脑血流动力学改变对高血压病患者EEG的影响

目的:探讨原发性高血压病患者脑血流动力学改变对EEG的影响。方法:采用经颅多普勒(TCD)、脑电图(EEG)对80例原发性高血压病患者进行检测,并作了统计观察。结果:TCD平均血流增快31例,EEG异常率达67.74%,血流缓慢23例,EEG异常率达69.57%,血流正常26例,EEG异常率仅7.69%,流速增快,流速减慢组EEG异常率明显高于血流正常组。结论:原发性高血压病患者当脑血流动力学发生改变时,对脑功能影响尤其明显。     

经颅多普勒对妊高征脑血流变化的研究

目的研究妊娠高血压综合征（简称妊高征）的脑血流速变化。方法利用经颅多普勒（TCD）检测,36例妊高征（观察组）,40例正常孕妇（对照组）的大脑中动脉的各项血流参数（Vs、Vd、Vm、PI）。结果①观察组脑血流速度增快或减慢,PI值增高与对照组之间的差异具有显著意义（P〈0.05=、（P〈0.01=②观察组中,轻、中度妊高征以收缩期血流速度增快为主,重度妊高征以平均血流速度减慢居多。两者PI比值均增高。结论TCD可监测妊高征患者脑血管痉挛程度,轻、中度妊高征血管痉挛程度轻以代偿增快为主,但PI比值增高。正常孕妇TCD血流速度增快,但PI比值正常。故可早期行TCD检查脑血流变化预防妊高征患者脑血管意外和子痫发生。     

经颅多普勒超声诊断（续）

偏头痛TCD表现： （1）偏头痛发作期和间歇期脑动脉血流速度增快者多见，减慢者少见，血流速度异常改变多见于单侧或双侧MCA和（或）ACA。Thie 1990年提出偏头痛患者血流速度异常标准为MCAV。大于100cm／s。ACAVm大于90cm／s，PCAVm大于80cm／s。血流速度增快为血管紧张度增高（血管功能性狭窄）所致，血流速度减慢可能是血管张力减低，血管扩张的表现。     

后循环缺血患者的脑血流动力学及神经电生理变化

目的:探讨后循环缺血(PCI)患者的脑血流动力学及神经电生理学的变化.方法:对134例经临床确诊的PCI患者依据临床症状及CT、MRI检查结果分为梗死组(58例)和非梗死组(76例),均进行经颅多普勒(TCD)及脑干听觉诱发电位(BAEP)检查,并与健康对照组(68例)进行对比.结果:134例PCI患者TCD异常98例,异常率为73.1%,主要异常表现为椎基底动脉系统血流速度降低或增快、血流频谱改变及PI值增高.其中梗死组TCD异常率(50/58,86.1%)高于非梗死组(48/76,63.2%),差异有显著意义(P<0.01).BAEP异常107例,异常率为79.7%,主要异常表现为Ⅰ、Ⅲ、Ⅴ波的潜伏期(PL)和Ⅲ-Ⅴ波的波间潜伏期(IPL)延长,脑干型所占比例较最高(44/134,32.8%),内耳型最低(25/134,18.5%),混合型介于其中(38/134,28.4%).梗死组Ⅲ波PL(3.97±0.23 ms)较非梗死组(3.78±0.25 ms)显著延长(P<0.05),梗死组Ⅴ波PL(5.94±0.31 ms)较非梗死组(5.65±0.29 ms)显著延长(P<0.01),梗死组Ⅲ-Ⅴ波IPL(2.19±0.21 ms)较非梗死组(1.92±0.22 ms)显著延长(P<0.01).结论:TCD可无创地检测PCI患者的血流动力学异常,具有较高的敏感性;BAEP能灵敏地检测出PCI患者的神经功能异常,其异常程度可部分反映病情的严重程度,联合应用TCD及BAEP可为PCI的诊断和病情评估提供重要的参考.     

150例偏头痛的经颅多普勒分析

目的：探讨经颅多普勒检查时偏头痛发作期和发作间期血流动力学改变的临床意义。方法：对150例偏头痛患者发作期和发作间期经颅多普勒检查结果进行对照研究。结果：偏头痛发作期脑血流量调节复杂，表现各不一致。发作期间，TCD上多表现为不同程度的血流速度增快。结论：本组结果发现不论处于头痛发作期或间歇期，TCD均可检测到脑血管动力学特征及脑血管的反应性，以推测脑血管的功能状态。TCD检测异常率达69％，对偏头痛临床诊疗有较大的帮助。     

TCD、MRA对儿童脑血管烟雾病诊断的对比研究

目的探讨经颅多普勒超声(TCD)在儿童烟雾病的特征表现并与核磁共振(MRA)对照比较其诊断价值.方法对6例由MRA确诊为烟雾病患儿的TCD检查资料比较分析.结果 6例患者TCD获得的检测结果具有一定的特征性,TCD所测出的病变血管与MRA证实的病变部位基本符合. TCD与MRA对照分析结果:①MRA显示血管狭窄,TCD均见相应动脉血流速度增快;②MRA显示血管严重狭窄,TCD显示该血管血流速度减慢、血流频谱降低或无血流信号;③椎动脉系统因其与颈内动脉系统由后交通动脉相连,当颈内动脉系统出现狭窄闭塞,椎动脉系统血流代偿性增快,也为TCD所证实.结论 TCD作为一种无创的检查手段,可以对烟雾病患者的脑血流进行追踪观察.对于烟雾病的早期诊断,具有重要的临床意义,并且具有明显优势.     

后循环缺血患者的脑干听觉诱发电位与经颅多普勒对比分析

目的:探讨后循环缺血患者的脑干听觉诱发电位(BAEP)及经颅多普勒(TCD)的变化并作对照分析。方法:对78例临床诊断为后循环缺血的患者进行BAEP和TCD的检测,并与健康对照组进行对比分析。结果:BAEP异常的有59例,异常率为76.0%。其中表现为脑干型35例(59.3%),混合型18例(30.5%)和内耳型6例(10.1%)。在TCD异常的55例,异常率为70.5%。主要表现在椎基底动脉系统血流速度减慢或增快;血流频谱改变及PI值增高。结论:BAEP能敏感地检出后循环缺血患者的听通道神经功能的异常,而TCD则可了解后循环缺血患者的椎基底动脉系统的血流动力异常情况,联合应用BAEP和TCD检测对后循环缺血的早期诊断、治疗和疗效观察有重要的参考价值。     

经颅多普勒超声下血流动力学与血管性认知功能障碍患者认知功能的相关性

目的:研究血管性认知功能障碍患者经颅多普勒超声(TCD)下血流动力学和认知功能之间的关联。方法:从本院选取43例血管性认知功能障碍患者,设为研究组;再选取43例认知功能正常的血管性疾病患者,设为对照组。比较两组大脑中动脉搏动指数(MCA-PI)、大脑中动脉平均血流速度(MCA-Vm)、大脑前动脉搏动指数(ACA-PI)、大脑前动脉平均血流速度(ACA-Vm)4项TCD下血流动力学指标和蒙特利尔认知功能评分量表(MoCA)。结果:研究组MCA-IP、ACA-PI明显高于对照组,差异均有统计学意义(t=6.864,2.501;P0.05);两组MCA-Vm、ACA-Vm进行比较,差异均无统计学意义(P0.05)。研究组的视空间与执行功能、命名、语言、抽象、延迟回忆评分和总分明显低于对照组,差异均有统计学意义(t=-10.978,-5.265,-4.609,-7.076,-2.033,-9.001,-6.254;P0.05)。对比两组的定向评分,两组差异均无统计学意义。MCA-IP与MoCA呈线性相关,且为负相关,回归系数是-7.824,差异具有统计学意义(t=-2.075,P0.05);而ACA-PI和MoCA评分无相关性。结论:TCD下血流动力学与血管性认知功能障碍患者的认知功能呈负相关系,反映了动脉血管阻力及患者认知功能障碍程度。     

去大脑皮层状态下脑功能、脑血流动力学观察

应用脑电图(EEG)、脑干听觉诱发电位(BAEP)、体感诱发电位(SEP)、经颅多普勒超声(TCD)等新技术,对两例去大脑皮层状态患者进行观察,旨在探讨会大脑皮层状态下脑功能及脑血流动力学改变。 一、病例 例1.张某,男,29岁,因右头面部枪弹伤行开颅探查、硬膜下及脑内血肿清除术后昏迷一年余,查体:生命体征平稳,呈浅昏迷状态,眼球浮动、分离,吞咽动作存在,四肢腱反射左侧活跃,有轻微自主屈曲动作,脑干反射存在,皮层功能消失。CT示右半球脑软化。EEG示:各导联均为10～20μv,1.5     

甲状腺机能亢进症的脑血流、脑功能观察

应用经颅多普勒和脑电图技术检测20例甲状腺机能亢进症病人,异常率分别为95％和70％,证实了本病在存在脑神经功能异常的同时,脑血流动力学亦发生明显异常。作者认为,虽然此两项技术对于临床诊断无特异性,但二者联合应用可为本病的诊断、治疗及预后提供客观指标。     

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.     

Beta-endorphin and drug-induced reward and reinforcement

Although drugs of abuse have different acute mechanisms of action, their brain pathways of reward exhibit common functional effects upon both acute and chronic administration. Long known for its analgesic effect, the opioid beta-endorphin is now shown to induce euphoria, and to have rewarding and reinforcing properties. In this review, we will summarize the present neurobiological and behavioral evidences that support involvement of beta-endorphin in drug-induced reward and reinforcement. Currently, evidence supports a prominent role for beta-endorphin in the reward pathways of cocaine and alcohol. The existing information indicating the importance of beta-endorphin neurotransmission in mediating the reward pathways of nicotine and THC, is thus far circumstantial. The studies described herein employed diverse techniques, such as biochemical measurements of beta-endorphin in various brain sites and plasma, and behavioral measurements, conducted following elimination (via administration of anti-beta-endorphin antibodies or using mutant mice) or augmentation (by intracerebral administration) of beta-endorphin. We suggest that the reward pathways for different addictive drugs converge to a common pathway in which beta-endorphin is a modulating element. beta-Endorphin is involved also with distress. However, reviewing the data collected so far implies a discrete role, beyond that of a stress response, for beta-endorphin in mediating the substance of abuse reward pathway. This may occur via interacting with the mesolimbic dopaminergic system and also by its interesting effects on learning and memory. The functional meaning of beta-endorphin in the process of drug-seeking behavior is discussed.     

PTEN与信号转导及肿瘤

ＴＥＮ[1] (ｐｈｏｓｐｈａｔａｓｅａｎｄｔｅｎｓｉｎｈｏｍｏｌｏｇｙｄｅｌｅｔｅｄｏｎｃｈｒｏｍｏｓｏｍｅｔｅｎ)又名ＭＭＡＣ1 [2 ] (ｍｕｔａｔｅｄｉｎｍｕｔｉｐｌｙａｄａｎｃｅｄｃａｎｃｅｒ 1 )和ＴＥＰ1 [3 ] (ＴＧＦ -βｒｅｇｕｌａｔｅｄａｎｄｅｐｉｔｈｅｌｉａｌｃｅｌｌ -ｒｉｃｈｅｄｐｈｏｓｐｈａｔａｓｅ 1 ) (以下均称为ＰＴＥＮ) ,是 1 997年由 3个研究小组先后发现的一个具有双特异磷酸酶活性的抑癌基因。ＰＴＥＮ基因异常广泛存在于人类多种恶性肿瘤 ,如恶性神经胶质瘤、前列腺癌、子宫内膜癌、黑色素瘤等…     

Tobacco and alcohol and the risk of head and neck cancer

Summary We carried out two case-control studies on the relative risk of head and neck cancer in association with tobacco and alcohol consumption. The first study carried out at the ENT Department of the University hospitals of Heidelberg and Giessen (FRG) comprised 200 male patients with squamous cell cancer of the head and neck and 800 control subjects matched for sex, age, and residential area (1:4 matching design). Of the tumour patients, 4.5% had never smoked, in contrast to 29.5% of the control group. The average tobacco and alcohol consumption of the patients was approximately twice as high as in the control subjects. The highest alcohol and tobacco consumption was observed in patients suffering from oropharyngeal cancer. Tobacco and alcohol increased the risk of head and neck cancer in a dose-dependent fashion and acted as independent risk factors. In heavy smokers (> 60 pack-years) a relative risk of 23.4 (alcohol adjusted) was calculated. Combined alcohol and tobacco consumption showed a synergistic effect. The risk ratio increased more in a multiplicative than in an additive manner. Oral and laryngeal cancer were associated with the highest tobacco-associated risk values. The highest ethanol-associated risk values were associated with oropharyngeal and laryngeal cancer. The second study was carried out at the ENT Department of the University of Heidelberg on 164 males with squamous cell carcinoma of the larynx and 656 control subjects matched for sex, age and residential area (1:4 matching design). Of the cases, 4.2% had never smoked, compared with 28.5% of the control subjects. The risk of laryngeal cancer by tobacco consumption was dose dependent, reaching a maximum value of 9.1 (adjusted for alcohol) for a consumption of more than 50 tobacco-years (TY). The relative risk of laryngeal cancer associated with alcohol intake was also dose dependent, reaching a value of 9.0 (adjusted for tobacco) for a mean daily consumption of more than 75 g alcohol. An analysis of subsite specific risks showed that heavy smokers (> 50 TY) carried a nearly ten times higher risk of supraglottic cancer than of glottic cancer. The risk of supraglottic cancer from alcohol consumption was also higher than that of glottic cancer.     

Postinfectious immunodeficiency and autoimmunity: pathogenic and clinical values and implications

Autoimmunity is still a mystery of clinical immunology and medicine as a whole. The etiology and pathogenesis of autoimmune disorders remain unclear and, thus, are assessed as a balance between hereditary predisposition, triggering factors and the appearance of autoantibodies and/or self-reactive T cells. Among the immunological armamentarium, molecular mimicry, based on self-reactive T- and B-cell activation by cross-reactive epitopes of infectious agents, is of special value. Hypotheses regarding the possible involvement of molecular mimicry in the development of postinfectious autoimmunity are currently very intriguing. They provide new approaches for identifying etiological agents that are associated with postinfectious autoimmunity, paired microbial- and tissue-linked epitopes targeted for autoimmune reaction determination, postinfectious autoimmunity pathogenesis recognition and specific prevention, and therapy for autoimmune disorder development.     

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.     

类赖氨酰氧化酶2与肿瘤转移和发生

类赖氨酰氧化酶2(lysyl oxidase-like 2,LOXL2)是赖氨酰氧化酶(lysyl oxidase,LOX)基因家族的成员之一,其表达产物能促进胶原沉积.LOXL2的过表达能促进纤维化,并与肿瘤侵袭、转移及不良预后有关.目前大部分学者认为LOXL2是一种转移促进基因,也有实验支持其是一种肿瘤抑制基因.研究发现LOXL2可以通过激活Snail/Ecadherin通路或Src/FAK通路促进转移.LOXL2有望作为肿瘤生物标志物,用于预后判断,成为一个新的治疗靶点.