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1.
目前,生物学研究已进人后基因组时代,一个以“蛋白质组”为研究重点的生命科学新时代已悄然到来。近年来,蛋白质组技术发展迅速,激光捕获微切割、蛋白质芯片、同位素包被亲和标记等新技术,促进了蛋白质组学的发展。综述了近年蛋白质组学相关新技术的进展及其应用情况。  相似文献   

2.
蛋白质组学在消化系统肿瘤中的应用   总被引:2,自引:1,他引:1  
随着人类基因组计划的完成,生命科学的研究重点又转移到基因功能产物——蛋白质的研究上来。“蛋白质组学(pmteomics)”逐渐成为后基因组时代生命科学的主要研究领域。它研究的是一个基因组所表达的全套蛋白质,包括一种细胞乃至一种生物在特定的时间和空间上表达的全部蛋白质。目前研究者们对蛋白质组的研究兴趣不断上升,  相似文献   

3.
FRET的理论基础及应用   总被引:6,自引:1,他引:6       下载免费PDF全文
2001年,《自然》和《科学》杂志先后公布了人类基因组的工作草图,人类从此进入了功能基因组时代。目前,研究生物大分子,特别是蛋白质的结构、功能、特点及其相互作用已经成为生命科学的工作重点,随着蛋白质研究的进展,一项古老的技术-荧光共振能量转移(fluorescenceresonanceen  相似文献   

4.
虚拟细胞研究进展及应用价值   总被引:6,自引:0,他引:6  
1 虚拟细胞产生背景及研究概况1. 1 产生背景 虚拟细胞的产生得益于 20世纪末生命科学和信息科学两大领域的迅猛发展。20世纪末期, 人类和许多模式生物基因组计划的完成引来了以基因功能研究为目的的后基因组时代。后基因组时代的研究任务可以分为两大方面: 一是综合运用各种"组学 "研究方法, 来获得有关生物体系统的大量信息。这些研究方法包括蛋白质组学、转录组学和代谢组学等, 它们的研究对象代表生物信息传递的不同水平。另一方面是应用复杂的计算模型对基因组学和上述 "组学"研究方法所得到的数据进行生物信息学分析。这些方法的综…  相似文献   

5.
目前,生物学研究已进入后基因组时代,一个以"蛋白质组"为研究重点的生命科学新时代已悄然到来.近年来,蛋白质组技术发展迅速,激光捕获微切割、蛋白质芯片、同位素包被亲和标记等新技术,促进了蛋白质组学的发展.综述了近年蛋白质组学相关新技术的进展及其应用情况.  相似文献   

6.
细胞芯片的研究进展   总被引:2,自引:0,他引:2  
细胞芯片技术是以活细胞作为研究对象的一种生物芯片技术。它是适应后基因组时代人类对生命科学探索的要求而产生的。作为细胞研究领域的一种新技术,其既保持传统的细胞研究方法的优点如原位检测等,又满足了高通量获取活细胞信息等方面的要求。本文中扼要介绍细胞芯片的概念以及几种已报道的细胞芯片,并对细胞免疫芯片进行了简述。  相似文献   

7.
CAR-T技术作为免疫治疗的一种,从最早期的第一代发展至目前的第4代,其细胞毒性和抗肿瘤免疫效应大大增强,但也暴露出相关安全问题,其在原发性肝癌治疗的相关研究中展现出一定优势,预示着在精准个体化肝癌治疗时代,免疫治疗尤其CAR-T技术联合手术治疗、放化疗和局部治疗等综合治入将会发挥更强有力的作用。  相似文献   

8.
边缘性人格障碍(BPD)是精神科常见的一种人格障碍,虽然目前对BPD的发病机制尚未完全明了,但已有研究提示基因与环境及两者的交互作用在BPD的发生发展中具有非常重要的作用。本文通过CNKI,MEDLINE和PsysNET等数据库上检索有关边缘性人格与环境、基因之间关系的研究文献,并对文献进行系统总结,发现目前已有较多研究结果支持了基因与环境之间的交互作用在BPD发生发展中的作用。然而,已有关于两者交互作用相关研究尚存在缺陷,需未来的研究进行完善。  相似文献   

9.
第十四届全国生物材料大会暨中国生物医学工程学会生物材料分会(CSBME-BMB)第十四届学术年会将于2013年9月22日至25日在西安召开。本次会议是我国生物医学材料界的一次高水平学术盛会。会议将汇集来自国内外不同大专院校、研究机构和工业企业等从事生物医学材料研究的专家学者,就目前我们生物医学材料研究的新理论、新方法、新材料、新装置、新发现以口头报告和墙报两种形式进行交流和研讨,充分反映我国目前生物医学材料研究及产业发展的最新动向。  相似文献   

10.
强迫障碍是临床上较难治愈的一种神经症。暴露反应∕仪式阻断治疗技术(Exposure and Response/Ritual Prevention,本文简称ERP)目前被证实是一种针对强迫障碍的最为有效的心理治疗方法。本文从ERP心理治疗的定义出发,阐述了ERP治疗强迫障碍的理论基础、操作原则、疗效分析与其他心理治疗方法的比较等,最后对强迫障碍ERP心理治疗目前存在问题和未来研究方向进行了探讨。  相似文献   

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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 injury1,2 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, researchers8,9 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,1012 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 al13,14 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,1618 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.1618 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.  相似文献   

13.
即早基因c-fos与脑血管病及学习记忆   总被引:5,自引:1,他引:5  
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.  相似文献   

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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.  相似文献   

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