钙/钙调素依赖性蛋白激酶-Ⅱ及其生物学作用

钙 /钙调素依赖性蛋白激酶 -Ⅱ (ｃａｌｃｉｕｍ/ｃａｌｍｏｄｕｌｉｎ -ｄｅｐｅｎｄｅｎｔｐｒｏｔｅｉｎｋｉｎａｓｅ -Ⅱ ,ＣａＭＫⅡ )是一种多功能蛋白激酶 ,存在于许多动物细胞内 ,尤其在神经组织中含量丰富。在脑部某些区域如海马内占其蛋白质总量的 2 % ,主要集中在突触部位。研究表明 :ＣａＭＫⅡ广泛参与基因转录调节、神经递质合成、骨架蛋白磷酸化 ,近年来ＣａＭＫⅡ在海马学习及记忆功能过程中的作用正得到广泛的研究。1　ＣａＭＫⅡ的分子结构与活性调节ＣａＭＫⅡ是不同动物种属脑内广泛存在的一种非脯氨酸指导的蛋白激酶。…     

癫痫手术治疗的皮层电图监测

目的：探讨皮层电图（ＥＣｏＧ）监测对切除癫痫病灶的应用价值及适应症。方法：对１０４例难治性癫痫患者使用盘状电极行ＥＣｏＧ监测下切除癫痫灶进行研究。结果：术前脑电图（ＥＥＧ）检查８６例异常（８２７％）。皮层电图１０２例异常（９８％）。术后随访３个月至４年,有８８例（８４６％）临床发作已控制,１６例发作次数明显减少。复查常规ＥＥＧ有痫样放电６例,慢波局限性改变５例,其余ＥＥＧ均为正常。术前术后ＥＥＧ阳性率相差显著。结论：在ＥＣｏＧ监测下切除癫痫灶具有一定的临床价值     

癫痫伴发焦虑抑郁患者脑神经递质活动的脑电超慢涨落图表现分析

目的:探讨癫痫伴焦虑抑郁患者脑神经递质活动的脑电超慢涨落图（EFG）表现并对其进行分析。 方法:以2014年1月~2015年12月我院治疗的30例癫痫伴焦虑抑郁患者（记为观察组）、同期于我院治疗的30例癫痫患者（无焦虑抑郁者记对照组）为对象,采用EFG分析仪检测两组研究对象脑内神经递质活动变化情况、脑功能状态差异。 结果:观察组仅5-HT较对照组明显低,其它指标两组之间比较无明显差异（P>0.05）;两组运动指数、兴奋抑郁指数及血管舒缩指数由高至低排序为:观察组＞对照组,两组之间比较差异显著（P<0.05）。 结论:癫痫伴焦虑抑郁患者的EFG表现为脑神经递质的活动异常、脑功能状态处于异常状态,而这些异常表现有助于癫痫伴焦虑抑郁的鉴别诊断。     

小儿癫痫及其发作类型、频率与脑细胞葡萄糖代谢的相关性研究

目的： 探讨小儿癫痫及其发作类型、频率与癫痫灶脑细胞葡萄糖代谢的相关性。方法: 对经临床、EEG及MRI检查确诊的86例癫痫患儿进行脑18F-FDG PET显像检测,以反映癫痫灶脑细胞葡萄糖代谢情况。结果: 与对照组比,癫痫组脑PET显像异常 (P<0.01);异常率为89.9% (77/86), 其中72例发作间期为低代谢显像,5例发作期为高代谢显像。不同发作类型癫痫患儿脑PET显像异常的脑区不同,婴儿痉挛症和Lennox-Gastaut syndrome 脑PET显像异常部位主要在双侧皮质,呈双侧大脑弥漫性皮质低代谢改变,复杂部分性发作患儿则主要为颞叶。脑PET显像异常与发作频率或病情呈正相关(P<0.01),即脑PET显像异常愈重,发作频率愈高或病情愈重;但与发病年龄无关(P>0.05)。结论: 癫痫患儿脑细胞葡萄糖代谢异常;不同发作类型的癫痫患儿脑细胞葡萄糖代谢异常的脑区不同;脑PET显像异常与发作频率或病情呈正相关。     

发作期及发作间期痫性放电对癫痫的诊断价值

目的探讨发作期及发作间期脑电图对癫痫诊断的意义。方法对５６例癫痫患者常规脑电图（ＲＥＥＧ）与２４ｈ脑电图（ＡＥＥＧ）进行比较研究。结果①ＲＥＥＧ的阳性率为３０％，而ＡＥＥＧ的阳性率为８６％；②不同类型癫痫在发作期和发作间期大脑活动的规律和特点，ＲＥＥＧ无１例记录到癫痫发作，而ＡＥＥＧ有２７例（４８％）记录到癫痫发作全过程的大脑电活动变化。结论发作期的ＥＥＧ对确定癫痫类型有重要意义，全身性癫痫在发作的同时发作波在两侧半球同时出现，而部分性发作患者在临床发作的同时ＥＥＧ常局限在某一脑叶有单个棘波发放，此棘波处是癫痫的病灶的部位，这种局限棘波可扩散至全脑而临床出现全身阵挛发作，此类患者为部分性癫痫并非全身性癫痫。     

去甲肾上腺素对大鼠腹腔巨噬细胞内IP_3、［Ca~（2＋）］_i和Ia抗原表达

本文应用细胞膜放射标记和离子交换层析法测定巨噬细胞（ＭФ）内肌醇－１，４，５－三磷酸（ＩＰ３）、用Ｃａ￣（２＋）指示剂的分光光谱法测定ＭФ内Ｃａ￣（２＋）浓度（［Ｃａ￣（２＋）］）、用ＡＰＡＡＰ桥联酶标法检测ＭФ表面Ｉａ抗原的表达，研究去甲肾上腺素（ＮＥ）对大鼠腹腔的ＭФ内ＩＰ３、［Ｃａ￣（２＋）］ｉ和ＭФ表面ｌａ抗原表达的影响。结果显示ＮＥ（１０￣（－８）ｍｏｌ／Ｌ）可显著增高ＭФ中ＩＰ＿３含量（４４２±２２ｃｐｍ／１０￣６ｃｅｌｌｓ，对照组１０２±８ｃｐｍ／１０￣６ｃｅｌｌｓ，Ｐ＜０．０１）；ＮＥ可使ＭФ内［Ｃａ￣（２＋）］ｉ显著增高（３２２±７８ｎｍｏｌ／Ｌ，对照组９７±１７ｎｍｏｌ／Ｌ，Ｐ＜０．０１）；ＮＥ可显著增高ＭФ表面Ｉ－Ａ、Ｉ－Ｅ抗原的表达（６４±８％、５８±６％，对照组５０±３％，４４±４％，Ｐ＜０．０１）。提示神经递质ＮＥ促进ＭФ表面Ｉａ抗原表达的作用可能是通过第二信使ＩＰ＿３和Ｃａ￣（２＋）介导的。     

癫痫脑电的双谱特性研究

双谱分析对于分析处理非高斯、非线性随机信号具有明显优点.脑电信号被认为具有非高斯、非线性的特性.本文对不同发作阶段癫痫患者的脑电信号进行双谱估计,进而研究不同生理条件下脑电的双谱特性.结果表明,不同发作阶段时癫痫脑电信号的高斯偏离程度明显不同,其中双相干系数能够区分不同发作阶段脑电的信号特征,有望成为临床监护和预报癫痫发作的一个指标.     

发作间期PET和SPECT检查对颞叶癫痫定位的诊断价值

目的：探讨发作间期１８Ｆ脱氧葡萄糖（ＦＤＧ）正电子发射断层扫描（ＰＥＴ）和９９ｍＴｃ已撑半胱氨酸（ＥＣＤ）单光子发射断层扫描（ＳＰＥＣＴ）对难治性颞叶癫痫（ＴＬＥ）的定位诊断价值。方法：５３例脑电图（ＥＥＧ）定位明确的难治性ＴＬＥ患者分别行发作间期１８ＦＦＤＧＰＥＴ和９９ｍＴｃＥＣＤＳＰＥＣＴ检查。其中２１例磁共振（ＭＲＩ）显示有结构性病变并与ＥＥＧ定位结果一致。结果：ＭＲＩ异常组均在ＰＥＴ和ＳＰＥＣＴ相应部位出现低代谢和低灌注表现。ＭＲＩ正常组，ＰＥＴ定位准确率为８４％，显著高于ＳＰＥＣＴ的５６％（Ｐ＜００５）。结论：对于无结构性病变的颞叶癫痫，发作间期ＰＥＴ检查有较高的定位诊断价值，ＳＰＥＣＴ的临床意义相对较小。     

NMDA受体在癫痫发病机制中的作用

癫痫是慢性反复发作短暂脑功能失调综合征,是神经科常见疾病之一。目前有关癫痫的发病机制尚未阐明。研究表明,癫痫的发生与兴奋性神经递质和抑制性神经递质的失衡有关。谷氨酸作为一种主要的兴奋性神经递质,通过受体介导的兴奋性机制在癫痫的发生过程中具有重要作用。谷氨酸受体可以分为促离子型和促代谢型2类。     

实验性癫痫大鼠海马内生长抑素对5—HT,NE能递质系统活动的影响

本实验在青霉素致痫大鼠模型上观察海马内微量注射半胱胺降低生长抑素后，癫痫发作强度和脑电总功能的变化，并用免疫组化和ＨＰＬＣ方法检测中缝背核５－ＨＴ，蓝斑核ＮＥ免疫阳性物质和海马内ＮＥ含量。结果发现致痫后２ｈ５－ＨＴ，ＮＥ免疫阳性物质显著减少，海马灌流液中ＮＥ含量增加，半胱胺降低海马内生长抑素３０％后，癫痫发作程序减轻，５－ＨＴ，ＮＥ免疫阳性物质和马ＮＥ含量与对照组相比无显著改变，提示海马内ＳＳ有致     

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.