纤维蛋白原或纤维蛋白参与动脉粥样硬化的炎症反应途径及其调控

动脉粥样硬化是一种发生于含有平滑肌的大、中动脉的疾病,它是心脑血管疾病最主要的病理基础。动脉粥样硬化形成机制尚不清楚,目前最被广泛接受的观点是Ross提出的“动脉粥样硬化是一种炎症性疾病”的学说,这种学说认为动脉粥样硬化是源于内皮功能障碍的慢性、进行性、炎症性疾病,动脉粥样硬化的各种改变被认为是在慢性炎症的不同阶段机体对损伤的一种反应。该学说的提出吸引了很多学者从炎症反应角度对动脉粥样硬化进程中的炎性分子作用机制进行研究,     

RANTES基因多态性与动脉粥样硬化疾病的研究进展

动脉粥样硬化的形成和发展是心脑血管疾病、糖尿病等重要的病理生理基础,而炎症反应在动脉粥样硬化的形成过程中具有重要的意义[1]。表达于动脉粥样硬化病变处的一些趋化因子在单核细胞迁移和巨噬细胞分化过程中可以起     

DNA甲基化酶3A在动脉粥样硬化中的作用机制

近来的研究显示，DNA甲基化酶3A（DNA methylase 3 alpha，DNMT3A）在动脉粥样硬化过 程中起着重要的调控作用，而动脉粥样硬化是冠心病及缺血性卒中等心脑血管疾病的重要病理基础。 体细胞DNMT3A 基因突变可能通过多种免疫细胞、作用机制影响动脉粥样硬化的发生、发展过程，是 心脑血管疾病一项尚未明确的重要危险因素。本文重点介绍DNMT3A在心脑血管疾病中的作用机制以 及其在心脑血管疾病诊疗中的应用前景。     

脂蛋白相关磷脂酶A2与缺血性脑血管疾病的研究进展

动脉粥样硬化(atherosclerosis,AS)是缺血性脑血管疾病的重要病理生理基础,防治动脉粥样硬化是目前医学领域急需解决的一个重大问题.对其机制的研究已从大体病理深入到细胞、分子和基因水平,而AS也由先前被认为主要是管道问题、退行性疾病,转变为一种多种因素导致的慢性炎症反应性疾病[1].炎症已经被公认是AS发展过程中的核心因素[2],炎症反应贯穿AS发生、发展的整个环节,在动脉粥样硬化斑块的起始、发展以及稳定性丧失及斑块破裂脱落中均起着重要的作用,所以积极寻找其发生、发展过程中的炎症标志物作为缺血性心脑血管疾病危险预测的指标,并以其为治疗靶点成为目前的研究热点.     

血管稳态对动脉粥样硬化发生发展影响的研究进展

动脉粥样硬化(AS)是心脑血管疾病的主要病理生理基础,其发生发展是在致病因素的作用下,内外环境改变,血管稳态失衡,从而导致血管功能及结构改变。本文以血管稳态这个角度,从血管壁、血液成分、炎症、表观遗传和营养物质五个方面对动脉粥样硬化机制进行阐述。     

白细胞膜微粒在动脉粥样硬化发生发展的作用

白细胞膜微粒是白细胞在活化、损伤或凋亡时,从其表面释放的富含脂质的膜囊泡,其在内皮细胞损伤、血管功能障碍、氧化应激、炎症反应及细胞之间的信号传导等方面发挥重要作用。近来研究发现,在动脉粥样硬化基础上发生的心脑血管疾病、血栓栓塞性疾病、代谢性疾病和恶性高血压病等疾病中白细胞膜微粒明显增高。文中就白细胞膜微粒对动脉粥样硬化发生发展的作用进行概述。     

PCSK9在肝细胞和脑组织中的不同生物作用

随着人们平均期望寿命的增长,心脑血管疾病成为常见病,而且其病死率越来越高.有效地预防心脑血管疾病的发生、发展成为当今医学研究的热点.动脉粥样硬化侵犯心、脑血管,是导致心脑血管疾病发生的主要原因[1].预防和控制动脉粥样硬化成为降低心脑血管疾病发生、发展的主要治疗措施.动脉粥样硬化属于多病因疾病,主要危险因素有高血压病、糖尿病、年龄、性别、吸烟等,脂质异常是最重要的危险因素之一[1].降低血清低密度脂蛋白胆固醇（low density lipoprotein-cholesterol,LDL C）浓度可以有效地预防冠心病、脑梗死的发生和再发生.     

血凝集素样氧化型低密度脂蛋白受体1与动脉粥样硬化性疾病的研究进展

正随着人口老龄化的不断加速,心脑血管疾病的发病率、致残率以及死亡率也在逐年升高。颅内血管动脉粥样硬化形成是心脑血管疾病的重要病理基础,脂质代谢紊乱是动脉粥样硬化形成的直接原因,其中氧化型低密度脂蛋白(oxidized low-density lipoprotein,ox-LDL)是重要的危险因子,血     

动脉粥样硬化及支架置入后炎症因子的变化与干预治疗★

动脉粥样硬化为一多因素疾病，慢性炎症介导其发生、发展的全过程。炎症过程的一些炎症因子，如C-反应蛋白，白细胞介素6，细胞黏附分子，肿瘤坏死因子α等，不但参与动脉粥样硬化相关疾病的发病过程，而且还可预示心血管事件发生的危险。炎症因子的水平对急性冠状动脉综合征等动脉粥样硬化性疾病的诊断、治疗和预后判断具有重要的价值。近年来的研究发现，在心脏支架置入后也存在着明显的炎症反应，这种炎症反应在内膜的重塑过程中、尤其是支架内再狭窄中起很重要的作用。因此，探讨炎症过程中的分子机制及其病理变化，研究药物对炎症反应的防治作用，将成为预防和治疗动脉粥样硬化及其并发症的新靶点。     

脂蛋白相关磷脂酶A_2在缺血性脑卒中中的临床应用

正脂蛋白相关磷脂酶A_2是一种血管特异性炎性因子,与动脉粥样硬化的发生发展密切相关,是当前心脑血管疾病研究的热点。本研究回顾国内外脂蛋白相关磷脂酶A_2在缺血性脑卒中方面的相关研究,探讨其对缺血性脑卒中的发病风险、病情严重程度及预后的预测价值,以指导脂蛋白相关磷脂酶A_2的临床应用。动脉粥样硬化是缺血性脑卒中最主要的病理生理机制,关于缺血性脑卒中危险因素的研究围绕动脉粥样硬化的发生发展过程展开。血管炎症是动脉粥样硬化的发病机制和     

Treatment Considerations in Anticonvulsant Monotherapy

Summary: The long-standing practice of polypharmacy in treating epilepsy is giving way to use of monotherapy. Monotherapy can improve seizure control as well as reduce the risk of serious idiosyncratic reactions, dose-related side effects, and complex drug interactions. Monotherapy also offers improved compliance and cost-effectiveness. The basis of monotherapy is accurate diagnosis and assessment of the patient's seizure type(s), followed by selection of a single appropriate anticonvulsant drug. Many patients currently treated with multiple anticonvulsants can be successfully converted to monotherapy with a carefully monitored program in which troublesome and redundant drugs are gradually withdrawn from the therapeutic regimen.     

Dextromethorphan: Cellular Effects Reducing Neuronal Hyperactivity

Summary: Dextromethorphan is a dextrorotary morphinan without affinity for opioid receptors, commonly used as an antitussive medication. During the past 5 years, interest in the compound and its demethylated derivative, dextrorphan, has been revived because additional neuroprotective and an-tiepileptic properties were found in in vitro studies, animal experiments, and a few clinical cases. Both morphinans are able to inhibit N -methyl-D-aspartate (NMDA) receptor channels and voltage-operated calcium and sodium channels with different potencies. The inhibition of the NMDA receptor is believed to be the predominant mechanism of action responsible for the anticonvulsant and neuroprotective properties of the compounds.     

Pediatric Epilepsy Surgery

Summary: The use of implantable arrays of epidural electrodes has made it possible to carry out extraoperative electrocorticography (ECoG) and functional localization in the awake child. This has permitted cortical excisions that are determined by criteria similar to those obtained during surgical procedures performed under local anesthesia in adults. In addition, the method also permits simultaneous ECoG and video monitoring during the child's symptomatic seizures, providing additional important localizing information that is impractical to obtain in operations under local anesthesia. We report our experience with 75 children, ages 5 months to 15 years, whom we have managed with epidural electrode arrays. The method of extraoperative ECoG is described and illustrative cases are presented to demonstrate its feasibility and utility in children. In addition, we call attention to gliomas as a common cause of chronic focal seizures in children. Of 49 children undergoing resection and followed for from 1 to 14 years (mean of 5.8 years), 32 (65%) are either seizure free or have had a significant reduction in seizure frequency that has unambiguously improved their quality of life. The results are analyzed further by relating the surgical outcome to each of the pathologic entities that caused the seizures. This analysis reveals the variety of neurological conditions that commonly cause intractable focal seizure disorder in children and distinguishes those pathologic entities in which the seizure disorder is apt to respond to surgical intervention from those that will not.     

Un nouveau cadre conceptuel de travail pour une psychiatrie revisitée ? Introduction à deux articles de E. Kandel

In two articles which appeared in the American Journal of Psychiatry and that were subsequently translated for Évolution Psychiatrique, E. Kandel examines the bases for a reinterpreted psychiatry that is prepared to confront the major challenge of the 3rd millenium: that of insight into the mind and brain. This requires a major reorganization of the discipline, which involves a reinvestment of the scientific approach and a critical  assessment of the data provided by psychoanalytical psychiatry and cognitive neurosciences. Seven concepts have therefore been proposed for interactive re-examination: consciousness, the unconscious, memory, emotion, development, desire, impulse. The dynamic relations existing between genetics and the environment allow one to see how evolutions are possible from actions at different levels, both psychotherapeutic and pharmacological. Imaging and other techniques provide additional objective information to the process of human interaction which remains the basis of psychiatry. A common framework for psychiatry and the neurosciences, a reconsideration and renewal of the psychoanalytical approach are both possible and necessary.     

Opioids and the developing organism: A comprehensive bibliography, 1984–1988

A comprehensive bibliography of the literature concerned with opioids and the developing organism for 1984-1988 is presented. Utilized with companion papers (Neurosci. Biobehav. Rev. 6:439-479; 1982; 8:387-403; 1984), these articles cover the clinical and laboratory references beginning in 1875. For the years 1984, 1985, 1986, 1987, and 1988, a total of 877 citations were recorded. A series of indexes accompanies the citations in order to make the literature more accessible. These indexes are divided into clinical and laboratory topics, and subdivided into such topics as the type of opioid explored and the general area of biological interest (e.g., physiology).     

La biologie et le futur de la psychanalyse : un nouveau cadre conceptuel de travail pour une psychiatrie revisitée

The American Journal of Psychiatry has received a number of letters in response to my earlier “Framework” article (1). Some of these are reprinted elsewhere in this issue, and I have answered them briefly there. However, one issue raised by some letters deserves a more detailed answer, and that relates to whether biology is at all relevant to psychoanalysis. To my mind, this issue is so central to the future of psychoanalysis that it cannot be addressed with a brief comment. I therefore have written this article in an attempt to outline the importance of biology for the future of psychoanalysis.     

Classification of methods in transcranial Electrical Stimulation (tES) and evolving strategy from historical approaches to contemporary innovations

Transcranial Electrical Stimulation (tES) encompasses all methods of non-invasive current application to the brain used in research and clinical practice. We present the first comprehensive and technical review, explaining the evolution of tES in both terminology and dosage over the past 100 years of research to present day. Current transcranial Pulsed Current Stimulation (tPCS) approaches such as Cranial Electrotherapy Stimulation (CES) descended from Electrosleep (ES) through Cranial Electro-stimulation Therapy (CET), Transcerebral Electrotherapy (TCET), and NeuroElectric Therapy (NET) while others like Transcutaneous Cranial Electrical Stimulation (TCES) descended from Electroanesthesia (EA) through Limoge, and Interferential Stimulation. Prior to a contemporary resurgence in interest, variations of transcranial Direct Current Stimulation were explored intermittently, including Polarizing current, Galvanic Vestibular Stimulation (GVS), and Transcranial Micropolarization. The development of these approaches alongside Electroconvulsive Therapy (ECT) and pharmacological developments are considered. Both the roots and unique features of contemporary approaches such as transcranial Alternating Current Stimulation (tACS) and transcranial Random Noise Stimulation (tRNS) are discussed. Trends and incremental developments in electrode montage and waveform spanning decades are presented leading to the present day. Commercial devices, seminal conferences, and regulatory decisions are noted. We conclude with six rules on how increasing medical and technological sophistication may now be leveraged for broader success and adoption of tES.     

Facteurs de risque environnementaux à la schizophrénie

Schizophrenia is currently a major concern, its prevalence being estimated at around 1% and its social consequences being severe. The elucidation of the pathophysiology of the disease is difficult due to the great variability of clinical expressions, the instability of the clinical symptoms during the evolution and the absence of reliable biological markers. The existence of a familial aggregation in schizophrenia is well known, the risk of presenting the disease for first-degree relatives of patients being 5 to 10 times higher than the risk observed in the general population. The genetic component was further confirmed by twin and adoption studies. Although the concordance for the disease is higher (40 to 70%) among monozygotic twins as compared with dizygotic twins (15%) it does not reach 100%, which implies that environmental factors modulate the effects of the genotype. However, the role of these factors and especially their interaction with genetic factors remain unclear but the implications of some specific environmental factors are well documented by recent research data. The current literature on sex differences in schizophrenia is consistent. Several studies have suggested that male and female patients may differ in age at the onset and expression of clinical symptoms. Complications during pregnancy or birth-giving may increase the risk of developing schizophrenia later in life. The major complications are oxygen deprivation during pregnancy, bleeding, maternal malnutrition or infection (exposure to influenza, for example). A low birth weight is associated with an increased risk of schizophrenia. Psychoses are more common among people living in an urban environment and among those born during winter months. Schizophrenia is probably more prevalent in people who are living promiscuously, are subject to toxic abuse, poor nutrition and stress but here more precise data are needed. Moreover, immigrants have a higher risk of developing psychotic disorders. In addition, head traumas are associated with an increased risk of schizophrenia. Though they are contentious, some studies suggest that substance abuse (cannabis use in European countries) is related to the development of schizophrenia, especially in people with genetic vulnerability. Moreover, substance misuse may worsen the symptoms. If the environment is sufficiently stressful, people with a high genetic vulnerability will develop some degree of mental illness, including schizophrenia. Conversely, a less stressful or a protective environment may decrease the risk of its onset in persons with a predisposition to schizophrenia.