乳腺癌治疗对骨质的影响及防治策略

骨折是骨质疏松最常见的并发症随着雌激素水平的降低,绝经后女性骨质疏松的发生风险逐年增加。乳腺癌的一些治疗方法会进一步降低患者血清雌激素水平,加速骨质的流失（即肿瘤治疗诱导的骨丢失）,从而增加患者罹患骨质疏松和骨折的风险。一系列研究已证实,化疗、内分泌治疗（尤其是芳香化酶抑制剂的使用）能显著增加乳腺癌患者骨质疏松及骨折的发生率。近年来,国内外相关组织相继发布了针对此类患者的骨质疏松预防和治疗指南,并推荐将其用于临床实践,尤其用于绝经后乳腺癌患者的临床治疗中。     

骨质疏松性骨折的若干问题

近年来,骨质疏松症领域内临床治疗、科研和预防均取得较大发展.适时、合理的预防和治疗措施可以减慢骨量的丢失,延缓骨衰老,保护骨健康,降低骨质疏松性骨折的风险.中国是世界上人口最多的国家,老龄化已接近发达国家.与2000年相比,2010年我国60岁及以上人口已由1.32亿增加至1.77亿.中国老年学会日前称,截至2011年7月1日,全国(不包港,澳,台地区)健在的百岁老人已达48 921人,比去年净增5 228人,增幅为11.97%.预计2020年全国老年人口将增加至2.45亿.     

骨质疏松症的遗传学研究及其基因定位的方法和现状

低创伤性骨折是老年人特别是老年妇女中一个主要的公众健康问题。骨质疏松症是一种具有脆性骨且易发生低创伤性骨折的疾病。在美国,由骨质疏松症引发的骨折每年超过130万例,超过40％的绝经后妇女平均至少要遭受一次骨质疏松性骨折。仅在美国每年由骨质疏松症引起的直接花费估计约为140亿美元。骨质量(Bone mass)是一个可测定骨折危险的主要因子。世界卫生组织(WHO)将骨质疏松症在数量上定义为:骨密度或骨质含量值低于年轻成年人平均值2.5个标准差。骨质量是由多个遗传因素和环境因素共同决定的复杂性状,并且很大程度上受遗传因素决定,其遗传率大于50％。进行骨遗传学研究对于全面地了解引起骨质量变化的主要决定因素是很重要的。     

健康教育在放疗病人中的实施

健康教育是以病人和家属为中心 ,通过护理人员有计划、有目的的宣传教育 ,使病人了解增进健康的知识 ,提高自我保健和预防能力 ,改变他们对健康教育的认识 ,配合治疗与护理 ,尽快恢复健康。我们在护理中实施了健康教育并收到了较好的效果 ,现将实施介绍如下。1　入院时宣传教育　患者入院后由主班护士负责向病人介绍主管医生、病区护士及护士长 ,介绍病区环境、医院的管理制度。如 :探视、陪护、作息制度等。使病人尽快的熟悉住院环境 ,消除陌生感 ;向病人讲解有关疾病的一般知识 ,如 :情绪对健康的影响 ,饮食对放疗的影响 ,主观因素在疾病…     

临终关怀和姑息治疗日

在“临终关怀之声”与世界各地的“临终关怀和姑息治疗学会”的联合倡导下,2005年10月8日将诞生第一个新的世界纪念日,即第一个“临终关怀和姑息治疗日”。因之,WHO对肿瘤工作也由“肿瘤预防、早期诊断、早期治疗”三项任务改为“肿瘤预防、早期诊断、综合治疗、姑息治疗”四项任务。临终关怀和姑息治疗日     

凡临床试验都应在中国临床试验注册中心注册北大核心CSCD

全球临床试验注册制度由世界各国政府共同决定由WHO领导建立。临床试验注册具有伦理和科学的双重意义,目的是为了尊重和珍惜所有试验参与者的贡献,他们的贡献用于改善全社会的医疗保健,因此,任何临床试验都与公众利益相关。     

癌症的预防和控制

由于世界范围内癌症总的发病率仍呈逐渐上升趋势，死亡率亦居高不下，经常居各国总死亡率的前三位乃至第一位，所以癌症对人类生命健康是一个严重的危害。各国均积极加以研究、预防和控制。癌症的预防和控制已被提到全民的卫生保健日程上来。世界卫生组织（WHO）现已协助各成员国制订肿瘤防治计划，并推动其实行。我国卫生部全国肿瘤防治研究办公室已组织专家制订了《1986－2000年全国肿瘤防治规划纲要》，并把控制癌症列为我国卫生战略重点之一。发达国家，如美国和欧洲地区都有了自己的规划或防癌准则。发展中的其它国家，如印度、古巴…     

第四届世界乳腺健康大会（境内代表）征文及参会的补充通知

由世界乳腺癌健康协会、中华医学会主办,中国工程院医药卫生学部、天津医科大学协办,中华医学会肿瘤学分会、天津医科大学附属肿瘤医院承办的第四届世界乳腺健康大会将于2007年10月18～21日在天津举行。本届大会,来自世界各国的医务工作者、科研工作者、教育工作者及护理人员将围绕乳腺癌的基础研究、预防、诊断、治疗、     

骨质疏松症的防治药物的现状与未来

骨质疏松症的防治在过去的几十年中有了非常迅速和显著的发展。就诊断来说,1994年以前骨质疏松症是在骨折发生后被诊断的。直到1994年世界卫生组织(WHO)首次提出骨质疏松症定义和     

骨疏康对去卵巢雌鼠骨质疏松症防治作用的研究

目的 为验证骨疏康颗粒防治原发性骨质疏松症(POP)的疗效和探讨其治疗机理。方法 以切除卵巢雌性大鼠复制绝经后骨质疏松症模型,观察该药对去卵巢大鼠抗失骨作用。实验分为模型组、骨疏康组、尼尔雌醇组和正常对照组。术后1周开始灌胃治疗,持续12周。结果 实验性骨质疏松症大鼠一般状态、器官指数、腰椎骨矿含量、胫骨骨组织形态计量学、股骨生物力学性能等指标明显异常,病理光镜和计算机图像分析显示POP病变典型。骨疏康颗粒对上述改变有明显缓解作用,综合疗效优于对照西药。结论 骨疏康颗粒可通过体内多方位调节作用达到预防和抑制骨质疏松症的发生和发展,具有较好的应用前景。     

Fatalistic beliefs about cancer prevention and three prevention behaviors.

BACKGROUND: A substantial proportion of US adults hold fatalistic beliefs about cancer prevention. Although evidence suggests that fatalistic beliefs discourage people from engaging in screening behaviors that can reduce their cancer risk, far less is known about associations between cancer fatalism and other prevention behaviors. We examined sociodemographic correlates of these beliefs and their associations with regular exercise, smoking, and fruit and vegetable consumption with a national sample of American adults. METHODS: Data were analyzed from the first wave of the Health Information National Trends Survey (HINTS 2003). HINTS used random-digit dialing to complete phone interviews with adult Americans (N = 6,369). RESULTS: Nearly half of respondents (47.1%) agreed that "It seems like almost everything causes cancer," 27.0% agreed that "There's not much people can do to lower their chances of getting cancer," and 71.5% agreed that "There are so many recommendations about preventing cancer, it's hard to know which ones to follow." These beliefs were stronger in subjects who were less educated but generally weaker among both African Americans and Hispanics relative to Whites. Fatalistic beliefs about cancer prevention were negatively associated with exercising weekly, not smoking, and eating five or more fruits and vegetables daily in multivariate analysis controlling for sociodemographic characteristics. CONCLUSIONS: Americans who hold fatalistic beliefs about cancer prevention may be at greater risk of cancer because they are less likely to engage in various prevention behaviors. Results have notable implications for future cancer communication and education efforts.     

Diet and cancer prevention

Research from several sources provides strong evidence that vegetables, fruits, and whole grains, dietary fibre, certain micronutrients, some fatty acids and physical activity protect against some cancers. In contrast, other factors, such as obesity, alcohol, some fatty acids and food preparation methods may increase risks. Unravelling the multitude of plausible mechanisms for the effects of dietary factors on cancer risk will likely necessitate that nutrition research moves beyond traditional epidemiological and metabolic studies. Nutritional sciences must build on recent advances in molecular biology and genetics to move the discipline from being largely 'observational' to focusing on 'cause and effect'. Such basic research is fundamental to cancer prevention strategies that incorporate effective dietary interventions for target populations.     

Fenretinide and cancer prevention

A characteristic feature of fenretinide is the ability to inhibit cell growth through the induction of apoptosis with mechanisms that may be both receptor-dependent and receptor-independent. Chemopreventive efficacy of fenretinide has been investigated in clinical trials targeted at different organs. Results of a phase III secondary prevention trial suggest a benefit in preventing second breast malignancies in premenopausal women with early breast cancer. A potential benefit of fenretinide with ovarian cancer and a reduction of new occurrences of leukoplakia have also been observed in clinical trials with this agent. However, no effects on DNA content of urothelial cells from bladder washings and on recurrence rate were noted in a study of patients with superficial bladder tumors. Future trials using surrogate biomarkers may aid in rapid evaluation of the chemopreventive activity of fenretinide with various targeted organs.     

Phytoestrogen and cancer prevention

Phytoestrogens are defined to be plant chemicals that modify estrogenic effects in the body by binding to the estrogen receptors in mammals. Isoflavones, coumestane, lignan, and prenylflavones are examples of these, with isoflavones from soy foods and lignans from rye being a major dietary contribution. Mechanisms of cancer prevention by these phytoestrogens are reviewed, and human epidemiological studies, especially for breast and prostate cancers, are summarized and the results discussed.     

Statins and cancer prevention

Randomized controlled trials for preventing cardiovascular disease indicated that statins had provocative and unexpected benefits for reducing colorectal cancer and melanoma. These findings have led to the intensive study of statins in cancer prevention, including recent, large population-based studies showing statin-associated reductions in overall, colorectal and prostate cancer. Understanding the complex cellular effects (for example, on angiogenesis and inflammation) and the underlying molecular mechanisms of statins (for example, 3-hydroxy-3-methylglutaryl coenzyme-A (HMG-CoA) reductase-dependent processes that involve geranylgeranylation of Rho proteins, and HMG-CoA-independent processes that involve lymphocyte-function-associated antigen 1) will advance the development of molecularly targeted agents for preventing cancer. This understanding might also help the development of drugs for other ageing-related diseases with interrelated molecular pathways.     

Diet and cancer prevention

Dietary effects are presumed to underlie many of the large international differences in incidence seen for most cancers. Apart from alcohol and a few micronutrients, however, the role of specific nutritional factors remains ill-defined. The evidence for a role of energy balance, physical inactivity, and obesity has strengthened, while for dietary fat it has weakened. Phytochemicals such as folate, lycopene and flavonoids are still the subject of active research. As the mechanisms underlying human carcinogenesis are better understood, dietary research will focus increasingly on intermediate markers such as the insulin-like growth factors and potentially carcinogenic metabolites.