bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mercury correlations among six tissues for four waterbird species breeding in San Francisco Bay, California, USA
Authors: Eagles-Smith Collin A , Ackerman Joshua T , Adelsbach Terrence L , Takekawa John Y , Miles A. Keith , Keister Robin A 
Published: April 2008

Abstract
Despite a large body of research concerning mercury (Hg) in birds, no single tissue has been used consistently to assess Hg exposure, and this has hampered comparisons across studies. We evaluated the relationships of Hg concentrations among tissues in four species of waterbirds (American avocets [Recurvirostra americana], black-necked stilts [Himantopus mexicanus], Caspian terns [Hydroprogne caspia; formerly Sterna caspia], and Forster's terns [Sterna forsteri]) and across three life stages (prebreeding adults, breeding adults, and chicks) in San Francisco Bay, California, USA. Across species and life stages, Hg concentrations (least square mean ± standard error) were highest in head feathers (6.45 ± 0.31 μg/g dry wt) and breast feathers (5.76 ± 0.28 μg/g dry wt), followed by kidney (4.54 ± 0.22 μg/g dry wt), liver (4.43 ± 0.21 μg/g dry wt), blood (3.10 ± 0.15 μg/g dry wt), and muscle (1.67 ± 0.08 μg/g dry wt). Relative Hg distribution among tissues, however, differed by species and life stage. Mercury concentrations were highly correlated among internal tissues (r2 ≥ 0.89). Conversely, the relationships between Hg in feathers and internal tissues were substantially weaker (r2 ≤ 0.42). Regression slopes sometimes differed among species and life stages, indicating that care must be used when predicting Hg concentrations in one tissue based on those in another. However, we found good agreement between predictions made using a general tissue-prediction equation and more specific equations developed for each species and life stage. Finally, our results suggest that blood is an excellent, nonlethal predictor of Hg concentrations in internal tissues but that feathers are relatively poor indicators of Hg concentrations in internal tissues.
Influence of lake characteristics on the biomagnification of persistent organic pollutants in lake trout food webs
Authors: Houde Magali , Muir Derek C. G , Kidd Karen A , Guildford Stephanie , Drouillard Ken , Evans Marlene S , Wang Xiaowa , Whittle D. Michael , Haffner Doug , Kling Hedy 
Published: April 2008

Abstract
The biomagnification of polychlorinated biphenyls (PCBs) and major organochlorine pesticides (OCPs) was studied using lake trout (Salvelinus namaycush) and other food web organisms collected from 17 lakes in Canada and the northeastern United States between 1998 and 2001. Whole lake trout (n = 357) concentrations of the sum (Σ) of 57 PCB congeners ranged between 1.67 and 2,890 ng/g wet weight (median 61.5 ng/g wet wt). Slimy sculpin had the highest mean concentrations of ΣPCB of all forage fish (32–73 ng/g wet wt). Positive relationships between log (lipid wt) concentrations of PCB congener 153, PCB congener 52, p,p'-dichlorodiphenyldichloroethylene, hexachlorobenzene, cis-chlordane, trans-nonachlor, or dieldrin and trophic level (determined using stable nitrogen isotope ratios) were found for most of the 17 food webs, indicating biomagnification of these PCBs and OCPs. The p,p'-dichlorodiphenyldichloroethylene had the highest trophic magnification factors (TMFs) of the 14 individual compounds studied, averaging 4.0 ± 1.8 across the 17 lakes, followed by trans-nonachlor (3.6 ± 1.5) and PCB congener 153 (3.4 ± 1.2). Average TMFs for 14 individual PCBs or OCPs were significantly correlated with log octanol–water partition coefficient, implying that the rate of accumulation along the food web is dependent on hydrophobicity and recalcitrance. Significant correlations (p &lt; 0.05) were found between TMFs of ΣPCBs, hexachlorobenzene, α-hexachlorocyclohexane, and lindane and lake area, latitude, and longitude, but not for 11 other PCBs or OCPs. Overall, the results of the present study show that biomagnification of PCBs and most OCPs, as measured by TMFs, is only weakly influenced by such factors as latitude and longitude. Exceptions are hexachlorocyclohexane isomers and hexachlorobenzene, which had generally greater TMFs in northern lakes, possibly due to lower rates of elimination and biotransformation in the food web.
siRNA-Mediated Reduction of Inhibitor of Nuclear Factor-κB Kinase Prevents Tumor Necrosis Factor-α–Induced Insulin Resistance in Human Skeletal Muscle
Authors: Austin Reginald L. , Rune Anna , Bouzakri Karim , Zierath Juleen R. , Krook Anna 
Published: April 2008

OBJECTIVE—Proinflammatory cytokines contribute to systemic low-grade inflammation and insulin resistance. Tumor necrosis factor (TNF)-α impedes insulin signaling in insulin target tissues. We determined the role of inhibitor of nuclear factor-κB kinase (IKK)β in TNF-α–induced impairments in insulin signaling and glucose metabolism in skeletal muscle.
RESEARCH DESIGN AND METHODS—Small interfering RNA (siRNA) was used to silence IKKβ gene expression in primary human skeletal muscle myotubes from nondiabetic subjects. siRNA gene silencing reduced IKKβ protein expression 73% (P &lt; 0.05). Myotubes were incubated in the absence or presence of insulin and/or TNF-α, and effects of IKKβ silencing on insulin signaling and glucose metabolism were determined.
RESULTS—Insulin increased glucose uptake 1.7-fold (P &lt; 0.05) and glucose incorporation into glycogen 3.8-fold (P &lt; 0.05) in myotubes from nondiabetic subjects. TNF-α exposure fully impaired insulin-mediated glucose uptake and metabolism. IKKβ siRNA protected against TNF-α–induced impairments in glucose metabolism, since insulin-induced increases in glucose uptake (1.5-fold; P &lt; 0.05) and glycogen synthesis (3.5-fold; P &lt; 0.05) were restored. Conversely, TNF-α–induced increases in insulin receptor substrate-1 serine phosphorylation (Ser312), Jun NH2-terminal kinase phosphorylation, and extracellular signal–related kinase-1/2 mitogen-activated protein kinase (MAPK) phosphorylation were unaltered by siRNA-mediated IKKβ reduction. siRNA-mediated IKKβ reduction prevented TNF-α–induced insulin resistance on Akt Ser473 and Thr308 phosphorylation and phosphorylation of the 160-kDa Akt substrate AS160. IKKβ silencing had no effect on cell differentiation. Finally, mRNA expression of GLUT1 or GLUT4 and protein expression of MAPK kinase kinase kinase isoform 4 (MAP4K4) was unaltered by IKKβ siRNA.
CONCLUSIONS—IKKβ silencing prevents TNF-α–induced impairments in insulin action on Akt phosphorylation and glucose uptake and metabolism in human skeletal muscle.
Heritability of Proliferative Diabetic Retinopathy
Authors: Hietala Kustaa , Forsblom Carol , Summanen Paula , Groop Per-Henrik ,   on behalf of the FinnDiane Study Group
Published: April 2008

OBJECTIVE—Diabetic nephropathy clusters in families, suggesting that genetic factors play a role in its pathogenesis. We investigated whether similar clustering exists for proliferative retinopathy in families with two or more siblings with type 1 diabetes.
RESEARCH DESIGN AND METHODS—The FinnDiane Study has characterized 20% (4,800 patients) of adults with type 1 diabetes in Finland. In 188 families, there were at least two siblings with type 1 diabetes. Ophthalmic records were obtained for 369 of 396 (93%) and fundus photographs for 251 of 369 (68%) patients. Retinopathy was graded based on photographs and/or repeated ophthalmic examinations using the Early Treatment of Diabetic Retinopathy grading scale.
RESULTS—Mean age at onset of diabetes was 14.3 ± 10.2 years, and mean duration was 25.9 ± 11.8 years. Proliferative retinopathy was found in 115 of 369 patients (31%). The familial risk of proliferative retinopathy was estimated in 168 of 188 sibships, adjusted for A1C, duration, and mean blood pressure. Proliferative retinopathy in the probands (48 of 168) was associated with an increased risk (odds ratio 2.76 [95% CI 1.25- 6.11], P = 0.01) of proliferative retinopathy in the siblings of probands (61 of 182). The heritability of proliferative retinopathy was h2 = 0.52 ± 0.31 (P &lt; 0.05).
CONCLUSIONS—We found a familial clustering of proliferative retinopathy in patients with type 1 diabetes. The observation cannot be accounted for by conventional risk factors, suggesting a genetic component in the pathogenesis of proliferative retinopathy in type 1 diabetes.
Activation of Peroxisome Proliferator–Activated Receptor β/δ Inhibits Lipopolysaccharide-Induced Cytokine Production in Adipocytes by Lowering Nuclear Factor-κB Activity via Extracellular Signal–Related Kinase 1/2
Authors: Rodríguez-Calvo Ricardo , Serrano Lucía , Coll Teresa , Moullan Norman , Sánchez Rosa M. , Merlos Manuel , Palomer Xavier , Laguna Juan C. , Michalik Liliane , Wahli Walter , Vázquez-Carrera Manuel 
Published: April 2008

OBJECTIVE—Chronic activation of the nuclear factor-κB (NF-κB) in white adipose tissue leads to increased production of pro-inflammatory cytokines, which are involved in the development of insulin resistance. It is presently unknown whether peroxisome proliferator–activated receptor (PPAR) β/δ activation prevents inflammation in adipocytes.
RESEARCH DESIGN AND METHODS AND RESULTS—First, we examined whether the PPARβ/δ agonist GW501516 prevents lipopolysaccharide (LPS)-induced cytokine production in differentiated 3T3-L1 adipocytes. Treatment with GW501516 blocked LPS-induced IL-6 expression and secretion by adipocytes and the subsequent activation of the signal transducer and activator of transcription 3 (STAT3)–Suppressor of cytokine signaling 3 (SOCS3) pathway. This effect was associated with the capacity of GW501516 to impede LPS-induced NF-κB activation. Second, in in vivo studies, white adipose tissue from Zucker diabetic fatty (ZDF) rats, compared with that of lean rats, showed reduced PPARβ/δ expression and PPAR DNA-binding activity, which was accompanied by enhanced IL-6 expression and NF-κB DNA-binding activity. Furthermore, IL-6 expression and NF-κB DNA-binding activity was higher in white adipose tissue from PPARβ/δ-null mice than in wild-type mice. Because mitogen-activated protein kinase–extracellular signal–related kinase (ERK)1/2 (MEK1/2) is involved in LPS-induced NF-κB activation in adipocytes, we explored whether PPARβ/δ prevented NF-κB activation by inhibiting this pathway. Interestingly, GW501516 prevented ERK1/2 phosphorylation by LPS. Furthermore, white adipose tissue from animal showing constitutively increased NF-κB activity, such as ZDF rats and PPARβ/δ-null mice, also showed enhanced phospho-ERK1/2 levels.
CONCLUSIONS—These findings indicate that activation of PPARβ/δ inhibits enhanced cytokine production in adipocytes by preventing NF-κB activation via ERK1/2, an effect that may help prevent insulin resistance.
High Prevalence of Diabetes and Cardiovascular Risk Factors Associated With Urbanization in India
Authors: Ramachandran Ambady , Mary Simon , Yamuna Annasami , Murugesan Narayanasamy , Snehalatha Chamukuttan 
Published: April 2008

OBJECTIVE—To compare prevalence of diabetes, impaired glucose tolerance (IGT), impaired fasting glucose (IFG), and cardiovascular risk factors between a city, a town, and periurban villages (PUVs) in southern India and to look for temporal changes in the city and PUVs.
RESEARCH DESIGN AND METHODS—Subjects aged ≥20 years were studied in Tamilnadu, India, in Chennai (city, n = 2,192; 1,053 men and 1,138 women), Kanchipuram (town, n = 2,290; 988 men and 1,302 women), and Panruti (PUVs, n = 2,584; 1,280 men and 1,304 women) in 2006. Demographic, socioeconomic, and anthropometric details; blood pressure; physical activity; diet habits; and lipids were studied. Risk associations with diabetes were analyzed using multiple logistic regression analyses. Present and previous data in the city and the PUVs were compared.
RESULTS—Mean BMI, waist circumference, and family history of diabetes were significantly lower in the PUVs. The PUVs had a lower prevalence of diabetes (9.2 [95% CI 8.0–10.5], P &lt; 0.0001) than the city (18.6 [16.6–20.5]) and town (16.4 [14.1–18.6]). Approximately 40% of subjects were newly diagnosed. Prevalence of impaired glucose tolerance (IGT) was higher (P &lt; 0.0001) in the city (7.4 [6.2–8.5]) than in the town (4.3 [3.3–5.3]) and the PUVs (5.5 [4.6–6.5]). Prevalence of IFG was generally low. Age, family history, and waist circumference were significantly associated with diabetes, while physical activity was not. Overweight, elevated waist circumference, hypertension, and dyslipidemia were more prevalent in the city.
CONCLUSIONS—In the city, diabetes increased from 13.9 to 18.6% in 6 years and IGT decreased significantly. The town and city had similar prevalences; the PUVs had lower diabetes prevalence, but prevalence had increased compared with that in a previous survey. Cardiometabolic abnormalities were more prevalent in urban populations.
High Birth Weight and Early Postnatal Weight Gain Protect Obese Children and Adolescents From Truncal Adiposity and Insulin Resistance
Authors: Bouhours-Nouet Natacha , Dufresne Sylvie , de Casson Florence Boux , Mathieu Elisabeth , Douay Olivier , Gatelais Frédérique , Rouleau Stéphanie , Coutant Régis 
Published: April 2008

OBJECTIVE—Low birth weight (LBW), no early catch-up weight, and subsequent fat accumulation have been associated with increased risks of insulin resistance from childhood onward and later cardiovascular disease. We sought to clarify the effects of high birth weight (HBW) and postnatal weight gain on insulin resistance.
RESEARCH DESIGN AND METHODS—A total of 117 obese children aged 10.4 ± 2.4 years were divided into three groups according to fetal growth after exclusion of maternal diabetes. They were comparable for age, sex, puberty, and percent body fat. Customized French birth weight standards, adjusted for maternal characteristics and gestation number, identified subjects with true altered fetal growth: 32 had increased fetal growth according to customized standards (HBWcust), 52 were eutrophic, and 33 had restricted fetal growth according to customized standards (LBWcust). Fat distribution by dual-energy X-ray absorptiometry, insulin sensitivity indexes from an oral glucose tolerance test (OGTT), and leptin, adiponectin, and visfatin levels were compared between groups.
RESULTS—The HBWcust subjects had a higher adiponectin level, higher whole-body insulin sensitivity index (WBISI), and lower hepatic insulin resistance index, lower insulin and free fatty acid concentrations during OGTT, and lower trunk fat percent than eutrophic (P &lt; 0.05) and LBWcust subjects (P &lt; 0.05). Besides birth weight, weight gain between 0 and 2 years was a positive predictor (P &lt; 0.05) of WBISI, whereas weight gain after 4 years was a negative predictor (P &lt; 0.05).
CONCLUSIONS—HBW and early weight gain may program insulin sensitivity and adipose tissue metabolism and contribute to so-called metabolically healthy obesity.
Estimating Physician Effects on Glycemic Control in the Treatment of Diabetes
Authors: Tuerk Peter W. , Mueller Martina , Egede Leonard E. 
Published: April 2008

OBJECTIVE—Researchers have only just begun to investigate physician-related effects on medical outcomes. Such research is necessary for developing empirically informed practice guidelines and policy. The primary goal of this study was to investigate whether glucose management in type 2 diabetes varies by randomly assigned physicians over the course of a year in treatment. A second goal of the study was to investigate whether physician-related effects vary across differential patient characteristics. A tertiary goal was to investigate potential patient-level effects on glucose management.
RESEARCH DESIGN AND METHODS—Hierarchical linear models were used to investigate A1C among 1,381 patients, nested within 42 randomly assigned primary care physicians at a Veterans Affairs medical center in the southeastern U.S. The primary outcome measure was change in A1C over the course of 1 year in treatment. On average, each study physician had 33 patients with diabetes.
RESULTS—Overall, physician-related factors were associated with statistically significant but modest variability in A1C change (2%), whereas patient-level factors accounted for the majority of variation in A1C change (98%). Physician effects varied by patient characteristics, mattering more for black patients, patients aged 65 years, and patients whose glucose management improved over the treatment year.
CONCLUSIONS—The results of this study indicate that differential physician effects have minimal impact on glycemic control. Results suggest that it is logical to support policies encouraging the development of patient-level behavioral interventions because that is the level that accounts for the majority of variance in glycemic control.
Determinants of New-Onset Diabetes Among 19,257 Hypertensive Patients Randomized in the Anglo-Scandinavian Cardiac Outcomes Trial–Blood Pressure Lowering Arm and the Relative Influence of Antihypertensive Medication
Authors: Gupta Ajay K. , Dahlof Bjorn , Dobson Joanna , Sever Peter S. , Wedel Hans , Poulter N.R. ,   on behalf of the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) Investigators
Published: April 2008

OBJECTIVE—The purpose of this study was to determine the baseline predictors of new-onset diabetes (NOD) in hypertensive patients and to develop a risk score to identify those at high risk of NOD.
RESEARCH DESIGN AND METHODS—Among 19,257 hypertensive patients in the Anglo-Scandinavian Cardiac Outcomes Trial–Blood Pressure Lowering Arm (ASCOT-BPLA) who were randomly assigned to receive one of two antihypertensive regimens (atenolol ± thiazide or amlodipine ± perindopril), 14,120 were at risk of developing diabetes at baseline. Of these, 1,366 (9.7%) subsequently developed NOD during median follow-up of 5.5 years. A multivariate Cox model was developed to identify the independent predictors of NOD and individual risk scores.
RESULTS—NOD was significantly associated with an increase in baseline fasting plasma glucose (FPG), BMI, serum triglycerides, and systolic blood pressure. In contrast, amlodipine ± perindopril in comparison with atenolol ± thiazide treatment (hazard ratio 0.66 [95% CI 0.59–0.74]), high HDL cholesterol, alcohol use, and age &gt;55 years were found to be significantly protective factors. FPG was the most powerful predictor with risk increasing by 5.8 times (95% CI 5.23–6.43) for each millimole per liter rise &gt;5 mmol/l. The risk of NOD increased steadily with increasing quartile of risk score, with a 19-fold increase (95% CI 14.3–25.4) among those in the highest compared with those in the lowest quartile. The model showed excellent internal validity and discriminative ability.
CONCLUSIONS—Baseline FPG &gt;5 mmol/l, BMI, and use of an atenolol ± diuretic regimen were among the major determinants of NOD in hypertensive patients. The model developed from these data allows accurate prediction of NOD among hypertensive subjects.
A1C in Children and Adolescents With Diabetes in Relation to Certain Clinical Parameters
Authors: Hanberger Lena , Samuelsson Ulf , Lindblad Bengt , Ludvigsson Johnny 
Published: April 2008

OBJECTIVE—We explored the relationship between A1C and insulin regimen, duration of diabetes, age, sex, and BMI as well as the differences between clinical mean A1C levels at pediatric diabetes clinics in Sweden.
RESEARCH DESIGN AND METHODS—Data from 18,651 clinical outpatient visits (1,033 girls and 1,147 boys) at 20 pediatric clinics during 2001 and 2002 registered in the Swedish Childhood Diabetes Registry SWEDIABKIDS, a national quality registry, were analyzed.
RESULTS—A1C was &lt;7.0% (target value ∼8% per Diabetes Control and Complications Trial/National Glycohemoglobin Standardization Program standards) at 35% of the visits. Girls had significantly higher mean A1C than boys during adolescence. High mean A1C was correlated with high mean insulin dose, long duration of diabetes, and older age. Mean A1C varied between clinics (6.8–8.2%). Differences between centers could not be explained by differences in diabetes duration, age, BMI, or insulin dose.
CONCLUSIONS—Adolescents with a high insulin dose and a long duration of diabetes, especially girls, need to be focused on. Differences in mean values between centers remained inexplicable and require further investigation.
Inclusion of Educational Messages in Laboratory Reports Aids to Complete the Diagnostic Workup of Hyperglycemia
Authors: Pérez-Jáuregui José , González-Cardel Ana María , Olay-Fuentes Gabriela , Reza-Albarrán Alfredo , Mehta Roopa , Aguilar-Salinas Carlos A. 
Published: April 2008

OBJECTIVE—To evaluate whether educational messages regarding oral glucose tolerance test (OGTT) indications in laboratory reports increase the number of OGTTs appropriately requested.
RESEARCH DESIGN AND METHODS—The following message was printed on the lab reports of individuals with a fasting plasma glucose (FPG) concentration between 5.5 and 6.9 mmol/l: “A FPG between 5.5 and 6.9 mmol/l is considered abnormal by the American Diabetes Association (impaired fasting glucose). An OGTT is recommended if the patient does not have a diagnosis of diabetes and suffers from conditions associated with an increased risk for having type 2 diabetes (i.e., overweight, high blood pressure, abnormal plasma lipids or family history of diabetes).” The number of educational messages printed was 81,099.
RESULTS—The intervention resulted in a significant increase in the number of OGTTs requested, from 78 ± 19 to 268 ± 48 tests per month. It also resulted in a greater proportion of case subjects that had an abnormal OGTT result.
CONCLUSIONS—Educational messages in laboratory reports aid in the diagnostic workup of hyperglycemia.
Differences in Metabolites in Pain-Processing Brain Regions in Patients With Diabetes and Painful Neuropathy
Authors: Sorensen Lea , Siddall Philip J. , Trenell Michael I. , Yue Dennis K. 
Published: April 2008

OBJECTIVE—Magnetic resonance spectroscopy (MRS) (specifically, 1H-MRS) has been used to show changes in the brain following peripheral nerve injury in subjects without diabetes. This study used 1H-MRS to examine the brain in subjects with or without painful diabetic neuropathy.
RESEARCH DESIGN AND METHODS—Twenty-six diabetic subjects (12 with and 14 without chronic neuropathic pain) were compared, with 18 subjects without diabetes and pain. The left thalamus, anterior cingulate cortex (ACC), and dorsolateral prefrontal cortex (DLPFC) were assessed using 1H-MRS.
RESULTS—In the DLPFC, diabetic subjects had a decrease in N-acetyl aspartate (NAA) and creatine relative to the control group. In the thalamus, there was a reduction of NAA in the diabetic group with pain compared with that in patients with diabetes and no pain.
CONCLUSION—Subjects with diabetes have metabolite differences in the brain compared with control subjects. Subjects with painful neuropathy showed reduced NAA in the thalamus, which may explain the genesis of pain in some cases.