Gap junctions play essential roles in the normal function of the heart and arteries, mediating the spread of the electrical impulse that stimulates synchronized contraction of the cardiac chambers, and contributing to co-ordination of function between cells of the arterial wall. Altered gap junctional coupling is implicated in the genesis of arrhythmia, a major cause of death in heart disease. Two abnormalities in myocardial gap junctions distribution at the border zone of infarcts and reduced levels of connexin43 (Cx43; alpha 1)--may lead to heterogeneous wavefront propagation and lowered conduction velocity, key factors that precipitate arrhythmia. In the major arteries, endothelial cells express Cx40 (alpha 5) and Cx37 (alpha 4) and, in some instances, also Cx43, whereas underlying medial smooth muscle cells express only Cx43. Increased Cx43 expression between medial smooth muscle cells is intimately linked to phenotypic transformation to the synthetic state in both early human coronary phenotypic transformation to the synthetic state in both early human coronary atherosclerosis, and in the response of the arterial wall to injury. The accumulating evidence suggests that gap junctions in both their guises--as pathways for cell-to-cell signalling in the vessel wall and as pathways for impulse conduction in the heart--may have key roles in the initial pathogenesis and eventual clinical manifestation of human cardiovascular disease.
This chapter contains section titled: Introduction The reason for protein sub-units The Coding Ratio Experimental Evidence The arrangement of protein sub-units Other Viruses References Discussion
While there has been a great deal of interest in the role of brain-derived neurotrophic factor (BDNF) in mood disorders and/or the mode of action of antidepressants, less is known about the role of other growth factors. This paper is focused on a group of growth factors, the fibroblast growth factor (FGF) family and their potential role in mood disorders.
A common single-nucleotide polymorphism in the human brain-derived neurotrophic factor (BDNF) gene, a methionine (Met) substitution for valine (Val) at codon 66 (Val66Met), is associated with alterations in brain anatomy and memory, but its relevance to clinical disorders is unclear. We generated a variant BDNF mouse (BDNF(MET/Met)) that reproduces the phenotypic hallmarks in humans with the variant allele. Variant BDNF(Met) was expressed in brain at normal levels, but its secretion from neurons was defective. In this context, the BDNF(Met/Met) mouse represents a unique model that directly links altered activity-dependent release of BDNF to a defined set of in vivo consequences. Our subsequent analyses of these mice elucidated a phenotype that had not been established in human carriers: increased anxiety. When placed in conflict settings, BDNF(Met/Met) mice display increased anxiety-related behaviours that were not normalized by the antidepressant, fluoxetine. A genetic variant BDNF may thus play a key role in genetic predispositions to anxiety and depressive disorders.
Free Access Cumulative Index to Volumes Book Editor(s):G. E. W. Wolstenholme O.B.E., M.A., B.Ch., G. E. W. Wolstenholme O.B.E., M.A., B.Ch.Search for more papers by this authorMaeve O'Connor B.A., Maeve O'Connor B.A.Search for more papers by this author First published: 01 January 1958 https://doi.org/10.1002/9780470719084.indcumBook Series:Novartis Foundation Symposia AboutPDFPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShareShare a linkShare onFacebookTwitterLinked InRedditWechat Ciba Foundation Symposium - Hormone Production in Endocrine Tumours (Colloquia on Endocrinology), Volume 12 RelatedInformation
The prelims comprise: The Excretion of Sodium: The Excretion of Potassium: The Excretion of Anions: References Discussion
This chapter contains section titled: Brain Development Genetic Regulation of Brain Development Regulation of Genetic Expression Summary and Conclusion Acknowledgement References Discussion References
This chapter contains section titled: Experimental Methods Results The Capacity for Information Transmission Some Speculation about Neural Discriminanda Summary and Conclusions References Discussion
Ciba Foundation Sessions on Central Adrenergic Mechanisms Book Editor(s):G. E. W. Wolstenholme O.B.E., M.A., M.B., M.R.C.P., G. E. W. Wolstenholme O.B.E., M.A., M.B., M.R.C.P.Search for more papers by this authorMaeve O'Connor B.A., Maeve O'Connor B.A.Search for more papers by this author First published: 01 January 1961 https://doi.org/10.1002/9780470719206.part10Book Series:Novartis Foundation Symposia AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Ciba Foundation Symposium ‐ Aetiology of Diabetes Mellitus and its Complications (Colloquia on Endocrinology) RelatedInformation
Chapter 21 Chairman's Closing Remarks Book Editor(s):G. E. W. Wolstenholme O.B.E., M.A., M.B., B.Ch., G. E. W. Wolstenholme O.B.E., M.A., M.B., B.Ch.Search for more papers by this authorMaeve O'Connor B.A., Maeve O'Connor B.A.Search for more papers by this author First published: 01 January 1958 https://doi.org/10.1002/9780470719107.ch21Book Series:Novartis Foundation Symposia AboutPDFPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShareShare a linkShare onFacebookTwitterLinked InRedditWechat Ciba Foundation Symposium - Water and Electrolyte Metabolism in Relation to Age and Sex (Colloquia on Ageing), Volume 4 RelatedInformation
Recent work has begun to identify neural stem and progenitor cells in the embryonic and adult brain, and is unravelling the mechanisms whereby new nerve cells are created and delivered to their correct locations. Radial glial (RG) cells, which are present in the developing mammalian brain, have been proposed to be neural stem cells because they produce multiple cell types. Furthermore, time-lapse imaging demonstrates that RG cells undergo asymmetric self-renewing divisions to produce immature neurons that migrate along their parent radial fibre to reach the developing cerebral cortex. RG cells also produce intermediate progenitor (IP) cells that undergo symmetric division in the subventricular zone of the embryonic cortex to produce pairs of neurons. The symmetric IP divisions increase cell number within the same cortical layer. This two-step process of neurogenesis suggests new mechanisms for the generation of cell diversity and cell number in the developing cortex and supports a model similar to that proposed for the development of the fruit fly CNS. In this model, a temporal sequence of gene expression changes in asymmetrically dividing self-renewed RG cells could lead to the differential inheritance of cell identity genes in cortical cells generated at different cell cycles.
The recovery process after acute brain damage has attracted little interest from either basic or clinical scientists who seem to be most concerned with the acute stage. Much might be learnt about the mechanisms of the nervous system from study of the recovery process. The number of patients with permanent brain damage is growing as the result of the increased survival rate from such common conditions as severe head injury and non-geriatric stroke. Response to this problem has largely come from other disciplines, and in the form of supportive care rather than scientific enquiry. Such an enquiry might seek to answer three outstanding questions. (1) What is the nature of the persisting disability? (2) Can more scientifically based rehabilitation, including physical, mental and social components, either accelerate the rate of recovery or reduce the degree of ultimate disability? (3) Can the ultimate outcome be predicted in the acute stage; and can the amount of further improvement be estimated in the later stages of recovery?
This chapter contains section titled: Signs and Symptoms Pathology of the Adrenal Gland X-Ray Visualization of the Adrenals The Treatment of Gushing' Syndrome References
