Who Furls the Umbrella on Rainy Days? The Role of Bank Ownership Type and Bank Size in SME Lending
In: Emerging markets, finance and trade: EMFT, Band 48, Heft sup2, S. 184-199
ISSN: 1558-0938
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In: Emerging markets, finance and trade: EMFT, Band 48, Heft sup2, S. 184-199
ISSN: 1558-0938
In: CEJ-D-22-00149
SSRN
In: PNAS nexus, Band 1, Heft 2
ISSN: 2752-6542
Abstract
Climate change is adversely impacting the burden of diarrheal diseases. Despite significant reduction in global prevalence, diarrheal disease remains a leading cause of morbidity and mortality among young children in low- and middle-income countries. Previous studies have shown that diarrheal disease is associated with meteorological conditions but the role of large-scale climate phenomena such as El Niño-Southern Oscillation (ENSO) and monsoon anomaly is less understood. We obtained 13 years (2002–2014) of diarrheal disease data from Nepal and investigated how the disease rate is associated with phases of ENSO (El Niño, La Niña, vs. ENSO neutral) monsoon rainfall anomaly (below normal, above normal, vs. normal), and changes in timing of monsoon onset, and withdrawal (early, late, vs. normal). Monsoon season was associated with a 21% increase in diarrheal disease rates (Incident Rate Ratios [IRR]: 1.21; 95% CI: 1.16–1.27). El Niño was associated with an 8% reduction in risk while the La Niña was associated with a 32% increase in under-5 diarrheal disease rates. Likewise, higher-than-normal monsoon rainfall was associated with increased rates of diarrheal disease, with considerably higher rates observed in the mountain region (IRR 1.51, 95% CI: 1.19–1.92). Our findings suggest that under-5 diarrheal disease burden in Nepal is significantly influenced by ENSO and changes in seasonal monsoon dynamics. Since both ENSO phases and monsoon can be predicted with considerably longer lead time compared to weather, our findings will pave the way for the development of more effective early warning systems for climate sensitive infectious diseases.
Tau is implicated in more than 20 neurodegenerative diseases, including Alzheimer's disease. Under pathological conditions, Tau dissociates from axonal microtubules and missorts to pre- and postsynaptic terminals. Patients suffer from early synaptic dysfunction prior to Tau aggregate formation, but the underlying mechanism is unclear. Here we show that pathogenic Tau binds to synaptic vesicles via its N-terminal domain and interferes with presynaptic functions, including synaptic vesicle mobility and release rate, lowering neurotransmission in fly and rat neurons. Pathological Tau mutants lacking the vesicle binding domain still localize to the presynaptic compartment but do not impair synaptic function in fly neurons. Moreover, an exogenously applied membrane-permeable peptide that competes for Tau-vesicle binding suppresses Tau-induced synaptic toxicity in rat neurons. Our work uncovers a presynaptic role of Tau that may be part of the early pathology in various Tauopathies and could be exploited therapeutically. ; We thank Colin Smith and Matthew Frosch for access to human tissue. We thank lab members of the Verstreken laboratory for helpful discussions, and Kristel Vennekens and An Snellinx for technical support. Support was provided by an ERC Starting Grant (260678), ERC Consolidator grant (646671), the Instituut voor Wetenschap en Technologie (IWT O&O grant), the Interuniversity Attraction Pole program by BELSPO, the research fund KU Leuven, a Methusalem grant of the Flemish government and VIB, Leuvens Universiteitsfonds (LUF) Opening the Future grant, and a Belgian-American Educational Foundation fellowship to J.M. T.S.-J., A.H. and R.J.J. receive funding from Alzheimer's Research UK, an anonymous foundation, and a Welcome Trust Institutional strategic support grant.
BASE
In: Air quality, atmosphere and health: an international journal, Band 17, Heft 7, S. 1535-1545
ISSN: 1873-9326