含糖饮料1年夺命18万人

正据英国《BBC新闻》(BBC NEWS)2015-06-30报道,一项刊载于《循环》(Circulation)的研究指出,汽水和其他含糖饮料1年可能造成全球184 000人死亡。这项报告分析与喝含糖饮料有关联的糖尿病、心血管疾病及癌症的全球性死亡风险。研究人员估计,全球约133 000人因为喝报告中所谓的含糖饮料而死于糖尿病,约45 000人因此死于心血管疾病,6 450人死于癌症。     

心理因素对癌症的影响

癌症是当代人类三大原因之一。在疾病谱中也占有重要的地位。据统计,目前全世界约有千余万人患有癌症,全年新发病例达一千余万人,数百万人死于非命。美国1974年的资料,每年死于癌症者就有36万人;日本1983年的资料,每年死于癌症者也有17.6万人。因此,癌症是种威胁人类健康和生命的严重疾病,已在世界医学领域中引起广泛重视。     

肠道菌群、饮食与结直肠癌发病相关联

正据Mehta RS 2017年1月26日(JAMA Oncol,2017 Jan 26.)报道,Dana-Farber癌症研究所和麻省总医院的研究人员通过研究发现,机体大肠中生存的微生物或许在饮食和特殊类型结直肠癌发病的关联中起到了关键的桥梁作用。研究人员重点对具核梭杆菌(Fusobacterium nucleatum)进行了研究,这种细菌是寄居在人类大肠中的常见细菌,同时其也被认为在结直肠癌发生过程中扮演着关键角色;通过对超过137 000例个体的饮食进行长达10年追踪,并且对1 000份结直肠癌样本     

DC-CIK联合化疗治疗非小细胞肺癌的研究进展

<正>据2015年最新报道,至2012年估计新增180万肺癌病例,约占癌症确诊总量的13%~([1])。肺癌是2012年男性癌症确诊和导致死亡最主要的原因。在女性中,肺癌是发达国家癌症死亡的主要原因,和发展中国家癌症死亡的第二大原因。而中国妇女即使吸烟率低于欧洲一些国家的妇女,但因为环境等多方面因素,肺癌患病率(每100 000人20.4例女性)却高于一些欧洲国家的女性发病率。其中非小     

癌症,不再相信眼泪

直到今天,癌对人类的威胁依然存在。直到今天,世界医学界尚未给这种顽疾开辟一条彻底的治疗佳径。 进入廿世纪,癌症已上升为人类生命的超级“杀手”,成为威胁人类最严重的灾难之一。据资料不完全统计,世界每年有六百万人患癌症,五百万人死于癌症;癌症在我国已上升为死亡序列的第三位。美国卫生研究院院长费富德克森指出:“今后廿五年内的主要挑战,将是癌症。”联合国教科文组织曾发布:世界上谁能攻克癌症,将为其塑一个与真人一     

癌症疼痛的治疗进展

癌症是当今严重威胁人类健康和生命的疾病之一。解除癌症疼痛对改善患者的生活质量非常有意义,了解癌性疼痛的发生机制和治疗方法对治好癌症疼痛起着基础作用。本文就癌痛的发生机制,癌痛治疗的方法和药物进行阐述。     

久坐增加女性癌症风险

正据美国WebM D医学新闻网(2015-06-29)报道,花太多时间坐着会增加女性癌症的概率,但对男性来说似乎没有类似的效果。主导美国癌症协会癌症预防研究的Alpa Patel博士表示,花较多闲暇时间坐着与女性整体癌症风险较高有关,尤其是多发性骨髓瘤、乳腺癌以及卵巢癌等;但坐着的时间与男性癌症风险没有关联性。这篇研究针对超过146 000名男女从1992年追踪至2009年,参与者开始时都没有癌症。在这段期间,近31 000名参与     

射频加温治疗肿瘤的机理和技术

工业的发展及人类生活环境的恶化,使威胁人类健康的癌症发病率也逐年上升。但随着科学技术的进步,对癌症的研究和治疗也提供了愈来愈多的方法。70年代兴起至今方兴未艾的射频加温治疗恶性肿瘤,国内外都有很多治疗成功的报道,并且有不少医疗研究单位对其机理进行了研究。     

癌症疼痛的治疗进展

癌症是当今严重威胁人类健康和生命的疾病之一.解除癌症疼痛对改善患者的生活质量非常有意义,了解癌性疼痛的发生机制和治疗方法对治好癌症疼痛起着基础作用.本文就癌痛的发生机制,癌痛治疗的方法和药物进行阐述.     

国际会议预报

第4届国际实体瘤染色体专题讨论会(Fourth International workshop on Chromosomes in Solid Tumors)定于1991年2月24日至27日在美国亚里桑那图森举行。大会报告:癌症成因的分子机理,与人类癌症有关的遗传图谱,癌症的分子遗传学与细胞遗传学,人类肿瘤的染色体带分析,荧光原位杂交分析,     

A novel fungal prenyl diphosphate synthase in the dimorphic zygomycete Mucor circinelloides

Two Mucor circinelloides structural genes involved in isoprenoid biosynthesis were isolated and characterised. The isoA gene encodes a typical eukaryotic farnesyl diphosphate synthase (EC 2.5.1.10), whereas the isoB gene deduced amino acid sequence shows similarity to fungal medium-chain prenyl diphosphate synthases. By functional complementation in Escherichia coli, the isoB gene product was shown to be a solanesyl diphosphate synthase (EC 2.5.1.11), which is the first fungal enzyme reported having this specificity. In addition, a M. circinelloides one-marker-per-chromosome map was completed by contour-clamped homogeneous electric field localisation of isoA, isoB and three other isoprenoid biosynthesis genes to individual chromosomes.Abbreviations FPP farnesyl diphosphate (or pyrophosphate) - GGPP geranylgeranyl diphosphate - PrenylPP prenyl diphosphate - DPP decaprenyl diphosphate - HPP hexaprenyl diphosphate - SPP solanesyl diphosphate     

Missense mutation of the COQ2 gene causes defects of bioenergetics and de novo pyrimidine synthesis

Coenzyme Q(10) (CoQ(10)) deficiency has been associated with an increasing number of clinical phenotypes that respond to CoQ(10) supplementation. In two siblings with encephalomyopathy, nephropathy and severe CoQ(10) deficiency, a homozygous mutation was identified in the CoQ(10) biosynthesis gene COQ2, encoding polyprenyl-pHB transferase. To confirm the pathogenicity of this mutation, we have demonstrated that human wild-type, but not mutant COQ2, functionally complements COQ2 defective yeast. In addition, an equivalent mutation introduced in the yeast COQ2 gene also decreases both CoQ(6) concentration and growth in respiratory-chain dependent medium. Polyprenyl-pHB transferase activity was 33-45% of controls in COQ2 mutant fibroblasts. CoQ-dependent mitochondrial complexes activities were restored in deficient fibroblasts by CoQ(10) supplementation, and growth rate was restored in these cells by either CoQ(10) or uridine supplementation. This work is the first direct demonstration of the pathogenicity of a COQ2 mutation involved in human disease, and establishes yeast as a useful model to study human CoQ(10) deficiency. Moreover, we demonstrate that CoQ(10) deficiency in addition to the bioenergetics defect also impairs de novo pyrimidine synthesis, which may contribute to the pathogenesis of the disease.     

The glycine 90 to aspartate alteration in the Abeta subunit of PP2A (PPP2R1B) associates with breast cancer and causes a deficit in protein function

Mutations of the PPP2R1B gene, which encodes the Abeta scaffolding subunit of serine/threonine protein phosphatase 2A (PP2A), have been identified in several types of cancer including lung and breast carcinoma. One of these mutations results in an alteration of glycine 90 to aspartic acid (G90D), which has been found in both tumor and genomic DNA, raising the possibility that it is associated with an increased risk for cancer. A novel microarray-based technology was used to screen for this single-nucleotide polymorphism in 387 cancer patients and 329 control individuals. These data were used for case-control and family-based comparisons in order to study the association of this polymorphism with susceptibility to lung carcinoma, breast carcinoma, and acute lymphoblastic leukemia. The frequency of the G90D polymorphism in breast cancer patients was significantly higher in cases (3%) than in controls (0.3%). The wild-type Abeta subunit interacted with the B56gamma (PPP2R5C), PR72 (PPP2R3A), and PR48 subunits of PP2A but did not interact with the B55alpha (PPP2R2A), B56alpha (PPP2R5A), or B56beta (PPP2R5B) regulatory subunits in an in vitro binding assay. The G90D alteration inhibited the interaction of Abeta with the B56gamma subunit but had no effect on binding to the PR72 subunit. These results provide evidence that the G90D alteration of the Abeta subunit of PP2A is associated with a low frequency of breast carcinoma and that the role of this alteration in transformation is likely to involve decreased interaction with the B56gamma regulatory subunit.     

Coenzyme Q10 can prolong C. elegans lifespan by lowering oxidative stress

The mev-1 gene encodes cytochrome b, a large subunit of the Complex II enzyme succinate-CoQ oxidoreductase. The mev-1(kn1) mutants are hypersensitive to oxidative stress and age precociously, probably because of elevated superoxide anion production in mitochondria. Coenzyme Q (CoQ) is essential for the mitochondrial respiratory chain. Here, we show that CoQ(10) and Vitamin E extended the life span of wild-type Caenorhabditis elegans. Conversely, only CoQ(10) recovered the life shortening effects seen in mev-1. We also show that CoQ(10) but not Vitamin E reduced superoxide anion levels in wild type and mev-1. Another previously described phenotype of mev-1 animals is the presence of supernumerary apoptotic cells. We now demonstrate that CoQ(10) (but not Vitamin E) suppressed these supernumerary apoptoses. Collectively these data suggest that exogenously supplied CoQ(10) can play a significant anti-aging function. It may do so either by acting as an antioxidant to dismutate the free radical superoxide anion or by reducing the uncoupling of reactions during election transport that could otherwise result in superoxide anion production. The latter activity has not been ascribed to CoQ(10); however, it is known that conditions that uncouple electron transport reactions can lead to elevated superoxide anion production.     

RNA阵列技术检测自发性高血压大鼠甲羟戊酸途径酶的基因表达

目的：探讨甲羟戊酸(MVA)途径的9个酶在不同周龄自发性高血压大鼠(SHR)发病过程中的基因表达变化特点。方法:提取2、4、6、8、10、12不同周龄雄性SHR以及正常血压大鼠(WKY)的心室肌、血管平滑肌、肝脏和肾脏4种组织的总RNA，共294个样品，利用高通量RNA阵列技术(RNA array)检测甲羟戊酸途径的9个酶的基因在不同周龄SHR和WKY大鼠中mRNA表达谱的改变。 结果:（1）SHR大鼠从第6周开始收缩压明显高于WKY(P<0.01)。 （2）12周龄SHR大鼠体内血清胆固醇浓度明显低于WKY大鼠，组织中的胆固醇浓度没有明显差异(P<0.01)。（3）在SHR大鼠心脏、血管、肝脏、肾脏组织中：MVA中间产物的合成酶如法呢醇焦磷酸合成酶(FDS)、异戊烯化焦磷酸化异构酶(IDI)、法呢醇转移酶α亚基(FT1)和β亚基(FT2)的表达明显高于WKY(P<0.01)。（4）SHR肾脏组织中羟甲基戊二酰辅酶A还原酶（HMGR）、甲羟戊酸激酶（MVK）、焦磷酸甲羟戊酸脱羧酶（MVD）、鲨烯合成酶（SQS）和鲨烯环氧化酶（SQ） 表达较为一致，早期(2-4 周)SHR大鼠的基因表达明显高于WKY，随着周龄增加SHR的表达进一步增高，且与WKY相比都有明显差异(P<0.01) 。（5）在心脏、血管和肝脏中，HMGR、MVK、MVD、SQS和SQ的基因表达无明显规律。结论:SHR大鼠随着周龄的增长甲羟戊酸途径中各酶基因表达的改变，以非胆固醇产物类合成酶(如IDI、FDS和FT1、FT2)表达增加为特点，这一改变是否与高血压有关尚待进一步验证。     

Coenzyme Q plays opposing roles on bacteria/fungi and viruses in Drosophila innate immunity

Coenzyme Q (CoQ or ubiquinone) is a lipid-soluble component of virtually all types of cell membranes and has been shown to play multiple metabolic functions. Several clinical diseases including encephalomyopathy, cerebellar ataxia and isolated myopathy were shown to be associated with CoQ deficiency. However, the role of CoQ in immunity has not been defined. In the present study, we showed that flies defective in CoQ biosynthetic gene coq2 were more susceptible to bacterial and fungal infections, while were more resistant to viruses. We found that Drosophila contained both CoQ9 and CoQ10, and food supplement of CoQ10 could partially rescue the impaired immune functions of coq2 mutants. Surprisingly, wild-type flies fed CoQ10 became more susceptible to viral infection, which suggested that extra caution should be taken when using CoQ10 as a food supplement. We further showed that CoQ was essential for normal induction of anti-microbial peptides and amplification of viruses. Our work determined CoQ content in Drosophila and described its function in immunity for the first time.     

The role of ubiquinone in Caenorhabditis elegans longevity

Aging is an irreversible physiological process that affects all living organisms. Different mutations in the insulin signaling pathway and caloric restriction have been shown to retard aging in Caenorhabditis elegans. In addition, mutations or RNAi silencing of components of the respiratory chain results in the modification of adult life span. Another class of genes that affect life span in C. elegans is the clock (clk) genes. Particularly interesting is clk-1, which encodes an enzyme required for ubiquinone (coenzyme Q, CoQ) biosynthesis. Down-regulation by RNAi silencing of the genes required for ubiquinone biosynthesis also extends life span in C. elegans, and CoQ supplied in the diet also affects nematode longevity in both clk-1 and wild-type strains. Although there are many aspects that can be considered in aging, we focus this review on the role of CoQ in the longevity of C. elegans. We will review the current information about the biosynthesis of CoQ and its dietary supplementation related to the extension of life span. We will also analyze the function of CoQ in the electron transport chain and reactive oxygen species production in the context of aging. We hypothesize that the role of CoQ on longevity of C. elegans supports the oxidative damage theory of aging.     

Tumor suppressive microRNA-133a regulates novel molecular networks in lung squamous cell carcinoma

Analysis of the microRNA (miRNA) expression signature of lung squamous cell carcinoma (lung-SCC) revealed that the expression levels of miR-133a were significantly reduced in cancer tissues compared with normal tissues. In this study, we focused on the functional significance of miR-133a in cancer cell lines derived from lung-SCC and the identification of miR-133a-regulated novel cancer networks in lung-SCC. Restoration of miR-133a expression in PC10 and H157 cell lines resulted in significant inhibition of cell proliferation, suggesting that miR-133a functions as a tumor suppressor. We used genome-wide gene expression analysis to identify the molecular targets of miR-133a regulation. Gene expression data and web-based searching revealed several candidate genes, including transgelin 2 (TAGLN2), actin-related protein2/3 complex, subunit 5, 16kDa (ARPC5), LAG1 homolog, ceramide synthase 2 (LASS2) and glutathione S-transferase pi 1 (GSTP1). ARPC5 and GSTP1 likely represent bona fide targets as their expression is elevated in lung-SCC clinical specimens. Furthermore, transient transfection of miR-133a, repressed ARPC5 and GSTP1 mRNA and protein levels. As cell proliferation was significantly inhibited in lung-SCC cells following RNAi knock down of either gene, ARPC5 and GSTP1 may function as oncogenes in the development of lung-SCC. The identification of a tumor suppressive miRNA and the novel cancer pathways it regulates could provide new insights into potential molecular mechanisms of lung-SCC carcinogenesis.     

Dual involvement of coenzyme Q10 in redox signaling and inhibition of death signaling in the rat heart mitochondria

Coenzyme Q10 (CoQ) has long been utilized as a cardioprotective agent in various heart diseases. One of the most important mechanisms by which CoQ exerts cardioprotection is aerobic ATP production as a mobile electron carrier in the mitochondrial electron transfer chain. The ability of CoQ to afford myocardial protection is also attributed to its antioxidant property. However, CoQ may also act as a pro-oxidant through the generation of reactive oxygen species. Although excess oxidative stress is known to induce death signaling via cytochrome c release from mitochondria, it is now apparent that a brief exposure to oxidative stress stimulates redox signaling for acquisition of tolerance to oxidative stress. Therefore, we have investigated dual involvement of CoQ in redox signaling generation through enhanced production of reactive oxygen species and death signaling inhibition through antioxidation. Mitochondria were isolated from the rat heart and incubated with CoQ (10 or 100 microM) or its vehicle HCO 60 for 1 h. H2O2 and cytochrome c release from respiring mitochondria were increased by antimycin A (2 microM), an inhibitor of complex III respiratory chain, or by high Ca2+ (10 microM). This enhanced release of H2O2 was associated with an increase in lipid peroxidation as measured with 4-hydroxy-2-nonenal-modified proteins and with large amplitude swelling of mitochondria. CoQ potentiated H2O2 release from antimycin A- or high Ca(2+)-treated mitochondria, but was capable of inhibiting lipid peroxidation and large amplitude swelling, and attenuated cytochrome c release from the mitochondria. In addition, CoQ increased ATP synthesis by mitochondria. These results suggest that CoQ plays dual roles in mitochondrial generation of intracellular signaling. CoQ acts as a pro-oxidant that participates in redox signaling. CoQ also acts as an antioxidant that inhibits permeability transition and cytochrome c release, and increases ATP synthesis, thereby attenuating death signaling toward apoptosis and necrosis.     

Coenzyme Q10 content in different parts of the normal human heart

Coenzyme Q10 (CoQ10) and citrate synthase (CS) activities were analysed in the myocardium of brain-dead organ donors (14-40 years). Different parts of the heart were studied: right and left auricular appendage, right and left atrium, right ventricle (septum and free wall) and left ventricle (septum, free wall, and papillary muscle). Freeze-dried, dissected myocardial samples were analysed for CoQ10 content by HPLC and CS activity by fluorometric technique. CoQ10 content in the normal human myocardium was lowest in auricular appendages and atria (0.25 +/- 0.06 mg X g-1 dry muscle), intermediate in right ventricle (0.37 +/- 0.05 mg X g-1 dm) and highest in left ventricle (0.42 +/- 0.07 mg X g-1 dm). CS activity showed the same relationship between these locations as CoQ10. The results suggest that there exist differences in CoQ10 content between different parts of the normal human myocardium. These differences were closely related to the differences in CS activity between corresponding parts. The differences between different parts of the heart may be related to divergent work demand, and the constant relationship between CS and CoQ10 may be related to their coupling to the mitochondrial oxidative metabolism.