骨疏康对1型糖尿病大鼠体外培养的破骨细胞影响的初步探讨

目的 探讨骨疏康对1型糖尿病大鼠体外培养的破骨细胞影响。方法 用RANKL和M-CSF诱导1型糖尿病大鼠的股骨骨髓进行体外培养生成类破骨细胞样细胞(OLC)。实验分为正常对照组,1型糖尿病组,正常对照+骨疏康组,1型糖尿病+骨疏康组。骨疏康的浓度为20μg/ml。细胞培养7天后,贴壁细胞固定,抗酒石酸盐酸性磷酸酶染色,破骨细胞计数。结果 1型糖尿病大鼠与正常大鼠组的破骨细胞数比较无明显差别(P>0.05);经骨疏康干预后,1型糖尿病大鼠与正常大鼠的破骨细胞数都明显减少(P<0.01)。结论 1型糖尿病早期破骨细胞形成与正常对照组无明显差异。中药骨疏康明显抑制正常大鼠和1型糖尿病大鼠的破骨细胞形成。     

17β-雌二醇对破骨细胞骨架和骨吸收功能影响的实验研究

目的　研究17β-雌二醇对体外培养破骨细胞细胞骨架的影响,以及这种影响与骨吸收功能之间的关系。方法　在破骨细胞培养液中加入不同浓度的17β-雌二醇,用F-actin特异性抗体进行免疫荧光染色,激光共聚焦显微镜观察破骨细胞细胞骨架的变化情况,同时用扫描电镜观察破骨细胞在骨片形成骨吸收陷窝数目及面积的变化。结果　随着17β-雌二醇浓度的升高,实验组破骨细胞F-actin相对荧光强度从(89 6±7 5)%下降至(34 7±5 4)% (与对照组荧光强度相比),细胞内微丝收缩变短,排列紊乱,细胞波状缘消失,破骨细胞伸展面积从(1289±53)μm2 /细胞核下降至(406±42)μm2 /细胞核,同时,骨吸收陷窝的数目和面积从(131 5 ±11 7)个/片和(2157±51)μm2 减少到(16 8±4 0 )个/片和(965±75)μm2。生理浓度(10-7mol/l)及其以上17β-雌二醇处理组与对照组比较,差异有显著性(P<0 01 )。结论　17β-雌二醇影响破骨细胞内细胞骨架的结构,下调F-actin的表达,降低破骨细胞的活动能力,从而抑制破骨细胞的骨吸收功能。     

同种异体骨移植后骨吸收和破骨细胞的形态学特点

目的探讨骨移植后骨吸收和破骨细胞的型态学特点。方法利用扫描电镜,结合光镜,观察8例临床植骨后因严重骨吸收被取出的标本,5例人类正常骨标本和20例大鼠肌内埋入的骨标本,分析严重骨吸收过程中破骨细胞和破骨区表面的形态学特征,以及破骨细胞的形态学演变。结果与正常对照骨标本不同,骨吸收部位有大量幼稚的单核破骨细胞聚集,伴有表面结构变异退变,内部纤维裸露和红细胞吞噬破骨区表现为局灶性切割而不是弥漫性骨质疏松。结论破骨的特点是出现单核破骨细胞和局灶性切割。     

骨移植并发感染时骨吸收的细胞学成分和植入骨辐照灭菌的作用

目的探讨骨移植后并发炎症感染时引起骨吸收的细胞成分。方法利用光镜、扫描电镜和光镜扫描电镜对比(LM/SEM)的方法,对10例感染骨标本进行观察,同时利用染菌和掺入内毒素的骨标本植入大鼠肌内进行验证。结果利用LM/SEM方法能在那些看似只有炎症细胞的骨吸收区发现破骨细胞,只是因其形态模糊而被光镜忽略。结论植入骨的吸收来自破骨细胞而不是炎症细胞。由于辐照灭菌不能消除染菌样品引起的炎症反应,辐照不能使内毒素灭活,因此控制骨产品的初始菌量是保证骨产品质量和降低植骨后出现炎症反应的重要措施。     

一种从骨巨细胞瘤组织中纯化破骨细胞的简单方法

目的从人骨巨细胞瘤组织中分离纯化及鉴定破骨细胞。方法我们利用0．25％胰酶-EDTA和Ⅰ型胶原酶从人骨巨细胞瘤组织中纯化出大量破骨细胞，并进行表型特征的鉴定：包括抗酒石酸酸性磷酸酶染色(TRAP染色)，采用RT-PCR方法检测降钙素受体、组织蛋白酶K和破骨细胞分化因子受体(RANK)表达。结果该方法所得细胞纯度可达79．7％，具有破骨细胞表型特征。结论该方法所得破骨细胞可用于生化和分子生物学研究，是进行骨代谢研究较好的破骨细胞来源。     

肺癌A549细胞诱导RAW264.7破骨细胞分化中AMPK信号通路的作用

目的:探讨AMPK信号通路在体外肺癌细胞诱导破骨细胞分化中的作用。方法:将肺癌A549细胞与RAW264.7细胞共培养后随机分为阴性对照组、阳性对照组、AICAR组,药物干预后行TRAP染色观察破骨细胞的分化,流式细胞仪观察破骨细胞细胞凋亡情况,qPCR检测破骨细胞AMPK、mTOR和CTSK mRNA的表达,Western blot检测破骨细胞AMPK、p-AMPK、mTOR和p-mTOR蛋白的表达。结果:与阴性对照组比较,AICAR组破骨细胞数明显减少,差异具有统计学意义（P＜0.05）;对诱导破骨细胞凋亡的作用无差异;上调AMPK的mRNA和蛋白表达,下调mTOR的mRNA和蛋白表达,差异具有统计学意义（P＜0.05）。结论:AICAR可以抑制肺癌细胞诱导破骨细胞分化,而AMPK/mTOR信号通路可能参与了肺癌细胞诱导破骨细胞分化过程。     

一种从骨巨细胞瘤组织中纯化破骨细胞的简单方法(英文)

目的从人骨巨细胞瘤组织中分离纯化及鉴定破骨细胞。方法我们利用0.25%胰酶-EDTA 和Ⅰ型胶原酶从人骨巨细胞瘤组织中纯化出大量破骨细胞,并进行表型特征的鉴定:包括抗酒石酸酸性磷酸酶染色(TRAP 染色),采用 RT-PCR 方法检测降钙素受体、组织蛋白酶 K 和破骨细胞分化因子受体(RANK)表达。结果该方法所得细胞纯度可达79.7%,具有破骨细胞表型特征。结论该方法所得破骨细胞可用于生化和分子生物学研究,是进行骨代谢研究较好的破骨细胞来源。     

骨松康含药血清对成骨细胞生物学活性的影响

目的 观察骨松康对体外培养成骨细胞增殖和分化的影响。方法 分离培养乳鼠颅骨成骨细胞，加入中药骨松康吸收后血清，流式细胞仪和碱性磷酸酶活性检测、骨钙素免疫组化染色、矿化结节计数分析其对成骨细胞增殖和分化的影响。结果以含药血清培养的成骨细胞，S期细胞比例增多，说明细胞DNA的合成增加；碱性磷酸酶活性及骨钙素表达增强；形成矿化结节数及分泌胰岛素样生长因子1（IGF-1）的含量均明显高于对照血清组（P〈0．01）。结论 骨松康含药血清能直接促进体外培养的大鼠成骨细胞的增殖、分泌和矿化，提高了成骨细胞骨形成功能。     

骨关节结核发病机制的相关实验研究

目的研究骨关节结核的发病机制。方法采用不同浓度结核分枝杆菌超声裂解产物体外诱导破骨细胞的生长;通过体外颅骨吸收实验,观察不同浓度结核分枝杆菌超声裂解产物诱导破骨细胞生成和钙离子释放的关系;体内注射结核分枝杆菌超声裂解产物,从血钙浓度和组织学方面观察骨质变化。结果结核分枝杆菌超声裂解产物能够在体外诱导破骨细胞生长,且破骨细胞数量的增加依赖细菌浓度的提高。钙离子释放与细菌诱导破骨细胞的数量相关,体内注射细菌能够引起破骨细胞数量增加、钙离子释放和骨质吸收。结论骨、关节结核的发病很可能与结核菌诱导破骨细胞增生有关。     

骨巨细胞瘤中单核基质细胞的分离培养及其性质研究

目的对骨巨细胞瘤中单核基质细胞的性质和来源进行探讨。方法体外分离培养8例骨巨细胞瘤的单核基质细胞，用胶原酶分离方法和差速贴壁法分离纯化细胞，将分离培养的骨巨细胞瘤单核基质细胞与狗股骨薄磨片共培养，观察骨巨细胞瘤单核基质细胞的噬骨能力、TRAP染色和RT—PCR检测降钙素受体（CTR）和细胞核因子KB受体活化因子（RANK）。结果利用酶消化的方法可以获得较高纯度的单核基质细胞；TRAP染色阳性；体外培养具有噬骨能力；采用RT—PCR方法可检测到降钙素受体和细胞核因子KB受体活化因子。结论利用胶原酶-Ⅱ消化的方法结合差速贴壁方法可以获得较纯的单核基质细胞，可用于生化和分子生物学研究，是进行骨巨细胞瘤细胞学研究的细胞来源。     

Religiosity and Physical and Emotional Functioning Among African American and White Colorectal and Lung Cancer Patients

The literature suggests that religiosity helps cope with illness. The present study examined the role of religiosity in functioning among African Americans and Whites with a cancer diagnosis. Patients were recruited from an existing study and mailed a religiosity survey. Participants (N = 269; 36% African American, 56% women) completed the mail survey, and interview data from the larger cohort was utilized in the analysis. Multivariate analyses indicated that in the overall sample religious behaviors were marginally and positively associated with mental health and negatively with depressive symptoms. Among women, religious behaviors were positively associated with mental health and negatively with depressive symptoms. Religiosity was not a predictor of study outcomes for men. Among African Americans, religious behaviors were positively associated with mental health and vitality. Among Whites, religious behaviors were negatively associated with depressive symptoms. These findings suggest a mixed role of religious involvement in cancer outcomes. The current findings may have applied potential in the areas of emotional functioning and depression.     

New and emerging radiosensitizers and radioprotectors

The combination of chemotherapy and radiation has led to clinical breakthroughs in several disease sites, and current work continues to define optimum combinations of proven chemotherapy as well as more recently available, noncytotoxic agents. Administration of systemic therapies allows modulation of radiation response to improve tumor control (radiosensitization) or to prevent normal tissue toxicity (radioprotection). Substantial progress has been made in identifying the targets of standard chemotherapeutic radiation sensitizers and protectors as well as in the introduction of a new generation of molecularly targeted therapies in combination with radiation. We have reviewed the most recent, predominantly early phase clinical trials combining systemic agents with radiation. Although the proof of an improved schedule ultimately needs to come from well-run Phase III trials, the search among schedules could be shortened by the use of surrogate endpoints such as presence of active drug metabolites in the tumor. This has been accomplished only in a few cases and needs to become a more standard part of radiation sensitizer and protector trials.     

Fruit and vegetables and cancer risk

The possibility that fruit and vegetables may help to reduce the risk of cancer has been studied for over 30 years, but no protective effects have been firmly established. For cancers of the upper gastrointestinal tract, epidemiological studies have generally observed that people with a relatively high intake of fruit and vegetables have a moderately reduced risk, but these observations must be interpreted cautiously because of potential confounding by smoking and alcohol. For lung cancer, recent large prospective analyses with detailed adjustment for smoking have not shown a convincing association between fruit and vegetable intake and reduced risk. For other common cancers, including colorectal, breast and prostate cancer, epidemiological studies suggest little or no association between total fruit and vegetable consumption and risk. It is still possible that there are benefits to be identified: there could be benefits in populations with low average intakes of fruit and vegetables, such that those eating moderate amounts have a lower cancer risk than those eating very low amounts, and there could also be effects of particular nutrients in certain fruits and vegetables, as fruit and vegetables have very varied composition. Nutritional principles indicate that healthy diets should include at least moderate amounts of fruit and vegetables, but the available data suggest that general increases in fruit and vegetable intake would not have much effect on cancer rates, at least in well-nourished populations. Current advice in relation to diet and cancer should include the recommendation to consume adequate amounts of fruit and vegetables, but should put most emphasis on the well-established adverse effects of obesity and high alcohol intakes.     

VEGF及KDR在大肠腺瘤和腺癌中的表达及意义

目的：探讨VEGF和KDR在大肠腺瘤和大肠腺癌中的表达及临床病理特征的关系。方法：大肠腺瘤和大肠腺癌组织标本各100例,采用免疫组织化学染色法检测VEGF和KDR在标本中的表达情况。结果：VEGF和KDR在大肠腺癌组中的阳性表达明显高于大肠腺瘤组（P〈0.05）;在正常大肠黏膜均未见VEGF和KDR表达的阳性染色;VEGF阳性表达组中KDR的阳性表达率为70%,显著高于VEGF阴性表达组中KDR的阳性表达率16%,两组比较有统计学意义（P〈0.01）。结论：大肠腺癌组织中KDR的表达与肿瘤大小、转移情况、浸润深度密切相关;VEGF和KDR在大肠腺瘤中的表达与患者的年龄、性别及分型均无相关性,而与增生程度相关（P〈0.05）。在大肠腺癌患者中VEGF及KDR表达更高,二者具有协同效应。     

肾上腺素能β受体与肿瘤生长及转移

大量研究表明肿瘤细胞可表达β受体，而一些神经递质、药物和社会心理因素可能通过β受体影响肿瘤的生长和转移，β受体激动剂、β受体阻滞剂以及抑郁等社会心理因素可加强或削弱这种作用。这为表达β受体肿瘤的治疗开辟了新的道路，提供了新的治疗靶点。     

Occupational and environmental radiation and cancer

Epidemiologic evidence on the relation between occupational and environmental radiation and cancer is reviewed. Studies of pioneering radiation workers, underground miners, and radium dial painters revealed excess cancer deaths and contributed to the setting of radiation protection standards and to theories of carcinogenesis. Occupational exposures today are generally much lower than in the past, thus any associated increases in cancer will be difficult to detect. Pooling investigations of these more recently exposed workers, however, has the potential to validate current estimates of risk used in radiation protection. New information on the effects of chronic radiation exposure also may come from studies in the former Soviet Union of Chernobyl clean-up workers and of workers at the Mayak nuclear facilities. Studies of environmental radiation exposures, other than radon, are largely inconclusive, due mainly to the difficulties in detecting the low risks associated with low dose exposures. Thyroid cancer, however, has been linked to environmental radiation from the Chernobyl accident and from nuclear weapons tests. Low-level radiation released during normal operations at nuclear plants has not been found to increase cancer rates in surrounding populations. Radon, a human carcinogen, is the most ubiquitous exposure to human populations; remediating high residential-radon levels is recommended, recognizing that the exposure can never be removed completely because it occurs naturally.     

Cell and tissue interactions in carcinogenesis and metastasis and their clinical significance

This review describes a new vision for future directions in the study of metastatic cancer biology and pathology. It is based upon clinical and experimental observations on the constituent cell lineages within a neoplasm and on tumour-host interactions. The vision incorporates information from studies in population biology, developmental biology and experimental pathology as well as investigations upon human malignant disease. The assembled information reveals that invasion and metastasis are supra-cellular manifestations of "emergent behavior" among combinations of normal and malignant cell lineages in vivo. Emergent behavior is a combinatorial interactive process in which a population displays new traits which cannot be achieved by individuals acting separately and which subside when the specific population mix disaggregates. Disruption of such pathological interactions in the field of a developing primary or secondary tumour is, therefore, required to disable the malignant population and arrest progression without tissue destruction. These conclusions originate, in part, from principles which govern the sociobiology and group behavior of bees, ants, fish, birds and human societies. In all these social organisms, external factors can disrupt signaling mechanisms and induce expanding self-perpetuating rogue behavior, leading to social disintegration. These principles also apply to cellular societies composing higher animals, which likewise need intrinsic rules to maintain social order and avoid anarchy, and recognition of this is essential for advancing future research on the mechanisms involved in carcinogenesis and metastasis. Summarised evidence is presented here to support the conclusion that miscommunications between cells and tissues in the region of the developing tumour and its metastases are the main direct perpetrators of malignant disease. Genetic lesions (mutations, deletions, translocations, reduplications, etc.), commonly seen in cancers, can significantly disrupt important molecular pathways in the networks of communications needed to sustain orderly tissue/organ structure and function. However, genetic lesions can also, themselves, be induced by abnormal cell interactions initiated by extrinsic carcinogenic agents such as chemicals, viruses, hormones and radiation. The evidence shows that, irrespective of the initiating cause, it is this miscommunication in the region of a developing tumour and its metastases that is ultimately responsible for the emergence and progression of the disease. The article describes how this information collectively, provides a framework for designing specific novel therapeutic approaches targeting the cell and tissue interactions driving tumour metastasis and its manifold effects on the whole body.     

Vitamin D and melanoma and non-melanoma skin cancer risk and prognosis: A comprehensive review and meta-analysis

Vitamin D is formed mainly in the skin upon exposure to sunlight and can as well be taken orally with food or through supplements. While sun exposure is a known risk factor for skin cancer development, vitamin D exerts anti-proliferative and pro-apoptotic effects on melanocytes and keratinocytes in vitro. To clarify the role of vitamin D in skin carcinogenesis, we performed a review of the literature and meta-analysis to evaluate the association of vitamin D serum levels and dietary intake with cutaneous melanoma (CM) and non-melanoma skin cancer (NMSC) risk and melanoma prognostic factors. Twenty papers were included for an overall 1420 CM and 2317 NMSC. The summary relative risks (SRRs) from random effects models for the association of highest versus lowest vitamin D serum levels was 1.46 (95% confidence interval (CI) 0.60–3.53) and 1.64 (95% CI 1.02–2.65) for CM and NMSC, respectively. The SRR for the highest versus lowest quintile of vitamin D intake was 0.86 (95% CI 0.63–1.13) for CM and 1.03 (95% CI 0.95–1.13) for NMSC. Data were suggestive of an inverse association between vitamin D blood levels and CM thickness at diagnosis. Further research is needed to investigate the effect of vitamin D on skin cancer risk in populations with different exposure to sunlight and dietary habits, and to evaluate whether vitamin D supplementation is effective in improving CM survival.