Road map towards the implementation of the United Nations Millennium Declaration: report of the Secretary-General

Includes bibliography

Fondo especial de las Naciones Unidas plan de operaciones tercer texto propuesto: proyecto regional: Costa Rica, El Salvador, Gutemela, Hoduras, Nicaragua y Panamá = United Nations Special Fund plan of operation third draft: regional: Costa Rica, El Salvador, Guatemala, Honduras, Nicaragua and Panamá

Designación del proyecto: ampliación y mejoramiento de los servicios hidrometeorologicos en el Istmo Centroamericano

A regional approach to the consultations held by the Secretary-General of the United Nations on part XI of the United Nations Convention on the Law of the Sea

Includes bibliography

Summary of resolutions recently adopted by CDCC and resolutions of ECLAC and other organs of the United Nations which might be of special interest to member countries of ECLAC/CDCC

This paper brings to the attention of member countries of the Caribbean Development and Cooperation Committee (CDCC) resolutions adopted by past sessions of the Committee, since 2000, and the process of their implementation. Resolutions 55 to 66 for the period 2000- 2006 have been extracted from the reports of the eighteenth to twenty first sessions of the CDCC Also included for the information of member countries are selected resolutions recently adopted by the Economic Commission for Latin America and the Caribbean (ECLAC) and other organs of the United Nations. These resolutions greatly influence the preparation of the programme of work and are expected guide the day-to-day functioning of the secretariat. It is a great source of information for delegations, given the perceived special relevance of the resolutions to the membership of the CDCC. The resolutions listed in this document are pertinent to all subprogrammes of ECLAC and indeed the CDCC subprogramme 12 of ECLAC. However, the content of these resolutions either marked no real advance on the outcomes of the corresponding conferences that were held within recent times or were cast in a globally relevant context that did not address specific concerns of Caribbean countries to any significant extent.

Increased expression of the auxiliary beta2-subunit of ventricular L-type Ca2+ channels leads to single-channel activity characteristic of heart failure

BACKGROUND: Increased activity of single ventricular L-type Ca(2+)-channels (L-VDCC) is a hallmark in human heart failure. Recent findings suggest differential modulation by several auxiliary beta-subunits as a possible explanation. METHODS AND RESULTS: By molecular and functional analyses of human and murine ventricles, we find that enhanced L-VDCC activity is accompanied by altered expression pattern of auxiliary L-VDCC beta-subunit gene products. In HEK293-cells we show differential modulation of single L-VDCC activity by coexpression of several human cardiac beta-subunits: Unlike beta(1) or beta(3) isoforms, beta(2a) and beta(2b) induce a high-activity channel behavior typical of failing myocytes. In accordance, beta(2)-subunit mRNA and protein are up-regulated in failing human myocardium. In a model of heart failure we find that mice overexpressing the human cardiac Ca(V)1.2 also reveal increased single-channel activity and sarcolemmal beta(2) expression when entering into the maladaptive stage of heart failure. Interestingly, these animals, when still young and non-failing ("Adaptive Phase"), reveal the opposite phenotype, viz: reduced single-channel activity accompanied by lowered beta(2) expression. Additional evidence for the cause-effect relationship between beta(2)-subunit expression and single L-VDCC activity is provided by newly engineered, double-transgenic mice bearing both constitutive Ca(V)1.2 and inducible beta(2) cardiac overexpression. Here in non-failing hearts induction of beta(2)-subunit overexpression mimicked the increase of single L-VDCC activity observed in murine and human chronic heart failure. CONCLUSIONS: Our study presents evidence of the pathobiochemical relevance of beta(2)-subunits for the electrophysiological phenotype of cardiac L-VDCC and thus provides an explanation for the single L-VDCC gating observed in human and murine heart failure.