Language processing from the perspective of electrical stimulation mapping

ABSTRACT

Electrical Stimulation (ES) is a neurostimulation technique that is used to localize language functions in the brain of people with intractable epilepsy and/or brain tumors. We reviewed 25 ES articles published between 1984 and 2018 and interpreted them from a cognitive neuropsychological perspective. Our aim was to highlight ES as a tool to further our understanding of cognitive models of language. We focused on associations and dissociations between cognitive functions within the framework of two non-neuroanatomically specified models of language. Also, we discussed parallels between the ES and the stroke literatures and showed how ES data can help us to generate hypotheses regarding how language is processed. A good understanding of cognitive models of language is essential to motivate task selection and to tailor surgical procedures, for example, by avoiding testing the same cognitive functions and understanding which functions may be more or less relevant to be tested during surgery.     

5-HT 102T/C多态性与Tourette综合征的病例对照及核心家系关联分析

目的 研究5－羟色胺受体102T／C多态性是否与Tourette综合征（TS）相关联,方法对157个核心家系样本采用病例－对照关联分析,传递不平衡检验方法,聚合酶链反应及RFLP等技术,根据TS与强迫症（obsessive compulsive disorder,OCD)的同病现象,将TS划分亚组进行与5－羟色胺受体102T／C多态性的关联分析。结果 合并OCD的TS与该位点的基因型102C／C（X2＝8．38,P＝0．004）及等位基因102C／（X2＝4．84,P＝0．028）存在关联,进一步采用传递不平衡分析,发现合并（美国精神疾病诊断和统计手册IV》论断标准的OCD的TS与该位点存在关联或连锁不平衡（X2＝5．12,,P＝0．02）,而在TS总体样本及单纯TS样本中未发现与该位点的关联,结论 5－羟色胺受体102T／C多态性与中国人群合并OCD的TS存在关联,合并OCD的TS可能是TS中相对独立的一个亚型。     

Program for generation of three-dimensional finite element mesh from magnetic resonance imaging scans of human limbs

A PC-AT based program for conversion of magnetic resonance imaging (MRI) scans into coordinate input for finite element mesh generation is presented. The program is written in Borland C + +3.1 and is compatible with every general-use personal computer, permitting the use of MS-DOS 3.0 or higher with a Microsoft mouse. The program is menu driven and does not demand specialised knowledge from the user. The system and memory requirements are minimal -- 640 kB RAM -- and it runs as a stand-alone program. A second program allows the construction of a three-dimensional representation of the limb sub-structure and generation of the FE mesh from the converted cross-sectional scans. The capabilities of the program are demonstrated using cross-sectional scans of the upper arm; the fat, muscle and bone contours were obtained to a very high level of precision (0.4 mm).     

Three novel mutations of the fibrillin-1 gene and ten single nucleotide polymorphisms of the fibrillin-3 gene in Marfan syndrome patients

Marfan syndrome (MFS) is an autosomal dominant disorder of the extracellular matrix. Allelic variations in the gene for fibrillin-1 (FBN1) have been shown to cause MFS. To date, over 550 mutations have been identified in patients with MFS and related connective tissue diseases. However, about a half of MFS cases do not possess mutations in the FBN1 gene. These findings raise the possibility that variants located in other genes cause or modify MFS. To explore this possibility, firstly we analyzed FBN1 allelic variants in 12 Japanese patients with MFS, and secondly we analyzed fibrillin-3 gene (FBN3) in patients without FBN1 mutations using conformation sensitive gel electrophoresis (CSGE) and direct sequencing analysis. We identified three novel FBN1 mutations and ten FBN3 single nucleotide polymorphisms (SNPs). In this report, we could not detect a responsible mutation of the FBN3 gene for MFS. Although the number of the cases in this report is small, at least these results suggest that disease-causing mutations in exon regions of the FBN3 gene are very rare in MFS.Nucleotide sequence data reported are available in the DDBJ/EMBL/GenBank databases under the accession numbers: AB177797, AB177798, AB177799, AB177800, AB177801, AB177802, AB177803     

Tritiated imipramine binding to platelets in manic subjects

We studied 21 patients with bipolar affective disorder and 25 healthy controls in order to determine if tritiated imipramine binding to platelets distinguished the manic from the depressed phase of bipolar disorder. Depressed patients had a significantly lower mean Bmax value (754 +/- 149 fmole/mg protein) than the manic and control groups (1112 +/- 248 and 1237 +/- 201 fmole/mg protein, respectively), which did not differ from each other. These differences could not be attributed to differences in age, sex, menopausal status, the presence of psychotic features or medication history among the subject groups. These findings confirm that decreased imipramine binding to platelets is a state marker for bipolar depression and not a trait marker of bipolar disorder.     

Sustained interleukin-6 signalling leads to the development of lymphoid organ-like structures in the lung

A variety of pathological changes are seen in lymphoproliferative disorders of the lung but the histogenesis of these abnormalities is not yet fully understood. We previously showed that adenovirus vector-mediated transient expression of both the human interleukin-6 (IL-6) and IL-6 receptor (IL-6R) genes, but not the IL-6 gene alone, in the rat lung induced lymphocytic alveolitis. In the present study, we explored the lung pathology of human IL-6 and IL-6R double transgenic mice to elucidate the effects of prolonged IL-6 signalling on the lung. The transgenic animals developed mononuclear cell accumulation in peribronchovascular regions, but little infiltration into alveolar spaces. Immunohistochemical analysis revealed that the cellular accumulations contained not only mixtures of inflammatory cells but also lymphoid tissue-like structures. As the expression of CXCL13/BLC, the indispensable chemokine for lymphoid organogenesis, was recognized in the B cell follicles of the pulmonary lesions, we speculate that this chemokine plays an inductive role in the development of the lymphoid tissue-like structures. These structures were distinguished from bronchus-associated lymphoid tissues (BALTs) by their location and by the lack of lymphoepithelium, which is a characteristic of BALT. These findings imply that IL-6 signalling may play a role in the pathogenesis of lymphoproliferative disorders of the lung.     

大学生的焦虑心理分析

为了解当前大学生的心理健康状况，本研究通过一项对河北某高校2071名在校大学生的SCL-90调查，结果表明。该校的大学生中，心理问题的发生率由高到低依次为焦虑、强迫、人际敏感等。针对焦虑现象比较突出这一特点，运用自编的半开放式量表进行访谈，对焦虑情绪进行分类和产生原因分析，并且希望以此为参考，去探讨对大学生焦虑问题的一些对策。     

湛江市城区7-12岁小学生社交恐惧症流行病学现状调查

目的:了解湛江市儿童社交恐惧症(Social anxiety disorder of childhood,SADC)的患病现况。方法:采取随机、分层、整群抽样的调查方法,使用中文修订版儿童社交焦虑量表(SASC)调查湛江市2409名小学生,对量表分大于2倍均数标准差的儿童进行面谈,依照中国精神障碍分类与诊断标准第三版(CCMD-3)的标准进行诊断。结果:湛江市儿童社交恐惧症患病率为2·74%。男、女生患病率分别为2·6%和2·9%,差异无显著性(χ2=0·11,P=0·744);各年级患病率在1·76%~4·32%之间,差异无显著性(χ2=5·47,P=0·361)。结论:湛江市儿童社交恐惧症患病率较高,应引起老师、家长及有关部门的重视。     

Hidden posttraumatic stress disorder in the mother of a boy with traumatic limb amputation

Posttraumatic stress disorder (PTSD) is usually diagnosed in the primary victim of a psychologically distressing event who demonstrates the criteria symptomatology. Presented here is a case study of PTSD symptoms in a mother whose 4-year-old boy underwent bilateral arm amputation. Discussed is how the mother became the primary PTSD victim and why the particular injury (electrical shock) can be explained as readily giving rise to her problems. Consultants to pediatric and trauma services are reminded that the primary patient's medical care may suffer if disorders such as PTSD are not recognized in those responsible for making treatment decisions for the young victim.     

Linkage analysis between manic-depressive illness and markers on the long arm of chromosome 11

The long arm of chromosome 11 is one of the most interesting regions in the search for major genes involved in the etiology of manic-depressive illness. Several candidate genes have been identified, including the gene encoding the dopamine D2 receptor, the M1 muscarinic receptor, and porfobillinogen deaminase. Furthermore, different families with co-segregation of psychiatric illness and structural chromosome abnormalities involving regions 11q21, 11q22.3, and 11q25 have been reported. Using narrow as well as broad phenotypic models, conservative genetic parameters, models with dominant or recessive modes of inheritance, and various methods to reduce misclassification, the present study did not find evidence for a major gene causing manic-depressive illness on the long arm of chromosome 11. In the broader phenotypic models multi-point analyses excluded at least 11q14 to 11q23.3, approximately 60 cM, even in one large family. Assuming homogeneity close linkage to DRD2 was excluded for all dominant models, and also in the affecteds-only analyses in the large family alone. © 1995 Wiley-Liss, Inc.