阿美替尼、安罗替尼靶向治疗非小细胞肺癌的前瞻性研究

目的:探究阿美替尼、安罗替尼靶向治疗非小细胞肺癌(Non-small cell lung carcinoma,NSCLC)的前瞻性对照研究.方法:将 2020 年 1 月至 2023 年 6 月在本院接受治疗的 92 例非小细胞肺癌患者作为研究对象,随机分为阿美替尼组和安罗替尼组,每组 46 例.阿美替尼组接受阿美替尼治疗,安罗替尼组接受安罗替尼治疗.比较两组治疗前后免疫指标、炎症因子水平、疗效和两组不良反应发生率.结果:治疗后阿美替尼组成熟T淋巴细胞和自然杀伤细胞的水平均高于安罗替尼组(P＜0.05);治疗后阿美替尼组的超敏C反应蛋白、白介素-6、白介素-8 水平均低于安罗替尼组(P＜0.05).结论:阿美替尼治疗NSCLC效果优于安罗替尼,改善患者体内免疫指标、炎症因子的水平.     

安罗替尼治疗老年肺癌患者疗效及安全性分析

目的:探讨安罗替尼对老年肺癌患者疗效及安全性分析.方法:回顾性收集2018年12月1日至2020年5月1日首都医科大学附属北京友谊医院收治的晚期肺癌老年患者73例,均使用安罗替尼治疗,观察患者无进展生存期(progression-free survival,PFS)、总生存期(overall survival,OS)以...     

癌胚抗原监测吉非替尼治疗晚期非小细胞肺癌的临床疗效初步研究

目的探讨吉非替尼治疗晚期非小细胞肺癌患者的临床疗效及安全性,观察治疗前后肿瘤标志物血清胚抗原变化。方法 2008年12月至2013年12月在我院治疗的晚期非小细胞肺癌患者36例,给予吉非替尼口服250mg/d,直至出现疾病进展或副作用不能耐受而停止治疗。结果 36例均可评定疗效,临床受益率为77.8%。11例获PR,17例获SD,11例获PD,总有效率30.6%,疾病控制率为77.8%。中位随访时间9个月（1~33月）。中位无进展生存期4个月,中位生存时间9个月。1年生存率38.9%,2年生存率22.2%。最长1例存活30.3个月。药物不良反应主要为：皮疹,腹泻,肝功能异常等。患者癌胚抗原治疗后较治疗前明显下降。结论吉非替尼治疗晚期非小细胞肺癌疗效较好,特别女性和腺癌更加明显,毒副反应相对较轻,血清癌胚抗原水平可以作为检测吉非替尼对晚期非小细胞肺癌疗效的指标。值得临床进一步推广使用。     

安罗替尼联合氯喹促进人非小细胞肺癌细胞系H1299凋亡

目的 探讨安罗替尼和氯喹(CQ)单用及联用对人非小细胞肺癌系H1299存活率、迁移、侵袭和凋亡的影响.方法 安罗替尼与CQ单用及两药联合处理H1299细胞,MTT法检测细胞的存活率;划痕愈合和Transwell小室法检测细胞迁移及侵袭能力;Hoechst 33342染色检测细胞凋亡;Western blot检测自噬标志...     

吉非替尼、厄洛替尼及埃克替尼治疗非小细胞肺癌应用价值比较

目的:比较吉非替尼、厄洛替尼及埃克替尼治疗非小细胞肺癌的应用价值.方法:回顾性分析2017年1月至2018年1月期间我院收治的102例Ⅳ期EGFR突变非小细胞肺癌患者的临床资料,根据治疗药物的不同将其分为吉非替尼组(n=34)、厄洛替尼组(n=34)以及埃克替尼组(n=34).在治疗开始1个月后对比三组近期疗效、无瘤生存率(三年)、经济学以及不良反应.结果:吉非替尼、厄洛替尼及埃克替尼三组有效率分别为(73.53％)、(76.47％)、(70.59％)(P>0.05);三组无瘤生存率分别为(79.41％、(70.58％)、(67.65％)(P<0.05);三组成本效果比分别为30.84、63.92、19.84;三组不良反应发生率比较无明显差异(P>0.05).结论:三组研究药物近期疗效相似,但生存率以及成本具有差异,在临床应用中,建议优先选择有药物经济学评价和成本-效果比高的药品.     

晚期肺腺癌的临床治疗与分析

非小细胞肺癌(NSCLC)是世界范围内发病率和死亡第较高的恶性肿瘤之一,其中腺癌所占比例逐年上升[1],由于大部分的患者就诊时已属晚期,故主要采用以化疗为主的综合治疗.我们自2007年3月至2009年3月采用厄洛替尼单药治疗晚期肺腺癌21例,取得较好疗效.     

盐酸埃克替尼联合 GP 化疗方案治疗对非小细胞肺癌患者临床疗效、免疫功能及毒副反应的影响

目的:分析盐酸埃克替尼联合吉西他滨联合顺铂(Gemcitabine combined with cisplatin,GP)化疗方案治疗对非小细胞肺癌患者临床疗效、免疫功能及毒副反应的影响.方法:选取2017年5月至2020年1月期间收入我院治疗的102例非小细胞型肺癌患者作为研究对象,根据治疗方法的差异将患者分为基础组和联合组,各51例.基础组采用GP化疗方案治疗,联合组在基础组的基础上增加口服盐酸埃克替尼;观察两组治疗效果、用药前后免疫功能以及毒副反应.结果:联合组客观有效率、疾病控制率明显高于基础组(P<0.05);用药后,两组患者的CD4+/CD8+与CD4+均上升,且联合组明显高于基础组(P<0.05);CD8+均下降,且联合组明显低于基础组(P<0.05);联合组的腹泻发生率明显高于基础组(P<0.05),其他毒副反应比较无差异(P>0.05).结论:盐酸埃克替尼联合GP化疗方案可提高非小细胞型肺癌临床疗效佳,保障免疫能力、安全性尚可.     

安罗替尼通过调控miR-16-5p/PD-1轴抑制人非小细胞肺癌细胞系增殖并促进凋亡

目的 探讨安罗替尼对非小细胞肺癌细胞增殖和凋亡的影响及其分子机制。方法 将非小细胞肺癌细胞系A549和H1299分别采用安罗替尼、miR-16-5p激动剂和/或PD-1过表达载体进行处理。CCK-8实验和EDU实验检测细胞增殖;流式细胞术检测细胞凋亡;RT-qPCR检测miR-16-5p相对表达量;Western blot检测程序性细胞死亡-1蛋白(PD-1)的表达。双荧光素酶报告实验确定miR-16-5p和PD-1的靶向关系。用A549细胞构建裸鼠成瘤模型,检测安罗替尼对体内肿瘤生长的影响。结果 安罗替尼在A549和H1299细胞中以剂量依赖的方式显著增加miR-16-5p表达,同时降低PD-1表达,并且抑制细胞增殖,促进细胞凋亡(P<0.05)。miR-16-5p过表达可抑制细胞增殖,促进细胞凋亡(P<0.05)。miR-16-5p能靶向PD-1,且负调控PD-1表达。siRNA下调PD-1表达后明显抑制细胞增殖,并促进细胞凋亡(P<0.05)。过表达PD-1则可逆转安罗替尼介导的miR-16-5p对A549和H1299细胞的促增殖和抗凋亡作用(P<0.05...     

中国人非小细胞肺癌EGFR和K-RAS基因突变情况的研究

目的研究中国人非小细胞肺癌表皮生长因子受体(epidermal growth factor receptor,EGFR)基因和K-RAS基因突变情况。方法通过PCR扩增和基因测序的方法检测了101例中国人非小细胞肺癌(non-small cell lung cancers,NSCLCs)EGFR第18、19和21外显子及K-RAS密码子12、13的突变情况,并观察分析了其突变与肺癌临床特征及吉非替尼(gefitinib,商品名:易瑞沙/Iressa)药物治疗肺癌的疗效间的关系。结果共检测到26例EGFR突变(25.7%),3例K-RAS突变(2.9%),并发现腺癌患者、非吸烟患者和女性患者EGFR突变率较高(分别为44.2%、65.7%和48.3%)。10例服用吉非替尼有效的患者9例伴有EGFR突变。结论中国人肺癌的EGFR突变率高于西方人,吉非替尼疗效与EGFR突变有关。     

吉非替尼联合培美曲塞治疗老年NSCLC患者的效果及其对肿瘤生物学指标、血流动力学的影响

目的:探究吉非替尼与培美曲塞联合应用于老年非小细胞肺癌(Non-small cell lung cancer,NSCLC)患者的效果观察.方法:选取本院我科85例老年中晚期NSCLC患者作为研究对象,采用抽签法分成两组,对照组42例采用培美曲塞治疗,观察组43例加用吉非替尼治疗,观察两组患者的临床疗效,肿瘤生物学指标、...     

Pain and Effusion and Quadriceps Activation and Strength

Context:

Quadriceps dysfunction is a common consequence of knee joint injury and disease, yet its causes remain elusive.

Objective:

To determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion affect the magnitude of quadriceps dysfunction.

Design:

Crossover study.

Setting:

University research laboratory.

Patients or Other Participants:

Fourteen (8 men, 6 women; age = 23.6 ± 4.8 years, height = 170.3 ± 9.16 cm, mass = 72.9 ± 11.84 kg) healthy volunteers.

Intervention(s):

All participants were tested under 4 randomized conditions: normal knee, effused knee, painful knee, and effused and painful knee.

Main Outcome Measure(s):

Quadriceps strength (Nm/kg) and activation (central activation ratio) were assessed after each condition was induced.

Results:

Quadriceps strength and activation were highest under the normal knee condition and differed from the 3 experimental knee conditions (P < .05). No differences were noted among the 3 experimental knee conditions for either variable (P > .05).

Conclusions:

Both pain and effusion led to quadriceps dysfunction, but the interaction of the 2 stimuli did not increase the magnitude of the strength or activation deficits. Therefore, pain and effusion can be considered equally potent in eliciting quadriceps inhibition. Given that pain and effusion accompany numerous knee conditions, the prevalence of quadriceps dysfunction is likely high.Key Words: arthrogenic muscle inhibition, central activation failure, voluntary activation, muscles

Key Points

• Knee pain and effusion resulted in arthrogenic muscle inhibition and weakness of the quadriceps.
• The simultaneous presence of pain and effusion did not increase the magnitude of quadriceps dysfunction.
• To reduce arthrogenic muscle inhibition and improve muscle strength, clinicians should employ interventions that target removing both pain and effusion.

Quadriceps weakness is a common consequence of traumatic knee joint injury^1,2 and chronic degenerative knee joint conditions.^3,4 Arthrogenic muscle inhibition (AMI), a neurologic decline in muscle activation, results in quadriceps weakness and hinders rehabilitation by preventing gains in strength.⁵ The inability to reverse AMI and restore muscle function can lead to decreased physical abilities,⁶ biomechanical deficits,⁷ and possibly reinjury.⁵ Furthermore, researchers^8,9 have suggested that quadriceps weakness resulting from AMI may place patients at risk for developing osteoarthritis in the knee. In light of the substantial influence of quadriceps AMI on these clinically relevant outcomes, we need to improve our understanding of the factors that contribute to this neurologic decline in muscle activity so efforts to target and reverse it can be implemented and gains in strength can be achieved more easily.Joint injury and disease are accompanied by numerous sequelae (ie, pain, swelling, tissue damage, inflammation), so ascertaining which one ultimately leads to neurologic muscle dysfunction is difficult. Whereas a joint effusion can result in AMI,^10–12 the effects of pain are less understood despite many clinicians attributing AMI to pain. Using techniques that introduce knee pain without accompanying injury may provide insights into the role of pain in eliciting AMI.The degree of knee joint damage may play a role in the quantity of AMI that manifests. Hurley et al^13,14 demonstrated that quadriceps AMI, measured using an interpolated-twitch technique, was greater in patients with extensive traumatic knee injury (eg, fractured tibial plateau, ruptured medial collateral ligament, and medial meniscectomy) than patients with isolated joint trauma (ie, isolated anterior cruciate ligament [ACL] rupture). Similarly, patients with more knee joint symptoms (ie, greater number of symptoms and increased severity of symptoms) may present with greater magnitudes of quadriceps inhibition. Recently, investigators¹⁵ have suggested that patients with more pain display less quadriceps strength, supporting this tenet. Given that effusion and pain often present simultaneously with joint injuries and diseases, such as ACL injury and osteoarthritis, examining both the isolated and cumulative effects of these sequelae appears warranted to determine if they influence the magnitude of muscle inhibition.Experimental joint-effusion and pain models are safe and effective experimental methods that allow for the isolated examination of their effects on muscle function. The effusion model, whereby sterile saline is injected directly into the knee joint capsule,⁷ produces a clinically relevant magnitude of the joint effusion that may be present with traumatic injury. Effusion is thought to activate group II afferents responding to stretch or pressure,^16–18 which in turn may facilitate group Ib interneurons and result in quadriceps AMI.⁵ The pain model involves injecting hypertonic saline into the infrapatellar fat pad to produce anteromedial knee pain similar to that described in patients with patellofemoral pain syndrome.¹⁹ Pain is considered to initiate AMI through activation of group III and IV afferents that act as nocioceptors to signal damage or potential damage to joint structures.^16–18 The firing of these afferents then may lead to facilitation of group Ib interneurons, the flexion reflex, or the gamma loop, ultimately resulting in quadriceps inhibition.²⁰ Thus, these models allow us to create symptoms that are associated with knee injury and have the added benefit of providing a way to examine their effects in isolation.Therefore, the purpose of our study was to determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion would affect the magnitude of quadriceps dysfunction. We hypothesized that pain alone would result in quadriceps inhibition and that the magnitude of inhibition would be greater when effusion and pain were present simultaneously.     

即早基因c-fos与脑血管病及学习记忆

即早基因c-fos是广泛存在于原核细胞和真核细胞的高度保守基因.在正常情况下,c-fos基因参与细胞生长、分化、信息传递、学习和记忆等生理过程,而在病理情况下c-fos基因表达及调控变化与多种疾病的发生和发展有关.C-fos在中枢神经系统的某些部位可有基础水平的表达,但表达很低,当受到如脑缺血、脑出血、痫性发作、应激等刺激后,其在数十分钟内做出反应,在对外界刺激-转录耦联的信忠传递过程中起着核内第三信使的重要作用.     

Opportunities and challenges in the prevention and control of cancer and other chronic diseases: children's diet and nutrition and weight and physical activity

OBJECTIVE: The purpose of this article is to review the role of behavioral research in disease prevention and control, with a particular emphasis on lifestyle- and behavior-related cancer and chronic disease risk factors--specifically, relationships among diet and nutrition and weight and physical activity with adult cancer, and tracking developmental origins of these health-promoting and health-compromising behaviors from childhood into adulthood. METHOD: After reviewing the background of the field of cancer prevention and control and establishing plausibility for the role of child health behavior in adult cancer risk, studies selected from the pediatric published literature are reviewed. Articles were retrieved, selected, and summarized to illustrate that results from separate but related fields of study are combinable to yield insights into the prevention and control of cancer and other chronic diseases in adulthood through the conduct of nonintervention and intervention research with children in clinical, public health, and other contexts. RESULTS: As illustrated by the evidence presented in this review, there are numerous reasons (biological, psychological, and social), opportunities (school and community, health care, and family settings), and approaches (nonintervention and intervention) to understand and impact behavior change in children's diet and nutrition and weight and physical activity. CONCLUSIONS: Further development and evaluation of behavioral science intervention protocols conducted with children are necessary to understand the efficacy of these approaches and their public health impact on proximal and distal cancer, cancer-related, and chronic disease outcomes before diffusion. It is clear that more attention should be paid to early life and early developmental phases in cancer prevention.