104 research outputs found

    The periodicity of violent and property crime in Tshwane, South Africa

    Get PDF
    In this article, we identify and analyze the periodicity of violent and property crimes committed in Tshwane, South Africa, from 2001 to 2006. This is done using Fourier analysis, an advanced explorative mathematical technique commonly used in the physical sciences to detect the presence of a frequency or periodicity in a large time-series data set. The use of this technique in criminology is in its infancy, and in this study, Fourier analysis is used to identify periodic moments in time at which the risk of being a victim of violent and property crime in the city of Tshwane is heightened. Results indicated that violent crime peaks roughly every 7 and 75 days over the 5-year study period, with a marginal peak every 150 days. Property crimes peak every 75 days and every 150 days. Periodic peaks of crime observed in this study are explained using the central tenets of routine activities theory. Fourier analysis is an underused, powerful data-driven mathematical tool that should be added to the methodological arsenal available to criminologists when analyzing the temporal dimension of crime.http://icj.sagepub.comGeography, Geoinformatics and Meteorolog

    Is it safer behind the gates? Crime and gated communities in South Africa

    Get PDF
    Gated communities have long been seen as a rational response to rising crime levels, yet very little is known about the extent to which residing in a gated community actually reduces an individuals’ risk of criminal victimisation. In this study, we use location quotients to compare the extent of burglary in gated communities with burglary across the entire city of Tshwane, South Africa, as well as compare burglary in gated communities with burglary occurring within a series of buffer intervals immediately surrounding these communities. Finally, we identify what physical characteristics of gated communities differentiate between high and low burglary in these enclaves. Prior to expectations, we found that gated communities (and their immediate surrounding areas) are associated with increased levels of burglary. There are, however, a number of physical characteristics of gated communities which are associated with much lower burglary levels. The implications of our work from a crime prevention and development planning perspective are discussed.http://link.springer.com/journal/10901/29/1hb201

    Parents\u27 Goals: An Analysis of Therapist Reasoning

    Get PDF
    Purpose: Illustrate the use of DDDM to develop parent-identified goals for occupational therapy and to identify underlying sensory integration factors hypothesized to be impacting participation

    Finishing the euchromatic sequence of the human genome

    Get PDF
    The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

    Evacetrapib and Cardiovascular Outcomes in High-Risk Vascular Disease

    Get PDF
    BACKGROUND: The cholesteryl ester transfer protein inhibitor evacetrapib substantially raises the high-density lipoprotein (HDL) cholesterol level, reduces the low-density lipoprotein (LDL) cholesterol level, and enhances cellular cholesterol efflux capacity. We sought to determine the effect of evacetrapib on major adverse cardiovascular outcomes in patients with high-risk vascular disease. METHODS: In a multicenter, randomized, double-blind, placebo-controlled phase 3 trial, we enrolled 12,092 patients who had at least one of the following conditions: an acute coronary syndrome within the previous 30 to 365 days, cerebrovascular atherosclerotic disease, peripheral vascular arterial disease, or diabetes mellitus with coronary artery disease. Patients were randomly assigned to receive either evacetrapib at a dose of 130 mg or matching placebo, administered daily, in addition to standard medical therapy. The primary efficacy end point was the first occurrence of any component of the composite of death from cardiovascular causes, myocardial infarction, stroke, coronary revascularization, or hospitalization for unstable angina. RESULTS: At 3 months, a 31.1% decrease in the mean LDL cholesterol level was observed with evacetrapib versus a 6.0% increase with placebo, and a 133.2% increase in the mean HDL cholesterol level was seen with evacetrapib versus a 1.6% increase with placebo. After 1363 of the planned 1670 primary end-point events had occurred, the data and safety monitoring board recommended that the trial be terminated early because of a lack of efficacy. After a median of 26 months of evacetrapib or placebo, a primary end-point event occurred in 12.9% of the patients in the evacetrapib group and in 12.8% of those in the placebo group (hazard ratio, 1.01; 95% confidence interval, 0.91 to 1.11; P=0.91). CONCLUSIONS: Although the cholesteryl ester transfer protein inhibitor evacetrapib had favorable effects on established lipid biomarkers, treatment with evacetrapib did not result in a lower rate of cardiovascular events than placebo among patients with high-risk vascular disease. (Funded by Eli Lilly; ACCELERATE ClinicalTrials.gov number, NCT01687998 .)

    Global, regional, and national age-sex-specific mortality for 282 causes of death in 195 countries and territories, 1980-2017: a systematic analysis for the Global Burden of Disease Study 2017.

    Get PDF
    BACKGROUND: Global development goals increasingly rely on country-specific estimates for benchmarking a nation's progress. To meet this need, the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2016 estimated global, regional, national, and, for selected locations, subnational cause-specific mortality beginning in the year 1980. Here we report an update to that study, making use of newly available data and improved methods. GBD 2017 provides a comprehensive assessment of cause-specific mortality for 282 causes in 195 countries and territories from 1980 to 2017. METHODS: The causes of death database is composed of vital registration (VR), verbal autopsy (VA), registry, survey, police, and surveillance data. GBD 2017 added ten VA studies, 127 country-years of VR data, 502 cancer-registry country-years, and an additional surveillance country-year. Expansions of the GBD cause of death hierarchy resulted in 18 additional causes estimated for GBD 2017. Newly available data led to subnational estimates for five additional countries-Ethiopia, Iran, New Zealand, Norway, and Russia. Deaths assigned International Classification of Diseases (ICD) codes for non-specific, implausible, or intermediate causes of death were reassigned to underlying causes by redistribution algorithms that were incorporated into uncertainty estimation. We used statistical modelling tools developed for GBD, including the Cause of Death Ensemble model (CODEm), to generate cause fractions and cause-specific death rates for each location, year, age, and sex. Instead of using UN estimates as in previous versions, GBD 2017 independently estimated population size and fertility rate for all locations. Years of life lost (YLLs) were then calculated as the sum of each death multiplied by the standard life expectancy at each age. All rates reported here are age-standardised
    corecore