183 research outputs found

    Iringa Regional and District Projections.

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    This report presents population projections for the period 2003 to 2025 for Iringa Region and its districts. The projections were made using a Cohort Component Method (Spectrum System), whereby three components responsible for population change, namely: mortality, fertility and migration were projected separately as well as HIV/AIDS prevalence. The projected components were then applied to 2002 midyear base population in order to come up with the desired projections from 2003 to 2025. The report gives mortality, fertility, migration and HIV/AIDS assumptions, and shows Iringa’s demographic and socio-economic future trends. The results include estimated population by sex in single years and five-year age groups as well as some demographic indicators. Population growth for the period 2003 to 2025 shows a decrease in growth rates. The projections show that population growth rate will decrease from 1.6 percent in 2003 (with a population of 1,520,891) to 0.4 percent in 2025 (with a population of 2,019,217). Sex Ratio at birth is projected to increase from 90 male births per 100 females in 2003 to 99 male births per 100 females in 2025. Mortality estimates show that Infant Mortality Rate (IMR) is expected to decline for both sexes from 127 deaths per 1,000 live births in 2003 to 78 deaths per 1,000 live births in 2025. Under Five Mortality Rate (U5MR) for both sexes will also decline from 207 deaths per 1,000 live births in 2003 to 122 deaths per 1,000 live births in the year 2025. The mortality projected estimates further show that the life expectancy at birth for both males and females stands at 45 years in 2003. Life expectancy at birth for Iringa will decline from 45 years in 2003 to 44 years in 2025 for both sexes. For male population, life expectancy at birth will remain at the same level of 45 years in year 2003 and year 2025, while for female population the life expectancy at birth will decline from 45 years in 2003 to 43 years in 2025. On fertility, TFR will decline from 4.9 children per woman in 2003 to 2.6 children per woman in 2025.\u

    Dar es Salaam Regional and District Projections.

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    This report presents population projections for the period 2003 to 2025 for Dar es Salaam Region. The projections were made using a Cohort Component Method (Spectrum System), whereby three components responsible for population change, namely: mortality, fertility and migration were projected separately as well as HIV/AIDS prevalence. The projected components were then applied to 2002 midyear base population in order to come up with the desired projections from 2003 to 2025. The report gives mortality, fertility, migration and HIV/AIDS assumptions, and shows Dar es Salaam’s demographic and socio-economic future trends. The results include estimated population by sex in single years and five-year age groups as well as some demographic indicators. Population growth for the period 2003 to 2025 shows a decrease in growth rates. The projections show that population growth rate will decrease from 1.99 percent in 2003 (with a population of 2,535,594) to 0.27 percent in 2025 (with a population of 3,055,456). Sex Ratio at birth is projected to increase slightly from 102 male per 100 females in 2003 to 103 male per 100 females in 2025. Mortality estimates show that Infant Mortality Rate (IMR) is expected to decline for both sexes from 80 deaths per 1,000 live births in 2003 to 49 deaths per 1,000 live births in 2025. Under Five Mortality Rate (U5MR) for both sexes will also decline from 122 deaths per 1,000 live births in 2003 to 71 deaths per 1,000 live births in the year 2025. As expected, the mortality projected estimates further show that the life expectancy at birth for females is higher compared to that of males. Life expectancy at birth for Dar es Salaam will decline from 55 years in 2003 to 52 years in 2025 for both sexes. For male population, life expectancy at birth will almost remain at 53 years for the whole period. For female population, the life expectancy at birth will decline from 57 years in 2003 to 52 years in 2025. On fertility, TFR will decline from 2.7 children per woman in 2003 to about 2 children per woman in 2025.\u

    GEANT4 : a simulation toolkit

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    Abstract Geant4 is a toolkit for simulating the passage of particles through matter. It includes a complete range of functionality including tracking, geometry, physics models and hits. The physics processes offered cover a comprehensive range, including electromagnetic, hadronic and optical processes, a large set of long-lived particles, materials and elements, over a wide energy range starting, in some cases, from 250 eV and extending in others to the TeV energy range. It has been designed and constructed to expose the physics models utilised, to handle complex geometries, and to enable its easy adaptation for optimal use in different sets of applications. The toolkit is the result of a worldwide collaboration of physicists and software engineers. It has been created exploiting software engineering and object-oriented technology and implemented in the C++ programming language. It has been used in applications in particle physics, nuclear physics, accelerator design, space engineering and medical physics. PACS: 07.05.Tp; 13; 2

    Defending the genome from the enemy within:mechanisms of retrotransposon suppression in the mouse germline

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    The viability of any species requires that the genome is kept stable as it is transmitted from generation to generation by the germ cells. One of the challenges to transgenerational genome stability is the potential mutagenic activity of transposable genetic elements, particularly retrotransposons. There are many different types of retrotransposon in mammalian genomes, and these target different points in germline development to amplify and integrate into new genomic locations. Germ cells, and their pluripotent developmental precursors, have evolved a variety of genome defence mechanisms that suppress retrotransposon activity and maintain genome stability across the generations. Here, we review recent advances in understanding how retrotransposon activity is suppressed in the mammalian germline, how genes involved in germline genome defence mechanisms are regulated, and the consequences of mutating these genome defence genes for the developing germline

    Multiple Translocation of the AVR-Pita Effector Gene among Chromosomes of the Rice Blast Fungus Magnaporthe oryzae and Related Species

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    Magnaporthe oryzae is the causal agent of rice blast disease, a devastating problem worldwide. This fungus has caused breakdown of resistance conferred by newly developed commercial cultivars. To address how the rice blast fungus adapts itself to new resistance genes so quickly, we examined chromosomal locations of AVR-Pita, a subtelomeric gene family corresponding to the Pita resistance gene, in various isolates of M. oryzae (including wheat and millet pathogens) and its related species. We found that AVR-Pita (AVR-Pita1 and AVR-Pita2) is highly variable in its genome location, occurring in chromosomes 1, 3, 4, 5, 6, 7, and supernumerary chromosomes, particularly in rice-infecting isolates. When expressed in M. oryzae, most of the AVR-Pita homologs could elicit Pita-mediated resistance, even those from non-rice isolates. AVR-Pita was flanked by a retrotransposon, which presumably contributed to its multiple translocation across the genome. On the other hand, family member AVR-Pita3, which lacks avirulence activity, was stably located on chromosome 7 in a vast majority of isolates. These results suggest that the diversification in genome location of AVR-Pita in the rice isolates is a consequence of recognition by Pita in rice. We propose a model that the multiple translocation of AVR-Pita may be associated with its frequent loss and recovery mediated by its transfer among individuals in asexual populations. This model implies that the high mobility of AVR-Pita is a key mechanism accounting for the rapid adaptation toward Pita. Dynamic adaptation of some fungal plant pathogens may be achieved by deletion and recovery of avirulence genes using a population as a unit of adaptation

    Prognostic significance of cortactin levels in head and neck squamous cell carcinoma: comparison with epidermal growth factor receptor status

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    Cortactin is an actin-binding Src substrate involved in cell motility and invasion. In this study, we sought to examine the prognostic importance of cortactin protein expression in head and neck squamous cell carcinoma (HNSCC). To do so, cortactin and EGF receptor (EGFR) expression was retrospectively evaluated by immunohistochemistry in a tissue microarray composed of 176 HNSCCs with a mean follow-up time of 5 years. Cortactin immunoreactivity was weak to absent in normal epithelial tissue. Overexpression of the protein in 77 out of 176 tumours (44%) was associated with more advanced tumour-node-metastasis stage and higher histologic grade. Cortactin overexpression was associated with significantly increased local recurrence rates (49 vs 28% for high and low expressing carcinomas, respectively), decreased disease-free survival (17 vs 61%), and decreased the 5-year overall survival of (21 vs 58%), independently of the EGFR status. In multivariate analysis, cortactin expression status remained an independent prognostic factor for local recurrence, disease-free survival, and overall survival. Importantly, we identified a subset of patients with cortactin-overexpressing tumours that displayed low EGFR levels and a survival rate that equalled that of patients with tumoral overexpression of both EGFR and cortactin. These findings identify cortactin as a relevant prognostic marker and may have implications for targeted therapies in patients with HNSCC

    Early Loss of Xist RNA Expression and Inactive X Chromosome Associated Chromatin Modification in Developing Primordial Germ Cells

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    The inactive X chromosome characteristic of female somatic lineages is reactivated during development of the female germ cell lineage. In mouse, analysis of protein products of X-linked genes and/or transgenes located on the X chromosome has indicated that reactivation occurs after primordial germ cells reach the genital ridges.We present evidence that the epigenetic reprogramming of the inactive X-chromosome is initiated earlier than was previously thought, around the time that primordial germ cells (PGCs) migrate through the hindgut. Specifically, we find that Xist RNA expression, the primary signal for establishment of chromosome silencing, is extinguished in migrating PGCs. This is accompanied by displacement of Polycomb-group repressor proteins Eed and Suz(12), and loss of the inactive X associated histone modification, methylation of histone H3 lysine 27.We conclude that X reactivation in primordial germ cells occurs progressively, initiated by extinction of Xist RNA around the time that germ cells migrate through the hindgut to the genital ridges. The events that we observe are reminiscent of X reactivation of the paternal X chromosome in inner cell mass cells of mouse pre-implantation embryos and suggest a unified model in which execution of the pluripotency program represses Xist RNA thereby triggering progressive reversal of epigenetic silencing of the X chromosome

    Nonhuman primates across sub-Saharan Africa are infected with the yaws bacterium Treponema pallidum subsp. pertenue

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    Dear Editor, The bacterium Treponema pallidum (TP) causes human syphilis (subsp. pallidum; TPA), bejel (subsp. endemicum; TEN), and yaws (subsp. pertenue; TPE) (1). Although syphilis has reached a worldwide distribution (2), bejel and yaws have remained endemic diseases. Bejel affects individuals in dry areas of Sahelian Africa and Saudi Arabia, whereas yaws affects those living in the humid tropics (1). Yaws is currently reported as endemic in 14 countries, and an additional 84 countries have a known history of yaws but lack recent epidemiological data (3,4). Although this disease was subject to global eradication efforts in the mid-20th century, it later reemerged in West Africa, Southern Asia, and the Pacific region (5). New large-scale treatment options triggered the ongoing second eradication campaign, the goal of which is to eradicate yaws globally by 2020 (5). References: (1) Giacani, L. & Lukehart, S.A. The endemic treponematoses. Clin. Microbiol. Rev. 27, 89–115 (2014). (2) Arora, N. et al. Origin of modern syphilis and emergence of a pandemic Treponema pallidum cluster. Nat. Microbiol. 2, 16245 (2016). (3) Marks, M. Yaws: towards the WHO eradication target. Trans. R Soc. Trop. Med. Hyg. 110, 319–320 (2016). (4) World Health Organization. Eradication of yaws: procedures for verification and certification of interruption of transmission (World Health Organization, Geneva, 2018). (5) Asiedu, K., Fitzpatrick, C. & Jannin, J. Eradication of yaws: historical efforts and achieving WHO’s 2020 target. PLoS Negl. Trop. Dis. 8, e3016 (2014)

    Measuring women's perceived ability to overcome barriers to healthcare seeking in Burkina Faso

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