An assessment of the Zimbabwe ministry of health and child welfare provider initiated HIV testing and counselling programme

Background Provider-initiated HIV testing and counselling (PITC) is widely recommended to ensure timely treatment of HIV. The Zimbabwe Ministry of Health introduced PITC in 2007. We aimed to evaluate institutional capacity to implement PITC and investigate patient and health care worker (HCW) perceptions of the PITC programme. Methods Purposive selection of health care institutions was conducted among those providing PITC. Study procedures included 1) assessment of implementation procedures and institutional capacity using a semi-structured questionnaire; 2) in-depth interviews with patients who had been offered HIV testing to explore perceptions of PITC, 3) Focus group discussions with HCW to explore views on PITC. Qualitative data was analysed according to Framework Analysis. Results Sixteen health care institutions were selected (two central, two provincial, six district hospitals; and six primary care clinics). All institutions at least offered PITC in part. The main challenges which prevented optimum implementation were shortages of staff trained in PITC, HIV rapid testing and counselling; shortages of appropriate counselling space, and, at the time of assessment, shortages of HIV test kits. Both health care workers and patients embraced PITC because they had noticed that it had saved lives through early detection and treatment of HIV. Although health care workers reported an increase in workload as a result of PITC, they felt this was offset by the reduced number of HIV-related admissions and satisfaction of working with healthier clients. Conclusion PITC has been embraced by patients and health care workers as a life-saving intervention. There is need to address shortages in material, human and structural resources to ensure optimum implementation

Averting biodiversity collapse in tropical forest protected areas

The rapid disruption of tropical forests probably imperils global biodiversity more than any other contemporary phenomenon¹⁻³. With deforestation advancing quickly, protected areas are increasingly becoming final refuges for threatened species and natural ecosystem processes. However, many protected areas in the tropics are themselves vulnerable to human encroachment and other environmental stresses⁴⁻⁹. As pressures mount, it is vital to know whether existing reserves can sustain their biodiversity. A critical constraint in addressing this question has been that data describing a broad array of biodiversity groups have been unavailable for a sufficiently large and representative sample of reserves. Here we present a uniquely comprehensive data set on changes over the past 20 to 30 years in 31 functional groups of species and 21 potential drivers of environmental change, for 60 protected areas stratified across the world’s major tropical regions. Our analysis reveals great variation in reserve ‘health’: about half of all reserves have been effective or performed passably, but the rest are experiencing an erosion of biodiversity that is often alarmingly widespread taxonomically and functionally. Habitat disruption, hunting and forest-product exploitation were the strongest predictors of declining reserve health. Crucially, environmental changes immediately outside reserves seemed nearly as important as those inside in determining their ecological fate, with changes inside reserves strongly mirroring those occurring around them. These findings suggest that tropical protected areas are often intimately linked ecologically to their surrounding habitats, and that a failure to stem broad-scale loss and degradation of such habitats could sharply increase the likelihood of serious biodiversity declines.Keywords: Ecology, Environmental scienc

Devastating Decline of Forest Elephants in Central Africa.

African forest elephants– taxonomically and functionally unique–are being poached at accelerating rates, but we lack range-wide information on the repercussions. Analysis of the largest survey dataset ever assembled for forest elephants (80 foot-surveys; covering 13,000 km; 91,600 person-days of fieldwork) revealed that population size declined by ca. 62% between 2002–2011, and the taxon lost 30% of its geographical range. The population is now less than 10% of its potential size, occupying less than 25% of its potential range. High human population density, hunting intensity, absence of law enforcement, poor governance, and proximity to expanding infrastructure are the strongest predictors of decline. To save the remaining African forest elephants, illegal poaching for ivory and encroachment into core elephant habitat must be stopped. In addition, the international demand for ivory, which fuels illegal trade, must be dramatically reduced

Major phytoplasma diseases of forest and urban trees

In the northern hemisphere, yellows, witches’ broom, and decline diseases of several forest and urban tree species are widespread and of considerable economic and ecological significance. Elm (Ulmus spp.) and alder (Alnus spp.) are affected by elm yellows (EY) and alder yellows (ALY), respectively. These diseases are mainly associated with the presence of closely related phytoplasmas, the EY agent ‘Candidatus Phytoplasma ulmi’ and the ALY agent, which are members of the EY or 16SrV group, subgroups 16SrV-A and 16SrV-C, respectively. Ash (Fraxinus spp.) is affected by ash yellows, a disease which occurs mainly in North America and is associated with the presence of ‘Candidatus Phytoplasma fraxini’, a member of subgroup 16SrVII-A. Poplar (Populus spp.), sandal (Santalum album), paulownia (Paulownia spp.), and mulberry (Morus spp.) are affected by yellows diseases associated with phytoplasmas of different 16SrI subgroups. Several species of conifers are affected by yellows and witches’ broom diseases associated with phytoplasmas belonging to at least five taxonomic groups (16SrI, 16SrIII, 16SrVI, 16SrIX, and 16SrXXI) and several different subgroups. A number of urban tree species grown in the Sabana de Bogotà (Colombia) are affected by decline diseases which are primarily associated with 16SrI and 16SrVII phytoplasmas. This chapter summarizes the current knowledge of major phytoplasma diseases of forest and urban trees grown in the northern hemisphere

Averting biodiversity collapse in tropical forest protected areas

The rapid disruption of tropical forests probably imperils global biodiversity more than any other contemporary phenomenon. With deforestation advancing quickly, protected areas are increasingly becoming final refuges for threatened species and natural ecosystem processes. However, many protected areas in the tropics are themselves vulnerable to human encroachment and other environmental stresses. As pressures mount, it is vital to know whether existing reserves can sustain their biodiversity. A critical constraint in addressing this question has been that data describing a broad array of biodiversity groups have been unavailable for a sufficiently large and representative sample of reserves. Here we present a uniquely comprehensive data set on changes over the past 20 to 30 years in 31 functional groups of species and 21 potential drivers of environmental change, for 60 protected areas stratified across the world’s major tropical regions. Our analysis reveals great variation in reserve ‘health’: about half of all reserves have been effective or performed passably, but the rest are experiencing an erosion of biodiversity that is often alarmingly widespread taxonomically and functionally. Habitat disruption, hunting and forest-product exploitation were the strongest predictors of declining reserve health. Crucially, environmental changes immediately outside reserves seemed nearly as important as those inside in determining their ecological fate, with changes inside reserves strongly mirroring those occurring around them. These findings suggest that tropical protected areas are often intimately linked ecologically to their surrounding habitats, and that a failure to stem broad-scale loss and degradation of such habitats could sharply increase the likelihood of serious biodiversity declines.William F. Laurance, D. Carolina Useche, Julio Rendeiro, Margareta Kalka, Corey J. A. Bradshaw, Sean P. Sloan, Susan G. Laurance, Mason Campbell, Kate Abernethy, Patricia Alvarez, Victor Arroyo-Rodriguez, Peter Ashton, Julieta Benítez-Malvido, Allard Blom, Kadiri S. Bobo, Charles H. Cannon, Min Cao, Richard Carroll, Colin Chapman, Rosamond Coates, Marina Cords, Finn Danielsen, Bart De Dijn, Eric Dinerstein, Maureen A. Donnelly, David Edwards, Felicity Edwards, Nina Farwig, Peter Fashing, Pierre-Michel Forget, Mercedes Foster, George Gale, David Harris, Rhett Harrison, John Hart, Sarah Karpanty, W. John Kress, Jagdish Krishnaswamy, Willis Logsdon, Jon Lovett, William Magnusson, Fiona Maisels, Andrew R. Marshall, Deedra McClearn, Divya Mudappa, Martin R. Nielsen, Richard Pearson, Nigel Pitman, Jan van der Ploeg, Andrew Plumptre, John Poulsen, Mauricio Quesada, Hugo Rainey, Douglas Robinson, Christiane Roetgers, Francesco Rovero, Frederick Scatena, Christian Schulze, Douglas Sheil, Thomas Struhsaker, John Terborgh, Duncan Thomas, Robert Timm, J. Nicolas Urbina-Cardona, Karthikeyan Vasudevan, S. Joseph Wright, Juan Carlos Arias-G., Luzmila Arroyo, Mark Ashton, Philippe Auzel, Dennis Babaasa, Fred Babweteera, Patrick Baker, Olaf Banki, Margot Bass, Inogwabini Bila-Isia, Stephen Blake, Warren Brockelman, Nicholas Brokaw, Carsten A. Brühl, Sarayudh Bunyavejchewin, Jung-Tai Chao, Jerome Chave, Ravi Chellam, Connie J. Clark, José Clavijo, Robert Congdon, Richard Corlett, H. S. Dattaraja, Chittaranjan Dave, Glyn Davies, Beatriz de Mello Beisiegel, Rosa de Nazaré Paes da Silva, Anthony Di Fiore, Arvin Diesmos, Rodolfo Dirzo, Diane Doran-Sheehy, Mitchell Eaton, Louise Emmons, Alejandro Estrada, Corneille Ewango, Linda Fedigan, François Feer, Barbara Fruth, Jacalyn Giacalone Willis, Uromi Goodale, Steven Goodman, Juan C. Guix, Paul Guthiga, William Haber, Keith Hamer, Ilka Herbinger, Jane Hill, Zhongliang Huang, I Fang Sun, Kalan Ickes, Akira Itoh, Natália Ivanauskas, Betsy Jackes, John Janovec, Daniel Janzen, Mo Jiangming, Chen Jin, Trevor Jones, Hermes Justiniano, Elisabeth Kalko, Aventino Kasangaki, Timothy Killeen, Hen-biau King, Erik Klop, Cheryl Knott, Inza Koné, Enoka Kudavidanage, José Lahoz da Silva Ribeiro, John Lattke, Richard Laval, Robert Lawton, Miguel Leal, Mark Leighton, Miguel Lentino, Cristiane Leonel, Jeremy Lindsell, Lee Ling-Ling, K. Eduard Linsenmair, Elizabeth Losos, Ariel Lugo, Jeremiah Lwanga, Andrew L. Mack, Marlucia Martins, W. Scott McGraw, Roan McNab, Luciano Montag, Jo Myers Thompson, Jacob Nabe-Nielsen, Michiko Nakagawa, Sanjay Nepal, Marilyn Norconk, Vojtech Novotny, Sean O'Donnell, Muse Opiang, Paul Ouboter, Kenneth Parker, N. Parthasarathy, Kátia Pisciotta, Dewi Prawiradilaga, Catherine Pringle, Subaraj Rajathurai, Ulrich Reichard, Gay Reinartz, Katherine Renton, Glen Reynolds, Vernon Reynolds, Erin Riley, Mark-Oliver Rödel, Jessica Rothman, Philip Round, Shoko Sakai, Tania Sanaiotti, Tommaso Savini, Gertrud Schaab, John Seidensticker, Alhaji Siaka, Miles R. Silman, Thomas B. Smith, Samuel Soares de Almeida, Navjot Sodhi, Craig Stanford, Kristine Stewart, Emma Stokes, Kathryn E. Stoner, Raman Sukumar, Martin Surbeck, Mathias Tobler, Teja Tscharntke, Andrea Turkalo, Govindaswamy Umapathy, Merlijn van Weerd, Jorge Vega Rivera, Meena Venkataraman, Linda Venn, Carlos Verea, Carolina Volkmer de Castilho, Matthias Waltert, Benjamin Wang, David Watts, William Weber, Paige West, David Whitacre, Ken Whitney, David Wilkie, Stephen Williams, Debra D. Wright, Patricia Wright, Lu Xiankai, Pralad Yonzon & Franky Zamzan

Identification of genetic risk loci and causal insights associated with Parkinson\u27s disease in African and African admixed populations: a genome-wide association study

\ua9 2023 Elsevier LtdBackground: An understanding of the genetic mechanisms underlying diseases in ancestrally diverse populations is an important step towards development of targeted treatments. Research in African and African admixed populations can enable mapping of complex traits, because of their genetic diversity, extensive population substructure, and distinct linkage disequilibrium patterns. We aimed to do a comprehensive genome-wide assessment in African and African admixed individuals to better understand the genetic architecture of Parkinson\u27s disease in these underserved populations. Methods: We performed a genome-wide association study (GWAS) in people of African and African admixed ancestry with and without Parkinson\u27s disease. Individuals were included from several cohorts that were available as a part of the Global Parkinson\u27s Genetics Program, the International Parkinson\u27s Disease Genomics Consortium Africa, and 23andMe. A diagnosis of Parkinson\u27s disease was confirmed clinically by a movement disorder specialist for every individual in each cohort, except for 23andMe, in which it was self-reported based on clinical diagnosis. We characterised ancestry-specific risk, differential haplotype structure and admixture, coding and structural genetic variation, and enzymatic activity. Findings: We included 197 918 individuals (1488 cases and 196 430 controls) in our genome-wide analysis. We identified a novel common risk factor for Parkinson\u27s disease (overall meta-analysis odds ratio for risk of Parkinson\u27s disease 1\ub758 [95% CI 1\ub737–1\ub780], p=2\ub7397 7 10−14) and age at onset at the GBA1 locus, rs3115534-G (age at onset β=–2\ub700 [SE=0\ub757], p=0\ub70005, for African ancestry; and β=–4\ub715 [0\ub758], p=0\ub7015, for African admixed ancestry), which was rare in non-African or non-African admixed populations. Downstream short-read and long-read whole-genome sequencing analyses did not reveal any coding or structural variant underlying the GWAS signal. The identified signal seems to be associated with decreased glucocerebrosidase activity. Interpretation: Our study identified a novel genetic risk factor in GBA1 in people of African ancestry, which has not been seen in European populations, and it could be a major mechanistic basis of Parkinson\u27s disease in African populations. This population-specific variant exerts substantial risk on Parkinson\u27s disease as compared with common variation identified through GWAS and it was found to be present in 39% of the cases assessed in this study. This finding highlights the importance of understanding ancestry-specific genetic risk in complex diseases, a particularly crucial point as the Parkinson\u27s disease field moves towards targeted treatments in clinical trials. The distinctive genetics of African populations highlights the need for equitable inclusion of ancestrally diverse groups in future trials, which will be a valuable step towards gaining insights into novel genetic determinants underlying the causes of Parkinson\u27s disease. This finding opens new avenues towards RNA-based and other therapeutic strategies aimed at reducing lifetime risk of Parkinson\u27s disease. Funding: The Global Parkinson\u27s Genetics Program, which is funded by the Aligning Science Across Parkinson\u27s initiative, and The Michael J Fox Foundation for Parkinson\u27s Research