Spin frustration and magnetic ordering in theS=12molecular antiferromagnetfcc−Cs3C60

We have investigated the low-temperature magnetic state of face-centered-cubic (fcc) Cs3C60, a Mott insulator and the first molecular analog of a geometrically frustrated Heisenberg fcc antiferromagnet with S=1/2 spins. Specific heat studies reveal the presence of both long-range antiferromagnetic ordering and a magnetically disordered state below TN=2.2 K, which is in agreement with local probe experiments. These results together with the strongly suppressed TN are unexpected for conventional atom-based fcc antiferromagnets, implying that the fulleride molecular degrees of freedom give rise to the unique magnetic ground state

GH peak response to GHRH-arginine: relationship to insulin resistance and other cardiovascular risk factors in a population of adults aged 50–90

OBJECTIVE: To assess the GH response to GHRH-arginine in apparently healthy adults in relation to cardiovascular risk factors. DESIGN: Cross-sectional. PATIENTS: Eighty-six male and female volunteers aged 50–90. MEASUREMENTS: GH peak response to GHRH-arginine and cardiovascular risk factors, including obesity, insulin resistance, low levels of high density lipoprotein (HDL) cholesterol, elevated triglycerides, and hypertension. The primary outcome measurement was GH response to GHRH-arginine. The relationship between GH peak responses and cardiovascular risk factors was determined after data collection. RESULTS: GH peaks were highly variable, ranging from 2·3 to 185 µg/l (14% with GH peaks < 9 µg/l). An increasing number of cardiovascular risk factors were associated with a lower mean GH peak (P < 0·0001). By univariate analysis, fasting glucose, insulin, body mass index (BMI), HDL cholesterol and triglycerides were significantly associated with GH peak (all P < 0·0001). Multiple regression analysis revealed that fasting glucose, fasting insulin, BMI, triglycerides and sex accounted for 54% of GH peak variability. The role of abdominal fat as it relates to GH peak was explored in a subset of 45 subjects. Trunk fat and abdominal subregion fat measured by dual energy X-ray absorptiometry (DXA) were inversely related to GH peak (P < 0·008 and 0·001, respectively). Analysis of this subgroup by multiple regression revealed that subregion abdominal fat became the significant obesity-related determinant of GH peak, but still lagged behind fasting insulin and glucose. CONCLUSIONS: GH response to secretagogues was highly variable in apparently healthy adults aged 50–90 years. Peak GH was significantly related to fasting glucose, insulin, BMI, HDL cholesterol, triglycerides, trunk fat and abdominal subregion fat, with fasting glucose ranking first by multiple regression analysis. There was a strong relationship between cardiovascular risk factors and low GH, with individual risk factors being additive. Although these data do not differentiate between low GH being a cause or an effect of these cardiovascular risk factors, they indicate that the relationship between low GH and increased cardiovascular risk may be physiologically important in the absence of pituitary disease

The relationship of bottle feeding and other sucking behaviors with speech disorder in Patagonian preschoolers

<p>Abstract</p> <p>Background</p> <p>Previous studies have shown that children's nonnutritive sucking habits may lead to delayed development of their oral anatomy and functioning. However, these findings were inconsistent. We investigated associations between use of bottles, pacifiers, and other sucking behaviors with speech disorders in children attending three preschools in Punta Arenas (Patagonia), Chile.</p> <p>Methods</p> <p>Information on infant feeding and sucking behaviors, age starting and stopping breast- and bottle-feeding, pacifier use, and other sucking behaviors, was collected from self-administered questionnaires completed by parents. Evaluation of speech problems was conducted at preschools with subsequent scoring by a licensed speech pathologist using age-normative standards.</p> <p>Results</p> <p>A total of 128 three- to five-year olds were assessed, 46% girls and 54% boys. Children were breastfed for an average of 25.2 (SD 9.6) months and used a bottle 24.4 (SD 15.2) months. Fifty-three children (41.7%) had or currently used a pacifier for an average of 11.4 (SD 17.3) months; 23 children (18.3%) were reported to have sucked their fingers. Delayed use of a bottle until after 9 months appeared to be protective for subsequent speech disorders. There was less than a one-third lower relative odds of subsequent speech disorders for children with a delayed use of a bottle compared to children without a delayed use of a bottle (OR: 0.32, 95% CI: 0.10-0.98). A three-fold increase in relative odds of speech disorder was found for finger-sucking behavior (OR: 2.99, 95% CI: 1.10-8.00) and for use of a pacifier for 3 or more years (OR: 3.42, 95% CI: 1.08-10.81).</p> <p>Conclusion</p> <p>The results suggest extended use of sucking outside of breastfeeding may have detrimental effects on speech development in young children.</p

Association Between Periodontitis and Impaired Fasting Glucose and Diabetes

OBJECTIVEMany studies have reported that periodontal disease is associated with diabetes, but its relation with impaired fasting glucose (IFG) has been understudied. This study investigated the relationship between chronic periodontitis, IFG, and diabetes in the U.S. population.RESEARCH DESIGN AND METHODSParticipants in the National Health and Nutrition Examination Survey III, aged ≥20 years, who received periodontal examinations and provided blood samples (n = 12,254) were grouped into quintiles of mean clinical attachment loss (CAL) and pocket depth, with the lowest category being the reference. Plasma fasting glucose was categorized into three groups (normal, <100 mg/dL; IFG, ≥100 but <126 mg/dL; and diabetic, ≥126 mg/dL). Sociodemographic factors and other potential risk factors were obtained by interview or examination. SAS 9.1 was used for statistical analysis accounting for the complex weighted sampling.RESULTSParticipants in the top quintile category of CAL had higher prevalence odds of IFG (odds ratio [OR] 1.55 [95% CI 1.16–2.07]) and diabetes (4.77 [2.69–8.46]) after adjustment for related confounders, compared with those in the bottom quintile. The highest quintile of pocket depth was positively associated with IFG (1.39 [1.00–1.92]) and diabetes (1.63 [1.10–2.42]) compared with the lowest quintile. ORs for CAL increased from the lowest to the highest quintile (P value test for trend <0.01) for all outcomes. The ORs for pocket depth also tended to rise across quintiles.CONCLUSIONSChronic periodontitis measured by CAL and pocket depth was positively associated in a linear relation with IFG and diabetes in U.S. adults

Knowing in general dental practice: Anticipation, constraint, and collective bricolage

National Institute for Health Research (NIHR) Oxford Biomedical Research Centre. Grant Number: BRC‐1215‐2000

Subdividing Y-chromosome haplogroup R1a1 reveals Norse Viking dispersal lineages in Britain

The influence of Viking-Age migrants to the British Isles is obvious in archaeological and place-names evidence, but their demographic impact has been unclear. Autosomal genetic analyses support Norse Viking contributions to parts of Britain, but show no signal corresponding to the Danelaw, the region under Scandinavian administrative control from the ninth to eleventh centuries. Y-chromosome haplogroup R1a1 has been considered as a possible marker for Viking migrations because of its high frequency in peninsular Scandinavia (Norway and Sweden). Here we select ten Y-SNPs to discriminate informatively among hg R1a1 sub-haplogroups in Europe, analyse these in 619 hg R1a1 Y chromosomes including 163 from the British Isles, and also type 23 short-tandem repeats (Y-STRs) to assess internal diversity. We find three specifically Western-European sub-haplogroups, two of which predominate in Norway and Sweden, and are also found in Britain; starlike features in the STR networks of these lineages indicate histories of expansion. We ask whether geographical distributions of hg R1a1 overall, and of the two sub-lineages in particular, correlate with regions of Scandinavian influence within Britain. Neither shows any frequency difference between regions that have higher (≥10%) or lower autosomal contributions from Norway and Sweden, but both are significantly overrepresented in the region corresponding to the Danelaw. These differences between autosomal and Y-chromosomal histories suggest either male-specific contribution, or the influence of patrilocality. Comparison of modern DNA with recently available ancient DNA data supports the interpretation that two sub-lineages of hg R1a1 spread with the Vikings from peninsular Scandinavia

Parent-of-origin-specific allelic associations among 106 genomic loci for age at menarche.

Age at menarche is a marker of timing of puberty in females. It varies widely between individuals, is a heritable trait and is associated with risks for obesity, type 2 diabetes, cardiovascular disease, breast cancer and all-cause mortality. Studies of rare human disorders of puberty and animal models point to a complex hypothalamic-pituitary-hormonal regulation, but the mechanisms that determine pubertal timing and underlie its links to disease risk remain unclear. Here, using genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies, we found robust evidence (P < 5 × 10(-8)) for 123 signals at 106 genomic loci associated with age at menarche. Many loci were associated with other pubertal traits in both sexes, and there was substantial overlap with genes implicated in body mass index and various diseases, including rare disorders of puberty. Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns. Pathway analyses implicated nuclear hormone receptors, particularly retinoic acid and γ-aminobutyric acid-B2 receptor signalling, among novel mechanisms that regulate pubertal timing in humans. Our findings suggest a genetic architecture involving at least hundreds of common variants in the coordinated timing of the pubertal transition