左心室辅助装置控制模式影响双心室搏动同步性的数值研究

右心室(RV)衰竭已成为左心室辅助装置(LVAD)治疗的一种致命并发症。由LVAD引起的双心室搏动的不同步是引发RV功能障碍的重要因素。本文采用数值方法研究LVAD的控制模式对左、右心室搏动同步性的影响。数值结果表明:左心室(LV)与RV的收缩持续时间在无泵模式下没有显著差异(分别为48.52%和51.77%)。连续模式下,LV收缩期明显短于RV收缩期(LV vs.RV:24.38%vs.49.16%)和无泵模式的LV收缩期。搏动模式下,LV收缩期明显短于RV收缩期(LV vs.RV:28.38%vs.50.41%)但长于连续模式的LV收缩期。反搏动模式中的LV、RV收缩期差异较小(LV vs.RV:43.13%vs.49.23%),而LV收缩期短于无泵模式,并且长于连续模式。与连续和搏动模式相比,由反搏动模式提供的收缩期转速(RS)降低显著地校正了LV收缩持续时间,连续模式下缩短的收缩持续时间在反搏动模式下被校正为LV和RV之间的重新同步。因此,本文认为LV和RV收缩的再同步有助于预防RV功能障碍。总之,使用在收缩期间降低RS的反搏动模式有望用于由LVAD引起的双心室搏动不同步的临床校正。     

慢性高输出量型心功能不全发展过程中心室舒、缩功能和顺应性的变化及其与心泵功能的关系

本文研究了大鼠慢性高输出量型心功能不全发展过程中心室舒,缩功能和顺应性的变化规律及其与心泵功能的关系。疾病模型采用动静脉造瘘(ACF)加单侧肾动脉缩窄(RAS)的方法建立。本实验中,全部ACF+RAS大鼠均呈现出慢性高输出量型心功能不全的特征,在静息状态下心脏指数(CI)显著升高,而心泵贮备功能(CORF)却不同程度地降低。结果表明:随心泵功能的恶化,心室的舒、缩功能进行性降低,心室的舒张顺应性显著升高,心室的舒,缩性能和顺应性在心功能不全发展的不同阶段对心泵功能所起的作用不同。     

大鼠实验性左室心肌梗塞对右室收缩性能的影响

对左室心肌梗塞(MI)是否会直接影响右室功能,至今尚有争议。本实验观察大鼠左室MI时右室dp/dt max的改变及其与左室dp/dt max和梗塞范围(IS)间的关系。结果发现冠脉结扎后1天,在左室dp/dt max显著降低的同时,右室dp/dt max也显著降低,且与左室dp/dt max呈显著的直线正相关,而与IS呈显著的直线负相关。在冠脉结扎后3天时,左室dp/dt max有显著恢复,但仍低于对照水平,而右室dp/dt max已恢复正常,且与左室的dp/dt max和IS间不再具有显著的直线相关关系。由此证明;在大鼠左室MI早期,右室收缩性能可受到直接影响,影响的程度与IS及左室收缩性能降低的程度相关;但当左室收缩性能恢复到一定程度时,这种影响消失。     

彩超探讨肺切除术对心脏血流动力学的影响

目的探讨肺切除术后病人心脏血流动力学改变.方法对42例肺切除术病人,于术前及术后应用彩色多普勒超声心动图,测定肺动脉(PA)、主动脉(AO)、左心房(LA)、右心房(RA)及左心室(LV)、右心室(RV)内径,左、右心功能等相关参数,并进行术前后对比分析.结果术后右心参数:射血前期(PEP)、射血期(PE)、肺动脉收缩压(PASP)明显增高(p<0.05),RA、RV、PA内径未见改变.左心参数:LA较术前小(p<0.05),左室射血分数(EF)、短轴缩短率(FS)、每搏量(SV)有所下降,心输出量(CO)有所升高.结论肺切除术对右心功能、肺动脉压影响较明显,对左心功能的影响值得注意.     

尼群地平及卡找普利治疗高血压肥厚左室后的功能变化

已形成式室肥厚的１４ｗｋ龄自发性高血压大鼠经用尼群地平或卡托普利治疗１４ｗｋ后，左室肥厚消退。肥厚消退后的左室收缩力无明显改变，但异丙基肾上腺素灌注后左室压力最大上升速度的增量增加并接近年龄配对的正常血压鼠；左室被弹性系数Ｋｍ值变相应降低，结果表明左室肥厚消退后，左室舒张功能改善，收缩速度储备力恢复，左室收缩力不变。     

三七总甙对大鼠烧伤后心肌细胞膜离子泵活性的影响

心肌细胞膜Na -K 泵、Ca2 -Mg2 泵通过消耗ATP,调节离子转运,直接参与心肌舒缩过程的调控;红细胞膜上的Na -K 泵与左心室收缩功能之间有高度相关性,而Ca2 -Mg2 泵则与心脏舒张及收缩功能均显著相关。本室既往研究发现大鼠在严重烧伤后心功能下降,三七总皂苷(PNS)能有效改善烧伤后心功能。为观察PNS对烫伤大鼠红细胞及心肌细胞     

人体心脏舒张最大吸力的模拟实验研究

目的:模拟研究人体心脏舒张早期潜存的心室最大负压.材料与方法:先在血液循环体外模拟装置上模拟正常生理情况下的左、右心室心动周期压力曲线,然后近似阻断房室瓣,分别测定左、右心室压力.结果:模拟实验得到的左、右心室心动周期压力曲线和正常生理情况下的左、右心室心动周期压力曲线非常接近.近似阻断房室瓣时,左、右心室舒张的负压平均值分别是-93.25 mmHg(-12.43 kPa)和-10.28 mmHg(-1.37 kPa).结论:(1)模拟得到的实验结果可以定性地说人体心脏舒张和静脉血液回流心生物动力学关系;(2)心脏舒张时心室压力的减低(负压)是形成静脉-心房-心室压力梯度的根本原因,心脏舒张所产生的舒张吸力是静脉血液回流心室的主要动力,即静脉血液回流心脏是心脏舒张吸力作用的结果;(3)心脏前负荷产生的机理应该是心脏舒张抽吸静脉血液回流心脏所需的吸力;(4)静脉血液在被抽吸回流心室腔的过程中对心室肌没有伸展作用,即Starling心定律没有心脏舒张动力学基础.     

尼群地平及卡托普利治疗高血压肥厚左室后的功能变化

已形成左室肥厚的１４ｗｋ龄自发性高血压大鼠（ＳＨＲ）经用尼群地平或卡托普利治疗１４ｗｋ后，左室肥厚消退。肥厚消退后的左室收缩力无明显改变，但异丙基肾上腺素灌注后左室压力最大上升速度的增量（Δｄｐ／ｄｔ－ｍａｘ）增加并接近年龄配对的正常血压鼠；左室被动弹性系数数Ｋｍ值亦相应降低。结果表明左室肥厚消退后，左室舒张功能改善，收缩速度储备力恢复，左室收缩力不变     

美心力对左室功能和血流动力学影响的实验研究

目的：探讨美心力（cAMP)对左室功能和血流动力学的影响。方法：建立心内植入压力、容积测定装置的犬模型。利用压力-容积关系分析美心力对左室功能和血流动力学的影响。结果：美心力明显减慢心率（HR）,降低总外周阻力（TSR）,使左室收缩末期压力（PES）、容积（VES）和舒张末期压力（PED）、容积（VED）明显下降;并加速左室舒张速度（Tc),使每搏容积（SV）及射血分数（EF）增加,对于左室PES-VES、左室压上升最大速率（dp/dtmax)-VED和心搏功（SW）-VED3种关系斜率及位置无影响。表明无正性肌力作用。结论：美心力无正性肌力作用。但能够降低心脏负荷,改善心肌舒张功能,增加心排血量。     

经胸实时三维超声心动图测量左、右心室心肌质量的动物实验研究

目的探讨经胸实时三维超声心动图(real-timethree-dimensionalechocardiography,RT-3DE)测量左、右心室心肌质量的准确性及优选测量时相。方法10头正常上海种白猪,猪龄均为2个月,其中雌性6头,雄性4头,体质量(20.60±1.88)kg。RT-3DE测定左心室心肌质量和右心室游离壁心肌质量,结果与实测值进行Pearson相关分析。结果①左心室心肌质量:RT-3DE在收缩末期及舒张末期测定的左心室心肌质量分别为(56.34±4.80)g、(57.02±4.86)g,实测值为(63.07±6.44)g。RT-3DE在收缩末期及舒张末期测定的左心室心肌质量结果分别与实测值进行相关分析,r分别为0.78、0.87,均存在较好的相关性,而以舒张末期测值相关性更高。②右心室游离壁心肌质量:RT-3DE在收缩末期及舒张末期测定的右心室游离壁心肌质量分别为(16.63±1.54)g和(19.07±1.95)g,实测值为(20.78±2.70)g。RT-3DE在收缩末期及舒张末期测定的右心室游离壁心肌质量结果分别与实测值进行相关分析,r分别为0.68、0.74,亦均存在较好的相关性,而以舒张末期测值相关性更高。结论RT-3DE可准确测量左、右心室心肌质量,尤以舒张末期测值更可靠。     

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.     

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.     

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.     

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.     

海洛因成瘾与学习记忆

海洛因成瘾是我国发病最高,危害最大的一种成瘾性疾病,而其中枢机制则是解决临床预防和治疗的关键,至今仍不清楚。既往工作表明,学习记忆功能在海洛因成瘾的中枢机制中居于重要的中心环节。本文在总结既往海洛因成瘾研究工作基础上联系学习记忆功能,试图从系统整合层次分析相关领域研究工作的不足和今后工作的发展方向。     

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.