Disaster Risks Research and Assessment to Promote Risk Reduction and Management

Natural hazard events lead to disasters when the events interact with exposed and vulnerable physical and social systems. Despite significant progress in scientific understanding of physical phenomena leading to natural hazards as well as of vulnerability and exposure, disaster losses due to natural events do not show a tendency to decrease. This tendency is associated with many factors including increase in populations and assets at risk as well as in frequency and/or magnitude of natural events, especially those related to hydro-meteorological and climatic hazards. But essentially disaster losses increase because some of the elements of the multidimensional dynamic disaster risk system are not accounted for risk assessments. A comprehensive integrated system analysis and periodic assessment of disaster risks at any scale, from local to global, based on knowledge and data/information accumulated so far, are essential scientific tools that can assist in recognition and reduction of disaster risks. This paper reviews and synthesizes the knowledge of natural hazards, vulnerabilities, and disaster risks and aims to highlight potential contributions of science to disaster risk reduction (DRR) in order to provide policy-makers with the knowledge necessary to assist disaster risk mitigation and disaster risk management (DRM)

Global risks: Pool knowledge to stem losses from disasters

Public awareness, rigorous risk research and aligned targets will help policy-makers to increase resilience against natural hazards, say Susan L. Cutter and colleagues

Functional consequences of perinatal exposure to3,4-methylenedioxymethamphetamine in rat brain

1. In this study we have examined methylenedioxymethamphetamine (MDMA)-induced toxicity in perinatal rat brain, related this to normal development of serotonin transporter sites (SERT), and determined whether early exposure to MDMA subsequently alters cerebral function in adults. 2. Perinatal development of SERT was visualized and quantified using [(3)H]-paroxetine binding autoradiography in embryonic and neonatal rat brain from embryonic day 15 (E15) to postnatal day 30 (P30). Cerebral glucose utilization (lCMR(glu)) was measured by 2-deoxyglucose autoradiography in adult rats. 3. [(3)H]-Paroxetine binding was observed in forebrain from E18. From birth (P0), binding was organized into neocortical columns (75% higher at P10 than in adult) which declined toward adult levels between P20 and P25. 4. MDMA treatment (20 mg kg(−1) s.c. twice daily for four days) commencing at developmental stages from E15 (treatment given to dams) to P20, had no effect upon [(3)H]-paroxetine binding measured at P40. Treatments started on P25 or later resulted in significant decreases in [(3)H]-paroxetine binding (⩾46%). This was coincident with the development of adult patterns of binding in forebrain. 5. Despite the lack of MDMA-induced neurotoxicity, rats treated in utero (E15) showed increased lCMR(glu) in locus coeruleus (+37%), and in areas receiving ascending noradrenergic innervation, such as anterior thalamus (+44%) and septal nucleus (+24%). 6. These studies confirm that the susceptibility of serotonergic terminals to the neurotoxic properties of MDMA is absent in the immediate perinatal period, but also suggests that in utero MDMA exposure produces significant long-term effects on cerebral function by a mechanism as yet unknown