in β‐glucoside metabolism indicates that there may be extensive heterogeneity in the species.     

Enamelin maps to human chromosome 4q21 within the autosomal dominant amelogenesis imperfecta locus

Amelogenesis imperfecta is a group of hereditary enamel defects. Of the autosomal dominant forms, only the local hypoplastic type has been mapped to human chromosome 4q 13-4q21. Enamelin is a large enamel matrix protein secreted by ameloblasts. The purpose of this study was to determine the human chromosomal localization of enamelin to establish an association with various forms of amelogenesis imperfecta. Chromosomal mapping was performed by polymerase chain reaction (PCR) amplification using somatic hybrid and deletion/derivation cell line panels with an enamelin primer set based on 100% conserved regions between pig and mouse cDNAs. Sequence-tagged site content mapping using eight markers within the critical local hypoplastic amelogenesis imperfecta region was then performed using an isolated human enamelin genomic BAC clone. The human enamelin amplicon was confirmed by DNA sequence analysis, revealing 81% and 73% identity to pig and mouse cDNAs, respectively. PCR amplification using a somatic cell hybrid panel placed enamelin on chromosome 4 with analysis of a regional chromosome 4 mapping panel refining the localization to 4q 13.1-q21.23. An identified human enamelin BAC genomic clone was shown to contain markers D4S2604 and D4S2670, as well as the first exon of the human ameloblastin gene, placing enamelin in the critical amelogenesis imperfecta locus between markers HIS1 and D4S2604 at 4q21. Our results suggest that enamelin is a strong candidate gene for this disease. Furthermore, human 4q21 may contain a second cluster of enamel matrix genes located proximally to the identified cluster of dentin and bone genes.