张瑞萍，高云阁，董晓昕，周学慧，王志高，崔庆超，翟树森

目的：调查127例住院患者的营养风险、营养不足发生情况及营养支持治疗现状,分析营养风险的发生与病期、年龄、血红蛋白、白蛋白及前白蛋白的关系。方法：对127例患者,于入院第2天采用营养风险筛查量表（nutrition risk screening 2002,NRS2002）进行营养风险及营养不足评估。并记录患者年龄、身高、体重、病期、血红蛋白、白蛋白、前白蛋白及患者的治疗情况,计算患者的体重指数（body mass index,BMI）及NRS2002评分。明确患者的年龄、病期、血红蛋白、白蛋白、前白蛋白与营养风险的关系。结果：127例恶性肿瘤患者营养不足（BMI ＜18．5kg／m2）25例,占19．69％;具有营养风险的患者（即 NRS2000评分≥3分者）为72例,发生率为56．69％。23例给予营养治疗,其中3例 NRS2002评分为1～2分,≥3分以上患者给予营养支持治疗20例（5例为终末期患者）,占27．78％,主要应用脂肪乳、氨基酸及葡萄糖治疗。年龄越大,发生营养风险的几率越高,贫血、白蛋白及前白蛋白水平降低增加营养风险的发生率,病期的早晚与营养风险无相关性。结论：肿瘤患者营养风险发生率高,营养支持治疗未得到重视,存在不恰当及不充分的营养支持治疗。积极纠正贫血及低蛋白血症是营养支持治疗的重要补充。     

晚期肿瘤患者营养风险及影响因素的研究

目的:探讨晚期肿瘤患者的营养风险及可能的影响因素。方法:收集2018年1月到2020年6月我院肿瘤内科收治的94例晚期肿瘤患者的临床资料，采用KPS评分评估患者的体力状况，采用营养风险筛查量表（NRS2002）筛查患者的营养风险，采用疼痛视觉模拟评分法(VAS)评估患者的疼痛程度，分析患者的营养风险情况及其可能的影响因素。结果:94例晚期肿瘤患者中有营养风险的患者(NRS2002评分≥3分的患者)共53例，占56.4%；年龄＞70岁患者共34例，有营养风险患者占70.6%，与年龄≤70岁患者具有显著统计学差异；KPS评分≤60分患者有37例，有73.0%患者存在营养风险，与KPS＞60分患者有显著统计学差异；不同BMI指数及疼痛程度的患者间有显著的统计学差异。消化系统肿瘤共有59例，有营养风险者占43例，总营养风险发生率达72.9%(43/59)。结论:晚期肿瘤患者营养风险的发生率较高，消化道肿瘤更显著，年龄、KPS评分、BMI指数、疼痛是其重要的影响因素。     

非霍奇金淋巴瘤患者营养不良状况调查研究

目的 调查吉林大学第三医院非霍奇金淋巴瘤患者营养风险、营养不良及营养治疗情况。方法 采用定点连续抽样方法，以2017年10月至2019年10月吉林大学第三医院非霍奇金淋巴瘤患者作为研究对象，在患者入院后48h内采用营养风险筛查2002（NRS 2002）进行营养风险筛查，调查营养不良发生率，记录患者住院期间营养治疗情况。结果 在入选的134例患者中，营养风险发生率为52.24%（n=70）；营养不良有两个来源：NRS 2002中营养状况评分≥3分评估营养不良发生率为13.43%（n=18），体质指数（BMI）<18.5kg/m2，结合一般状况较差者比例10.45%（n=14）；男、女患者在营养风险、营养不足营养不良发生率方面差异无统计学意义（P>0.05）；≥60周岁患者营养风险及营养不良发生率高于<60周岁患者（P<0.05）；营养风险患者营养治疗的比例为54.29%。结论 非霍奇金淋巴瘤患者营养风险、营养不良发生率较高，营养治疗比例有待提升；NRS 2002可以将这部分患者筛查出来，为临床合理营养治疗提供依据。     

放射治疗中心恶性肿瘤患者营养状况的横断面调查研究

目的调查恶性肿瘤放射治疗住院患者的营养风险和营养不良发生率。方法选取2017年8月至2017年10月就诊于重庆大学附属肿瘤医院放射治疗中心的恶性肿瘤患者330例为研究对象,采用连续定点抽样调查的方法,对患者进行NRS 2002、PS-SGA、人体测量指标和实验室检测等数据收集。结果330例患者完成营养调查,其中,男性227例,女性103例（68.8% vs 31.2%）,年龄（54.0±11.4）岁,有营养风险（NRS 2002≥3分）发生率为28.8%,营养不良（PG-SGA ≥4分）发生率为52.7%,鼻咽癌患者营养风险检出率最高为（29.3%）,其次为肺癌（28.1%）、口腔癌（18.1%）和食管癌（15.2%）。BMI与PG-SGA评分呈负相关,NRS 2002评分与PG-SGA评分呈正相关。年龄（≥65岁）、白蛋白（<40g/L）、 前白蛋白（<150g/L）、卡氏功能状态评分（<80分）是营养风险和重度营养不良的危险因素（P<0.05）。结论放射治疗中心的恶性肿瘤患者营养风险发生率属于中等水平,营养不良发生率较高,建议加强放疗患者的营养管理,结合患者的营养状况,PG-SGA评分可作为营养干预的参考标准。     

胃肠道肿瘤患者的营养状况与术后感染情况的分析

目的 探究胃肠道肿瘤患者的营养状况，并分析患者的营养状况对术后感染的影响。方法 收集2016年1月至2019年3月重庆医科大学附属永川医院行肿瘤手术治疗的271例胃肠道肿瘤患者的相关资料，运用营养风险筛查2002（NRS 2002）在患者术前进行营养风险筛查，根据筛查结果分为有营养风险组（121例）与无营养风险组（150例），比较两组患者一般观察指标以及术后感染、入住重症监护病房之间的差异，并分析患者术后感染的发生与术前营养状况、年龄、术前血液学指标、手术情况、肿瘤情况等多因素的相关性。结果 胃肠道肿瘤患者术前营养风险的发生率为44.6%，有营养风险组的术前总蛋白、白蛋白、血红蛋白以及淋巴细胞总数均低于无营养风险组，且差异有统计学意义（P<0.05）；术后有营养风险组感染发生率为27.3%（33/121），无营养风险组术后感染发生率为14.7%（22/150），两组差异有统计学意义。多因素Logistic回归分析显示术后感染的危险因素与NRS 2002 ≥ 3分、饮酒史、手术时长 ≥ 6h相关，差异有统计学意义（P<0.05）。结论 胃肠道肿瘤患者术前营养风险的发生率高，NRS 2002评分低的患者术后感染发生率较高，应该积极采取措施改善患者的营养状况。     

个性化营养诊疗在晚期肿瘤患者中的应用研究

目的 探讨基于肿瘤营养诊疗系统的个性化营养诊疗在晚期肿瘤化疗患者中的应用价值。方法 选取2019年1月至6月于北京市朝阳区桓兴肿瘤医院新入院的晚期肿瘤化疗患者作为研究对象，所有患者新入院时采用营养风险筛查量表2002进行营养风险筛查，对于存在营养风险的102例患者（NRS 2002≥3分）采用信封法将患者随机分为对照组（n=51）和观察组（n=51）。对照组患者由营养支持小组进行全程营养管理，观察组患者采用肿瘤营养诊疗系统进行个性化营养诊疗。比较两组患者两个周期化疗前后营养状况变化及化疗不良反应发生情况。结果 两个周期化疗后，两组患者体重、肌肉量、四肢骨骼肌指数均保持稳定，与化疗前相比均未有显著性差异（P>0.05）。对照组患者相比于化疗前，血红蛋白［（99.17±12.54）g/L vs （115.26±13.14）g/L］、白蛋白［（34.2±2.33）g/L vs （37.8±2.16）g/L］和前白蛋白［（19.48±3.02）mg/dl vs （26.14±3.21）mg/dl］水平显著提升，差异均有统计学意义（P<0.05）；观察组患者相比于化疗前，血红蛋白［（110.08±15.74）g/L vs （122.91±23.08）g/L］、白蛋白［（37.20±3.18）g/L vs （42.01±5.73）g/L］和前白蛋白［（24.13±2.56）mg/dl vs （29.14±3.74）mg/dl］水平显著提升，差异均有统计学意义（P<0.05）。此外，两组患者出现骨髓抑制（5.9% vs 3.9%）、白细胞减少（5.9% vs 7.8%），以及消化道反应（15.7 vs 19.6%）的情况均没有显著性差异（P>0.05）。结论 基于肿瘤营养诊疗系统的个性化营养诊疗与营养支持小组有助于维持晚期肿瘤患者在两个周期化疗过程中的营养状况，增加化疗耐受性。     

重庆市某医院常见恶性肿瘤住院患者营养状况调查

目的 调查重庆市人民医院常见恶性肿瘤住院患者的营养状况。方法 采用营养风险筛2002、PG-SGA、体格测 量、实验室检测等方法对重庆市人民医院自 2015 年 5 月 4 日至 2015 年 12 月 31 日的 311 例 16 种常见恶性肿瘤住院患者进 行营养风险筛查、营养评估,并调查这些患者的营养治疗情况。结果 311 例患者中,有营养风险（NRS 2002 ≥ 3 分）的 为 44.37%（138/311）。以 PG-SGA 评分评估患者营养状况,结果显示,52.73%（164/311) 的肿瘤患者存在中度营养不良 (PG-SGA ≥ 4 分 ),其中31.19%（97/311）为重度营养不良（PG-SGA ≥ 9 分 );消化道肿瘤患者营养不良的发生率比非消 化道肿瘤患者高（65.41% vs. 43.26%,χ2=13.417,P＜0.001）;多元线性回归分析体质指数、血清白蛋白、血清前白蛋白、 最近 1 个月体重下降百分比、左小腿围、非利手握力与 PG-SGA 评分之间有相关性（P 均＜ 0.001）,其中左小腿围、最近 1 个月体重下降百分比与PG-SGA 评分相关性最好（回归系数B 分别为-0.872、0.861,P ＜ 0.001 ）,血红蛋白、上臂肌 围与 PG-SGA 评分相关性不具统计学意义（P 分别为0.268,0.218）;中、重度营养不良患者的营养治疗率仅为43.90% （72/164）,营养治疗以单独肠外营养治疗为主,占 91.7%（66/72）,肠内营养联合肠外营养占 6.94%（5/72）,单独肠内 营养治疗仅1 例,占营养治疗患者的1.38%（1/72）。结论 52.73% 的常见恶性肿瘤患者存在中、重度营养不良。PG-SGA 评分是评估肿瘤患者营养不良简便、有效的工具,营养不良的患者营养治疗率低,且以肠外营养为主,肠内营养治疗率极低。 建议对恶性肿瘤患者进行入院后的营养风险筛查以及包括 PG-SGA 评分在内的全面营养评估,并给予正确的营养治疗。     

胃癌患者82例营养风险筛查及相关因素分析

摘 要： ［目的］ 应用欧洲营养筛查方法(NRS 2002) 分析胃癌患者营养风险。［方法］ 收集胃癌患者82例,患者入院48h进行营养风险筛查,采用NRS2002评估表进行评分。NRS2002总分≥3分为存在营养风险。［结果］ 在82例住院胃癌患者中,NRS 2002 营养风险筛查评分为(2.51±1.08)分,NRS2002≥3分24例,营养风险发生率为29.3%。随着患者临床分期的升高,营养风险发生率随之升高,Ⅰ期患者营养风险发生率为5.9%,而Ⅳ期患者的营养风险发生率为57.1%。营养风险发生率与患者的年龄、居住地和医疗费用相关。营养不良者（BMI＜18.5kg/m2）发生营养风险发生率为100%,但25.9%（14/54）患者的BMI 虽处于正常范围仍存在营养风险。NRS 2002≥3分存在营养风险的患者平均住院天数为(14.4±9.2)d,明显长于NRS 2002＜3分无营养风险的患者的(9.0±4.8)d (P＝0.041)。［结论］ NRS2002 对住院患者营养风险和营养支持率的调查可有效鉴别住院患者的营养风险,并为营养支持提供依据。     

癌性疼痛患者营养状况与血清C反应蛋白的相关性

目的 研究癌性疼痛患者营养状况、炎性反应水平及各项指标间的相关性。方法 选取146例癌痛患者为研究对象，采用NRS、NRS-2002、PG-SGA、人体测量、血液学检查等方法进行疼痛评估、营养风险筛查和营养状况评估，研究不同疼痛程度患者营养状态、炎性反应水平等各项指标的差异及相关性。结果 两组不同NRS评分患者NRS-2002、PG-SGA、胆碱酯酶差异均有统计学意义（均P<0.05）。两组不同C反应蛋白浓度患者的前白蛋白、白蛋白、血红蛋白、胆碱酯酶、白细胞、中性粒细胞比例、淋巴细胞总数差异有统计学意义（P<0.05）。相关性分析提示：NRS与胆碱酯酶、淋巴细胞总数和BMI呈负相关（P=0.000, P=0.003, P=0.000），与NRS-2002、PG-SGA呈正相关（P=0.003, P=0.000）。C反应蛋白浓度与前白蛋白、白蛋白、胆碱酯酶、血红蛋白、淋巴细胞总数呈负相关（P=0.000, P=0.000, P=0.000, P=0.002, P=0.004），与NRS-2002、PG-SGA呈正相关（P=0.020, P=0.028）。结论 癌性疼痛患者的营养风险和营养不良发生率都较高，具有较高血清C反应蛋白浓度的癌性疼痛患者的营养状况更差。     

营养风险筛查2002在晚期肿瘤患者营养状况筛查中的运用

目的 运用营养风险筛查2002对我院晚期肿瘤住院患者进行营养评估调研,统计患者的营养不足率、营养风险发生率和营养支持情况,探讨不同癌种患者的营养状况及临床指标差异,为个体化营养支持提供科学依据。方法 筛选符合要求的2016年1月—2017年2月入院的晚期肿瘤住院患者,进行营养问卷调查、人体测量、记录相关实验室检查指标,应用营养风险筛查2002(Nutritional risk screening,NRS2002)对患者进行营养风险筛查。结果 517例晚期肿瘤患者的营养不足率为19.54%,营养风险发生率为49.52%,无营养风险的患者接受营养支持的比例为14.56%,有营养风险的患者进行营养支持的比例为63.67%。有营养风险的患者平均住院时间为(14.43±11.82)天,无营养风险的患者为(8.29±6.93)天。消化道肿瘤患者的营养风险发生率高于其他癌种。结论 NRS2002作为有效的营养筛查工具,可协助临床医师筛查肿瘤科住院患者潜在的营养风险,为患者制定合理的营养支持提供依据。     

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.     

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.     

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。     

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.     

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。     

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.