bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mesenteric Fat Thickness Is an Independent Determinant of Metabolic Syndrome and Identifies Subjects With Increased Carotid Intima-Media Thickness
Authors: Liu Kin Hung , Chan Yu Leung , Chan Wing Bun , Chan Juliana Chung Ngor , Chu Chiu Wing Winnie 
Published: May 2006

OBJECTIVE—Mesenteric fat, a reflection of visceral adiposity, may play an important role in the pathogenesis of metabolic syndrome and cardiovascular diseases (CVD). In this study, we examined the independent relationship between mesenteric fat thickness and metabolic syndrome and defined its optimal cutoff value to identify high-risk subjects for metabolic syndrome and CVD.
RESEARCH DESIGN AND METHODS—A total of 290 Chinese subjects had an ultrasound examination for measurements of thickness of mesenteric, preperitoneal, and subcutaneous fat as well as carotid intima-media thickness (IMT). Anthropometric measurements and metabolic risk profile were assessed by physical examination and blood taking.
RESULTS—Twenty (6.9%) subjects had metabolic syndrome according to the National Cholesterol Education Panel Adult Treatment Panel III criteria with Asian definitions for central obesity (waist circumference &gt;80 cm in women and &gt;90 cm in men). Mesenteric fat thickness had significant correlations (P &lt; 0.05) with various metabolic variables. On multivariate regression, mesenteric fat thickness was an independent determinant of all components of metabolic syndrome after adjustment for age, sex, homeostasis model assessment of insulin resistance, and other fat deposits. The odds ratio of metabolic syndrome was increased by 1.35 (95% CI 1.10–1.66)-fold for every 1-mm increase in mesenteric fat thickness. On receiver-operating characteristic curve analysis, mesenteric fat thickness of ≥10 mm was the optimal cutoff value to identify metabolic syndrome, with sensitivity of 70% and specificity of 75%. Subjects with mesenteric fat thickness ≥10 mm had higher carotid IMT than those with thickness &lt;10 mm (0.73 ± 0.19 vs. 0.64 ± 0.16 mm, P = 0.001).
CONCLUSIONS—Mesenteric fat thickness was an independent determinant of metabolic syndrome and identified subjects with increased carotid IMT.
The Importance of Waist Circumference in the Definition of Metabolic Syndrome
Authors: Katzmarzyk Peter T. , Janssen Ian , Ross Robert , Church Timothy S. , Blair Steven N. 
Published: May 2006

OBJECTIVE—The purpose of this study was to compare the predictive ability of the National Cholesterol Education Panel (NCEP), revised NCEP (NCEP-R), and International Diabetes Federation (IDF) metabolic syndrome criteria for mortality risk, and to examine the effects of waist circumference on mortality within the context of these criteria.
RESEARCH DESIGN AND METHODS—The sample included 20,789 white, non-Hispanic men 20–83 years of age from the Aerobics Center Longitudinal Study. The main outcome measures were all-cause and cardiovascular disease (CVD) mortality over 11.4 years of follow-up.
RESULTS—The proportions of men with the metabolic syndrome were 19.7, 27, and 30% at baseline, respectively, according to NCEP, NCEP-R, and IDF criteria. A total of 632 deaths (213 CVD) occurred. The relative risks (RRs) and 95% CIs of all-cause mortality were 1.36 (1.14–1.62), 1.31 (1.11–1.54), and 1.26 (1.07–1.49) for the NCEP, NCEP-R, and IDF definitions, respectively. The corresponding RRs for CVD mortality were 1.79 (1.35–2.37), 1.67 (1.27–2.19), and 1.67 (1.27–2.20). Additionally, there was a significant trend for a higher risk of CVD mortality across waist circumference categories (&lt;94, 94–102, and &gt;102 cm) among men with at least two additional metabolic syndrome risk factors (P = 0.01).
CONCLUSIONS—The prediction of mortality with IDF and NCEP metabolic syndrome criteria was comparable in men. Waist circumference is a valuable component of metabolic syndrome; however, the IDF requirement of an elevated waist circumference warrants caution given that a large proportion of men with normal waist circumference have multiple risk factors and an increased risk of mortality.
High-Sensitivity C-Reactive Protein and Coronary Heart Disease Mortality in Patients With Type 2 Diabetes
Authors: Soinio Minna , Marniemi Jukka , Laakso Markku , Lehto Seppo , Rönnemaa Tapani 
Published: May 2006

OBJECTIVE—To investigate in a follow-up study whether high-sensitivity C-reactive protein (hs-CRP) predicts coronary heart disease (CHD) events in subjects with type 2 diabetes.
RESEARCH DESIGN AND METHODS—The original study population consisted of 1,059 patients with type 2 diabetes (age 45–64 years). Mean duration of diabetes was 8 years. CRP values were available from 1,045 subjects, of whom 878 were free of myocardial infarction (MI) at baseline. CHD mortality and the incidence of nonfatal MI were assessed in a 7-year follow-up.
RESULTS—Altogether, 157 patients died from CHD and 254 had a nonfatal or fatal CHD event. Patients with hs-CRP &gt;3 mg/l had a higher risk for CHD death than patients with hs-CRP ≤3 mg/l (19.8 and 12.9%, respectively, P = 0.004). In Cox regression analysis, patients with high hs-CRP had a relative risk of 1.72 for CHD death even after the adjustment for confounding factors (P = 0.002). Among subjects who were free from MI at baseline, those with a high hs-CRP level had relative risks of 1.83 (P = 0.003) and 1.84 (P = 0.004) for CHD death in univariate and multivariate analyses, respectively.
CONCLUSIONS—In this large cohort of type 2 diabetic patients, hs-CRP was an independent risk factor for CHD deaths.
Familial Clustering for Features of the Metabolic Syndrome
Authors: Tang Weihong , Hong Yuling , Province Michael A. , Rich Stephen S. , Hopkins Paul N. , Arnett Donna K. , Pankow James S. , Miller Michael B. , Eckfeldt John H. 
Published: May 2006

OBJECTIVE—Metabolic syndrome–related traits (obesity, glucose intolerance/insulin resistance, dyslipidemia, and hypertension) have been shown to be genetically correlated. It is less clear, however, if the genetic correlation extends to novel risk factors associated with inflammation, impaired fibrinolytic activity, and hyperuricemia. We present a bivariate genetic analysis of MetS-related traits including both traditional and novel risk factors.
RESEARCH DESIGN AND METHODS—Genetic correlations were estimated using a variance components procedure in 1,940 nondiabetic white individuals from 445 families in the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study. Twelve MetS-related traits, including BMI, waist circumference, blood pressure, white blood cell count, fasting serum triglycerides, HDL cholesterol, insulin, glucose, plasminogen activator inhibitor-1 antigen, uric acid, and C-reactive protein, were measured and adjusted for covariates, including lifestyle variables.
RESULTS—Significant genetic correlations were detected among BMI, waist circumference, HDL cholesterol, triglycerides, insulin, and plasminogen activator inhibitor-1 antigen and between uric acid and all of the above variables except insulin. C-reactive protein and white blood cell count were genetically correlated with each other, and both showed significant genetic correlations with waist circumference and insulin. Fasting glucose was not significantly genetically correlated with any of the other traits.
CONCLUSIONS—These results suggest that pleiotropic effects of genes or shared family environment contribute to the familial clustering of MetS-related traits.
Patterns of Metabolic Progression to Type 1 Diabetes in the Diabetes Prevention Trial–Type 1
Authors: Sosenko Jay M. , Palmer Jerry P. , Greenbaum Carla J. , Mahon Jeffrey , Cowie Catherine , Krischer Jeffrey P. , Chase H. Peter , White Neil H. , Buckingham Bruce , Herold Kevan C. , Cuthbertson David , Skyler Jay S. ,   the Diabetes Prevention Trial–Type 1 Study Group
Published: May 2006

OBJECTIVE—There is little information regarding the pattern of metabolic deterioration before the onset of type 1 diabetes. The goal of this study was to utilize data from the Diabetes Prevention Trial–Type 1 (DPT-1) to obtain a picture of the metabolic progression to type 1 diabetes over a period of approximately 2.5 years before its diagnosis.RESEARCH DESIGN AND METHODS—Fifty-four DPT-1 participants (22 in the parenteral trial and 32 in the oral trial) were studied. All had oral glucose tolerance tests (OGTTs) at 6-month intervals from approximately 30 to 6 months before diagnosis. The vast majority also had OGTTs at diagnosis. Changes in OGTT glucose and C-peptide indexes from 30 to 6 months before diagnosis were examined by calculating slopes of the indexes for each individual over that time period. Changes from 6 months before diagnosis to diagnosis were examined by paired comparisons of the OGTT metabolic indexes between the time points.RESULTS—Glucose levels increased gradually from 30 to 6 months before diagnosis in both the parenteral and oral groups (P &lt; 0.001 for all indexes). Area under the curve (AUC) C-peptide (P &lt; 0.05) and AUC C-peptide–to–AUC glucose ratio (P &lt; 0.001) values decreased in the oral group; peak C-peptide–to–2-h glucose ratio values decreased in both groups (P &lt; 0.001). In participants who also had OGTTs at diagnosis, AUC C-peptide (parenteral group, P &lt; 0.05) and peak C-peptide (oral group, P &lt; 0.05) values decreased from the last 6 months before diagnosis; stimulated C-peptide–to–glucose ratio values decreased in both groups (P &lt; 0.001). Conversely, fasting C-peptide levels increased in both groups (oral group, P &lt; 0.01). Fasting C-peptide–to–fasting glucose ratio values remained constant throughout the 30-month follow-up.CONCLUSIONS—These data indicate that over a period of at least 2 years, glucose tolerance gradually deteriorates as stimulated C-peptide levels slowly decline in a substantial number of individuals who develop type 1 diabetes. However, fasting C-peptide levels are maintained, even at diagnosis.
Diabetic Cardiomyopathy and Subclinical Cardiovascular Disease
Authors: Bertoni Alain G. , Goff David C. , D’Agostino Ralph B. , Liu Kiang , Hundley W. Gregory , Lima Joao A. , Polak Joseph F. , Saad Mohammed F. , Szklo Moyses , Tracy Russell P. , Siscovick David S. 
Published: May 2006

OBJECTIVE—Studies have demonstrated increased left ventricular mass (LVM) and diastolic dysfunction among diabetic patients without clinical cardiovascular disease (CVD), but few have assessed the potential contribution of subclinical CVD to ventricular abnormalities in diabetes. We examined whether diabetic cardiomyopathy is associated with subclinical atherosclerosis and if abnormalities are found with impaired fasting glucose (IFG).
RESEARCH DESIGN AND METHODS—LVM, end-diastolic volume (EDV), and stroke volume were measured by magnetic resonance imaging (MRI), and atherosclerosis was assessed by coronary artery calcium and carotid intima-media wall thickness in 4,991 participants in the Multi-Ethnic Study of Atherosclerosis, a cohort study of adults aged 45–84 without prior CVD. Multivariable linear regression was used to analyze the association between MRI measures and glucose status.
RESULTS—Increased LVM was observed in white, black, and Hispanic participants with diabetes but not among Chinese participants. After adjustment for weight, height, CVD risk factors, and subclinical atherosclerosis, ethnicity-specific differences in ventricular parameters were present. Among whites and Chinese with diabetes, LVM was similar to that in normal subjects; EDV and stroke volume were reduced. In blacks with diabetes, EDV and stroke volume were reduced, and LVM was increased (+5.6 g, P &lt; 0.05). Among Hispanics with diabetes, EDV and stroke volume were similar to normal, but LVM was increased (+5.5 g, P &lt; 0.05). After adjustment, IFG was associated with a decrease in EDV and stroke volume in whites and blacks only; however, no significant differences in LVM were observed.
CONCLUSIONS—Ethnicity-specific differences in LVM, EDV, and stroke volume are associated with abnormal glucose metabolism and are independent of subclinical CVD.
Age at Onset of Childhood-Onset Type 1 Diabetes and the Development of End-Stage Renal Disease
Authors: Svensson Maria , Nyström Lennarth , Schön Staffan , Dahlquist Gisela ,   on behalf of the Swedish Childhood Diabetes Study and the Swedish Registry for Active Treatment of Uraemia
Published: May 2006

OBJECTIVE—To analyze the impact of age at onset on the development of end-stage renal disease (ESRD) due to diabetic nephropathy in a nationwide population-based cohort with childhood-onset type 1 diabetes.
RESEARCH DESIGN AND METHODS—A record linkage between two nationwide registers, the Swedish Childhood Diabetes Registry, including 12,032 cases with childhood-onset diabetes, and the Swedish Registry for Active Treatment of Uraemia was performed. Log-rank test was used to test differences between cumulative risk curves of developing ESRD due to diabetic nephropathy in three different strata of age at onset (0–4, 5–9, and 10–14 years).
RESULTS—At a maximum follow-up of 27 years, 33 patients had developed ESRD due to diabetic nephropathy and all had a diabetes duration &gt;15 years. In total, 4,414 patients had diabetes duration &gt;15 years, and thus the risk in this cohort to develop ESRD was 33 of 4,414 (0.7%). A significant difference in risk of developing ESRD was found between the youngest (0–4 years) and the two older (5–9 and 10–14 years) age-at-onset strata (P = 0.03 and P = 0.001, respectively). A significant difference in the risk of developing ESRD was also found between children with prepubertal (0–4 and 5–9 years, n = 2,424) and pubertal (10–14 years, n = 2000) onset of diabetes (P = 0.002). No patient with onset of diabetes before 5 years of age had developed ESRD.
CONCLUSIONS—With a median duration of 21 years in this population-based Swedish cohort with childhood-onset diabetes, &lt;1% of the patients had developed ESRD due to diabetic nephropathy, and a prepubertal onset of diabetes seems to prolong the time to development of ESRD.
Hyperglycemia and Diabetes in Patients With Schizophrenia or Schizoaffective Disorders
Authors: Cohen Dan , Stolk Ronald P. , Grobbee Diederick E. , Gispen-de Wied Christine C. 
Published: May 2006

OBJECTIVE—Pharmacoepidemiological studies have shown an increased prevalence of diabetes in patients with schizophrenia. To address this issue, we decided to assess glucose metabolism in a population of patients with schizophrenia or schizoaffective disorder.
RESEARCH DESIGN AND METHODS—Oral glucose tolerance tests (OGTTs) were performed in 200 unselected in- and outpatients. Insulin sensitivity and β-cell function were assessed using the homeostasis model assessment (HOMA) indexes and 30-min glucose and insulin levels.
RESULTS—The mainly Western European (87.7%) study population had a mean age of 40.8 years, was 70% male, and had a mean fasting glucose of 5.1 mmol/l and a mean fasting insulin of 14.8 mU/l. Hyperglycemia was present in 7% of the population: 1.5% with impaired fasting glucose and 5.5% with impaired glucose tolerance. The prevalence of diabetes was 14.5%, of which 8% was previously known and 6.5% was newly diagnosed. Compared with a 1.5% prevalence of diabetes in the age-matched general Dutch population, the prevalence of identified cases was significantly increased in the study population. Comparable figures on the prevalence of hyperglycemia in the general population are not available. Insulin resistance was increased in the study population as a whole (HOMA of insulin resistance: 3.1–3.5), irrespective of the use of antipsychotic medication and, if used, irrespective of its type (typical or atypical). No indication of β-cell defect was found, whereas a nonsignificant increased insulin resistance was found with antipsychotic medication.
CONCLUSIONS—OGTTs in 200 mainly Caucasian patients with schizophrenia or schizoaffective disorder, mean age 41 years, showed that 7% suffered from hyperglycemia and 14.5% from diabetes. The prevalence of diabetes was significantly increased compared with the general population. No differential effect of antipsychotic monotherapy in diabetogenic effects was found. Therefore, a modification of the consensus statement on antipsychotic drugs, obesity, and diabetes is proposed, i.e., measurement of fasting glucose in all patients with schizophrenia, irrespective of prescribed antipsychotic drug.
The Hyperglycemia: Intensive Insulin Infusion In Infarction (HI-5) Study
Authors: Cheung N. Wah , Wong Vincent W. , McLean Mark 
Published: May 2006

OBJECTIVE—There is conflicting evidence regarding the benefit of intravenous insulin therapy on mortality following acute myocardial infarction (AMI). The goal of the current study was to determine whether improved glycemic control, achieved through an insulin/dextrose infusion with a variable rate of insulin, reduces mortality among hyperglycemic patients with AMI.
RESEARCH DESIGN AND METHODS—Subjects suffering AMI with either known diabetes or without diabetes but blood glucose level (BGL) ≥7.8 mmol/l were randomized to receive insulin/dextrose infusion therapy for at least 24 h to maintain a BGL &lt;10 mmol/l or conventional therapy.
RESULTS—A total of 240 subjects were recruited. Insulin/dextrose infusion did not reduce mortality at the inpatient stage (4.8 vs. conventional 3.5%, P = 0.75), 3 months (7.1 vs 4.4%, P = 0.42), or 6 months (7.9 vs. 6.1%, P = 0.62). There was, however, a lower incidence of cardiac failure (12.7 vs. 22.8%, P = 0.04) and reinfarction within 3 months (2.4 vs. 6.1%, P = 0.05). When analyzed by mean BGL achieved during the first 24 h, mortality was lower among subjects with a mean BGL ≤8 mmol/l, compared with subjects with a mean BGL &gt;8 mmol/l (2 vs. 11% at 6 months, P = 0.02).
CONCLUSIONS—We did not find a reduction in mortality among patients who received insulin/dextrose infusion therapy. However, it remains possible that tight glycemic control with insulin therapy following AMI improves outcomes.
The Relationship Among Pain, Sensory Loss, and Small Nerve Fibers in Diabetes
Authors: Sorensen Lea , Molyneaux Lynda , Yue Dennis K. 
Published: May 2006

OBJECTIVE—Many individuals with diabetes experience neuropathic pain, often without objective signs of large-fiber neuropathy. We examined intraepidermal nerve fibers (IENFs) to evaluate the role of small nerve fibers in the genesis of neuropathic pain.
RESEARCH DESIGN AND METHODS—Twenty-five diabetic subjects with neuropathic pain and 13 without were studied. The pain was present for at least 6 months for which no other cause could be found. Punch skin biopsies were obtained from the distal leg. IENFs were stained using antibody to protein gene product 9.5 and counted with confocal microscopy. Neuropathy was graded by vibration perception and cold detection thresholds and the Michigan Neuropathy Screening Instrument.
RESULTS—In the total cohort, IENF density was significantly lower in those with pain compared with those without (3 [1–6] vs. 10 [3–19], respectively, P = 0.02). There were significant inverse correlations between IENF and severity of neuropathy, with the pain group having a flatter gradient than their pain-free counterparts (P &lt; 0.02). The difference in IENF density was greatest in subjects with less objective evidence of neuropathy (P ≤ 0.01).
CONCLUSIONS—More severe loss of IENF is associated with the presence of neuropathic pain only in those with little or no objective sign of neuropathy. Thus, loss of IENF cannot explain pain in all cases, suggesting that different mechanisms underpin the genesis of pain at various stages of neuropathy.
Highly Luminescent CuI Complexes for Light‐Emitting Electrochemical Cells (Adv. Mater. 10/2006)
Authors: Armaroli N. , Accorsi G. , Holler M. , Moudam O. , Nierengarten J.‐F. , Zhou Z. , Wegh R. T. , Welter R. 
Published: May 2006

AbstractThe crystal structure of a Cu(I) complex having two nitrogen (blue) and two phosphor (yellow) coordinating atoms is depicted. This class of complexes exhibits intense green photo‐and electroluminescence as well as triplet lifetimes on the microsecond timescale. These features make them attractive candidates for light‐emitting devices based on cheap, abundant, and environmentally sustainable metal elements, as shown by Armaroli, Nierengarten, Wegh, and co‐workers on p. 1313.
Myeloperoxidase accumulates at the neutrophil surface and enhances cell metabolism and oxidant release during pregnancy
Authors: Kindzelskii Andrei L. , Clark Andrea J. , Espinoza Jimmy , Maeda Nobuyo , Aratani Yasuaki , Romero Roberto , Petty Howard R. 
Published: May 2006

AbstractPregnancy is a unique immunological state. Pregnancy neutrophils differ from those of non‐pregnant women as they cannot be fully activated for oxidant production, but yet have higher levels of unstimulated oxidant production. Although reduced activation is due to decreased hexose monophosphate shunt activity, the mechanism enhancing basal oxidant levels is unknown. We hypothesize that myeloperoxidase (MPO) trafficking affects the basal oxidant release by maternal neutrophils. Immunofluorescence microscopy has demonstrated MPO at the surface of pregnancy neutrophils, whereas non‐pregnancy cells do not exhibit surface MPO. Adherent pregnancy neutrophils were characterized by high‐amplitude metabolic oscillations, which were blocked by MPO inactivation. Conversely, metabolic oscillatory amplitudes of control neutrophils were heightened by incubation with PMA or exogenous MPO. Importantly, MPO decoration of cell surfaces and high‐amplitude metabolic oscillations were observed for neutrophils from pregnant but not from non‐pregnant mice. However, cells from pregnant MPO knockout mice did not exhibit MPO expression or high‐amplitude metabolic oscillations. Unstimulated neutrophils from pregnant women were found to release reactive oxygen metabolites (ROM) and reactive nitrogen intermediates (RNI), but cells from non‐pregnant women did not. MPO inhibition returned ROM and RNI formation to non‐pregnant levels. Hence, MPO trafficking influences metabolic activity and oxidant production in pregnancy.
The Reactivity of Hexa(N‐methylideneimine)CoIII Complexes towards Nucleophiles: Structure and Mechanism
Authors: Kuppert Dirk , Comba Peter , Hegetschweiler Kaspar 
Published: May 2006

AbstractThe reactivity of the hexa(N‐methylideneimine)CoIII complex [Co‐hmi‐(taci)2]3+ (taci = 1,3,5‐triamino‐1,3,5‐trideoxy‐cis‐inositol) towards the nucleophiles ammonia, aniline and cyanide was investigated and the main products were identified by spectroscopic methods and by a crystal structure analysis. The relative energies of the complexes formed and those of possible stereo isomers were analysed by means of molecular mechanics calculations. In the reaction with NH3, two condensation products, [Co(La)]3+ and [Co(Lb)]3+, were identified with the two taci moieties linked by one or two N=CH–N(H)‐CH2–NH bridges, respectively. The reaction with aniline yielded the complex [Co(Lc)(Ld)]3+ (where Lc is a mono‐N‐methylated and Ld a phenylformamidine‐substituted taci), whereas the reaction with cyanide resulted in the formation of [Co(Le)]3+ having an NH–CH2–C(NH2)=N bridge between the two taci subunits. A mechanism that accounts for the different types of products can be suggested as follows: In [Co(La)]3+, [Co(Lb)]3+ and [Co(Lc)(Ld)]3+, N‐methylation was observed and this can be interpreted in terms of an intramolecular Cannizzaro type hydride shift. For [Co(La)]3+ and [Co(Lb)]3+ two subsequent addition steps of the nucleophile to adjacent imino groups must take place prior to the hydride shift, whereas for [Co(Lc)(Ld)]3+ the hydride shift appears to have already occurred after the first addition step of aniline to an imino group. Formation of [Co(Le)]3+ can be explained in terms of a nucleophilic attack of CN– to an imino group and a subsequent attack of a deprotonated amino group (which must have previously been formed by hydrolysis of a methylideneimino group) to the nitrile C‐atom. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)