Credit Booms and Busts in the Caribbean

Since 1970, private sector credit has grown quite rapidly in the Caribbean. More recently, between 2004 and 2006, total real credit in the Caribbean has risen by a cumulative 55.7 percent, or approximately 19 percent per annum. In some countries, the rate of expansion has even been stronger, which is of concern given the likely negative macroeconomic consequences of credit booms. This paper attempts to identify the factors that have led to credit booms and conversely busts in the Caribbean, employing annual data for 13 Caribbean countries covering the period 1970 to 2006 in the analysis. This study employs a panel count data regression approach. Three key groups of variables are considered: (1) macroeconomic developments; (2) macroeconomic policy, and (3) external shocks. The reported results suggest that macroeconomic developments were the main determinants of credit booms in the Caribbean, with low inflation, high growth in GDP per capita, investment booms as well as less developed financial systems leading to the emergence of credit booms and conversely for busts.Credit Booms, Credit Busts, Caribbean, Count Data Model

Climate Change and Tourism Features in the Caribbean

The tourist industry is widely recognised as the key engine of growth in the Caribbean, representing a significant source of foreign exchange earnings and employment. The present study provides an assessment of how climate change could likely impact on regional tourism features. The analysis is undertaken by comparing historical tourism climatic indices to those obtained under the various climate change scenarios. The results suggest that the biggest losers, in terms of deteriorations in their climatic features, are likely to be the Caribbean, Central America and South America.Tourism climate index; Climate Change; Caribbean

Adenosine receptor signaling: a key to opening the blood–brain door

International audienceAbstractThe aim of this review is to outline evidence that adenosine receptor (AR) activation can modulate blood–brain barrier (BBB) permeability and the implications for disease states and drug delivery. Barriers of the central nervous system (CNS) constitute a protective and regulatory interface between the CNS and the rest of the organism. Such barriers allow for the maintenance of the homeostasis of the CNS milieu. Among them, the BBB is a highly efficient permeability barrier that separates the brain micro-environment from the circulating blood. It is made up of tight junction-connected endothelial cells with specialized transporters to selectively control the passage of nutrients required for neural homeostasis and function, while preventing the entry of neurotoxic factors. The identification of cellular and molecular mechanisms involved in the development and function of CNS barriers is required for a better understanding of CNS homeostasis in both physiological and pathological settings. It has long been recognized that the endogenous purine nucleoside adenosine is a potent modulator of a large number of neurological functions. More recently, experimental studies conducted with human/mouse brain primary endothelial cells as well as with mouse models, indicate that adenosine markedly regulates BBB permeability. Extracellular adenosine, which is efficiently generated through the catabolism of ATP via the CD39/CD73 ecto-nucleotidase axis, promotes BBB permeability by signaling through A1 and A2A ARs expressed on BBB cells. In line with this hypothesis, induction of AR signaling by selective agonists efficiently augments BBB permeability in a transient manner and promotes the entry of macromolecules into the CNS. Conversely, antagonism of AR signaling blocks the entry of inflammatory cells and soluble factors into the brain. Thus, AR modulation of the BBB appears as a system susceptible to tighten as well as to permeabilize the BBB. Collectively, these findings point to AR manipulation as a pertinent avenue of research for novel strategies aiming at efficiently delivering therapeutic drugs/cells into the CNS, or at restricting the entry of inflammatory immune cells into the brain in some diseases such as multiple sclerosis

An Outbreak of Pseudomonas aeruginosa Pneumonia and Bloodstream Infection Associated With Intermittent Otitis Externa in a Healthcare Worker

Arstract Objectives: To investigate an outbreak of Pseudomonas aeruginosa pneumonia and bloodstream infection among four neonates, determine risk factors for infection, and implement preventive strategies. Design: Retrospective case finding; prospective surveillance cultures of patients, personnel, and environmental sites; molecular typing by pulsed-field gel electrophoresis; and a matched case-control study. Patients and Setting: Neonates in the level-III neonatal intensive care unit of a tertiary-care pediatric institution. Interventions: Cohorting of patients with positive results for P. aeruginosa, work restrictions for staff with positive results, implementation of an alcohol-based hand product, review of infection control policies and procedures, and closure of the unit until completion of the investigation. Results: Seven (4%) of 190 environmental cultures and 5 (3%) of 178 cultures of individual healthcare workers' hands grew P. aeruginosa. All four outbreak isolates and one previous bloodstream isolate were genotypically identical, as were the P. aeruginosa isolates from the hands and external auditory canal of a healthcare worker with intermittent otitis externa. Four of 5 case-patients versus 5 of 15 matched control-patients had been cared for by this healthcare worker (P = .05). The healthcare worker was treated and no further cases occurred. Conclusions: These findings suggest that a healthcare worker with intermittent otitis externa may have caused this cluster of fatal P. aeruginosa infections, adding the external ear to the list of colonized body sites that may serve as a source of potentially pathogenic organism

Extracellular adenosine signaling induces CX3CL1 expression in the brain to promote experimental autoimmune encephalomyelitis

BACKGROUND: Multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE) are debilitating neuroinflammatory diseases mediated by lymphocyte entry into the central nervous system (CNS). While it is not known what triggers lymphocyte entry into the CNS during neuroinflammation, blockade of lymphocyte migration has been shown to be effective in controlling neuroinflammatory diseases. Since we have previously shown that extracellular adenosine is a key mediator of lymphocyte migration into the CNS during EAE progression, we wanted to determine which factors are regulated by adenosine to modulate EAE development. METHODS: We performed a genetic analysis of wild type and CD73−/− (that are unable to produce extracellular adenosine and are protected from EAE development) to identify factors that are both important for EAE development and controlled by extracellular adenosine signaling. RESULTS: We show that extracellular adenosine triggered lymphocyte migration into the CNS by inducing the expression of the specialized chemokine/adhesion molecule CX3CL1 at the choroid plexus. In wild type mice, CX3CL1 is upregulated in the brain on Day 10 post EAE induction, which corresponds with initial CNS lymphocyte infiltration and the acute stage of EAE. Conversely, mice that cannot synthesize extracellular adenosine (CD73−/− mice) do not upregulate CX3CL1 in the brain following EAE induction and are protected from EAE development and its associated lymphocyte infiltration. Additionally, blockade of the A2A adenosine receptor following EAE induction prevents disease development and the induction of brain CX3CL1 expression. The CX3CL1 induced during EAE is found on the choroid plexus, which is the barrier between the blood and cerebral spinal fluid in the brain and is a prime entry point into the CNS for immune cells. Furthermore, CX3CL1 expression can be induced in the brains of mice and in choroid plexus cell line following A2A adenosine receptor agonist administration. Most importantly, we show that CX3CL1 blockade protects against EAE development and inhibits lymphocyte entry into the CNS. CONCLUSIONS: We conclude that extracellular adenosine is an endogenous modulator of neuroinflammation during EAE that induces CX3CL1 at the choroid plexus to trigger lymphocyte entry into the brain

CD73 Is Critical for the Resolution of Murine Colonic Inflammation

CD73 is a glycosyl-phosphatidylinositol-(GPI-) linked membrane protein that catalyzes the extracellular dephosphorylation of adenosine monophosphate (AMP) to adenosine. Adenosine is a negative regulator of inflammation and prevents excessive cellular damage. We investigated the role of extracellular adenosine in the intestinal mucosa during the development of Dextran-Sulfate-Sodium-(DSS-)salt-induced colitis in mice that lack CD73 (CD73−/−) and are unable to synthesize extracellular adenosine. We have found that, compared to wild-type (WT) mice, CD73−/− mice are highly susceptible to DSS-induced colitis. CD73−/− mice exhibit pronounced weight loss, slower weight recovery, an increase in gut permeability, a decrease in expression of tight junctional adhesion molecules, as well as unresolved inflammation following the removal of DSS. Moreover, colonic epithelia in CD73−/− mice exhibited increased TLR9 expression, high levels of IL-1β and TNF-α, and constitutive activation of NF-κB. We conclude that CD73 expression in the colon is critical for regulating the magnitude and the resolution of colonic immune responses.National Institutes of Health (U.S.) (grant A1072434-A2)National Institutes of Health (U.S.) (grant R01NS063011