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1.
AIDS Care ; 21 Suppl 1: 60-75, 2009.
Article in English | MEDLINE | ID: mdl-22380980

ABSTRACT

Investing in social protection in sub-Saharan Africa has taken on a new urgency as HIV and AIDS interact with other drivers of poverty to simultaneously destabilise livelihoods systems and family and community safety nets. Cash transfer programmes already reach millions of people in South Africa, and in other countries in southern and East Africa plans are underway to reach tens and eventually hundreds of thousands more. Cash transfers worldwide have demonstrated large impacts on the education, health and nutrition of children. While the strongest evidence is from conditional cash transfer evaluations in Latin America and Asia, important results are emerging in the newer African programmes. Cash transfers can be implemented in conjunction with other services involving education, health, nutrition, social welfare and others, including those related to HIV and AIDS. HIV/AIDS-affected families are diverse with respect to household structure, ability to work and access to assets, arguing for a mix of approaches, including food assistance and income-generation programmes. However, cash transfers appear to offer the best strategy for scaling up to a national system of social protection, by reaching families who are the most capacity constrained, in large numbers, relatively quickly. These are important considerations for communities hard-hit by HIV and AIDS, given the extent and nature of deprivation, the long-term risk to human capital and the current political willingness to act.


Subject(s)
Acquired Immunodeficiency Syndrome/epidemiology , Education , HIV Seropositivity/epidemiology , Health Services Accessibility , Medical Assistance , Nutritional Status , Acquired Immunodeficiency Syndrome/economics , Adolescent , Adult , Africa South of the Sahara/epidemiology , Child , Child, Preschool , Education/economics , Female , Financing, Government , HIV Seropositivity/economics , Health Services Accessibility/economics , Health Services Accessibility/statistics & numerical data , Humans , Infant , Infant, Newborn , Male , Medical Assistance/economics , Middle Aged , Poverty Areas , Public Policy , Social Welfare , Young Adult
2.
Gastroenterology ; 115(4): 988-96, 1998 Oct.
Article in English | MEDLINE | ID: mdl-9753502

ABSTRACT

BACKGROUND & AIMS: The presence of cholecystokinin (CCK)-B/gastrin receptors in the pancreas of higher mammals including humans has been shown, but their physiological function in the normal pancreas is unknown. The aim of this study was to investigate whether they couple to the secretory machinery of normal acinar cells. METHODS: A transgenic mouse strain expressing the human CCK-B/gastrin receptor in the exocrine pancreas was created. The transgenic construction used the promoter region of the elastase I gene and the human CCK-B/gastrin receptor gene. Analysis of ElasCCKB mice included polymerase chain reaction and receptor autoradiography. Molecular and binding features of the CCK-B/gastrin receptor were determined by Western blot and radioligand binding studies. Amylase secretion and inositol phosphate production assays were used in functional characterization. RESULTS: The CCK-B/gastrin receptor was expressed in the exocrine pancreas and had typical molecular and binding features. CCK and sulfated gastrin stimulated enzyme secretion with identical potencies and efficacies. They activated phospholipase C, but CCK was 60-fold less potent than sulfated gastrin. CONCLUSIONS: The data show that the CCK-B/gastrin receptor mediates exocytosis in acinar cells and can differentially couple to phospholipase C depending on the agonist. The ElasCCKB mice provide a useful model to study phospholipase C-dependent and -independent intracellular transduction pathways leading to pancreatic exocrine secretion.


Subject(s)
Pancreas/metabolism , Receptors, Cholecystokinin/physiology , Amylases/metabolism , Animals , Cell Membrane/metabolism , Humans , Mice , Mice, Transgenic/genetics , Pancreatic Elastase/genetics , Rats , Receptor, Cholecystokinin B , Receptors, Cholecystokinin/genetics , Receptors, Cholecystokinin/metabolism , Type C Phospholipases/metabolism
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