Ending Extreme Poverty and Sharing Prosperity: Progress and Policies

To guide its work toward a "world free of poverty," the World Bank Group in 2013 established two clear goals: end extreme poverty by 2030 and promote shared prosperity. Along with the requirement to pursue these goals sustainably -- economically, environmentally, and socially -- the two goals are comprehensive in nature. They are fully aligned to support the Sustainable Development Goals (SDGs) set by the United Nations to replace the Millennium Development Goals (MDGs). To evaluate progress, the two goals are measured by two overall indicators: a reduction in the global headcount ratio of extreme poverty (the population share of those whose income is below the international poverty line) to 3 percent by 2030, and the promotion of income growth in the bottom 40 (B40) percent of the population in each country.This Policy Research Note updates the assessment of progress toward these two goals in a sustainable manner. The poverty goal is examined through three lenses: the evolution of income poverty based on the new international poverty line that has been re-estimated at $1.90 a day; an assessment of person-equivalent income poverty, a new intuitive indicator that combines the incidence with the depth of poverty; and a review of the breadth of poverty, recognizing that income shortfalls often coexist with multiple non-income deprivations. The shared prosperity goal is examined on the basis of the latest comparison of (comparable) household data on B40 income growth. As part of its analysis of the two goals, this note also comments on the status of defining and monitoring sustainability in its economic, environmental and social aspects

Exercise-Induced Cognitive Plasticity, Implications for Mild Cognitive Impairment and Alzheimer’s Disease

Lifestyle factors such as intellectual stimulation, cognitive and social engagement, nutrition, and various types of exercise appear to reduce the risk for common age-associated disorders such as Alzheimer’s disease (AD) and vascular dementia. In fact, many studies have suggested that promoting physical activity can have a protective effect against cognitive deterioration later in life. Slowing or a deterioration of walking speed is associated with a poor performance in tests assessing psychomotor speed and verbal fluency in elderly individuals. Fitness training influences a wide range of cognitive processes, and the largest positive impact observed is for executive (a.k.a. frontal lobe) functions. Studies show that exercise improves additional cognitive functions such as tasks mediated by the hippocampus, and result in major changes in plasticity in the hippocampus. Interestingly, this exercise-induced plasticity is also pronounced in APOE ε4 carriers who express a risk factor for late-onset AD that may modulate the effect of treatments. Based on AD staging by Braak and Braak (1991) and Braak et al. (1993) we propose that the effects of exercise occur in two temporo-spatial continua of events. The “inward” continuum from isocortex (neocortex) to entorhinal cortex/hippocampus for amyloidosis and a reciprocal “outward” continuum for neurofibrillary alterations. The exercise-induced hypertrophy of the hippocampus at the core of these continua is evaluated in terms of potential for prevention to stave off neuronal degeneration. Exercise-induced production of growth factors such as the brain-derived neurotrophic factor (BDNF) has been shown to enhance neurogenesis and to play a key role in positive cognitive effects. Insulin-like growth factor (IGF-1) may mediate the exercise-induced response to exercise on BDNF, neurogenesis, and cognitive performance. It is also postulated to regulate brain amyloid β (Aβ) levels by increased clearance via the choroid plexus. Growth factors, specifically fibroblast growth factor and IGF-1 receptors and/or their downstream signaling pathways may interact with the Klotho gene which functions as an aging suppressor gene. Neurons may not be the only cells affected by exercise. Glia (astrocytes and microglia), neurovascular units and the Fourth Element may also be affected in a differential fashion by the AD process. Analyses of these factors, as suggested by the multi-dimensional matrix approach, are needed to improve our understanding of this complex multi-factorial process, which is increasingly relevant to conquering the escalating and intersecting world-wide epidemics of dementia, diabetes, and sarcopenia that threaten the global healthcare system. Physical activity and interventions aimed at enhancing and/or mimicking the effects of exercise are likely to play a significant role in mitigating these epidemics, together with the embryonic efforts to develop cognitive rehabilitation for neurodegenerative disorders

Role of physical and mental training in brain network configuration

Continuous remodeling of proteins of excitatory neurons is fine-tuning the scaling and strength of excitatory synapses up or down via regulation of intra-cellular metabolic and regulatory networks of the genome-transcriptome-proteome interface. Alzheimer's disease is a model of energy cost-driven small-world network disorder as the network global efficiency is impaired by the deposition of an informed agent, the amyloid-β, selectively targeting high-degree nodes. In schizophrenia, the interconnectivity and density of rich-club networks are significantly reduced. Training-induced homeostatic synaptogenesis-enhancement produces a reconfiguration of brain networks into greater small-worldness. Creation of synaptic connections in a macro-network, and, at the intra-cellular scale, micro-networks regulate the physiological mechanisms for the preferential attachment of synapses. The strongest molecular relationship of exercise and functional connectivity was identified for brain-derived neurotrophic factor (BDNF). The allele variant, rs7294919, also shows a powerful relationship with the hippocampal volume. How the brain achieves this unique quest of reconfiguration remains a puzzle. What are the underlying mechanisms of synaptogenesis promoting communications brain ↔ muscle and brain ↔ brain in such trainings? What is the respective role of independent mental, physical or combined-mental-physical trainings? Physical practice seems to be playing an instrumental role in the cognitive enhancement (brain ↔ muscle com.). However, mental training, meditation or virtual reality (films, games) require only minimal motor activity and cardio-respiratory stimulation. Therefore, other potential paths (brain ↔ brain com.) molding brain networks are nonetheless essential. Patients with motor neuron disease/injury (e.g. amyotrophic lateral sclerosis, traumatism) also achieve successful cognitive enhancement albeit they may only elicit mental practic

PREFERENTIAL TRADE OF AGRICULTURAL COMMODITIES IN THE CARIBBEAN BASIN

Preferential agricultural trade under the Caribbean Basin Initiative has been beneficial to participating countries, particularly for differentiated goods. Goods that have not performed well were either subject to policy changes, eroding preferences and deteriorating market trends or structural changes that diminished CBI exports.International Relations/Trade,

Report on Comprehensive City Plan for Sarasota, Florida

Sarasota, Florida Report on comprehensive city plan for Sarasota, Florida. John Nolen, City Planner. Philip W. Foster, Associate. Cambridge, Mass. : John Nolen, 1925

Enhanced Thermoelectric Power in Graphene: Violation of the Mott Relation By Inelastic Scattering

We report the enhancement of the thermoelectric power (TEP) in graphene with extremely low disorder. At high temperature we observe that the TEP is substantially larger than the prediction of the Mott relation, approaching to the hydrodynamic limit due to strong inelastic scattering among the charge carriers. However, closer to room temperature the inelastic carrier-optical-phonon scattering becomes more significant and limits the TEP below the hydrodynamic prediction. We support our observation by employing a Boltzmann theory incorporating disorder, electron interactions, and optical phonons.Comment: 5 pages, 4 figure

Combining Information on Multiple Detection Techniques to Estimate the Effect of Patent Foramen Ovale on Susceptibility to Decompression Illness

The assembly and the maintenance of the International Space Station is expected to require hundreds of extravehicular excursions (EVA's) in the next 10 years. During an EVA, in order to allow movement and bending of limbs, spacesuit pressures are reduced to about 4.3 psi. as compared with about 14.7 psi. for normal atmospheric pressure at sea level. However, the exposure of astronauts to reduced pressures in spacesuits, is conducive to fonnation and growth of gas bubbles within venous blood or tissues, which could cause decompression illness (DCI), a pathology best known to occur among deep-sea divers when they return to the surface. To reduce the risk of DCI, astronauts adjust to the reduced pressure in stages for a prolonged time known as a "pre-breathe" period prior to their extravehicular activity. Despite the use of pre-breathe protocols, an increased risk of DCI can arise for about 25% of humans who have a small hole, known as a patent foramen ovale (PFO), between two chambers of the heart. The atrial septum's fossa oval is, an embryological remnant of a flap between the septae primum and secundum allows fetal right atrial blood to pass into the left atrium, and usually closes after birth (Hagen, et al,. 1984). If fusion does not occur, a valve-like opening, the foramen ovale persists between the two atria. It has been suggested that astronauts with PFO's might be at greater risk of stroke or other serious neurological DCI because bubbles from a venous site may traverse a PFO, travel to the aorta and then enter the cerebral circulatory system causing a stroke (Figure 1). Astronauts are not now screened for PFO's, however consideration is being given to doing so. Here, we study three main methods abbreviated here as "ITE", "TCD" and "TEE", for detecting PFO's in living subjects. All involve the introduction of bubbles into a vein, immediately after which a sensory probe attempts to detect the bubbles in systemic circulation. Presence of the injected bubbles in the systemic circulation is indicative of a PFO. More detailed descriptions are given after the explanation of PFO's under Figure I. Even if a true PFO affects the risk of DCI, there remains a question of how effective screening would be if the detection method has errors of omission and/or commission. Of the three methods studied here, TEE is the "gold standard", matching autopsy results with near-perfect sensitivity and specificity (Schneider, et al. , 1996). However TEE is also the most difficult method to implement, requiring an internal esophagal probe, and is therefore not widely used. Currently, the easiest to use and most common PFO detection method is TTE, which uses an external chest probe. This method has a specificity of near 100%, but suffers from a low sensitivity rate (about 30%). More recently, TCD has been developed, which uses ultrasound probes to detect the presence of bubbles in cerebral arteries. Studies indicate that TCD is quite effective, having a sensitivity of about 91% and a specificity of about 93% (Droste, et al., 1999) when applied correctly, however implementation is difficult and requires considerable training