Accessibility across transport modes and residential developments in Nairobi

A key goal of urban transportation planning is to provide people with access to a greater number of opportunities for interaction with people and places. Measures of accessibility are gaining attention globally for use in planning, yet few studies measure accessibility in cities in low-income countries, and even fewer incorporate semi-formal bus systems, also called paratransit. Drawing on rich datasets available for Nairobi, Kenya this analysis quantifies place-based accessibility for walking, paratransit, and driving using three different measures: a mobility measure quantifying how many other locations in Nairobi can be reached in 60 min, a contour measure quantifying the number of health facilities that can be reached in 60 min, and a gravity measure quantifying the number of health facilities weighted by a time-decay function. Health facilities are used because they are an essential service that people need physical access to and as a representation of the spatial distribution of activities more broadly. The findings show that place-based accessibility is highest for driving, then paratransit, then walking, and that there are high levels of access to health facilities near the Central Business District (CBD) for all modes. Additionally, paratransit accessibility is comparatively better in the contour and gravity measures, which may mean that paratransit is efficiently providing access based on the spatial distribution of services. The contour measure results are also compared across different residential levels, which are grouped based on neighborhood characteristics and ordered by income. Counterintuitively, the wealthiest areas have very low levels of place-based accessibility for all modes, while poor areas have comparatively better walking access to health facilities. Interestingly, the medium low residential level, characterized in part by tenement apartment buildings, has significantly higher accessibility than other residential types. One way to reduce inequality in access across income groups is to increase spatial accessibility for the modes used by low- and middle-income households, for example with policies that prioritize public transport and non-motorized travel, integrate paratransit with land use development, and provide safe, efficient, and affordable options

Spatial variation of fine particulate matter levels in Nairobi before and during the COVID-19 curfew: implications for environmental justice

Abstract: The temporary decrease of fine particulate matter (PM2.5) concentrations in many parts of the world due to the COVID-19 lockdown spurred discussions on urban air pollution and health. However there has been little focus on sub-Saharan Africa, as few African cities have air quality monitors and if they do, these data are often not publicly available. Spatial differentials of changes in PM2.5 concentrations as a result of COVID also remain largely unstudied. To address this gap, we use a serendipitous mobile air quality monitoring deployment of eight Sensirion SPS 30 sensors on motorbikes in the city of Nairobi starting on 16 March 2020, before a COVID-19 curfew was imposed on 25 March and continuing until 5 May 2020. We developed a random-forest model to estimate PM2.5 surfaces for the entire city of Nairobi before and during the COVID-19 curfew. The highest PM2.5 concentrations during both periods were observed in the poor neighborhoods of Kariobangi, Mathare, Umoja, and Dandora, located to the east of the city center. Changes in PM2.5 were heterogeneous over space. PM2.5 concentrations increased during the curfew in rapidly urbanizing, the lower-middle-class neighborhoods of Kahawa, Kasarani, and Ruaraka, likely because residents switched from LPG to biomass fuels due to loss of income. Our results indicate that COVID-19 and policies to address it may have exacerbated existing air pollution inequalities in the city of Nairobi. The quantitative results are preliminary, due to sampling limitations and measurement uncertainties, as the available data came exclusively from low-cost sensors. This research serves to highlight that spatial data that is essential for understanding structural inequalities reflected in uneven air pollution burdens and differential impacts of events like the COVID pandemic. With the help of carefully deployed low-cost sensors with improved spatial sampling and at least one reference-quality monitor for calibration, we can collect data that is critical for developing targeted interventions that address environmental injustice in the African context

Meta-analysis of genome-wide association studies from the CHARGE consortium identifies common variants associated with carotid intima media thickness and plaque

Carotid intima media thickness (cIMT) and plaque determined by ultrasonography are established measures of subclinical atherosclerosis that each predicts future cardiovascular disease events. We conducted a meta-analysis of genome-wide association data in 31,211 participants of European ancestry from nine large studies in the setting of the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium. We then sought additional evidence to support our findings among 11,273 individuals using data from seven additional studies. In the combined meta-analysis, we identified three genomic regions associated with common carotid intima media thickness and two different regions associated with the presence of carotid plaque (P < 5 × 10 -8). The associated SNPs mapped in or near genes related to cellular signaling, lipid metabolism and blood pressure homeostasis, and two of the regions were associated with coronary artery disease (P < 0.006) in the Coronary Artery Disease Genome-Wide Replication and Meta-Analysis (CARDIoGRAM) consortium. Our findings may provide new insight into pathways leading to subclinical atherosclerosis and subsequent cardiovascular events

Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis.

Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis

New loci associated with birth weight identify genetic links between intrauterine growth and adult height and metabolism.

Birth weight within the normal range is associated with a variety of adult-onset diseases, but the mechanisms behind these associations are poorly understood. Previous genome-wide association studies of birth weight identified a variant in the ADCY5 gene associated both with birth weight and type 2 diabetes and a second variant, near CCNL1, with no obvious link to adult traits. In an expanded genome-wide association meta-analysis and follow-up study of birth weight (of up to 69,308 individuals of European descent from 43 studies), we have now extended the number of loci associated at genome-wide significance to 7, accounting for a similar proportion of variance as maternal smoking. Five of the loci are known to be associated with other phenotypes: ADCY5 and CDKAL1 with type 2 diabetes, ADRB1 with adult blood pressure and HMGA2 and LCORL with adult height. Our findings highlight genetic links between fetal growth and postnatal growth and metabolism

[Avian cytogenetics goes functional] Third report on chicken genes and chromosomes 2015

High-density gridded libraries of large-insert clones using bacterial artificial chromosome (BAC) and other vectors are essential tools for genetic and genomic research in chicken and other avian species... Taken together, these studies demonstrate that applications of large-insert clones and BAC libraries derived from birds are, and will continue to be, effective tools to aid high-throughput and state-of-the-art genomic efforts and the important biological insight that arises from them

Genome-wide meta-analysis of common variant differences between men and women

The male-to-female sex ratio at birth is constant across world populations with an average of 1.06 (106 male to 100 female live births) for populations of European descent. The sex ratio is considered to be affected by numerous biological and environmental factors and to have a heritable component. The aim of this study was to investigate the presence of common allele modest effects at autosomal and chromosome X variants that could explain the observed sex ratio at birth. We conducted a large-scale genome-wide association scan (GWAS) meta-analysis across 51 studies, comprising overall 114 863 individuals (61 094 women and 53 769 men) of European ancestry and 2 623 828 common (minor allele frequency >0.05) single-nucleotide polymorphisms (SNPs). Allele frequencies were compared between men and women for directly-typed and imputed variants within each study. Forward-time simulations for unlinked, neutral, autosomal, common loci were performed under the demographic model for European populations with a fixed sex ratio and a random mating scheme to assess the probability of detecting significant allele frequency differences. We do not detect any genome-wide significant (P < 5 × 10−8) common SNP differences between men and women in this well-powered meta-analysis. The simulated data provided results entirely consistent with these findings. This large-scale investigation across ∼115 000 individuals shows no detectable contribution from common genetic variants to the observed skew in the sex ratio. The absence of sex-specific differences is useful in guiding genetic association study design, for example when using mixed controls for sex-biased trait

Genome-wide association study identifies six new loci influencing pulse pressure and mean arterial pressure.

Numerous genetic loci have been associated with systolic blood pressure (SBP) and diastolic blood pressure (DBP) in Europeans. We now report genome-wide association studies of pulse pressure (PP) and mean arterial pressure (MAP). In discovery (N = 74,064) and follow-up studies (N = 48,607), we identified at genome-wide significance (P = 2.7 × 10(-8) to P = 2.3 × 10(-13)) four new PP loci (at 4q12 near CHIC2, 7q22.3 near PIK3CG, 8q24.12 in NOV and 11q24.3 near ADAMTS8), two new MAP loci (3p21.31 in MAP4 and 10q25.3 near ADRB1) and one locus associated with both of these traits (2q24.3 near FIGN) that has also recently been associated with SBP in east Asians. For three of the new PP loci, the estimated effect for SBP was opposite of that for DBP, in contrast to the majority of common SBP- and DBP-associated variants, which show concordant effects on both traits. These findings suggest new genetic pathways underlying blood pressure variation, some of which may differentially influence SBP and DBP