右美托咪定复合瑞芬太尼用于脑功能区胶质瘤切除术中唤醒麻醉的临床观察

目的：观察右美托咪定复合瑞芬太尼在神经外科脑功能区胶质瘤术唤醒麻醉中的效果。方法：选择40例需行脑功能区胶质瘤切除的患者,（ASA）I-Ⅱ级,随机分为右美托咪定复合瑞芬太尼观察组（A组）（n=20）和丙泊酚复合瑞芬太尼对照组（B组）（n=20）,并应用两组方法行脑功能区胶质瘤切除手术术中唤醒麻醉。记录两组在术前（T0）及唤醒期间（T1）血压、心率、脉搏氧饱和度和呼吸频率的变化、唤醒时间、呛咳次数、体动次数。术后2d、7d、14d随访病人,了解患者精神伤害情况。结果：A、B两组术前血压、心率和呼吸抑制情况比较无差异（P〉0．05）,唤醒期间A组SBP、MAP、HR和呼吸抑制情况显著低于B组,有统计学意义（P〈0．05）,唤醒时间A组较短,明显短于B组（P〈0．05）,且呛咳次数及体动次数A组低于B组（P〈0．05）。精神伤害的发生率两组无差异（P〉0．05）。结论：右美托咪定复合瑞芬太尼应用于脑功能区胶质瘤切除术术中唤醒麻醉对病人血流动力学影响较小,病人苏醒快,不良事件发生率低,较丙泊酚复合瑞芬太尼有一定优势。     

右美托咪定与丙泊酚复合麻醉对脑膜瘤手术患者的麻醉效果及对血流动力学及脑组织的保护作用

目的 探讨右美托咪定与丙泊酚复合麻醉对脑膜瘤手术患者的麻醉效果及对血流动力学及脑组织的保护作用。方法 收集脑膜瘤手术患者120例,采用随机数字表法进行分组,即丙泊酚组和右美托咪定组,均60例。丙泊酚组对脑膜瘤手术患者采用丙泊酚注射液[3～10 mg/(kg·h)]麻醉,右美托咪定组对脑膜瘤手术患者采用盐酸右美托咪定注射液[0.2～1.0μg/(kg·h)]麻醉。分别于麻醉诱导前(T0)、切开硬脑膜时(T1)、去除肿瘤组织时(T2)、手术结束时(T3)、术后1 d(T4)监测患者HR、MAP、ScVO2、NSE、S100β指标,并记录苏醒时间、拔管时间、警觉/镇静(OAA/S)评分,同时进行安全性评估。结果 (1)T0、T4时刻2组HR、MAP比较,P>0.05;T1、T2、T3时刻2组HR、MAP比较,P<0.05,且右美托咪定组HR、MAP数值均显著低于丙泊酚组(P<0.05)。(2)T0时刻2组ScVO2、NSE、S100β水平比较,P>0.05;T1、T2、T3、T4时刻2组ScVO2、NSE、S100β水平比较,P<0.05,且右美托咪定组ScVO...     

不同麻醉药物对肺癌根治术患者全麻苏醒期躁动的影响

目的评价不同麻醉药物对肺癌根治术患者全麻苏醒期躁动的影响。方法择期全麻下行肺癌根治术患者84例,随机分为4组(n=21):生理盐水对照组(C组)、地佐辛组(D1组)、右美托咪定组(D2组)、地佐辛联合右美托咪定组(D3组)。分别于麻醉诱导前15 min时(T1)、气管导管拔除前15 min(T2)、气管导管拔除即刻(T3)和气管导管拔除后15 min时(T4)采集患者血样测定血浆中IL-10、TNF-α和C-反应蛋白(CRP)浓度,并记录患者镇静程度、躁动程度及其发生率。结果与T1比较,T2-T4时C组、D1组和D2组血浆IL-10、TNF-α和CRP浓度升高,D3组血浆IL-10浓度升高(P<0.05);与C组比较,D1、D2和D3组T2-T4时血浆IL-10浓度升高,TNF-α和CRP浓度降低,Ramsay评分升高,躁动发生率降低(P<0.05);与D3组比较,C、D1和D2组T2-T4时血浆IL-10浓度降低,TNF-α和CRP浓度升高,Ramsay评分降低,躁动发生率升高(P<0.05)。结论地佐辛、右美托咪定可有效降低肺癌根治术患者全麻苏醒期躁动发生率及抑制炎症的发生,且两种药物联合应用效果优于单独使用。     

右美托咪定对单侧乳癌改良根治术患者麻醉苏醒期躁动和术后疼痛的影响

目的:观察右美托咪定对单侧乳癌改良根治术患者麻醉苏醒期躁动和术后疼痛的影响。方法:纳入84例实施单侧乳癌改良根治术的女性患者,随机分为两组,对照组（瑞芬太尼-七氟烷组）:常规麻醉诱导成功后予靶控输注瑞芬太尼与七氟烷吸入维持麻醉;观察组（右美托咪定-瑞芬太尼-七氟烷组）:从麻醉诱导开始,泵注右美托咪定维持至手术结束,其余麻醉诱导及维持用药同对照组。观察测定两组患者麻醉复苏期血流动力学变化与躁动评分,以及术后6 h、12 h、24 h、48 h疼痛评分。结果:两组患者手术结束前5 min （T0）的收缩压、心率和氧饱和度差异均无统计学意义（均 P>0.05）,但拔管时间和苏醒时间上存在差异（P<0.05）。然而对比两组患者苏醒拔管前（T1）、拔管后即刻（T2）和拔管后 5 min（T3）的生命体征数据,与观察组相比,对照组患者各期的收缩压均明显升高（均 P<0.05）,心率均明显增快（均 P<0.05）。观察组患者麻醉复苏期躁动评分和躁动发生率均明显低于对照组（P<0.05）。观察组患者术后6 h、12 h、24 h疼痛评分均低于对照组（均 P<0.05）。结论:右美托咪定可使麻醉复苏期血流动力学更加稳定,并可减轻乳癌改良根治术患者麻醉复苏期躁动和术后疼痛的发生,临床效果确切,而且患者获得了更好的麻醉体验,值得临床推广。     

右美托咪定与丙泊酚对前列腺癌行腹腔镜手术患者术中血液动力学影响比较

目的探讨右美托咪定与丙泊酚对前列腺癌行腹腔镜手术患者术中血液动力学影响。方法选择60例前列腺癌行腹腔镜手术患者为研究对象,按照其麻醉用药的差异将其分为实验组与对照组(每组各30例患者),实验组患者在麻醉诱导前15 min泵注盐酸右美托咪定注射液0.5μg/kg,并持续泵注盐酸右美托咪定注射液0.2μg/kg/h至手术结束前40 min,对照组按照实验组剂量泵注生理盐水,术中对两组患者开展脑电双频指数(BIS)监测并根据该指标调节患者麻醉药物用量,观察两组患者用药前(T0)、给药15 min(T1)、插管时(T2)、气腹完成时(T3)、拔管时(T4)、拔管后30 min(T5)几个时间点的心率(HR)、收缩压(SBP)、舒张压(DBP)变化,记录两组患者麻醉药物用量,对比两组患者呼吸恢复时间、睁眼时间、拔管时间以及各类不良反应发生率。结果①与同组T0比较,实验组T1~T4时HR、SBP和DBP明显下降(P<0.05),对照组T2~T5时HR、SBP和DBP明显升高(P<0.05),组间比较实验组T1~T5时HR、SBP和DBP明显更低(P<0.05);②实验组丙泊酚和枸橼酸芬太尼注射液用量低于对照组(P<0.05);③术后实验组呼吸恢复时间、睁眼时间和拔管时间明显低于对照组(P<0.05);④术后实验组躁动发生率低于对照组;⑤术后不良反应发生率实验组明显低于对照组(P<0.05)。结论对前列腺癌行腹腔镜手术患者联用右美托咪定与丙泊酚可有效稳定患者术中血液动力学,有助于减少术中患者应激反应,维持患者循环稳定,减少麻醉药物用量,同时还能够加快患者术后复苏,降低围手术期麻醉躁动和不良反应发生率。     

小剂量右美托咪定在腹腔镜妇科手术中的应用

[目的]观察小剂量右美托咪定对腹腔镜妇科手术中的血流动力学和镇静镇痛药物用量的影响.[方法]选择全麻下行腹腔镜妇科手术的患者60例,美国麻醉医师协会(ASA)分级为Ⅰ～Ⅱ级,随机分为右美托咪定组(D组)和对照组(C组),每组各30例.记录诱导前(T0)、诱导后(T1)、插管后即刻(T2)、插管后10min(T3)、插管后30min(T4)和插管后50min (T5)的收缩压(SBP)、舒张压(DBP)、平均动脉压(MAP)和心率(HR).记录两组维持相同麻醉深度的丙泊酚、舒芬太尼和顺式阿曲库铵用量及不良反应发生情况.[结果]D组T3和T4的SBP、DBP、MAP均低于C组(P＜0.05).D组T3和T4的HR低于C组(P＜0.01).D组患者丙泊酚和舒芬太尼用量明显少于C组(P＜0.01).D组不良反应的发生率与C组无明显差别.[结论]小剂量右美托咪定能稳定腹腔镜妇科手术术中的血流动力学,减少镇静镇痛药物用量,不良反应少.     

不同剂量右美托咪啶复合依托咪酯对胃癌根治术后患者疼痛及感染的影响

目的 比较不同剂量右美托咪啶复合依托咪酯对胃癌根治术患者临床疗效及术后疼痛及感染的影响.方法 选取行胃癌根治术的患者78例作为研究对象,采用随机数字表法分为A、B、C3组.A组给予依托咪酯麻醉,B组给予低剂量右美托咪啶复合依托咪酯麻醉,C组给予高剂量右美托咪啶复合依托咪酯麻醉.比较3组患者血流动力学、麻醉情况、术后疼痛与感染以及不良反应发生率.结果 不同时间点,A组患者血流动力学指标变化幅度明显较B、C组大(P＜0.05).3组患者在自主呼吸恢复时间、呼之睁眼时间和拔管时间等麻醉情况方面比较均无统计学差异(P＞0.05).A组患者疼痛患者及感染以及不良反应发生率远远高于B组及C组,差异有统计学意义(P＜0.05).结论 右美托咪啶复合依托咪酯对于胃癌根治术患者具有良好麻醉效果,可减少患者术后疼痛及感染,减少不良反应发生.小剂量右美托咪啶即可发挥作用,故推荐临床使用小剂量治疗方案.     

右美托咪定对老年腹腔镜卵巢癌根治术患者术后苏醒与认知功能的影响研究

目的 探讨右美托咪定对老年腹腔镜卵巢癌根治术患者术后苏醒与认知功能的影响.方法 选取全身麻醉气管插管下行腹腔镜卵巢癌根治术的100例老年患者,按照随机数字表法分为观察组和对照组,每组50例.对照组患者使用咪达唑仑麻醉镇静,观察组患者使用右美托咪定麻醉镇静,比较麻醉拔管时两组患者的血浆S-100B蛋白、NSE水平,术后6 h ESS、MMSE评分,麻醉苏醒时间、麻醉拔管时间、复苏室停留时间及围麻醉期术中知晓、术后认知功能障碍的发生情况.结果 麻醉拔管时,观察组患者的血浆S-100B蛋白、NSE水平均明显低于对照组;术后6 h,观察组患者的ESS、MMSE评分均明显高于对照组;观察组麻醉苏醒时间、麻醉拔管时间、复苏室停留时间均明显短于对照组,差异均有统计学意义(P﹤0.01).观察组患者术中知晓、术后认知功能障碍的发生率均低于对照组,差异均有统计学意义(P﹤0.05).结论 围麻醉期使用右美托咪定,可以有效地促进老年腹腔镜卵巢癌根治术患者的麻醉苏醒,减少认知功能障碍的发生率.     

右美托咪定滴鼻联合舒芬太尼在儿童肿瘤放射治疗中的应用研究

目的:比较右美托咪定滴鼻联合舒芬太尼和单独使用水合氯醛在儿童肿瘤放射治疗过程中的疗效。方法:选取2018年11月至2019年9月深圳市人民医院行肿瘤放疗的48例患儿作为研究对象,随机分组为接受右美托咪定滴鼻联合舒芬太尼组(DS组)和口服水合氯醛组(C组)。观察比较两组镇静起效时间、苏醒时间和放射治疗时间,以及镇静前后平均动脉血压(MAP)、心率(HR)和血氧饱和度(SpO2)的变化情况,并统计两组不良反应发生情况。结果:研究纳入48例患儿,其中DS组24例和C组23例纳入最终分析。与C组相比,DS组患儿恢复时间更短,MAP、HR和不良反应发生率更低。两组患儿用药起效时间、治疗时间的差异无统计学意义(P>0.05)。结论:右美托咪定滴鼻联合舒芬太尼能安全地应用于儿童肿瘤放射治疗并缩短恢复时间。     

不同麻醉药物配伍对行腹腔镜下肿瘤切除手术的老年患者血流动力学及术后认知功能的影响

目的 分析不同麻醉药物配伍对行腹腔镜下肿瘤切除手术的老年患者血流动力学及术后认知功能的影响.方法 选取78例行腹腔镜下肿瘤切除术的老年患者为研究对象,随机将患者分为实验组和对照组,每组各39例,分别于手术治疗前给予2组患者不同麻醉药物配伍进行麻醉.实验组患者接受七氟醚、瑞芬太尼联合右美托咪定3种麻醉药物配伍麻醉,对照组患者接受异氟醚、芬太尼联合咪唑安定3种麻醉药物配伍麻醉,监测2组患者的血流动力学指标变化,比较2组患者术后认知功能评分.结果 实验组患者在麻醉诱导后、插管时及拔管后的血压、心率、左室射血分数及左室短轴缩短率等血流动力学指标优于对照组,且2组在麻醉诱导后、插管时及拔管后的血压及左室射血分数组间比较差异有统计学意义,在麻醉诱导后的心率及左室短轴缩短率组间比较差异有统计学意义(P<0.05).实验组患者术后定向力恢复时间、自主呼吸恢复时间及术后简易精神量表评分均优于对照组,且差异有统计学意义(P<0.05).结论 七氟醚、瑞芬太尼联合右美托咪定麻醉药物配伍及异氟醚、芬太尼联合咪唑安定麻醉药物配伍均有利于稳定老年患者腹腔镜下恶性肿瘤切除术前麻醉诱导期的血流动力学指标,但七氟醚、瑞芬太尼联合右美托咪定麻醉药物配伍的临床效果更好,更利于患者术后认知功能的恢复,临床安全性较好.     

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.     

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.     

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.