A unique human-fox burial from a pre-Natufian cemetery in the Levant (Jordan)

New human burials from northern Jordan provide important insights into the appearance of cemeteries and the nature of human-animal relationships within mortuary contexts during the Epipalaeolithic period (c. 23,000-11,600 cal BP) in the Levant, reinforcing a socio-ideological relationship that goes beyond predator-prey. Previous work suggests that archaeological features indicative of social complexity occur suddenly during the latest Epipalaeolithic phase, the Natufian (c. 14,500-11,600 cal BP). These features include sedentism, cemeteries, architecture, food production, including animal domestication, and burials with elaborate mortuary treatments. Our findings from the pre-Natufian (Middle Epipalaeolithic) cemetery of 'Uyun al-Hammam demonstrate that joint human-animal mortuary practices appear earlier in the Epipalaeolithic. We describe the earliest human-fox burial in the Near East, where the remains of dogs have been found associated with human burials at a number of Natufian sites. This is the first time that a fox has been documented in association with human interments pre-dating the Natufian and with a particular suite of grave goods. Analysis of the human and animal bones and their associated artefacts provides critical data on the nature and timing of these newly-developing relationships between people and animals prior to the appearance of domesticated dogs in the Natufian.     

Two 19th-century chronobiologists: Thomas Laycock and Edward Smith.

This article describes the works of two 19th-century chronobiologists. Thomas Laycock (1812-1876), who held the Chair of Medicine in Edinburgh from 1855-1876, published a series of seven articles in Lancet, all dedicated to periodicities in "vital phenomena." Laycock considered the understanding of periodicities essential for the advancement of the treatment of diseases. Edward Smith (1818-1874) was a pioneer in experimental chronobiology. In his 1861 book entitled: Health and disease as influenced by daily, seasonal and other cyclical changes in the human, Smith summarized a large number of experiments in which he investigated the occurrence of periodicities in pulse rate, urine flow, urea excretion, and respiration. From his experimental results and those of others, Smith drew practical conclusions regarding patients' care, the timing of drug administration, and the design of night work.     

The Black Death in Hereford,England: A demographic analysis of the Cathedral 14th-century plague mass graves and associated parish cemetery

Objectives

This study explores the paleoepidemiology of the Black Death (1348–52 AD) mass graves from Hereford, England, via osteological analysis. Hereford plague mortality is evaluated in the local context of the medieval city and examined alongside other Black Death burials.

Methods

The Hereford Cathedral site includes mass graves relating to the Black Death and a 12th-16th century parish cemetery. In total, 177 adult skeletons were analyzed macroscopically: 73 from the mass graves and 104 from the parish cemetery. Skeletal age-at-death was assessed using transition analysis, and sex and stress markers were analyzed.

Results

The age-at-death distributions for the mass graves and parish cemetery were significantly different (p = 0.0496). Within the mass graves, young adults (15–24 years) were substantially over-represented, and mortality peaked at 25–34 years. From 35 years of age onwards, there was little variation in the mortality profiles for the mass graves and parish cemetery. Males and females had similar representation across burial types. Linear enamel hypoplasia was more prevalent within the mass graves (p = 0.0340) whereas cribra orbitalia and tibial periostitis were underrepresented.

Conclusions

Mortality within the Hereford mass graves peaked at a slightly older age than is seen within plague burials from London, but the overall profiles are similar. This demonstrates that young adults were disproportionately at risk of dying from plague compared with other age groups. Our findings regarding stress markers may indicate that enamel hypoplasia is more strongly associated with vulnerability to plague than cribra orbitalia or tibial periostitis.     

Heroin addiction in African Americans: a hypothesis-driven association study

Heroin addiction is a chronic complex disease with a substantial genetic contribution. This study was designed to identify gene variants associated with heroin addiction in African Americans. The emphasis was on genes involved in reward modulation, behavioral control, cognitive function, signal transduction and stress response. We have performed a case–control association analysis by screening with 1350 variants of 130 genes. The sample consisted of 202 former severe heroin addicts in methadone treatment and 167 healthy controls with no history of drug abuse. Single nucleotide polymorphism (SNP), haplotype and multi-SNP genotype pattern analyses were performed. Seventeen SNPs showed point-wise significant association with heroin addiction (nominal P < 0.01). These SNPs are from genes encoding several receptors: adrenergic ( ADRA1A ), arginine vasopressin ( AVPR1A ), cholinergic ( CHRM2 ), dopamine (DRD1 ), GABA-A ( GABRB3 ), glutamate ( GRIN2A ) and serotonin ( HTR3A ) as well as alcohol dehydrogenase ( ADH7 ), glutamic acid decarboxylase ( GAD1 and GAD2 ), the nucleoside transporter ( SLC29A1 ) and diazepam-binding inhibitor ( DBI ). The most significant result of the analyses was obtained for the GRIN2A haplotype G-A-T (rs4587976-rs1071502-rs1366076) with protective effect ( P _uncorrected = 9.6E- 05, P _corrected = 0.058). This study corroborates several reported associations with alcohol and drug addiction as well as other related disorders and extends the list of variants that may affect the development of heroin addiction. Further studies will be necessary to replicate these associations and to elucidate the roles of these variants in drug addiction vulnerability.     

Extracellular water: greater expansion with age in African Americans.

Aging is associated with the onset of chronic diseases that lead to pathological expansion of the extracellular water (ECW) compartment. Healthy aging, in the absence of disease, is also reportedly accompanied by a relative expansion of the ECW compartment, although the studies on which this observation is based are few in number, applied different ECW measurement methods, included small ethnically homogeneous subject samples, and failed to adjust ECW for non-age-related influencing factors. The aim of the current study was to examine, in a large (n = 1,538) ethnically diverse [African American (AA), Asian, Caucasian, Hispanic] subject group the cross-sectional relationships between ECW and age after controlling first for other potential factors that may influence fluid distribution. ECW and intracellular water (ICW) were derived from measured total body water (isotope dilution) and potassium (40K whole body counting). The cross-sectional relationships between ECW, ICW, and ECW/ICW (E/I), and age were developed using multiple regression modelling methods. Body weight, weight squared, height, age, sex, race, and interactions were all significant ECW predictors. The slope of the observed race x age interaction was significantly greater in AA (beta = 0.0005, P = 0.005) than in the three other race groups. Race, sex, and age differences in fluid distribution persisted after adjusting for body composition in a subgroup (n = 994) with dual-energy X-ray absorptiometry lean soft tissue and fat measurements. A relative ECW expansion (i.e., E/I) was present with greater age in most sex-race groups, although the effect was not significantly larger in AA males (P > 0.05) compared with the other race groups, except Asians (P < 0.05). For females, a larger E/I-age effect was found in AA compared with the other race groups, but only the comparison against Hispanics was significant (P < 0.05). The ECW compartment and E/I are thus variably larger, according to race, in healthy older subjects independent of sex, lean soft tissue, and fat mass.     

Two 19th-century Chronobiologists: Thomas Laycock and Edward Smith by P. Lavie

Lavie has written an admirably clear account of some of the work of Laycock and Smith, two researchers whom he considers to be pioneers of chronobiology. In making an assessment of this claim, we will consider two areas in particular: collecting data and interpreting results.     

Admixture in a biologically African caste of black Americans

Social and historical factors account for much of the variation in European ancestry among different Black American populations, including that of McNary, Arizona. The Black population of McNary is socioculturally and geographically isolated. Admixture estimates based upon reflectometry and serological data suggest that this population has less than 5% European ancestry. Anthropometric and hemoglobin data also suggest that this population is more African in ancestry than other Black American populations. Admixture estimates for the population are complicated by several factors. Genetic drift has probably affected Black McNary; estimated effective population size (Ne) is 52.11 and the coefficient of breeding isolation is less than 50. Frequencies of the alleles B, O, and r support this hypothesis; they are quite atypical for a Black American group. Selective migration and occupational selection may also have influenced the current genetic composition of Black McNary. Over 80% of the Black residents of McNary were born in backwoods lumbering towns in the American South. Most Black families in McNary trace their economic reliance on lumbering back several generations. Historical sources and demographic data from Black McNary suggest that Southern Black millworking families formed an endogamous unit that produced this caste, which has a relatively small amount of European ancestry.     

The Quality of Mental Health Care for African Americans

In response to the Surgeon General's request for more research on racial disparities in mental health care, especially research that includes high-need populations (e.g., the homeless, incarcerated, children in foster care, and substance abusers), we examined racial disparities in the provision of mental health counseling, psychotherapy, and pharmacotherapy in hospital outpatient settings using nationally representative data from the 1997 National Hospital Ambulatory Medical Care Survey (NHAMCS). After controlling for diagnosis and other factors, we found that African Americans were less likely than whites to receive mental health counseling and psychotherapy, but more likely than whites to receive pharmacotherapy. We also found that substance abuse clinics were more likely than primary care and specialty mental health clinics to provide mental health counseling and psychotherapy. However, specialty mental health clinics were the only clinics to provide pharmacotherapy. Future research should examine racial disparities in a variety of settings, controlling for diagnosis as well as other factors.     

A comparison of type 2 diabetes risk allele load between African Americans and European Americans

The prevalence of type 2 diabetes (T2D) is greater in populations of African descent compared to European-descent populations. Genetic risk factors may underlie the disparity in disease prevalence. Genome-wide association studies (GWAS) have identified >60 common genetic variants that contribute to T2D risk in populations of European, Asian, African and Hispanic descent. These studies have not comprehensively examined population differences in cumulative risk allele load. To investigate the relationship between risk allele load and T2D risk, 46 T2D single nucleotide polymorphisms (SNPs) in 43 loci from GWAS in European, Asian, and African-derived populations were genotyped in 1,990 African Americans (n = 963 T2D cases, n = 1,027 controls) and 1,644 European Americans (n = 719 T2D cases, n = 925 controls) ascertained and recruited using a common protocol in the southeast United States. A genetic risk score (GRS) was constructed from the cumulative risk alleles for each individual. In African American subjects, risk allele frequencies ranged from 0.024 to 0.964. Risk alleles from 26 SNPs demonstrated directional consistency with previous studies, and 3 SNPs from ADAMTS9, TCF7L2, and ZFAND6 showed nominal evidence of association (p < 0.05). African American individuals carried 38–67 (53.7 ± 4.0, mean ± SD) risk alleles. In European American subjects, risk allele frequencies ranged from 0.084 to 0.996. Risk alleles from 36 SNPs demonstrated directional consistency, and 10 SNPs from BCL11A, PSMD6, ADAMTS9, ZFAND3, ANK1, CDKN2A/B, TCF7L2, PRC1, FTO, and BCAR1 showed evidence of association (p < 0.05). European American individuals carried 38–65 (50.9 ± 4.4) risk alleles. African Americans have a significantly greater burden of 2.8 risk alleles (p = 3.97 × 10^?89) compared to European Americans. However, GRS modeling showed that cumulative risk allele load was associated with risk of T2D in European Americans, but only marginally in African Americans. This result suggests that there are ethnic-specific differences in genetic architecture underlying T2D, and that these differences complicate our understanding of how risk allele load impacts disease susceptibility.     

Sailing against the Wind: African Americans and Women in U.S. Education

Sailing against the Wind: African Americans and Women in U.S. Education. Kofi Lomotey. Albany: State University of New York Press, 1997. 186 pp.     

The Genetic Ancestry of African Americans,Latinos, and European Americans across the United States

Over the past 500 years, North America has been the site of ongoing mixing of Native Americans, European settlers, and Africans (brought largely by the trans-Atlantic slave trade), shaping the early history of what became the United States. We studied the genetic ancestry of 5,269 self-described African Americans, 8,663 Latinos, and 148,789 European Americans who are 23andMe customers and show that the legacy of these historical interactions is visible in the genetic ancestry of present-day Americans. We document pervasive mixed ancestry and asymmetrical male and female ancestry contributions in all groups studied. We show that regional ancestry differences reflect historical events, such as early Spanish colonization, waves of immigration from many regions of Europe, and forced relocation of Native Americans within the US. This study sheds light on the fine-scale differences in ancestry within and across the United States and informs our understanding of the relationship between racial and ethnic identities and genetic ancestry.     

Fine-mapping the genetic basis of CRP regulation in African Americans: a Bayesian approach

Basal levels of C-reactive protein (CRP) have been associated with disease, particularly future cardiovascular events. Twin studies estimate 50% CRP heritability, so the identification of genetic variants influencing CRP expression is important. Existing studies in populations of European ancestry have identified numerous cis-acting variants but leave significant ambiguity over the identity of the key functional polymorphisms. We addressed this issue by typing a dense map of CRP single-nucleotide polymorphisms (SNPs), and quantifying serum CRP in 594 unrelated African Americans. We used Bayesian model choice analysis to select the combination of SNPs best explaining basal CRP and found strong support for triallelic rs3091244 alone, with the T allele acting in an additive manner (Bayes factor > 100 vs. null model), with additional support for a model incorporating both rs3091244 and rs12728740. Admixture analysis suggested SNP rs12728740 segregated with haplotypes predicted to be of recent European origin. Using a cladistic approach we confirmed the importance of rs3091244(T) by demonstrating a significant partition of haplotype effect based on the rs3091244(C/T) mutation (F = 8.91, P = 0.006). We argue that weaker linkage disequilibrium across the African American CRP locus compared with Europeans has allowed us to establish an unambiguous functional role for rs3091244(T), while also recognising the potential for additional functional mutations present in the European genome. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

African ancestry and its correlation to type 2 diabetes in African Americans: a genetic admixture analysis in three U.S. population cohorts

The risk of type 2 diabetes is approximately 2-fold higher in African Americans than in European Americans even after adjusting for known environmental risk factors, including socioeconomic status (SES), suggesting that genetic factors may explain some of this population difference in disease risk. However, relatively few genetic studies have examined this hypothesis in a large sample of African Americans with and without diabetes. Therefore, we performed an admixture analysis using 2,189 ancestry-informative markers in 7,021 African Americans (2,373 with type 2 diabetes and 4,648 without) from the Atherosclerosis Risk in Communities Study, the Jackson Heart Study, and the Multiethnic Cohort to 1) determine the association of type 2 diabetes and its related quantitative traits with African ancestry controlling for measures of SES and 2) identify genetic loci for type 2 diabetes through a genome-wide admixture mapping scan. The median percentage of African ancestry of diabetic participants was slightly greater than that of non-diabetic participants (study-adjusted difference = 1.6%, P<0.001). The odds ratio for diabetes comparing participants in the highest vs. lowest tertile of African ancestry was 1.33 (95% confidence interval 1.13-1.55), after adjustment for age, sex, study, body mass index (BMI), and SES. Admixture scans identified two potential loci for diabetes at 12p13.31 (LOD = 4.0) and 13q14.3 (Z score = 4.5, P = 6.6 × 10(-6)). In conclusion, genetic ancestry has a significant association with type 2 diabetes above and beyond its association with non-genetic risk factors for type 2 diabetes in African Americans, but no single gene with a major effect is sufficient to explain a large portion of the observed population difference in risk of diabetes. There undoubtedly is a complex interplay among specific genetic loci and non-genetic factors, which may both be associated with overall admixture, leading to the observed ethnic differences in diabetes risk.