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The wireless power transfer (WPT) technique plays an important role in powering remote devices. The power delivered to the load (PDL) and power transfer efficiency (PTE) are both obtained by knowing the parameters of the WPT system. The knowledge of such parameters and its variability can aid the designer to establish the most important parameters for maximizing the PDL or PTE. This paper presents a variability analysis of PDL and PTE when the WPT parameters change their values. Each parameter can be measured with an associated variability range. The variations in the PDL and PTE functions are computed by using this range of variability of the input parameters. The sensitivities of PDL and PTE with respect to each parameter are also identified with the presented analysis. Experimental measurements were taken on an inductive link, which was specially designed for a recharging battery system of a wireless sensor node with a 5-mm gap between the transmitting and receiving coils. The results pointed out that only small ranges on the input rated values can be tolerated to avoid significant distortions on the output distribution and thus the deviation of the optimal operation point. [ABSTRACT FROM AUTHOR]

Objectives: To examine the specific distribution of liver fat content, visceral and subcutaneous adiposity in normal glucose tolerance (NGT/NGT), isolated impaired fasting glucose (iIFG), isolated impaired glucose tolerance (iIGT) and combined conditions (IFG+IGT), as well as with newly diagnosed type 2 diabetes (nT2D).Design: Multicenter, international observational study: cross-sectional analysis.Subjects: Two thousand five hundred and fifteen patients (50.0% women, 54.5% non-Caucasian) without previously known diabetes were recruited from 29 countries. Abdominal fat distribution was measured by computed tomography (CT). Liver fat was estimated using the CT-liver mean attenuation.Results: Compared with NGT/NGT patients, increased visceral adiposity was found in iIFG, iIGT, IFG+IGT and nT2D; estimated liver fat progressively increased across these conditions. A one-s.d. increase in visceral adiposity was associated with an increased risk of having iIFG (men: odds ratio (OR) 1.41 (95% confidence interval (CI) 1.15-1.74), women: OR 1.62 (1.29-2.04)), iIGT (men: OR 1.59 (1.15-2.01), women: OR 1.30 (0.96-1.76)), IFG+IGT (men: OR 1.64 (1.27-2.13), women: OR 1.83 (1.36-2.48)) and nT2D (men: OR 1.80 (1.35-2.42), women: OR 1.73 (1.25-2.41)). A one-s.d. increase in estimated liver fat was associated with iIGT (men: OR 1.46 (1.12-1.90), women: OR 1.81 (1.41-2.35)), IFG+IGT (men: OR 1.42 (1.14-1.77), women: OR 1.74 (1.35-2.26)) and nT2D (men: OR 1.77 (1.40-2.27), women: OR 2.38 (1.81-3.18)). Subcutaneous abdominal adipose tissue showed an inverse relationship with nT2D in women (OR 0.63 (0.45-0.88)).Conclusions: Liver fat was associated with iIGT but not with iIFG, whereas visceral adiposity was associated with both. Liver fat and visceral adiposity were associated with nT2D, whereas subcutaneous adiposity showed an inverse relationship with nT2D in women. [ABSTRACT FROM AUTHOR]

Aims/hypothesis: Markers of liver injury, such as alanine aminotransferase (ALT), have been associated with atherogenic lipoprotein changes. We examined the extent to which this association was explained by insulin resistance, adiposity, glucose tolerance and chronic inflammation. Methods: In this analysis we included 824 non-diabetic participants (age 40-69 years) in the Insulin Resistance Atherosclerosis Study. No participants reported excessive alcohol intake or treatment with lipid-lowering medications. Lipoproteins and apolipoproteins were measured by conventional methods and lipoprotein heterogeneity by nuclear magnetic resonance (NMR) spectroscopy. Results: ALT had a positive relationship with triacylglycerols, LDL-to-HDL-cholesterol ratio and apolipoprotein B (ApoB) after adjusting for demographic variables ( p < 0.001 for all three relationships). ALT was also associated with the following NMR lipoproteins: positively with large VLDL ( p < 0.001), intermediate-density lipoprotein (IDL) ( p < 0.001) and small LDL subclass particles ( p < 0.001), and VLDL particle size ( p < 0.001); and negatively with large LDL subclass particles ( p < 0.05) and LDL ( p < 0.001) and HDL particle sizes ( p < 0.01). ALT remained associated with IDL and small LDL subclass particles and ApoB after adjusting for glucose tolerance, adiposity, directly measured insulin sensitivity and C-reactive protein. Conclusions/interpretation: ALT is associated with a wide range of atherogenic lipoprotein changes, which are partially explained by insulin resistance, adiposity, glucose tolerance and chronic inflammation. Because of the significant variability in the relationship between ALT and liver fat, further studies are needed to assess the extent of the lipoprotein changes using a direct measure of liver fat. [ABSTRACT FROM AUTHOR]

Aims/hypothesis: Insulin clearance may decline as an early mechanism compensating for deteriorating insulin sensitivity. However, no previous studies have investigated the association between subclinical inflammation or impaired fibrinolysis and insulin clearance. We examined the association between plasminogen activator inhibitor (PAI)-1, C-reactive protein (CRP), TNF-α, leptin and fibrinogen and the progression of metabolic clearance rate of insulin (MCRI) over time. Methods: We studied 784 non-diabetic white, Hispanic and African-American individuals in the Insulin Resistance Atherosclerosis Study (IRAS). Insulin sensitivity, acute insulin response and MCRI were determined from frequently sampled intravenous glucose tolerance tests at baseline and at 5-year follow-up. Inflammatory and fibrinolytic proteins were measured in fasting plasma at baseline. Results: MCRI had declined significantly by 29% at the 5-year follow-up. We observed a significant association between higher plasma PAI-1 levels and the decline in MCRI in multivariable-adjusted regression models ( β = −0.045 [95% CI −0.081, −0.0091]). Higher plasma CRP and leptin levels were associated with a decline in MCRI in unadjusted models, but these associations were non-significant after adjusting for BMI and waist circumference ( β = −0.016 [95% CI −0.041, 0.0083] for CRP; β = −0.044 [95% CI −0.10, 0.011] for leptin). A higher plasma TNF-α concentration was associated with a decline in MCRI in unadjusted ( β = −0.071 [95% CI −0.14, −0.00087]) but not in multivariable-adjusted ( β = −0.056 [95% CI −0.13, 0.017]) models. Plasma fibrinogen level was not associated with the change in MCRI. Conclusions/interpretation: We identified that higher plasma PAI-1 (but not CRP, TNF-α, leptin or fibrinogen) levels independently predicted the progressive decline of insulin clearance in the multiethnic cohort of the IRAS. [ABSTRACT FROM AUTHOR]

Aims: Associations of proinsulin-to-insulin ratios with incident type 2 diabetes have been inconsistent. The use of C-peptide as the denominator in the ratio may allow for better prediction because C-peptide concentration is not affected by hepatic insulin clearance. The objective of this paper was to compare fasting intact and split proinsulin-to-insulin ratios (PI/I, SPI/I) with intact and split proinsulin-to-C-peptide ratios (PI/C-pep, SPI/C-pep) in the prediction of type 2 diabetes. Methods: Prospective data on 818 multi-ethnic adults without diabetes at baseline from the Insulin Resistance Atherosclerosis Study (IRAS) were used. Insulin sensitivity (S) and acute insulin response (AIR) were determined from frequently sampled intravenous glucose tolerance tests, and fasting intact and split proinsulin were measured using specific two-site monoclonal antibody-based immunoradiometric assays. Associations of proinsulin ratios with type 2 diabetes were determined using logistic regression and differences in prediction were assessed by comparing areas under the receiver operating characteristic curve (AROCs). Results: In logistic regression analyses, PI/C-pep and SPI/C-pep were more strongly associated with incident type 2 diabetes ( n = 128) than PI/I and SPI/I, and were significantly better predictors of diabetes in AROC analyses (PI/C-pep = 0.662 vs PI/I = 0.603, p = 0.02; SPI/C-pep = 0.690 vs SPI/I = 0.631, p = 0.01). Both PI/C-pep and SPI/C-pep were associated with type 2 diabetes after adjustment for age, sex, ethnicity, waist circumference, impaired glucose tolerance, lipids and S. Both PI/C-pep and SPI/C-pep were significantly associated with incident type 2 diabetes in models that included AIR. Conclusions: Proinsulin-to-C-peptide ratios were stronger predictors of diabetes in comparison with proinsulin-to-insulin ratios. These findings support the use of C-peptide as the denominator for proinsulin ratios, to more accurately reflect the degree of disproportional hyperproinsulinaemia. [ABSTRACT FROM AUTHOR]

Objective:Previous studies have replicated the association of variants within FTO (fat mass- and obesity-associated) intron 1 with obesity and adiposity quantitative traits in populations of European ancestry. Non-European populations, however, have not been so intensively studied. The goal of this investigation was to examine the association of FTO single-nucleotide polymorphisms (SNPs), prominent in the literature in a multiethnic sample of non-Hispanic White American (n=458), Hispanic American (n=373) and African American (n=288) subjects from the Insulin Resistance Atherosclerosis Study (IRAS). This cohort provides the unique ability to evaluate how variation within FTO influences measures of adiposity and glucose homeostasis in three different ethnicities, which were ascertained and examined using a common protocol.Design:A total of 26 FTO SNPs were genotyped, including those consistently associated in the literature (rs9939609, rs8050136, rs1121980, rs1421085, rs17817449 and rs3751812), and tested for association with adiposity and glucose homeostasis traits.Results:For the adiposity phenotypes, these and other SNPs were associated with body mass index (BMI) in both non-Hispanic Whites (P-values ranging from 0.015 to 0.048) and Hispanic Americans (P-values ranging from 7.1 × 10−6 to 0.027). In Hispanic Americans, four other SNPs (rs8047395, rs10852521, rs8057044 and rs8044769) still showed evidence of association after multiple comparisons adjustment (P-values ranging from 5.0 × 10−5 to 5.2 × 10−4). The historically associated BMI SNPs were not associated in the African Americans, but rs1108102 was associated with BMI (P-value of 5.4 × 10−4) after accounting for multiple comparisons. For glucose homeostasis traits, associations were seen with acute insulin response in non-Hispanic Whites and African Americans. However, all associations with glucose homeostasis measures were no longer significant after adjusting for multiple comparisons.Conclusion:These results replicate the association of FTO intron 1 variants with BMI in non-Hispanic Whites and Hispanic Americans but show little evidence of association in African Americans, suggesting that the effect of FTO variants on adiposity phenotypes shows genetic heterogeneity dependent on ethnicity. [ABSTRACT FROM AUTHOR]

ims/hypothesis: Although protective relationships between coffee consumption and type 2 diabetes mellitus have consistently been observed, few studies have examined the relationships between coffee consumption and underlying pathophysiological defects that characterise diabetes aetiology. The aim of this study was to explore the associations between caffeinated and decaffeinated coffee consumption and measures of insulin sensitivity and secretion. Methods: The study population included 954 multi-ethnic non-diabetic adults from the Insulin Resistance Atherosclerosis Study (IRAS). Multiple regression analyses were performed to examine the cross-sectional relationships between caffeinated and decaffeinated coffee intake and insulin sensitivity and acute insulin response, measured by a frequently sampled intravenous glucose tolerance test, 2 h postload glucose measured by OGTT, fasting insulin, and proinsulin to C-peptide ratios. Results: Caffeinated coffee intake was positively associated with insulin sensitivity ( β = 0.054; SE = 0.026; p = 0.04) and inversely related to 2 h postload glucose ( β = −0.37; SE = 0.10; p = 0.0003) in fully adjusted models. Caffeinated coffee intake was not associated with acute insulin response or proinsulin ratios. Decaffeinated coffee intake was inversely related to 2 h postload glucose ( β = −0.47; SE = 0.18; p = 0.0096) and positively related to acute insulin response ( β = 0.191; SE = 0.077; p = 0.0132). Decaffeinated coffee intake was inversely related to the ratios of both intact and split proinsulin to C-peptide ( β = −0.150; SE = 0.061; p = 0.0148; β = −0.254; SE = 0.068; p = 0.0002, respectively). Conclusions/interpretation: In this cross-sectional study, caffeinated coffee was positively related to insulin sensitivity and decaffeinated coffee was favourably related to measures of beta cell function. These results provide pathophysiological insight as to how coffee could impact the risk of type 2 diabetes mellitus. [ABSTRACT FROM AUTHOR]

The majority of type 2 diabetes genome-wide association studies (GWAS) to date have been performed in European-derived populations and have identified few variants that mediate their effect through insulin resistance. The aim of this study was to evaluate two quantitative, directly assessed measures of insulin resistance, namely insulin sensitivity index (SI) and insulin disposition index (DI), in Hispanic-American participants using an agnostic, high-density single nucleotide polymorphism (SNP) scan, and to validate these findings in additional samples. A two-stage GWAS was performed in Hispanic-American samples from the Insulin Resistance Atherosclerosis Family Study. In Stage 1, 317,000 SNPs were assessed using 229 DNA samples. SNPs with evidence of association with glucose homeostasis and adiposity traits were then genotyped on the entire set of Hispanic-American samples ( n = 1,190). This report focuses on the glucose homeostasis traits: SI and DI. Although evidence of association did not reach genome-wide significance ( p = 5 × 10−7), in the combined analysis SNPs had admixture-adjusted p values of pADD = 0.00010–0.0020 with 8 to 41% differences in genotypic means for SI and DI. Several candidate loci were identified that are nominally associated with SI and/or DI in Hispanic-American participants. Replication of these findings in independent cohorts and additional focused analysis of these loci is warranted. [ABSTRACT FROM AUTHOR]

Central obesity, insulin resistance and beta cell dysfunction are independent risk factors for incident type 2 diabetes, although few studies have used detailed measures of these disorders. Our objective was to study the association of directly measured visceral and subcutaneous adipose tissue (VAT, SAT), insulin sensitivity ( SI) and the acute insulin response (AIR) with incident type 2 diabetes. Participants were 1,230 Hispanic-Americans and African-Americans in the Insulin Resistance Atherosclerosis Study (IRAS) Family Study who were free of type 2 diabetes at baseline (2000–2002). SI and AIR were determined from frequently sampled IVGTTs with minimal model analysis. VAT and SAT were determined by computed tomography. Impaired fasting glucose and type 2 diabetes were defined according to American Diabetes Association criteria. Incident type 2 diabetes was diagnosed in 90 participants after 5 years. After adjustment for age, sex, ethnicity, centre, impaired fasting glucose, triacylglycerol, HDL-cholesterol and systolic BP, both SI and AIR were inversely associated with type 2 diabetes ( SI, OR 0.53, 95% CI 0.39–0.73; AIR, OR 0.22, 95% CI 0.14–0.34 per SD; both p < 0.001), while both VAT and SAT were positively associated with type 2 diabetes (VAT, OR 1.68, 95% CI 1.22–2.33; SAT, OR 1.49, 95% CI 1.13–1.99; both p < 0.01). In a model including all four factors, SI and AIR ( SI, OR 0.55, 95% CI 0.37–0.80; AIR, OR 0.21, 95% CI 0.13–0.33; both p < 0.01) were significant predictors of type 2 diabetes, although associations with VAT and SAT were no longer significant. A significant sex × VAT interaction indicated a stronger association of VAT with type 2 diabetes in women than in men. Insulin resistance, beta cell dysfunction and VAT predicted incident type 2 diabetes, with evidence of a stronger association of VAT with type 2 diabetes among women. [ABSTRACT FROM AUTHOR]

This study sought to identify genes and regions in the human genome that are associated with the acute insulin response to glucose (AIRg), an important predictor of type 2 diabetes, in Hispanic-American participants from the Insulin Resistance Atherosclerosis Family Study (IRAS FS). A two-stage genome-wide association scan (GWAS) was performed in IRAS FS Hispanic-American samples. In the first stage, 317K single nucleotide polymorphisms (SNPs) were assessed in 229 Hispanic-American DNA samples from 34 families from San Antonio, TX, USA. SNPs with the most significant associations with AIRg were genotyped in the entire set of IRAS FS Hispanic-American samples ( n = 1,190). In chromosomal regions with evidence of association, additional SNPs were genotyped to capture variation in genes. No individual SNP achieved genome-wide levels of significance ( p < 5 × 10−7); however, two regions (chromosomes 6p21 and 20p11) had multiple highly ranked SNPs that were associated with AIRg. Additional genotyping in these regions supported the initial evidence of variants contributing to variation in AIRg. One region resides in a gene desert between PXT1 and KCTD20 on 6p21, while the region on 20p11 has several viable candidate genes ( ENTPD6, PYGB, GINS1 and RP4-691N24.1). A GWAS in Hispanic-American samples identified several candidate genes and loci that may be associated with AIRg. These associations explain a small component of variation in AIRg. The genes identified are involved in phosphorylation and ion transport, and provide preliminary evidence that these processes are important in beta cell response. [ABSTRACT FROM AUTHOR]

Metabolic abnormalities frequently develop prior to the diagnosis of type 2 diabetes and chronic kidney disease. However, it is not known whether GFR predicts the onset of type 2 diabetes. Incident diabetes was ascertained in the Insulin Resistance Atherosclerosis Study (IRAS) ( n = 864; age 40–69 years; median follow-up 5.2 years [4.5–6.6 years]; 141 incident cases of diabetes). GFR was estimated by the Modification of Diet in Renal Disease equation. We assessed the relationship between GFR and incident diabetes by logistic regression analysis. Results were adjusted for age, sex, ethnicity, clinic location, BMI, systolic blood pressure, antihypertensive treatment, family history of diabetes, insulin sensitivity and secretion, albumin to creatinine ratio, and levels of triacylglycerols, HDL-cholesterol, plasminogen activator inhibitor-1, and fasting and 2 h glucose. The relationship between GFR and incident diabetes was not linear. This relationship was statistically significant ( p = 0.039) using a restricted cubic polynomial spline for GFR as a regression modelling strategy. Participants were stratified by GFR quintiles. Mean values for GFR from the first to the fifth quintile were 60.8, 71.6, 79.8, 88.2 and 109.0 ml min−1 1.73 m−2. Relative to the fourth quintile, the odds ratios of incident diabetes for the first, second, third and fifth quintiles were 2.32 (95% CI 1.06–5.05), 1.76 (95% CI 0.80–3.88), 1.26 (95% CI 0.56–2.84) and 2.59 (95% CI 1.18–5.65), respectively. Individuals in the upper and lower ranges of GFR are at increased risk of future diabetes. GFR and type 2 diabetes may share common pathogenic mechanisms. [ABSTRACT FROM AUTHOR]

Objective:Obesity is widely accepted to be influenced by both environmental and genetic factors. Several recent studies have used the positional cloning approach in an attempt to discover genes contributing to obesity. In the IRAS Family Study a genomewide scan was performed on 1425 individuals of Hispanic descent (90 extended pedigree families) to identify regions of the genome linked to obesity phenotypes.Methods:Nonparametric QTL linkage analysis was performed using a variance components approach. The genome scan was performed in two phases: an initial genome scan in 45 families and a replication scan in 45 families. Fine mapping and candidate gene analyses were also performed. General estimating equations (GEE1) and quantitative pedigree disequilibrium tests (QPDT) were used for association analysis of single SNP and haplotype data.Results:Evidence for linkage to obesity traits was observed in each scan on the long arm of chromosome 17. When data from both scans was combined, a region on chromosome 17q was identified with evidence of linkage to visceral adipose tissue (VAT; LOD 3.11), waist circumference (WAIST) (LOD 2.5) and body mass index (BMI) (LOD 2.81). Nine additional microsatellite markers were identified and genotyped on all Hispanic individuals, with a mean marker density of approximately 1 marker/3 cM. Evidence of linkage remained significant with LOD 3.05 for VAT, LOD 2.44 for BMI and LOD 1.92 for WAIST. Fine mapping analyses suggest the possibility of two different obesity loci. In addition, the LOD – 1 interval of the major VAT peak decreased from 83–108 to 95–111 cM. Three positional candidate genes under the peak: somatostatin receptor 2 (SSTR2), galanin receptor 2 (GALR2), and growth hormone bound protein receptor 2 (GRB2) were chosen for detailed evaluation. Multiple polymorphisms within each candidate were genotyped and tested for association with the obesity phenotypes. Little evidence of association was detected between polymorphisms and obesity traits.Conclusion:In conclusion, replication of linkage and fine mapping suggest that a region on chromosome 17q contains a gene (or genes) that contributes to the genetic etiology of obesity with the strongest evidence for linkage to VAT. Candidate genes in the region do not appear to account for the evidence of linkage. Additional studies are necessary to identify the obesity-related polymorphisms.International Journal of Obesity (2006) 30, 1433–1441. doi:10.1038/sj.ijo.0803298; published online 7 March 2006 [ABSTRACT FROM AUTHOR]

Summary:Fludarabine is a nonmyeloablative immunosuppressant increasingly used as a component of alternative reduced-intensity conditioning regimens prior to allogeneic stem cell transplantation (SCT). However, we have previously shown that 2-fluoroadenine 9-beta-D-arabinofuranoside (F-Ara) as the active metabolized form of fludarabine induces damage, activation and allogenicity in human microvascular endothelial cells (HMEC). We had also identified the pharmaceutic compound Defibrotide (DF), originally used in the treatment of veno-occlusive disease and thrombotic microangiopathy, as being protective against F-Ara-induced dysfunction of HMEC, importantly, without affecting the antileukemic effect of F-Ara. In the present report, we show that a recently developed derivative of DF, Oligotide, similarly downregulates F-Ara-induced activation and damage of HMEC as well as their antigenicity for allogeneic CD8+T cells. In addition, Oligotide could also block F-Ara-mediated transendothelial migration of peripheral blood cells across the HMEC barrier. Taken together, these observations argue for a potential clinical use of both DF and Oligotide in pre transplant conditioning.Bone Marrow Transplantation (2005) 35, 915-920. doi:10.1038/sj.bmt.1704930 Published online 21 March 2005 [ABSTRACT FROM AUTHOR]

In obese people, an increase of plasma leptin levels is well-known and is seen as a consequence of the increased body fat mass. Moreover, a relationship between fasting concentrations of leptin and insulin has been described. Hyperinsulinemia is considered to be indicative of insulin resistance. We aimed at elucidating the interrelations between leptin, insulin and insulin resistance in type 2 diabetic patients. Under metabolic ward conditions, we investigated 21 moderately overweight men with type 2 diabetes. The patients had a mean age of 49.1 years, a mean body mass index (BMI) of 26.8 kg/m2, and a mean diabetes duration of 82.5 months. All patients were treated with diet alone. We measured fasting leptin and insulin levels, body composition by determination of total body water, and insulin resistance by euglycemic hyperinsulinemic clamp technique. At univariate analysis, fasting leptin level significantly and positively correlated with BMI (r=0.49, p=0.02) and with fasting insulin (r=0.69, p=0.001), while it negatively correlated with the glucose disposal rate (r=−0.62, p=0.002). Furthermore, leptin was inversely correlated with HDL-cholesterol (r=−0.45, p=0.04). When excluding the influence of body fat mass or of BMI in partial correlation analysis, the correlations between leptin and insulin or insulin sensitivity remained significant. The relationship between insulin resistance (as measured directly in the clamp experiments) and leptin concentrations was also shown by subdividing the diabetic patients according to tertiles of insulin sensitivity. The highest fasting leptin levels were observed in those patients with the most expressed insulin resistance. Our data point to a functional relationship between insulin resistance and leptin concentrations in insulin-resistant type 2 diabetic men, independently of body composition. This relationship is believed to be mediated by insulin. [ABSTRACT FROM AUTHOR]

The potassium doped monophosphate tungsten bronzes KxP4W8O32 are two-dimensional metals which show a metal-to-metal transition at a critical temperature which depends on the doping level. The metal-to-metal transition is accompanied by the formation of a commensurate charge density wave with wave vector ( π/b,0) which is independent of the doping level. Undoped P4W8O32, on the other hand, has two metal-to-metal transitions which are connected to the formation of incommensurate charge density waves. We measured the infrared reflectivity of the series KxP4W8O32 ( x = 0 - 1.57) in the spectral range from 100 to 10 000 cm-1 for room temperature and well below the critical temperature. Polarization-dependent infrared spectra find a two-dimensional behavior in the normal and the charge density wave state and show signatures of hybridization between one- and two-dimensional conduction bands. In undoped P4W8O32 the essentials of the charge density wave state can be understood from the nesting vectors of the calculated Fermi surface and two gaps are observed in the infrared spectra. The gap sizes are a factor of about 2.5 bigger than the predictions from mean-field theory in the weak-coupling limit which suggests medium- or strong electron-phonon coupling. For potassium doped KxP4W8O32 one gap is observed in the charge density wave state. The energetics of the charge density formation may be dominated by the energy required for the lattice modulation. [ABSTRACT FROM AUTHOR]

In recent years insight has been gained into the electronic structure of layered cuprates using angle-resolved photoelectron spectroscopy. In many of these studies it is assumed that the electron-photon matrix element follows the trends set by the atomic photoionization cross sections and does not influence lineshape, dispersion and the k-dependence of the spectral intensity. In this study using Sr2CuO2Cl2 as an example it will be shown that the electron-photon matrix element can have a strong impact on both strength and shape of a feature in an angle-resolved photoelectron spectrum of a layered cuprate which can strongly affect information on character and the momentum-dependence of the energy and spectral weight of a state deduced from the spectra. The results of this study put an emphasis on the need to employ the whole parameter range of the ARPES method to get reliable information on the spectral function of cuprates for which purpose synchrotron radiation is an uniquely suited tool. [ABSTRACT FROM AUTHOR]

The first electron-removal states of the layered cuprate Ba2Cu3O4Cl2 were measured using angle-resolved photoelectron spectroscopy. The symmetry and energy-momentum relations of the lowest-lying states were determined and interpreted in terms of the motion of a single hole in the two different planar Cu-O subsystems of the Cu3O4 plane. One subsystem is antiferromagnetic as in the undoped parent compounds of the high-temperature superconductors and the other is paramagnetic and corresponds to the strongly overdoped case. The data are compared to theoretical results on hole dynamics in two-dimensional antiferromagnetic or paramagnetic spin backgrounds. The lineshape, symmetry and dispersion of the first electron-removal states of Ba2Cu3O4Cl2 can be described in terms of Zhang-Rice singlets within a single band model. The photohole lifetime in the paramagnetic subsystem of the Cu3O4 plane is much smaller than with an antiferromagnetic spin background. [ABSTRACT FROM AUTHOR]

Aims/hypothesis. Proinsulin concentrations are increased relative to insulin concentrations in subjects with Type II (non-insulin-dependent) diabetes mellitus. This could be secondary to hyperglycaemia or insulin resistance or due to a defect in insulin secretion. Methods. We investigated the association between fasting insulin, intact proinsulin and the intact proinsulin: insulin ratio with insulin sensitivity, estimated by a frequently sampled intravenous glucose tolerance test and the minimal model and with acute insulin response (AIR) in 182 newly diagnosed Type II diabetic subjects aged 40 to 69 years. None of the subjects was receiving hypoglycaemic medication. Results. Insulin sensitivity correlated inversely with fasting insulin ( r s = –0.42) and intact proinsulin ( r s = –0.32) ( p < 0.001). The intact proinsulin:insulin ratio was not correlated with insulin sensitivity. AIR correlated positively with intact proinsulin ( r s = 0.23) and inversely with the intact proinsulin:insulin ratio ( r s = –0.29, p < 0.001). Fasting glucose correlated positively with intact proinsulin ( r s = 0.34) and the intact proinsulin:insulin ratio ( r s = 0.24, p < 0.001). The intact proinsulin:insulin ratio increased by decreasing AIR (quartiles of AIR from high to low: 7.8, 8.2, 9.7 and 12.1 %, p < 0.001). This association was independent of age, sex, ethnicity, body mass index, fasting glucose, and insulin sensitivity. Conclusion/interpretation. Insulin resistance (low insulin sensitivity) was not related to the intact proinsulin:insulin ratio in subjects with Type II diabetes. In contrast, both low AIR and high fasting glucose concentrations were associated with a disproportionate increase in proinsulin concentration. These results suggest that increased intact proinsulin:insulin ratio is a marker of a defect in insulin secretion in Type II diabetic subjects. [Diabetologia (1999) 42: 1060–1066] [ABSTRACT FROM AUTHOR]

INTRODUCTION: Leptin (the product of the human OB gene) is increased in obese individuals, suggesting resistance to its effect. However, there is considerable variability in leptin levels at each level of body mass index (BMI), suggesting that genetic and environmental factors may regulate leptin concentrations. Previous data have suggested that leptin levels are associated with insulin resistance and in a few reports with impaired insulin secretion. We examined whether non-diabetic subjects, with elevated specific insulin and proinsulin levels, had increased leptin levels. METHODS: We used a radioimmunoassay (RIA) to measure serum leptin levels in 197 non-diabetic Mexican Americans and non-Hispanic whites from the San Antonio Heart Study. We also evaluated whether leptin levels were associated with impaired insulin secretion or increased beta cell stress, as evaluated by the fasting proinsulin/insulin ratio. (Higher fasting proinsulin/insulin ratios are thought to reflect impaired insulin secretion.) RESULTS: Leptin levels were significantly correlated with fasting specific insulin (r=0.55, P<0.001) and proinsulin (r=0.57, P<0.001) and inversely with the proinsulin/insulin ratio (r=-0.154, P=0.035) after adjustment for age, gender, ethnicity and 2 h glucose. These associations were similar in men and women and in Mexican Americans and in non-Hispanic whites. After further adjustment for BMI and waist-to-hip ratio (WHR), leptin levels remained significantly correlated with specific insulin (r=0.31, P<0.001) and proinsulin (r=0.24, P<0.001) although the magnitude of the associations were considerably attenuated. CONCLUSION: We conclude that specific insulin and proinsulin are positively related to leptin levels and that these associations are to some degree independent of obesity and body fat distribution. Thus, subjects with increased insulin levels may be relatively resistant to the effects of leptin. However, leptin levels are associated with a decrease in... [ABSTRACT FROM AUTHOR]

BACKGROUND: Leptin, a hormone which is produced by adipose tissue, has been shown to inhibit food intake and increase energy expenditure. In humans, leptin levels are correlated with body fat. In addition, leptin levels decline in subjects who lose weight. Yet few data exist on whether leptin levels predict weight change, except for a recent report suggesting that low leptin levels predict weight gain in very obese middle-aged Pima Indians. METHODS: We have examined the association between baseline leptin levels and subsequent weight gain over 3.25 y in 180 non-diabetic participants in the Mexico City Diabetes Study. RESULTS: At baseline, the correlation between leptin levels and body mass index (BMI) was 0.712 in men and 0.691 in women (both P<0.001). Subjects were matched on age (±2 y), gender and BMI (±2 kg/m2) at baseline. Baseline BMI was 25.3 kg/m2 in men and 27.2 kg/m2 in women. Baseline leptin levels (ng/ml) did not predict weight gain in either men (weight gainers: 4.3; weight stable: 5.8; and weight losers: 5.2) or women (weight gainers: 17.4; weight stable: 17.7; and weight losers: 17.4). CONCLUSIONS: We conclude that baseline leptin levels did not predict weight change in moderately obese individuals. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Leptin is a hormone regulating weight in the mouse. Leptin regulates food intake and appetite. Leptin concentrations are increased in obese individuals suggesting resistance to its effect. However, there is considerable variability in leptin levels at each level of adiposity suggesting that environmental and genetic factors may regulate leptin concentrations. We examined whether subjects with decreased insulin sensitivity have increased leptin levels. METHODS: We used a radioimmunoassay to measure serum leptin levels and the hyperinsulinemic euglycemic clamp (with indirect calorimetry) to measure insulin sensitivity in 87 normoglycemic relatively lean men. RESULTS: Leptin levels were significantly correlated with fasting insulin (r=0.58), insulin area (r=0.45), overall (r=-0.57), non-oxidative (r=-0.51) and oxidative (r=-0.51) whole body glucose disposal (all P-values<0.001). After adjustment for body mass index, leptin levels remained significantly correlated with fasting insulin (r=0.44), insulin area (r=0.40), overall (r=-0.40), non-oxidative (r=-0.28) and oxidative (r=-0.33) whole body glucose disposal although the magnitude of the associations was considerably decreased. Leptin levels were significantly related to insulin sensitivity in both less obese and more obese subjects. CONCLUSIONS: We conclude that leptin concentrations are related to insulin resistance and insulin concentrations in relatively lean normoglycemic men and these associations are to some extent independent of body mass index. Thus, subjects with insulin resistance may be relatively resistant to the effects of leptin. [ABSTRACT FROM AUTHOR]

OBJECTIVE: It has been suggested that insulin could regulate the secretion of leptin, the ob gene product, but the findings have been contradictory. Therefore, we studied the association between leptin and insulin secretion and insulin sensitivity in impaired glucose tolerance (IGT). SUBJECTS: 39 obese subjects (17 men, 22 women, body mass index (BMI) 30.6±0.6 kg/m2, age 54±1 y, mean±s.e.m.) with IGT. MEASUREMENTS: Leptin, insulin sensitivity and first-phase insulin response (frequently sampled intravenous glucose tolerance test), anthropometry, infrared densitometric assay. RESULTS: Leptin correlated with BMI (r=0.36, P=0.022), fat percent (r=0.74, P<0.001) and fat mass (r=0.53, P<0.001). After adjustment for sex and fat mass, leptin showed no significant linear correlation with fasting insulin, insulin sensitivity or first-phase insulin response. CONCLUSION: In obese IGT subjects fat mass is the main correlate of serum leptin concentration. First-phase insulin response or the degree of insulin resistance are not associated with leptin in IGT. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Leptin is the product of ob gene shown to regulate body fat in mice. It is produced by human adipose tissue as well, but its physiological functions in man are not known. We explored if there is a relationship in obese humans with serum leptin and energy and fuel metabolism. DESIGN: Cross-sectional study including 45 obese (10 men, 35 women; age and body mass index: 42±7y and 35.1 ± 3.6 kg/m², respectively). MEASUREMENTS: Food intake by a four-day-food record, blood samples for serum leptin concentrations and resting energy expenditure by indirect calorimetry. RESULTS: Leptin concentrations showed an inverse association (adjusted for fat mass, age and sex) with resting energy expenditure, respiratory quotient and carbohydrate oxidation rate (r = -0.324, P < 0.05; r = -0.420, P < 0.01; r = 0.478, P = < 0.01, respectively), and interestingly, also with dietary fat intake (unadjusted r = -0.30, P < 0.05). Especially, leptin concentrations were elevated in those with Iow resting energy expenditure and respiratory quotient (below the median). CONCLUSION: Serum leptin concentrations in obese subjects showed an inverse association with resting energy expenditure, respiratory quotient and carbohydrate oxidation rate. The physiological significance of these associations is unclear at the moment but could indicate that obese subjects show resistance to the actions of leptin also outside the brain in terms of regulating metabolic rate and fuel metabolism. [ABSTRACT FROM AUTHOR]

Although insulin resistance and decreased insulin secretion are characteristic of established non-insulin-dependent diabetes mellitus (NIDDM), which of these metabolic abnormalities is the primary determinant of NIDDM is still controversial. A disproportionate increase in the proinsulin to insulin ratio has been proposed as a marker of compromised insulin secretion. We examined the association of fasting immunoreactive insulin (which cross-reacts with proinsulin), specific insulin (which does not cross-react with proinsulin), total immunoreactive proinsulin (or insulin precursors), and the fasting proinsulin/specific insulin ratio to the risk of developing NIDDM in the 3.25-year follow-up of the Mexico City Diabetes Study. These measurements were made in 85 subjects who subsequently converted to NIDDM (prediabetic subjects) and in 85 age and gender matched subjects who remained non-diabetic at follow-up (control subjects). Immunoreactive insulin, proinsulin and the proinsulin/specific insulin ratio were significantly higher in prediabetic than in control subjects. However, the relation between specific insulin and the development of NIDDM was weaker than for proinsulin or immunoreactive insulin. After further adjustment for obesity, body fat distribution and glucose tolerance status, proinsulin and the proinsulin/specific insulin ratio, but not specific or immunoreactive insulin, predicted conversion to NIDDM. A high proinsulin/specific insulin ratio predicted conversion to NIDDM both in subjects with normal and those with impaired glucose tolerance at baseline. We conclude that in prediabetic subjects increased proinsulin, a marker of islet cell distress or compromised insulin secretion, is associated with rapid conversion (within 3.25 years) to NIDDM even in obese populations. [Diabetologia (1997) 40: 830–837] [ABSTRACT FROM AUTHOR]

Men with non-insulin-dependent diabetes mellitus (NIDDM) have a twofold increased risk of coronary heart disease and women with NIDDM have a fourfold increased risk. The reasons for this higher relative risk in NIDDM women than in NIDDM men is not completely understood. Since some studies suggest that duration of clinical diabetes and degree of hyperglycaemia have only a modest effect on coronary heart disease risk, we hypothesized that women who eventually convert to NIDDM might have a more atherogenic pattern of lipids and blood pressure relative to subjects who do not convert than male converters, even in the prediabetic period. We examined this issue in Mexican-American subjects in the 8-year follow-up of the San Antonio Heart Study. Seventy-nine out of 801 men converted to NIDDM compared to 133 out of 1131 women. In both men and women, conversion to NIDDM was significantly associated with increased body mass index, fasting insulin and glucose, higher triglyceride and blood pressure and lower high density lipoprotein (HDL) cholesterol. The relative differences between converters and non-converters was significantly greater for women than for men; this interaction term for gender by conversion status was statistically significant for fasting insulin, triglyceride, HDL cholesterol and diastolic blood pressure. Thus, the higher relative risk for coronary heart disease in women with NIDDM relative to men with NIDDM may be partially due to their greater burden of cardiovascular risk factors even prior to the onset of diabetes. [Diabetologia (1997) 40: 711–717] [ABSTRACT FROM AUTHOR]

Mexican Americans have an increased risk of non-insulin-dependent diabetes mellitus (NIDDM) relative to non-Hispanic whites which is only partially explained by their excess overall obesity and unfavourable body fat distribution. Non-diabetic Mexican Americans have hyperinsulinaemia and insulin resistance relative to non-Hispanic whites. We therefore hypothesized that the insulin resistance might be a more important predictor of NIDDM in high-risk populations characterized by obesity and insulin resistance, while compromised insulin secretion might be a more important risk factor for NIDDM in low-risk populations. We assessed the ability of ethnicity (Mexican American vs non-Hispanic white), age, overall adiposity (body mass index [BMI]), unfavourable body fat distribution (as assessed by waist-to-hip ratio [WHR]), glucose tolerance (impaired glucose tolerance vs normal glucose tolerance), fasting insulin and compromised insulin secretion (as assessed by increment in insulin to the increment in glucose over the first 30 min of an oral glucose tolerance test (ΔI30/ΔG30)) to predict future NIDDM. In the 8-year follow-up of the San Antonio Heart Study, NIDDM developed in 11.7 % (107/914) of Mexican Americans and in 5.0 % (18/362) of non-Hispanic whites ( p < 0.001). Multivariate predictors of NIDDM by multiple logistic regression analysis included increased age, BMI, WHR, fasting insulin and impaired glucose tolerance and decreased insulin secretion. The strongest independent predictors of NIDDM were high fasting insulin and decreased insulin secretion. These risk factors predicted NIDDM equally well in high and low-risk populations. [Diabetologia (1997) 40: 62–66] [ABSTRACT FROM AUTHOR]

The relative importance of insulin resistance and abnormal insulin secretion as risk factors for the development of impaired glucose tolerance (IGT) is controversial. Few prospective data are available on metabolic precursors of IGT. We examined the relation of fasting serum insulin level (as a marker of insulin resistance) and change in insulin/glucose ratio (Δ I /ΔG) over the first 30 min after glucose ingestion (as a marker of insulin secretion) as predictors of the 7-year development of IGT in 839 Mexican Americans and non-Hispanic whites with normal glucose tolerance at baseline from the San Antonio Heart Study. IGT eventually developed in 148 subjects. When modelled separately, fasting serum insulin (odds ratio (OR)=2.60,95 % confidence interval (CI)=1.58,4.28, p<0.005), but not Δ I /ΔG (OR=0.80, 95 % CI=0.50,1.27, p=0.339) predicted the development of IGT. However, when both variables were included in the same logistic regression model, fasting serum insulin (OR=3.50, 95 % CI=1.97,6.21, p<0.001) and low Δ I /ΔG (OR=0.48, 95 % CI=0.28,0.82, p=0.008) both predicted IGT. These results were basically unchanged after further adjustment for obesity, body fat distribution and fasting plasma glucose level. We conclude that both decreased insulin secretion (as assessed by low Δ I /ΔG) and increased insulin resistance (as assessed by fasting serum insulin) predict the development of IGT and are thus early precursors of non-insulin-dependent diabetes mellitus; further studies of insulin secretion should take into account the level of basal insulin resistance. [ABSTRACT FROM AUTHOR]

Recently, the presence of small dense low density lipoprotein (LDL) has been postulated to be a stronger risk factor for coronary heart disease than large LDL. While small dense LDL has been associated with individual components of the insulin resistance syndrome such as hypertension, high triglyceride level, low high density (HDL) cholesterol, and diabetess mellitus, there has been little work exploring whether LDL size is decreased in subjects with multiple metabolic disorders. We examined the association of LDL size and pattern to specific insulin (which does not cross-react with proinsulin), proinsulin, increased triglyceride, decreased HDL, hypertension and impaired glucose tolerance in 488 non-diabetic subjects from the San Antonio Heart Study. LDL size was significantly related to specific insulin, proinsulin and the fasting proinsulin/insulin ratio. Small dense LDL was significantly associated with high triglyceride level, decreased HDL cholesterol, hypertension and impaired glucose tolerance. LDL size (å) decreased in a stepwise fashion with increasing number of the metabolic disorders described above (zero 262.6±9.4; one 257.0±9.3; two 256.4±9.4; three 249.0±9.1; and four 244.9±9.0). These results were similar in men and women and in non-Hispanic whites and Mexican Americans. The association between LDL size and the number of metabolic disorders remained statistically significant even after adjustment for obesity, body fat distribution, gender, ethnicity, proinsulin and insulin concentrations. Furthermore, decreases in LDL size are also significantly associated with both a selective beta-cell defect (as estimated by the fasting proinsulin/insulin ratio) and insulin resistance (as estimated by the fasting insulin concentrations) although the association was some-what stronger for the latter. We conclude that small dense LDL may form part of the insulin resistance syndrome in non-diabetic subjects. [ABSTRACT FROM AUTHOR]

Insulin resistance and impaired insulin secretion are thought to be the primary defects in the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM). Disproportionately increased proinsulin relative to insulin levels are suggested to be an early indicator of a failing pancreas. We examined the relationship of fasting specific insulin, proinsulin, and 32, 33 split proinsulin concentrations, and the proinsulin: insulin ratio to the risk of developing NIDDM 3.5 years later in 65-74-year-old non-diabetic Finnish subjects participating in a populationbased study ( n=892) on diabetes and heart disease. Altogether 69 subjects developed NIDDM over a 3.5-year follow-up (cases). The cases were compared to randomly-selected gender-matched control subjects ( n=69) and control subjects matched for gender, glucose tolerance status (normal or impaired), and body mass index ( n=69). There were no differences in insulin concentrations between cases and random or matched control subjects [median and interquartile range; 123 (77-154), 108 (74-143), 118 (83-145) pmol/l, p=0.271]. Random control subjects had lower proinsulin and 32,33 split proinsulin concentrations and split proinsulin: insulin ratios compared to cases [5.7 (3.8-9.0) vs 7.3 (4.8-10.0) pmol/l, p=0.005; 7.3 (4.5-13.0) vs 10.4 (7.1-18.0) pmol/l, p=0.002; 0.073 (0.057-0.110) vs 0.097 (0.060-0.135), p=0.003]. Matched control subjects had lower proinsulin concentrations and proinsulin: insulin ratios compared to cases [5.9 (4.0-7.7) vs 7.3 (4.8-10.0) pmol/l, p=0.019; 0.048 (0.035-0.071) vs 0.064 (0.045-0.100), p=0.008]. When cases were compared to matched control subjects a 1 SD increase in baseline proinsulin: insulin ratio was associated with a 1.37-fold risk ( p=0.020) of developing diabetes. Moreover, this association was independent of fasting glucose concentration at baseline. Thus, in elderly prediabetic subjects disproportionately increased proinsulin concentration, an indicator of defective insulin secretion, is associated with conversion to diabetes over a short time period. [ABSTRACT FROM AUTHOR]

Microalbuminuria is associated with increased cardiovascular mortality in both diabetic and non-diabetic subjects. A number of studies have indicated that insulin resistance, increased blood pressure and dyslipidaemia precede the onset of clinical diabetes. We examined various correlates of microalbuminuria in 1,298 non-diabetic subjects who participated in the Mexico city Diabetes Study, a population-based study of diabetes and cardiovascular risk factors. Both parental history of diabetes and impaired glucose tolerance were significantly associated with microalbuminuria. These results were not explained by differences in age or blood pressure between subjects with or without a parental history of diabetes or impaired glucose tolerance. In addition, subjects with microalbuminuria had increased 2-h insulin and triglyceride concentrations, a higher prevalence of hypertension, and decreased high density lipoprotein cholesterol concentrations relative to subjects without microalbuminuria. These results suggest that microalbuminuria may be a feature of the prediabetic state. [ABSTRACT FROM AUTHOR]

In a population-based survey of 2,930 subjects, prevalence rates for obesity, Type 2 (non-insulin-dependent) diabetes mellitus, impaired glucose tolerance, hypertension, hypertriglyceridaemia, and hypercholesterolaemia were 54.3, 9.3, 11.1, 9.8, 10.3 and 9.2%, respectively. The prevalence, however, of each of these conditions in its isolated form (free of the other five) was 29.0% for obesity, 1.3% for Type 2 diabetes, 1.8% for impaired glucose tolerance, 1.5% for hypertension, 1.0% for hypertriglyceridaemia, and 1.7% for hypercholesterolaemia. Two-by-two associations were even rarer. The large differences in prevalence between isolated and mixed forms indicate a major overlap among the six disorders in multiple combinations. In the isolated form, each condition was characterized by hyperinsulinaemia (both fasting and 2 h after oral glucose), suggesting the presence of insulin resistance. In addition, in any isolated condition most of the variables categorising other members of the sextet were still significantly altered in comparison with 1,049 normal subjects. In the whole of the subjects who presented with one or another disorder (1,881 of 2,930 or 64%), marked fasting and post-glucose hyperinsulinaemia was associated with higher body mass index, waist:hip ratio, fasting and post-glucose glycaemia, systolic and diastolic blood pressure, serum triglycerides and total cholesterol levels, and with lower HDL-cholesterol concentrations (all p <0.001). We conclude that (1) insulin sensitivity, glucose tolerance, blood pressure, body fat mass and distribution, and serum lipids are a network of mutually interrelated functions; and (2) an insulin resistance syndrome underlies each and all of the six disorders carrying an increased risk of coronary artery disease. [ABSTRACT FROM AUTHOR]

To define the kinetics of chylomicron apolipoprotein-B catabolism in diabetic subjects with lipaemia, autologous chylomicrons (S 400) harvested from plasma following an oral fat load were radioiodinated and re-injected. The radioactivity in the tetramethylurea-insoluble, non-lipid S>400 lipoprotein fraction was followed in serial samples over 60-72h on a fat-free, isocaloric diet in: (1) five normal subjects; (2) four hypertriglyceridaemic, non-diabetic subjects; and (3) five diabetic patients (one subject, No. 3, was studied twice). The plasma apolipoprotein-B decay curve for the S f 400 fraction disclosed biphasic disappearance: a rapid first phase (residence time 0.8-1.9 h) accounting for the large majority of removal (60%-95%) and a slower second phase (residence time 3.6-47.6 h), accounting for the remainder. Total chylomicron apolipoprotein-B residence times were similar in normolipidaemic (1.8-7.3 h) and hypertriglyceridaemic (2.3-10.3 h) non-diabetic subjects and the mildly hypertriglyceridaemic diabetic patients (5.6 and 5.8 h). In the untreated lipaemic diabetic subjects (Nos. 1 and 2), only a single, much slower phase was observed (total chylomicron apolipoprotein-B residence time 38.5-58 h). Adipose tissue biopsy in one of these subjects (No. 1) disclosed profoundly low lipoprotein lipase activity. The lipaemic diabetic subject (No. 3) studied early during treatment showed an intermediate pattern. These studies suggest a key role for insulin-dependent, lipoprotein lipase-mediated triglyceride hydrolysis in the removal of chylomicrons from plasma. [ABSTRACT FROM AUTHOR]

Obesity and Type 2 (non-insulin-dependent) diabetes mellitus are common in the Mexican American population. It is not clear whether this is merely a specific instance of the more general phenomenon of excess Type 2 diabetes and obesity among poor people, or whether Mexican Americans have a discrete genetic susceptibility to Type 2 diabetes. The latter consideration arises because Mexican Americans are of mixed native American and European ancestry and native Americans may have a genetic predisposition to Type 2 diabetes which Mexican Americans could share. We studied 936 Mexican Americans and 398 Anglo-Americans randomly selected from three socially and culturally distinct neighbourhoods in San Antonio, Texas. Three categories of obesity - lean, average, and obese were defined using the Anglo-American distribution of the sum of the triceps and subscapular skinfold. Mexican Americans were two to four times as likely to fall into the obese category as Anglo-Americans, but within categories, the two ethnic groups were closely matched in terms of sum of skinfolds. The prevalence of Type 2 diabetes, however, was significantly greater in Mexican Americans than in Anglo-Americans even when the comparisons were made within the three obesity categories. The summary prevalence ratio, controlling for obesity, was 2.54 for men ( p=0.004) and 1.70 for women ( p=0.036). Thus, lean Mexican Americans are still at greater risk of Type 2 diabetes than equally lean Anglo-Americans. Conversely, although Type 2 diabetes prevalence increases as expected with increasing obesity in both ethnic groups, obese Anglo-Americans are still relatively protected compared with equally obese Mexican Americans. Plasma glucose was significantly higher in Mexican Americans than in Anglo-Americans even after controlling for obesity. These results indicate that, although obesity contributes to Type 2 diabetes in Mexican Americans, it does not by itself explain the entire excess prevalence rate. [ABSTRACT FROM AUTHOR]

Although hypercholesterolemia has been recognized as a risk factor for coronary heart disease (CHD) for decades, only in recent years have clinical trials definitively shown the efficacy of lowering serum cholesterol to prevent the occurrence or worsening of CHD. In 1985, an NIH consensus conference published guidelines for the diagnosis and treatment of hypercholesterolemia. Prior to 1985, physicians and lay people alike were not yet convinced of the necessity to know one's cholesterol level, nor did they know what levels should be treated. In a community-based survey of cardiovascular risk factors, known as the San Antonio Heart Study, in which 1,932 Mexican-Americans (MAs) and 1,133 non-Hispanic whites (NHWs) were examined between 1979 and 1985, the authors found that only 36/501 MAs (7%) and 54/312 NHWs (17%) in the moderate- or high-risk categories were aware that their cholesterols were high. Of the total number aware, including those whose cholesterol levels were in the low-risk range, only 23/97 MAs (24%) and 29/108 NHWs (27%) were receiving dietary or drug treatment. Of those being treated, only 9/23 MAs (39%) and 12/29 NHWs (41%) were effectively controlled. Mexican-Americans were less likely to be aware of their hypercholesterolemia than non-Hispanic whites, but both ethnic groups had low levels of treatment. [ABSTRACT FROM AUTHOR]

Fibre reinforced composite materials incorporating thermoplastic matrices are gaining increasing popularity in many industrial applications. One of the potential preforms for the manufacture of technical components is commingled yarn composed of reinforcement and matrix in fibre form. These are often employed in the pultrusion process. Another innovative preform consists of polymer powder preimpregnated sheath surrounding fibre bundles. To achieve adequate mechanical properties of the final product it is essential, when producing laminates by a process such as pultrusion with both types of preform, that sufficient matrix impregnation is achieved. The prevention of voids and dry-spots in the laminate requires a theoretical understanding of the mechanisms involved. On a microscopic scale, several finite element (FE) models can be used to simulate the progress of the matrix flow into the interstitial spaces between the single reinforcement fibres. In the present simulations, a hexagonal and a square arrangement account for two of the various fibre packings occurring in a laminate. It permits an estimation of the impregnation performance of commingled and powder impregnated yarns. For each preform the shear rate, to which the polymer matrix is subjected during the impregnation and consolidation process, can be predicted. [ABSTRACT FROM AUTHOR]

We report the results of a detailed study of the occupied and unoccupied electronic structure of dimers of the new heterofullerene by means of photoemission and electron energy-loss spectroscopy. A close similarity is found between the electronic structures of pristine and with an additional broadening of the spectra in the former due to the distortion of the fullerene cage caused both by dimerization and the chemical substitution. Both the occupied and unoccupied electronic states, as well as the interband transitions between them, attest to the high degree of molecular character retained in the solid state. Comparison of the shake-up structures in the and X-ray photoemission spectra confirm that the highest lying occupied states in the heterofullerene have a strong degree of N character, whereas the lowest lying unoccupied states have mainly C character. We also present the optical conductivity of the heterofullerene (derived from the loss function), which shows an optical gap of 1.4 eV, some 0.4 eV smaller than that of . [ABSTRACT FROM AUTHOR]

Increased androgenicity as assessed by increased testosterone and decreased SHBG is strongly associated with an unfavorable body fat distribution and increased glucose and insulin concentrations and insulin resistance in both pre-and postmenopausal women. However, the temporal direction of the association between androgens and insulin is uncertain. In men, the association between SHBG and insulin levels is much weaker and is probably inverse. International Journal of Obesity (2000) 24, Suppl 2, S56–S58. [ABSTRACT FROM AUTHOR]