血管内皮生长因子及其受体在子宫内膜异位症中的表达和意义

目的:研究血管内皮生长因子(Vascular endothelial growth factor,VEGF)及其受体(Vascular endothelial growth factor receptor1,VEGFR1)在子宫内膜异位症(内异症)患者子宫在位内膜、异位内膜及正常对照组内膜组织中的表达,探讨其在子宫内膜异位症中的作用机制.方法:采用免疫组织化学及Western blot方法检测34例异位症患者在位内膜、异位内膜(内异症组)及34例正常内膜(对照组)组织中VEGF及其受体VEGFR1蛋白的定位及表达.结果:异症组在位及异位子宫内膜组织腺上皮细胞及间质细胞中均有VEGF及VEGFR1蛋白表达,且均高于同期对照组内膜,差异有统计学意义;对照组分泌期内膜VEGF及VEGFR1蛋白表达高于增生期,呈现周期性变化,而内异症组在位及异位内膜VEGF及VEGFR1蛋白表达失去周期性变化,分泌期与增生期均高表达,差异无统计学意义.Western blot检测结果与免疫组化结果一致.结论:内异症患者在位及异位内膜组织中VEGF、VEGFR1蛋白高表达可能与内异症的发生发展有关.     

子宫内膜异位症模型大鼠子宫内膜雌、孕激素受体表达的变化

利用大鼠子宫内膜异位症 (内异症 )动物模型 ,采用逆转录聚合酶链反应 (RT PCR)技术 ,检测子宫内膜雌激素受体 (ER)和孕激素受体 (PR)mRNAs的表达 ,探讨内异症的发病机理及激素治疗的可能性。结果表明 ,内异症模型组大鼠异位内膜ER、PRmRNAs的表达低于在位内膜及对照组正常子宫内膜 ,与后两者比较差异有显著性意义(P <0 0 1 ) ;而模型组在位内膜ER、PRmRNAs的表达与正常对照组比较差异无显著性意义。内异症模型组异位内膜ER PRmRNA比值大于在位内膜及正常子宫内膜ER PRmRNA比值 (P <0 0 1 )。提示内异症大鼠异位内膜ERmRNA表达的降低在内异症的发生与发展中起着一定的作用     

子宫内膜异位症异位内膜IL-6基因表达的研究

目的　探讨子宫内膜异位症 (内异症 )异位内膜白细胞介素 6 (IL 6 )mRNA表达的变化。方法　利用大鼠内异症动物模型 ,采用逆转录聚合酶链反应 (RT PCR)技术 ,检测子宫内膜IL 6mRNA表达情况。结果　正常对照组、内异症模型组在位及异位子宫内膜IL 6mRNA的表达明显不同 ,内异症异位子宫内膜的表达高于内异症在位子宫内膜 ;正常子宫内膜IL 6mRNA的表达较前两者均低。同一时间点各组间比较差异具有显著性意义 (P <0 0 1)。结论　内异症异位内膜IL 6mRNA表达明显增加     

内异症子宫内膜ER、PR基因表达的研究

目的/:v探讨子宫内膜异位症(内异症)子宫内膜雌激素受体(ER)、孕激素受体(PR)基因表达在内异症发病中的作用。方法:利用大鼠内异症动物模型,采用逆转录聚合酶链反应(RT-PCR)技术,检测子宫内膜ER和PRmRNAs的表达情况。结果:内异症模型组大鼠异位内膜ER、PRmRNAs的表达显著低于在位内膜及对照组正常子宫内膜(P＜0.01);而模型组在位内膜ER、PRmRNAs的表达与正常对照组比较差异无显著(P＞0.05)。内异症模型组异位内膜ER/PRmRNA比值大于在位内膜及正常子宫内膜ER/PRmRNA比值(P＜0.01)。结论:内异症大鼠异位内膜ERmRNA表达的相对增高在内异症的发生与发展中起着一定的作用。     

子宫内膜异位症患者在位和异位内膜上皮细胞ER-α、ER-β的检测

目的探讨ER-α和ER-β在内异症患者在位及异位内膜上皮细胞中的表达与子宫内膜异位症发生机制的关系。方法通过体外细胞培养,利用流式细胞仪检测ER-α和ER-β在正常子宫内膜上皮细胞及内异症患者在位及异位内膜上皮细胞中表达。结果在正常子宫内膜上皮细胞及内异症患者在位及异位内膜上皮细胞中均检测到ER-α和ER-β的表达。而且在正常对照组和在位内膜组上皮细胞中ER-β明显高于ER-α。结论在子宫内膜异位症患者在位内膜,异位内膜上皮细胞中ER-α和ER-β表达有明显差异,表明除了已知的ER-α对子宫内膜增殖和分化的作用,ER-β可能对子宫内膜的功能也有重要影响,并提出深入研究二者之间的关系对子宫内膜异位症的发生发展,临床生物特性,治疗及预后有重要价值。     

galectin-3在子宫内膜异位症患者在位内膜中的表达及意义

目的：探讨galectin-3在子宫内膜异位症（内异症）患者在位子宫内膜中的表达及意义.方法：分别采用免疫组化和实时定量逆转录-聚合酶链反应（Real-time RT-PCR）检测内异症患者在位内膜及正常对照中galectin-3蛋白及mRNA的表达,比较其表达差异.结果：galectin-3蛋白定位于子宫内膜的腔上皮细胞、腺上皮细胞和间质细胞.与正常对照相比,galectin-3 mRNA及蛋白在内异症在位内膜中的表达显著下降（P＜0.05）.其表达在分泌期高于增生期.结论：内异症患者在位子宫内膜galectin-3低表达可能与其子宫内膜容受性的改变有关,从而导致了内异症不孕.     

凋亡相关蛋白Bcl-2/Bax与子宫内膜异位症的相关性研究

目的研究子宫内膜异位症(内异症)及子宫腺肌症患者在位及异位内膜组织中细胞凋亡相关蛋白Bcl-2、Bax表达及其凋亡率比较。方法采用免疫组化法检测各组织标本中Bcl-2、Bax的表达,流式细胞仪测定各组织的细胞凋亡率。结果(1)在正常和正位内膜组织中,Bcl-2或Bax表达相同(P>0.05),具有明显周期性变化,均为增生期高于分泌期(P<0.05);(2)子宫腺肌病和腹壁异位内膜中,Bcl-2或Bax均持续表达,无周期性变化(P>0.05);(3)卵巢内异症的异位内膜,Bcl-2和Bax极少表达;(4)流式结果显示正常子宫内膜、在位内膜凋亡率与异位内膜组织凋亡率有显著性差异(P<0.05)。结论①Bcl-2或Bax在正常和在位子宫内膜的周期性表达,提示它们可能参与月经周期调节;②子宫腺肌病及腹壁异位内膜腺上皮细胞Bcl-2持续存在,使之得以长期增殖而发病;③卵巢内异症极少表达Bcl-2可能是促成细胞凋亡形成,引起巧克力囊肿的原因。     

胎盘生长因子(PLGF)及其受体血管内皮生长因子受体-1(VEGFR-1)在子宫内膜异位症中的表达及意义

目的探讨胎盘生长因子(PLGF)及其受体血管内皮生长因子受体-1(VEGFR-1)与子宫内膜异位症(endom etriosis,EMS)发病的相关性。方法用免疫组织化学染色法检测28例子宫内膜异位症患者的在位子宫内膜和异位子宫内膜(增生期、分泌期各14例),以及28例正常子宫内膜(增生期15例,分泌期13例)中PLGF及其受体VEGFR-1的表达。结果PLGF、VEGFR-1在各组内膜中均有表达,分泌期表达高于增生期,有显著差异。EMS的异位子宫内膜中的表达显著高于其在位子宫内膜和正常子宫内膜;EMS的在位子宫内膜和正常子宫内膜之间比较无明显差异。结论PLGF、VEGFR-1可能参与子宫内膜异位症的发病过程。     

神经纤维在子宫内膜异位症患者在位及异位内膜的分布

目的探讨子宫内膜异位症患者在位及异位内膜神经纤维的表达,并观察其与内异症疼痛症状的关系。方法选取2013年4月至2014年5月就诊于深圳市妇幼保健院,并通过腹腔镜手术确诊的子宫内膜异位症患者55例作为患病组,根据VAS评分分为疼痛组(38例)和无痛组(17例),同期因子宫肌瘤或CINⅢ级行全子宫切除并否认有痛经史的患者30例作为对照组,通过蛋白基因产物9.5免疫组化法比较内异症患者的在位内膜、异位内膜及对照组患者的在位内膜中神经纤维的表达。结果子宫内膜异位症患者的在位及异位内膜的神经纤维表达均高于对照组(t=9.62,P0.05;t=8.92,P0.05),疼痛组在位及异位内膜的神经纤维表达均高于无痛组(t=8.09,P0.05;t=4.96,P0.05),并且异位内膜中神经纤维的表达与痛经的严重程度有关(r=0.546,P=0.000)。结论神经纤维在子宫内膜异位症患者在位及异位内膜的表达增高,并与痛经的严重程度有一定的相关性。     

树突状细胞在子宫内膜异位症内膜组织中的变化

目的检测不成熟树突状细胞(im DCs)及成熟树突状细胞(m DCs)的标记物CD1a和CD83在子宫内膜异位症(EMS)内膜组织中的表达,探讨不同发育阶段的DCs在子宫内膜异位症发生发展中的作用。方法选取病理检查确诊的"巧克力囊肿"患者30例,分别取其异位内膜组织(异位内膜组)和在位内膜组织(在位内膜组),同时选取30例非内异症内膜组织为对照组。免疫组织化学法检测CD1a、CD83蛋白表达和分布,免疫印迹法检测CD1a、CD83蛋白表达量。结果 CD1a和CD83阳性细胞均分布于固有层基质细胞间及血管周围;CD1a蛋白在对照组、在位内膜组、异位内膜组表达依次升高,组间比较差异均有统计学意义(P0.01);CD83蛋白在对照组、在位内膜组、异位内膜组表达依次减少,差异均有统计学意义(P0.01)。结论子宫内膜异位症患者子宫内膜局部im DCs增多、m DCs减少,可能在子宫内膜异位症中发挥作用。     

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.