Introducing experiences from African pastoralist communities to cope with climate change risks, hazards and extremes: Fostering poverty reduction
AuthorsFilho, Walter Leal; email: email@example.com
Taddese, Habitamu; email: firstname.lastname@example.org
Balehegn, Mulubrhan; email: email@example.com
Nzengya, Daniel; email: firstname.lastname@example.org
Debela, Nega; email: Nega.email@example.com
Abayineh, Amare; email: firstname.lastname@example.org
Mworozi, Edison; email: email@example.com
Osei, Sampson; email: firstname.lastname@example.org
Ayal, Desalegn Y.; email: email@example.com
Nagy, Gustavo J.; email: firstname.lastname@example.org
Yannick, Nsani; email: email@example.com
Kimu, Saizi; email: firstname.lastname@example.org
Balogun, Abdul-Lateef; email: email@example.com
Alemu, Esubalew Abate; email: firstname.lastname@example.org
Li, Chunlan; email: email@example.com
Sidsaph, Henry; email: firstname.lastname@example.org
Wolf, Franziska; email: Franziska.Wolf@haw-hamburg.de
MetadataShow full item record
AbstractAbstract Pastoralist communities all over Africa have been facing a variety of social and economic problems, as well as climate risks and hazards for many years. They have also been suffering from climate change and extremes events, along with a variety of weather and climate threats, which pose many challenges to herders. On the one hand, pastoralist communities have little influence on policy decisions; however, on the other hand, they suffer to a significant extent from such policies, which limit their options for sustainable development and poverty alleviation. Also, the socio-cultural legacy of herders, and their role in food security and provision of ecosystem services, as well as their efforts towards climate change adaptation, are little documented, particularly in Eastern and Southern African countries. There is a perceived need for international studies on the risks and impacts of climate change and extreme events on the sustainability of pastoralist communities in Africa, especially in eastern and southern Africa. Based on the need to address this research gap, this paper describes the climate change risks and challenges that climate threats pose to the sustainability and livelihoods of pastoralist communities in eastern and southern Africa. Also, it discusses the extent to which such problems affect their well-being and income. Additionally, the paper reports on the socioeconomic vulnerability indices at country-level. Also, it identifies specific problems pastoralists face, and a variety of climate adaptation strategies to extreme events through field survey among pastoralist communities in a sample of five countries, namely Ethiopia, Kenya, Malawi, Uganda, and Zimbabwe. The study has shown that the long-term sustainability of the livelihoods of pastoral communities is currently endangered by climate change and the risks and hazards it brings about, which may worsen poverty among this social group. Also, the study suggests that a more systematic and structured approach is needed when assessing the climate vulnerability of individual pastoral communities, since this may help in designing suitable disaster risk reduction strategies. Moreover, the paper shows that it is also necessary to understand better the socio-ecological systems (SES) of the various communities, and how their livelihoods are influenced by the changing conditions imposed by a changing climate.
CitationInternational Journal of Disaster Risk Reduction, page 101738
DescriptionFrom Elsevier via Jisc Publications Router
History: accepted 2020-06-19, issue date 2020-07-05
Article version: AM
Publication status: Accepted
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No Difference in Penetrance between Truncating and Missense/Aberrant Splicing Pathogenic Variants in MLH1 and MSH2: A Prospective Lynch Syndrome Database StudyDominguez-Valentin, Mev; orcid: 0000-0001-7856-0057; email: Mev.Dominguez.Valentin@rr-research.no; Plazzer, John-Paul; orcid: 0000-0001-5114-4301; email: email@example.com; Sampson, Julian R.; email: Sampson@cardiff.ac.uk; Engel, Christoph; orcid: 0000-0002-7247-282X; email: firstname.lastname@example.org; Aretz, Stefan; orcid: 0000-0002-5228-1890; email: email@example.com; Jenkins, Mark A.; email: firstname.lastname@example.org; Sunde, Lone; email: email@example.com; Bernstein, Inge; email: firstname.lastname@example.org; Capella, Gabriel; orcid: 0000-0002-4669-7320; email: email@example.com; Balaguer, Francesc; orcid: 0000-0002-0206-0539; email: firstname.lastname@example.org; et al. (MDPI, 2021-06-28)Background. Lynch syndrome is the most common genetic predisposition for hereditary cancer. Carriers of pathogenic changes in mismatch repair (MMR) genes have an increased risk of developing colorectal (CRC), endometrial, ovarian, urinary tract, prostate, and other cancers, depending on which gene is malfunctioning. In Lynch syndrome, differences in cancer incidence (penetrance) according to the gene involved have led to the stratification of cancer surveillance. By contrast, any differences in penetrance determined by the type of pathogenic variant remain unknown. Objective. To determine cumulative incidences of cancer in carriers of truncating and missense or aberrant splicing pathogenic variants of the MLH1 and MSH2 genes. Methods. Carriers of pathogenic variants of MLH1 (path_MLH1) and MSH2 (path_MSH2) genes filed in the Prospective Lynch Syndrome Database (PLSD) were categorized as truncating or missense/aberrant splicing according to the InSiGHT criteria for pathogenicity. Results. Among 5199 carriers, 1045 had missense or aberrant splicing variants, and 3930 had truncating variants. Prospective observation years for the two groups were 8205 and 34,141 years, respectively, after which there were no significant differences in incidences for cancer overall or for colorectal cancer or endometrial cancers separately. Conclusion. Truncating and missense or aberrant splicing pathogenic variants were associated with similar average cumulative incidences of cancer in carriers of path MLH1 and path_MSH2.
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Elevated Circulating and Placental SPINT2 Is Associated with Placental DysfunctionMurphy, Ciara N.; orcid: 0000-0001-6996-7250; email: email@example.com; Walker, Susan P.; email: firstname.lastname@example.org; MacDonald, Teresa M.; email: email@example.com; Keenan, Emerson; orcid: 0000-0003-1966-2293; email: firstname.lastname@example.org; Hannan, Natalie J.; email: email@example.com; Wlodek, Mary E.; orcid: 0000-0002-8490-9099; email: firstname.lastname@example.org; Myers, Jenny; email: Jenny.Myers@manchester.ac.uk; Briffa, Jessica F.; email: email@example.com; Romano, Tania; orcid: 0000-0002-8581-2256; email: firstname.lastname@example.org; Roddy Mitchell, Alexandra; email: email@example.com; et al. (MDPI, 2021-07-12)Biomarkers for placental dysfunction are currently lacking. We recently identified SPINT1 as a novel biomarker; SPINT2 is a functionally related placental protease inhibitor. This study aimed to characterise SPINT2 expression in placental insufficiency. Circulating SPINT2 was assessed in three prospective cohorts, collected at the following: (1) term delivery (n = 227), (2) 36 weeks (n = 364), and (3) 24–34 weeks’ (n = 294) gestation. SPINT2 was also measured in the plasma and placentas of women with established placental disease at preterm (34 weeks) delivery. Using first-trimester human trophoblast stem cells, SPINT2 expression was assessed in hypoxia/normoxia (1% vs. 8% O2), and following inflammatory cytokine treatment (TNFα, IL-6). Placental SPINT2 mRNA was measured in a rat model of late-gestational foetal growth restriction. At 36 weeks, circulating SPINT2 was elevated in patients who later developed preeclampsia (p = 0.028; median = 2233 pg/mL vs. controls, median = 1644 pg/mL), or delivered a small-for-gestational-age infant (p = 0.002; median = 2109 pg/mL vs. controls, median = 1614 pg/mL). SPINT2 was elevated in the placentas of patients who required delivery for preterm preeclampsia (p = 0.025). Though inflammatory cytokines had no effect, hypoxia increased SPINT2 in cytotrophoblast stem cells, and its expression was elevated in the placental labyrinth of growth-restricted rats. These findings suggest elevated SPINT2 is associated with placental insufficiency.