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Risk loci identified through genome-wide association studies have explained about 25% of the phenotypic variations in nonsyndromic orofacial clefts (nsOFCs) on the liability scale. Despite the notable sex differences in the incidences of the different cleft types, investigation of loci for sex-specific effects has been understudied. To explore the sex-specific effects in genetic etiology of nsOFCs, we conducted a genome-wide gene × sex (GxSex) interaction study in a sub-Saharan African orofacial cleft cohort. The sample included 1,019 nonsyndromic orofacial cleft cases (814 cleft lip with or without cleft palate and 205 cleft palate only) and 2,159 controls recruited from 3 sites (Ethiopia, Ghana, and Nigeria). An additive logistic model was used to examine the joint effects of the genotype and GxSex interaction. Furthermore, we examined loci with suggestive significance ( P 2df = 1.16E-08, pGxSex = 1.49E-09, odds ratio [OR] = 0.44, 95% CI = 0.34 to 0.57). For males, the risk of cleft lip with or without cleft palate at this locus decreases with additional copies of the minor allele ( p

Novel or rare damaging mutations have been implicated in the developmental pathogenesis of nonsyndromic cleft lip with or without cleft palate (nsCL ± P). Thus, we investigated the human genome for high-impact mutations that could explain the risk of nsCL ± P in our cohorts.We conducted next-generation sequencing (NGS) analysis of 130 nsCL ± P case-parent African trios to identify pathogenic variants that contribute to the risk of clefting. We replicated this analysis using whole-exome sequence data from a Brazilian nsCL ± P cohort. Computational analyses were then used to predict the mechanism by which these variants could result in increased risks for nsCL ± P.We discovered damaging mutations within theThis is the first report on the contribution of

The majority (85%) of nonsyndromic cleft lip with or without cleft palate (nsCL/P) cases occur sporadically, suggesting a role for de novo mutations (DNMs) in the etiology of nsCL/P. To identify high impact DNMs that contribute to the risk of nsCL/P, we conducted whole genome sequencing (WGS) analyses in 130 African case-parent trios (affected probands and unaffected parents). We identified 162 high confidence protein-altering DNMs that contribute to the risk of nsCL/P. These include novel loss-of-function DNMs in the ACTL6A, ARHGAP10, MINK1, TMEM5 and TTN genes; as well as missense variants in ACAN, DHRS3, DLX6, EPHB2, FKBP10, KMT2D, RECQL4, SEMA3C, SEMA4D, SHH, TP63, and TULP4. Experimental evidence showed that ACAN, DHRS3, DLX6, EPHB2, FKBP10, KMT2D, MINK1, RECQL4, SEMA3C, SEMA4D, SHH, TP63, and TTN genes contribute to facial development and mutations in these genes could contribute to CL/P. Association studies have identified TULP4 as a potential cleft candidate gene, while ARHGAP10 interacts with CTNNB1 to control WNT signaling. DLX6, EPHB2, SEMA3C and SEMA4D harbor novel damaging DNMs that may affect their role in neural crest migration and palatal development. This discovery of pathogenic DNMs also confirms the power of WGS analysis of trios in the discovery of potential pathogenic variants.

Novel or rare damaging mutations have been implicated in the developmental pathogenesis of nonsyndromic cleft lip with or without cleft palate (nsCL ± P). Thus, we investigated the human genome for high-impact mutations that could explain the risk of nsCL ± P in our cohorts. We conducted next-generation sequencing (NGS) analysis of 130 nsCL ± P case-parent African trios to identify pathogenic variants that contribute to the risk of clefting. We replicated this analysis using whole-exome sequence data from a Brazilian nsCL ± P cohort. Computational analyses were then used to predict the mechanism by which these variants could result in increased risks for nsCL ± P. We discovered damaging mutations within the AFDN gene, a cell adhesion molecule (CAMs) that was previously shown to contribute to cleft palate in mice. These mutations include p.Met1164Ile, p.Thr453Asn, p.Pro1638Ala, p.Arg669Gln, p.Ala1717Val, and p.Arg1596His. We also discovered a novel splicing p.Leu1588Leu mutation in this protein. Computational analysis suggests that these amino acid changes affect the interactions with other cleft-associated genes including nectins (PVRL1, PVRL2, PVRL3, and PVRL4) CDH1, CTNNA1, and CTNND1. This is the first report on the contribution of AFDN to the risk for nsCL ± P in humans. AFDN encodes AFADIN, an important CAM that forms calcium-independent complexes with nectins 1 and 4 (encoded by the genes PVRL1 and PVRL4). This discovery shows the power of NGS analysis of multiethnic cleft samples in combination with a computational approach in the understanding of the pathogenesis of nsCL ± P.

Objectives Cleft lip with/without cleft palate and cleft palate only are congenital birth defects where the upper lip and/or palate fail to fuse properly during embryonic facial development. Affecting ~1.2/1000 live births world-wide, these orofacial clefts impose significant social and financial burdens on affected individuals and their families. Orofacial clefts have a complex etiology resulting from genetic variants combined with environmental covariates. Recent genome-wide association studies and whole-exome sequencing for orofacial clefts identified significant genetic associations and variants in several genes. Of these, we investigated the role of common/rare variants in SHH, RORA, MRPL53, ACVR1, and GDF11. Materials and methods We sequenced these five genes in 1255 multi-ethnic cleft lip with/without palate and cleft palate only samples in order to find variants that may provide potential explanations for the missing heritability of orofacial clefts. Rare and novel variants were further analyzed using in-silico predictive tools. Results 19 total variants of interest were found, with variant types including stop-gain, missense, synonymous, intronic, and splice-site variants. Of these, 3 novel missense variants were found, one in SHH, one in RORA, and one in GDF11. Conclusion This study provides evidence that variants in SHH, RORA, MRPL53, ACVR1, and GDF11 may contribute to risk of orofacial clefts in various populations.

Introduction: Malnutrition in children is one of the most prevalent global health challenges, and malnourished children have a higher risk of death from childhood diseases. Early childhood caries (ECC) is the most common chronic disease of childhood. Complications from ECC such as pain, loss of tooth/teeth, and infection can undermine a child’s nutrition and growth. Aim: This study aims to evaluate the severity of decay, missing, and filled tooth (dmft) by nutritional status using the z scores of the anthropometric measurements: height for age (HFA), weight for age (WFA), weight for height (WFH), and body mass index for age (BMIA) among children with ECC in Nigeria. Study Design: This is a cross-sectional study conducted in 5 local government areas (LGAs) in Lagos State, Nigeria. A multistage sampling technique was used. Results: A total of 273 cases of ECC were included in the analyses (mean age 4.19 ± 0.96 y). Overall, the mean dmft was 3.04 ± 2.28, and most (96%) were accounted for by untreated decay. The distribution of dmft within the different z score categories of BMIA (+3 = obese) showed the highest dmft scores among the combined severely wasted and wasted groups, lowest among children with normal z scores, and intermediate in the overweight and obese groups. There was a significant negative correlation between BMIA z score, WFH z score, and dmft ( r = −0.181, P < 0.05 and r = −0.143, P < 0.05, respectively). However, the correlations between HFA z score, WFA z score, and dmft were positive but not significant ( r = 0.048, P = 0.44 and r = 0.022, P = 0.77, respectively). Conclusion: Our study showed an increased severity of dental caries among severely wasted or wasted children with ECC compared to those of normal or overweight. Knowledge Transfer Statement: The results from this study will raise awareness among clinicians and policy makers on the need for a primary prevention program for early childhood caries in countries with high burden of malnutrition and limited resources. Also, it will help draw the attention of clinicians to the caries status of malnourished children that can be managed to improve the nutritional outcomes.

Background Early childhood caries (ECC) is a rapidly progressing form of dental infection and a significant public health problem, especially among socially and economically disadvantaged populations. This study aimed to assess the risk factors for ECC among a cohort of Sub-Saharan African children and to determine the role of genetics in the etiology of ECC. Methods A sample of 691 children (338 with ECC, 353 without ECC, age Results Of the 338 children with ECC, 64 (18.9%) had Severe-Early Childhood Caries (S-ECC). Children aged 48–59 months comprised the highest proportion of subjects with ECC (165; 48.8%) and S-ECC (24; 37.5%) while female subjects had higher dt (3.13 ± 2.56) and dmft values 3.27 ± 2.64. ECC was significantly more prevalent among children who were breastfed at night ≥ 12 months (OR 3.30; CI 0.39, 4.75), those with no previous dental visit (OR 1.71; CI 0.24, 2.77), those who used sweetened pacifiers (OR 1.85; CI 0.91, 3.79) and those who daily consumed sugar-sweetened drinks/snacks (OR 1.35; CI 0.09, 18.51). A suggestive increased risk for ECC (OR 1.26, p = 0. 0.0397) was observed for the genetic variant rs11239282 on chromosome 10. We also observed a suggestive reduced risk for ECC (OR 0.80, p = 0.03) for the rs131777 on chromosome 22. None of the genetic variants were significant after correction for multiple testing (Bonferroni p value p = 0.004). Conclusions Prolonged night-time breastfeeding, poor utilization of dental services and daily consumption of sugar were risk factors for ECC. Larger sample size is needed to confirm the results of the genetic analysis and to conduct genome wide studies in order to discover new risk loci for ECC.

We describe use of Fort Collins, Colorado, and nearby areas by bats in 2001–2005, and link patterns in bat ecology with concurrent public health surveillance for rabies. Our analyses are based on evaluation of summary statistics, and information-theoretic support for results of simple logistic regression. Based on captures in mist nets, the city bat fauna differed from that of the adjacent mountains, and was dominated by big brown bats (Eptesicus fuscus). Species, age, and sex composition of bats submitted for rabies testing locally and along the urbanizing Front Range Corridor were similar to those of the mist-net captures and reflected the annual cycle of reproduction and activity of big brown bats. Few submissions occurred November- March, when these bats hibernated elsewhere. In summer females roosted in buildings in colonies and dominated health samples; fledging of young corresponded to a summer peak in health submissions with no increase in rabies prevalence. Roosting ecology of big brown bats in buildings was similar to that reported for natural sites, including colony size, roost-switching behavior, fidelity to roosts in a small area, and attributes important for roost selection. Attrition in roosts occurred from structural modifications of buildings to exclude colonies by citizens, but without major effects on long-term bat reproduction or survival. Bats foraged in areas set aside for nature conservation. A pattern of lower diversity in urban bat communities with dominance by big brown bats may occur widely in the USA, and is consistent with national public health records for rabies surveillance.

Determining what products and services customers find of value is a crucial aspect of marketing. Our society members are "customers," with the Society's marketing efforts having primary focus on satisfying their needs while meeting the broader goals of their Society. Since any organization must operate within the boundaries of its mission and/or goals, we revisit the goals of the IEEE Communications Society (ComSoc) first, which are two-fold: (1) Scholarly - scientific and directed toward the advancement of the theory, practice, and application of communications engineering and related arts and sciences. (2) Professional - promoting high professional standards, development of competency and the advancement of the standings of members of the professions.

We used epidemiologic data for human West Nile virus (WNV) disease in Colorado from 2003 and 2007 to determine 1) the degree to which estimates of vector-borne disease occurrence is influenced by spatial scale of data aggregation (county versus census tract), and 2) the extent of concordance between spatial risk patterns based on case counts versus incidence. Statistical analyses showed that county, compared with census tract, accounted for approximately 50% of the overall variance in WNV disease incidence, and approximately 33% for the subset of cases classified as West Nile neuroinvasive disease. These findings indicate that sub-county scale presentation provides valuable risk information for stakeholders. There was high concordance between spatial patterns of WNV disease incidence and case counts for census tract (83%) but not for county (50%) or zip code (31%). We discuss how these findings impact on practices to develop spatial epidemiologic data for vector-borne diseases and present data to stakeholders.

We examined seasonal patterns for entomological measures of risk for exposure to Culex vectors and West Nile virus (family Flaviviridae, genus Flavivirus, WNV) in relation to human WNV disease cases in a five-county area of northeastern Colorado during 2006-2007. Studies along habitat/elevation gradients in 2006 showed that the seasonal activity period is shortened and peak numbers occur later in the summer for Culex tarsalis Coquillett females in foothills-montane areas >1600 m compared with plains areas 1600 m. The vector index for abundance of WNV-infected Cx. tarsalis females for the plains sites combined exceeded 0.50 from mid-July to mid-August, with at least one site exceeding 1.00 from early July to late August. Finally, we found that abundance of Cx. tarsalis females and the vector index for infected females were strongly associated with weekly numbers of WNV disease cases with onset 4-7 wk later (female abundance) or 1-2 wk later (vector index).

Human plague risks (Yersinia pestis infection) are greatest when epizootics cause high mortality among this bacterium's natural rodent hosts. Therefore, health departments in plague-endemic areas commonly establish animal-based surveillance programs to monitor Y. pestis infection among plague hosts and vectors. The primary objectives of our study were to determine whether passive animal-based plague surveillance samples collected in Colorado from 1991 to 2005 were sampled from high human plague risk areas and whether these samples provided information useful for predicting human plague case locations. By comparing locations of plague-positive animal samples with a previously constructed GIS-based plague risk model, we determined that the majority of plague-positive Gunnison's prairie dogs (100%) and non-prairie dog sciurids (85.82%), and moderately high percentages of sigmodontine rodents (71.4%), domestic cats (69.3%), coyotes (62.9%), and domestic dogs (62.5%) were recovered within 1 km of the nearest area posing high peridomestic risk to humans. In contrast, the majority of white-tailed prairie dog (66.7%), leporid (cottontailed and jack rabbits) (71.4%), and black-tailed prairie dog (93.0%) samples originated more than 1 km from the nearest human risk habitat. Plague-positive animals or their fleas were rarely (one of 19 cases) collected within 2 km of a case exposure site during the 24 months preceding the dates of illness onset for these cases. Low spatial accuracy for identifying epizootic activity prior to human plague cases suggested that other mammalian species or their fleas are likely more important sources of human infection in high plague risk areas. To address this issue, epidemiological observations and multi-locus variable number tandem repeat analyses (MLVA) were used to preliminarily identify chipmunks as an under-sampled, but potentially important, species for human plague risk in Colorado.

In the absence of a vaccine for use in humans against West Nile virus (WNV), mosquito control and personal protection against mosquito bites are the only measures available to prevent disease. Improved spatial targeting is desirable for costly mosquito and WNV surveillance and control schemes. We used a multivariate regression modeling approach to develop spatial models predicting high risk of exposure to WNV in western and eastern Colorado based on associations between Geographic Information System-derived environmental data and zip code of residence for 3,659 human WNV disease cases from 2002 to 2006. Models were robust, with user accuracies for correct classification of high risk areas of 67-80%. The importance of selecting a suitable model development area in an ecologically and climatically diverse environment was shown by models based on data from the eastern plains landscape performing poorly in the mountainous western part of Colorado and vice versa.

Assessments of spatial risk of exposure to vector-borne pathogens that combine vector and human disease data are needed for areas encompassing large tracts of public land with low population bases. We addressed this need for West Nile virus (WNV) disease in the northern Colorado Front Range by developing not only a spatial model for entomological risk of exposure to Culex tarsalis WNV vectors and an epidemiological risk map for WNV disease but also a novel risk-classification index combining data for these independently derived measures of entomological and epidemiological risk. Risk of vector exposure was high in the densely populated eastern plains portion of the Front Range but low in cooler montane areas to the west that are sparsely populated but used heavily for recreation in the summer. The entomological risk model performed well when applied to the western, mountainous part of Colorado and validated against epidemiologic data.

Plague is a rare but highly virulent flea-borne zoonotic disease caused by the Gram-negative bacterium Yersinia pestis Yersin. Identifying areas at high risk of human exposure to the etiological agent of plague could provide a useful tool for targeting limited public health resources and reduce the likelihood of misdiagnosis by raising awareness of the disease. We created logistic regression models to identify landscape features associated with areas where humans have acquired plague from 1957 to 2004 in the four-corners region of the United States (Arizona, Colorado, New Mexico, and Utah), and we extrapolated those models within a geographical information system to predict where plague cases are likely to occur within the southwestern United States disease focus. The probability of an area being classified as high-risk plague habitat increased with elevation up to approximately 2300 m and declined as elevation increased thereafter, and declined with distance from key habitat types (e.g., southern Rocky Mountain pinon--juniper [Pinus edulis Engelm. and Juniperus spp.], Colorado plateau pinon--juniper woodland, Rocky Mountain ponderosa pine (Pinus ponderosa P.& C. Lawson var. scopulorum), and southern Rocky Mountain juniper woodland and savanna). The overall accuracy of the model was >82%. Our most conservative model predicted that 14.4% of the four-corners region represented a high risk of peridomestic exposure to Y. pestis.

Colorado death certificate data from 1979 through 2001 show that the risk for Creutzfeldt-Jakob disease did not increase for residents of counties where chronic wasting disease is endemic among deer and elk., The transmission of the prion disease bovine spongiform encephalopathy (BSE) to humans raises concern about chronic wasting disease (CWD), a prion disease of deer and elk. In 7 Colorado counties with high CWD prevalence, 75% of state hunting licenses are issued locally, which suggests that residents consume most regionally harvested game. We used Colorado death certificate data from 1979 through 2001 to evaluate rates of death from the human prion disease Creutzfeldt-Jakob disease (CJD). The relative risk (RR) of CJD for CWD-endemic county residents was not significantly increased (RR 0.81, 95% confidence interval [CI] 0.40–1.63), and the rate of CJD did not increase over time (5-year RR 0.92, 95% CI 0.73–1.16). In Colorado, human prion disease resulting from CWD exposure is rare or nonexistent. However, given uncertainties about the incubation period, exposure, and clinical presentation, the possibility that the CWD agent might cause human disease cannot be eliminated.

Background Risk factors for complications of West Nile virus disease and prognosis in hospitalized patients are incompletely understood. Methods Demographic characteristics and data regarding potential risk factors, hospitalization, and dispositions were abstracted from medical records for residents of 4 Colorado counties who were hospitalized in 2003 with West Nile virus disease. Univariate and multivariate analyses were used to identify factors associated with West Nile encephalitis (WNE), limb weakness, or death by comparing factors among persons with the outcome of interest with factors among those without the outcome of interest. Results Medical records of 221 patients were reviewed; 103 had West Nile meningitis, 65 had WNE, and 53 had West Nile fever. Respiratory failure, limb weakness, and cardiac arrhythmia occurred in all groups, with significantly more cases of each in the WNE group. Age, alcohol abuse, and diabetes were associated with WNE. Age and WNE were associated with limb weakness. The mortality rate in the WNE group was 18%; age, immunosuppression, requirement of mechanical ventilation, and history of stroke were associated with death. Only 21% of patients with WNE who survived returned to a prehospitalization level of function. The estimated incidence of West Nile fever cases that required hospitalization was 6.0 cases per 100,000 persons; West Nile fever was associated with arrhythmia, limb weakness, and respiratory failure. Conclusions Persons with diabetes and a reported history of alcohol abuse and older persons appear to be at increased risk of developing WNE. Patients with WNE who have a history of stroke, who require mechanical ventilation, or who are immunosuppressed appear to be more likely to die. Respiratory failure, limb weakness, and arrhythmia occurred in all 3 categories, but there were significantly more cases of all in the WNE group.

West Nile virus (WNV) is a reemerging pathogen that causes fatal encephalitis in several species, including mouse and human. Recently, we showed that the chemokine receptor CCR5 is critical for survival of mice infected with WNV, acting at the level of leukocyte trafficking to the brain. To test whether this receptor is also protective in man, we determined the frequency of CCR5Δ32, a defective CCR5 allele found predominantly in Caucasians, in two independent cohorts of patients, one from Arizona and the other from Colorado, who had laboratory-confirmed, symptomatic WNV infection. The distribution of CCR5Δ32 in a control population of healthy United States Caucasian random blood donors was in Hardy-Weinberg equilibrium and CCR5Δ32 homozygotes represented 1.0% of the total group (n = 1,318). In contrast, CCR5Δ32 homozygotes represented 4.2% of Caucasians in the Arizona cohort (odds ratios [OR] = 4.4 [95% confidence interval [CI], 1.6–11.8], P = 0.0013) and 8.3% of Caucasians in the Colorado cohort (OR = 9.1 [95% CI, 3.4–24.8], P < 0.0001). CCR5Δ32 homozygosity was significantly associated with fatal outcome in the Arizona cohort (OR = 13.2 [95% CI, 1.9–89.9], P = 0.03). We conclude that CCR5 mediates resistance to symptomatic WNV infection. Because CCR5 is also the major HIV coreceptor, these findings have important implications for the safety of CCR5-blocking agents under development for HIV/AIDS.

Molecular epidemiological studies have linked many cryptic human rabies cases in the United States with exposure to rabies virus (RV) variants associated with insectivorous bats. In Colorado, bats accounted for 98% of all reported animal rabies cases between 1977 and 1996. The genetic divergence of RV was investigated in bat and terrestrial animal specimens that were submitted for rabies diagnosis to the Colorado Department of Public Health and Environment (CDPHE), Colorado, USA. RV isolates from animal specimens across the United States were also included in the analysis. Phylogenetic analyses were performed on partial nucleoprotein (N) gene sequences, which revealed seven principal clades. RV associated with the colonial big brown bat, Eptesicus fuscus, an bats of the genus Myotis were found to segregate into two distinct clades (I and IV). Clade I was harbored by E. fuscus and Myotis species, but was also identified in terrestrial animals such as domestic cats and striped skunks (Mephitis mephitis). Clade IV was divided into subclades IVA, IVB, and IVC; IVA was identified in E. fuscus, and Myotis species bats, and also in a fox; subclades IVB and IVC circulated predominantly in E. fuscus. Clade II was formed by big free-tailed bat (Nyctinomops macrotis) and striped skunk (Mephitis mephitis) samples. Clade III included RVs that are maintained by generally solitary, migratory bats such as the silver-haired bat (Lasionycteris noctivagans) and bats of the genus Lasiurus. Big brown bats were found to harbor this RV variant. None of the Colorado specimens segregated with clades V and VII that harbor RVs associated with terrestrial animals. Different species of bats had the same RV variant, indicating active inter-species rabies transmission. In Colorado, animal rabies occurs principally in bats, and the identification of bat RVs in cat, gray fox Urocyon cinereoargenteus), and striped skunks demonstrated the importance of rabies spillover from bats to domestic and terrestrial wildlife species.

Hantavirus pulmonary syndrome (HPS) occurs in most infections with Sin Nombre virus and other North American hantaviruses. We report five cases of acute hantavirus infection that did not fit the HPS case definition. The patients had characteristic prodromal symptoms without severe pulmonary involvement. These cases suggest that surveillance for HPS may need to be expanded.

We evaluated three commercial systems (RapID Yeast Plus System; Innovative Diagnostic Systems, Norcross, Ga.; API 20C Aux; bioMerieux-Vitek, Hazelwood, Mo.; and Vitek Yeast Biochemical Card, bioMerieux-Vitek) against an auxinographic and microscopic morphologic reference method for the ability to identify yeasts commonly isolated in our clinical microbiology laboratory. Two-hundred one yeast isolates were compared in the study. The RapID Yeast Plus System was significantly better than either API 20C Aux (193 versus 167 correct identifications; P < 0.0001) or the Vitek Yeast Biochemical Card (193 versus 173 correct identifications; P = 0.003) for obtaining correct identifications to the species level without additional testing. There was no significant difference between results obtained with API 20C Aux and the Vitek Yeast Biochemical Card system ( P = 0.39). The API 20C Aux system did not correctly identify any of the Candida krusei isolates ( n = 23) without supplemental testing and accounted for the major differences between the API 20C Aux and RapID Yeast Plus systems. Overall, the RapID Yeast Plus System was easy to use and is a good system for the routine identification of clinically relevant yeasts.

L'auteur impregne des idees de P. Freire dans Pedagogie des opprimes a travaille 10 ans dans l'enseignement superieur au Zimbabwe, il enseigne maintenant en Afrique du Sud dans une organisation non gouvernementale qui souscrit a l'analyse critique de P. Freire. Cette experience lui permet de comparer les evolutions des systemes educatifs des deux pays qui ont recu le systeme colonial anglais d'education en heritage. Comment s'operent les changements deux ans apres les premieres elections democratiques dans les deux pays? : Une expansion rapide de la reponse a la demande d'education au Zimbabwe et tres peu d'initiatives politiques pour ameliorer l'offre d'education en Afrique du sud. L'auteur explicite et argumente ces constatations en ce qu'elles augurent des evolutions futures.

Khanya College, a small tertiary access programme in Johannesburg, South Africa began operation in 1986. Making use of Freirian methodology and targeting activists involved in the anti‐apartheid struggle, the college has made a serious attempt to embody the notion of education for liberation. However, the college has faced serious constraints due to the conservative nature of the education system within which Khanya was forced to operate. Despite these constraints the college has succeeded in producing a number of politically active professionals as well as developing working relationships with mass organizations in the country. With the advent of democratic rule in South Africa in 1994, the college has been forced to evaluate its strategic orientation. The conclusion of Khanya has been to try to develop into a larger scale, comprehensive community college which still adheres to the ethos and methodology which inspired Khanya's founding.

West Nile virus (WNV) has become established across the Americas with recent heightened activity causing significant human illness. Surveillance methods to predict the risk of human infection are urgently needed to initiate timely preventative measures and justify the expense of implementing costly or unpopular control measures, such as aerial spraying or curfews. We quantified the links between mosquito surveillance data and the spatiotemporal patterns of 3,827 human WNV cases reported over 5 years in Colorado from 2003 to 2007. Mosquito data were strongly predictive of variation in the number of human WNV infections several weeks in advance in both a spatiotemporal statewide analysis and temporal variation within counties with substantial numbers of human cases. We outline several ways to further improve the predictive power of these data and we quantify the loss of information if no funds are available for testing mosquitoes for WNV. These results demonstrate that mosquito surveillance provides a valuable public health tool for assessing the risk of human arboviral infections, allocating limited public health resources, and justifying emergency control actions.

Most mortality associated with West Nile virus (WNV) disease occurs during the acute or early convalescent phases of illness. However, some reports suggest mortality may be elevated for months or longer after acute illness. The objective of this study was to assess the survival of a cohort of patients hospitalized with WNV disease in Colorado in 2003 up to 4 years after illness onset. We calculated age-adjusted standardized mortality ratios (SMRs) to evaluate excess mortality, evaluated reported causes of death in those who died, and analyzed potential covariates of delayed mortality. By 1 year after illness onset, 4% of the 201 patients had died (SMR, 2.7; 95% confidence interval [CI], 1.3-5.2), and 12% had died by 4 years after onset (SMR, 2.0; 95% CI, 1.3-3.0). Among those who had died, the most common immediate and contributory causes of death included pulmonary disease and cardiovascular disease; cancer, hepatic disease, and renal disease were mentioned less frequently. In multivariate analysis, age (hazard ratio [HR], 2.0 per 10-year increase; 95% CI, 1.4-2.7), autoimmune disease (HR, 3.0; 95% CI, 1.1-7.9), ever-use of tobacco (HR, 3.0; 95% CI, 1.3-7.0), encephalitis during acute WNV illness (HR, 2.6; 95% CI, 1.1-6.4), and endotracheal intubation during acute illness (HR 4.8; 95% CI, 1.9-12.1) were found to be independently associated with mortality. Our finding of an approximate twofold increase in mortality for up to 3 years after acute illness reinforces the need for prevention measures against WNV infection among at-risk groups to reduce acute as well as longer-term adverse outcomes.

This article examines the effects of independence on domestic workers in Zimbabwe during the years 1980–1990. In this period the government took numerous steps to improve the conditions of domestic workers. Among the most important of these were the creation of a legalised system of labour relations and the support of the formation of a domestic workers’ union. Yet, despite these measures, changes in the Zimbabwean political economy minimised the effect of government policy. By 1990 inflation, unemployment, and lack of political interest in the domestic sector meant that many conditions similar to those of the colonial era were reappearing in household labour relations. However, whereas during the colonial era race was a major factor underlying household power relations, after 1980 class came to be the dominant force.

MCSoC are comprised of a rich set of processor cores, specialized hardware accelerators, and I/O interfaces. Focusing only on functional verification is risky because the motivation for building such systems in the first place is to achieve high levels of system throughput: a functionally correct MCSoC that does not exhibit sufficient performance will fail in the market. Furthermore, focusing performance verification on individual system components (e.g., measuring processor core performance or hardware accelerator performance in isolation) is insufficient due to (1) the degree of resource contention that occurs in the MCSoC, and (2) the degree of configuration flexibility that is typically afforded by an MCSoC. These factors motivate system-level performance verification of MCSoC. This paper presents an important industrial case study of MCSoC performance verification, highlighting the methodology used, the lessons learned, and recommendations for improvement.

In the absence of a vaccine for use in humans against West Nile virus (WNV), mosquito control and personal protection against mosquito bites are the only measures available to prevent disease. Improved spatial targeting is desirable for costly mosquito and WNV surveillance and control schemes. We used a multivariate regression modeling approach to develop spatial models predicting high risk of exposure to WNV in western and eastern Colorado based on associations between Geographic Information System–derived environmental data and zip code of residence for 3,659 human WNV disease cases from 2002 to 2006. Models were robust, with user accuracies for correct classification of high risk areas of 67–80%. The importance of selecting a suitable model development area in an ecologically and climatically diverse environment was shown by models based on data from the eastern plains landscape performing poorly in the mountainous western part of Colorado and vice versa.

Assessments of spatial risk of exposure to vector-borne pathogens that combine vector and human disease data are needed for areas encompassing large tracts of public land with low population bases. We addressed this need for West Nile virus (WNV) disease in the northern Colorado Front Range by developing not only a spatial model for entomological risk of exposure to Culex tarsalis WNV vectors and an epidemiological risk map for WNV disease but also a novel risk-classification index combining data for these independently derived measures of entomological and epidemiological risk. Risk of vector exposure was high in the densely populated eastern plains portion of the Front Range but low in cooler montane areas to the west that are sparsely populated but used heavily for recreation in the summer. The entomological risk model performed well when applied to the western, mountainous part of Colorado and validated against epidemiologic data.

International audience; Long-term neurocognitive and functional impairments following West Nile virus (WNV) disease are poorly understood. We assessed quality-of-life indices and neurocognitive performance in a cohort of 54 persons recovering from one of three WNV disease syndromes (fever [WNF], meningitis [WNM], or encephalitis [WNE]) approximately 1.5 years following acute illness. We compared findings between the three syndromic groups; the study cohort and a demographically similar group of 55 controls from a study of chronic fatigue syndrome (CFS); and the study cohort and a `normative' control population based on cognitive test data. Persistent symptoms, diminished quality of life, and functional impairment were reported by 50% of WNF patients, and 75% each of WNM and WNE patients. Overall, objective neurocognitive performance did not differ significantly between the three syndromic groups, or between the study cohort and the CFS controls or the normative controls. In some neurocognitive subtests, the study cohort scored below the 15th percentile when compared with normative control data. Most persons who returned to independent living following hospitalization for WNV illness had persistent subjective complaints, but had normal cognitive function. However, a minority displayed subtle neurocognitive deficits more than 18 months following acute disease.