bluuebunny/crossref_metadata_2025_split huggingface dataset:
Salivary Antioxidants in Patients With Type 1 or 2 Diabetes and Inflammatory Periodontal Disease: A Case‐Control Study
Authors: Gümüş Pınar , Buduneli Nurcan , Çetinkalp Şevki , Hawkins Samuel I. , Renaud Diane , Kinane Denis F. , Scott David A. 
Published: September 2009

Background: The purpose of this study was to evaluate and compare salivary concentrations of reduced, oxidized glutathione, uric acid, ascorbic acid, and total antioxidant capacity in subjects with diabetes and systemically healthy subjects with inflammatory periodontal disease.Methods: Sixteen patients with type 1 diabetes mellitus (DM), 25 patients with type 2 DM, and 24 systemically healthy patients, all with inflammatory periodontal disease, were recruited. Whole‐saliva samples were obtained, and full‐mouth clinical periodontal measurements, including plaque index, probing depth, gingival recession, clinical attachment level, and bleeding on probing, were recorded at six sites per tooth. Saliva flow rate and salivary levels of reduced and oxidized glutathione, vitamin C, uric acid, and total antioxidant capacity were determined. Data were analyzed statistically by non‐parametric tests.Results: The subjects with type 2 DM had fewer teeth and more sites with probing depths >4 mm than the patients with type 1 DM (both P <0.01). The mean salivary reduced‐glutathione concentration was lower in patients with type 1 DM than in the other two groups (both P <0.05). No significant differences in the salivary concentrations of the other antioxidants measured were found among the groups (P >0.05). Oxidized glutathione levels in the patients with type 1 DM were significantly lower than in the systemically healthy group (P = 0.007). In both groups with diabetes, salivary reduced‐glutathione levels correlated positively with probing depth, and total antioxidant capacity correlated with salivary flow rate (P <0.01).Conclusion: The decrease in salivary reduced‐glutathione levels in patients with type 1 DM may have a role in periodontal tissue destruction by predisposing tissues to oxidative stress.
Low-Fat Versus Low-Carbohydrate Weight Reduction Diets
Authors: Bradley Una , Spence Michelle , Courtney C. Hamish , McKinley Michelle C. , Ennis Cieran N. , McCance David R. , McEneny Jane , Bell Patrick M. , Young Ian S. , Hunter Steven J. 
Published: September 2009

OBJECTIVE
Low-fat hypocaloric diets reduce insulin resistance and prevent type 2 diabetes in those at risk. Low-carbohydrate, high-fat diets are advocated as an alternative, but reciprocal increases in dietary fat may have detrimental effects on insulin resistance and offset the benefits of weight reduction.

RESEARCH DESIGN AND METHODS
We investigated a low-fat (20% fat, 60% carbohydrate) versus a low-carbohydrate (60% fat, 20% carbohydrate) weight reduction diet in 24 overweight/obese subjects ([mean ± SD] BMI 33.6 ± 3.7 kg/m2, aged 39 ± 10 years) in an 8-week randomized controlled trial. All food was weighed and distributed, and intake was calculated to produce a 500 kcal/day energy deficit. Insulin action was assessed by the euglycemic clamp and insulin secretion by meal tolerance test. Body composition, adipokine levels, and vascular compliance by pulse-wave analysis were also measured.

RESULTS
Significant weight loss occurred in both groups (P &lt; 0.01), with no difference between groups (P = 0.40). Peripheral glucose uptake increased, but there was no difference between groups (P = 0.28), and suppression of endogenous glucose production was also similar between groups. Meal tolerance–related insulin secretion decreased with weight loss with no difference between groups (P = 0.71). The change in overall systemic arterial stiffness was, however, significantly different between diets (P = 0.04); this reflected a significant decrease in augmentation index following the low-fat diet, compared with a nonsignificant increase within the low-carbohydrate group.

CONCLUSIONS
This study demonstrates comparable effects on insulin resistance of low-fat and low-carbohydrate diets independent of macronutrient content. The difference in augmentation index may imply a negative effect of low-carbohydrate diets on vascular risk.
The microRNA Signature in Response to Insulin Reveals Its Implication in the Transcriptional Action of Insulin in Human Skeletal Muscle and the Role of a Sterol Regulatory Element–Binding Protein-1c/Myocyte Enhancer Factor 2C Pathway
Authors: Granjon Aurélie , Gustin Marie-Paule , Rieusset Jennifer , Lefai Etienne , Meugnier Emmanuelle , Güller Isabelle , Cerutti Catherine , Paultre Christian , Disse Emmanuel , Rabasa-Lhoret Rémi , Laville Martine , Vidal Hubert , Rome Sophie 
Published: September 2009

OBJECTIVE
Factors governing microRNA expressions in response to changes of cellular environment are still largely unknown. Our aim was to determine whether insulin, the major hormone controlling whole-body energy homeostasis, is involved in the regulation of microRNA expressions in human skeletal muscle.

RESEARCH DESIGN AND METHODS
We carried out comparative microRNA (miRNA) expression profiles in human skeletal muscle biopsies before and after a 3-h euglycemic-hyperinsulinemic clamp, with TaqMan low-density arrays. Then, using DNA microarrays, we determined the response to insulin of the miRNA putative target genes in order to determine their role in the transcriptional action of insulin. We further characterized the mechanism of action of insulin on two representative miRNAs, miR-1 and miR-133a, in human muscle cells.

RESULTS
Insulin downregulated the expressions of 39 distinct miRNAs in human skeletal muscle. Their potential target mRNAs coded for proteins that were mainly involved in insulin signaling and ubiquitination-mediated proteolysis. Bioinformatic analysis suggested that combinations of different downregulated miRNAs worked in concert to regulate gene expressions in response to insulin. We further demonstrated that sterol regulatory element–binding protein (SREBP)-1c and myocyte enhancer factor 2C were involved in the effect of insulin on miR-1 and miR-133a expression. Interestingly, we found an impaired regulation of miRNAs by insulin in the skeletal muscle of type 2 diabetic patients, likely as consequences of altered SREBP-1c activation.

CONCLUSIONS
This work demonstrates a new role of insulin in the regulation of miRNAs in human skeletal muscle and suggests a possible implication of these new modulators in insulin resistance.
Deletion of GPR40 Impairs Glucose-Induced Insulin Secretion In Vivo in Mice Without Affecting Intracellular Fuel Metabolism in Islets
Authors: Alquier Thierry , Peyot Marie-Line , Latour Martin G. , Kebede Melkam , Sorensen Christina M. , Gesta Stephane , Ronald Kahn C. , Smith Richard D. , Jetton Thomas L. , Metz Thomas O. , Prentki Marc , Poitout Vincent 
Published: September 2009

OBJECTIVE
The G-protein–coupled receptor GPR40 mediates fatty acid potentiation of glucose-stimulated insulin secretion, but its contribution to insulin secretion in vivo and mechanisms of action remain uncertain. This study was aimed to ascertain whether GPR40 controls insulin secretion in vivo and modulates intracellular fuel metabolism in islets.

RESEARCH DESIGN AND METHODS
Insulin secretion and sensitivity were assessed in GPR40 knockout mice and their wild-type littermates by hyperglycemic clamps and hyperinsulinemic euglycemic clamps, respectively. Transcriptomic analysis, metabolic studies, and lipid profiling were used to ascertain whether GPR40 modulates intracellular fuel metabolism in islets.

RESULTS
Both glucose- and arginine-stimulated insulin secretion in vivo were decreased by ∼60% in GPR40 knockout fasted and fed mice, without changes in insulin sensitivity. Neither gene expression profiles nor intracellular metabolism of glucose and palmitate in isolated islets were affected by GPR40 deletion. Lipid profiling of isolated islets revealed that the increase in triglyceride and decrease in lyso-phosphatidylethanolamine species in response to palmitate in vitro was similar in wild-type and knockout islets. In contrast, the increase in intracellular inositol phosphate levels observed in wild-type islets in response to fatty acids in vitro was absent in knockout islets.

CONCLUSIONS
These results indicate that deletion of GPR40 impairs insulin secretion in vivo not only in response to fatty acids but also to glucose and arginine, without altering intracellular fuel metabolism in islets, via a mechanism that may involve the generation of inositol phosphates downstream of GPR40 activation.
Glucose Deprivation Regulates KATP Channel Trafficking via AMP-Activated Protein Kinase in Pancreatic β-Cells
Authors: Lim Ajin , Park Sun-Hyun , Sohn Jong-Woo , Jeon Ju-Hong , Park Jae-Hyung , Song Dae-Kyu , Lee Suk-Ho , Ho Won-Kyung 
Published: September 2009

OBJECTIVE
AMP-activated protein kinase (AMPK) and the ATP-sensitive K+ (KATP) channel are metabolic sensors that become activated during metabolic stress. AMPK is an important regulator of metabolism, whereas the KATP channel is a regulator of cellular excitability. Cross talk between these systems is poorly understood.

RESEARCH DESIGN AND METHODS
Rat pancreatic β-cells or INS-1 cells were pretreated for 2 h at various concentrations of glucose. Maximum KATP conductance (Gmax) was monitored by whole-cell measurements after intracellular ATP washout using ATP-free internal solutions. KATP channel activity (NPo) was monitored by inside-out patch recordings in the presence of diazoxide. Distributions of KATP channel proteins (Kir6.2 and SUR1) were examined using immunofluorescence imaging and surface biotinylation studies. Insulin secretion from rat pancreatic islets was measured using an enzyme immunoassay.

RESULTS
Gmax and NPo in cells pretreated with glucose-free or 3 mmol/l glucose solutions were significantly higher than in cells pretreated in 11.1 mmol/l glucose solutions. Immunofluorescence imaging and biotinylation studies revealed that glucose deprivation induced an increase in the surface level of Kir6.2 without affecting the total cellular amount. Increases in Gmax and the surface level of Kir6.2 were inhibited by compound C, an AMPK inhibitor, and siAMPK transfection. The effects of glucose deprivation on KATP channels were mimicked by an AMPK activator. Glucose deprivation reduced insulin secretion, but this response was attenuated by compound C.

CONCLUSIONS
KATP channel trafficking is regulated by energy status via AMPK, and this mechanism may play a key role in inhibiting insulin secretion under low energy status.
Haptoglobin Genotype and Renal Function Decline in Type 1 Diabetes
Authors: Costacou Tina , Ferrell Robert E. , Ellis Demetrius , Orchard Trevor J. 
Published: September 2009

OBJECTIVE
Haptoglobin (Hp) binds free Hb, inhibiting Hb-induced oxidative damage. As oxidative stress has been associated with microvascular complications, we evaluated the relationship between Hp genotype and microalbuminuria, macroalbuminuria, end-stage renal disease (ESRD), and early renal function decline in type 1 diabetes.

RESEARCH DESIGN AND METHODS
Participants from the Epidemiology of Diabetes Complications Study with DNA available were studied for the incidence of microalbuminuria (albumin excretion rate [AER] 20–200 μg/min), macroalbuminuria (AER &gt;200 μg/min), ESRD (renal dialysis or transplantation), and renal function decline (a decline ≥30 ml/min per 1.73 m2 from baseline estimated [by the Cockcroft-Gault equation] glomerular filtration rate [eGFR] in those with baseline eGFR &gt;60 ml/min per 1.73 m2).

RESULTS
The proportions with the Hp 2/2, 2/1, and 1/1 genotype were 43.4, 44.4, and 12.1%, respectively. During 18 years of follow-up, the incidence of eGFR decline, microalbuminuria, macroalbuminuria, and ESRD was 42.0, 40.5, 16.7, and 12.2%, respectively. No significant univariate differences were observed by Hp genotype. However, in multivariable Cox models, an ∼twofold increased risk was observed for the Hp 2/2 compared with the Hp 1/1 genotype for eGFR decline (hazard ratio 1.79 [95% CI 1.06–3.00]) and ESRD (2.74 [1.17–6.45]); no significant associations were observed for microalbuminuria or macroalbuminuria.

CONCLUSIONS
These data suggest that although Hp genotype is not associated with albuminuria per se, it may be an independent determinant of early renal function decline and progression to ESRD. Understanding these apparent contradictory findings may provide further insight into the pathogenesis of renal disease in type 1 diabetes.
Psychosocial Stress at Work Doubles the Risk of Type 2 Diabetes in Middle-Aged Women
Authors: Heraclides Alexandros , Chandola Tarani , Witte Daniel R. , Brunner Eric J. 
Published: September 2009

OBJECTIVE
To investigate the effect of psychosocial stress at work on risk of type 2 diabetes, adjusting for conventional risk factors, among a sample of British, white-collar, middle-aged men and women.

RESEARCH DESIGN AND METHODS
This was a prospective analysis (1991–2004) from the Whitehall II cohort study. The current sample consists of 5,895 Caucasian middle-aged civil servants free from diabetes at baseline. Type 2 diabetes was ascertained by an oral glucose tolerance test supplemented by self-reports at baseline and four consecutive waves of data collection including two screening phases. The job strain and iso-strain models were used to assess psychosocial work stress.

RESULTS
Iso-strain in the workplace was associated with a twofold higher risk of type 2 diabetes in age-adjusted analysis in women but not in men (hazard ratio 1.94 [95% CI 1.17–3.21). This effect remained robust to adjustment for socioeconomic position and outside work stressors and was only attenuated by 20% after adjustment for health behaviors, obesity, and other type 2 diabetes risk factors.

CONCLUSIONS
Psychosocial work stress was an independent predictor of type 2 diabetes among women after a 15-year follow-up. This association was not explained by potential confounding and mediating factors. More evidence from prospective studies using the same work stress models is needed to support the current findings and provide further information on sex differences.
Reduction of Tire Groove Noise Using Slot Resonators
Authors: Fujiwara S. , Yumii K. , Saguchi T. , Kato K. 
Published: September 2009

Abstract
Circumferential tire grooves form pipes in the contact patch and generate the nuisance noise, for which the fundamental natural frequency is approximately 1000 Hz for passenger car tires. The frequency coincides with the peak of pass-by noise spectrum. Therefore, controlling the groove resonance is of a main motivation of this paper to reduce environmental noise. If one lateral slot end is terminated in tread rib and if the other end merges to a circumferential groove, it is found that the slot performs as a side-branch or a Helmholtz subresonator to counteract to the pipe resonance. The slot parameters, such as cavity volume and the change in section area, determine the resonant frequency and effectively influence on the acoustic characteristics of whole groove space. Optimal slot geometry is widely investigated by using numerical analysis and validated by experiments. It is shown that the proposed tread design can significantly reduce groove noise without sacrificing other performances.
Structure and Parameterization of MF-Swift, a Magic Formula-based Rigid Ring Tire Model
Authors: Schmeitz A. J. C. , Versteden W. D. 
Published: September 2009

Abstract
Vehicle dynamic simulations require accurate, fast, reliable, and easy-to-parameterize tire models. For this purpose, TNO developed MF-Swift in close cooperation with the technical universities of Delft and Eindhoven. MF-Swift is based on the well-known magic formula model of Pacejka but extending to higher frequencies (60–100 Hz), shorter wavelengths (&gt;0.2 m), and rolling over obstacles by adding a rigid ring and obstacle enveloping model. During the development of MF-Swift, great emphasis was given to experimental validation using dedicated laboratory experiments. With increasing use of MF-Swift in the automotive industry, easy and reliable parameterization has become more important. Therefore, recent efforts have focused on improving the parameter identification process so that it can be conducted with little user interaction and with measurements obtained from industry common test facilities. This paper will discuss the theory behind the improved MF-Swift parameter identification process.
Evaluation of quantitative trait loci for hip dysplasia in Labrador Retrievers
Authors: Phavaphutanon Janjira , Mateescu Raluca G. , Tsai Kate L. , Schweitzer Peter A. , Corey Elizabeth E. , Vernier-Singer Margaret A. , Williams Alma J. , Dykes Nathan L. , Murphy Keith E. , Lust George , Todhunter Rory J. 
Published: September 2009

Abstract
Objective—To identify the quantitative trait loci (QTL) that contribute to hip dysplasia in dogs.
Animals—192 Labrador Retrievers.
Procedures—Hip dysplasia was measured by use of the Norberg angle (NA), dorsolateral subluxation (DLS) score, and distraction index (DI). Genome-wide screening was conducted by use of 276 unique microsatellites. Linkage analysis was performed with a variance-based linear model. Logarithm of the odds (LOD) scores were reported when values were > 2.0.
Results—Canis familiaris autosomes (CFAs) 01, 02, 10, 20, 22, and 32 harbored significant QTL at LOD scores > 2.0. Among the 6 QTL, the QTL on CFA02 had not been reported to harbor QTL for hip dysplasia. The highest LOD score of 3.32 on CFA20 contributed to the second principal component of the DLS score and NA of the right hip joint. The QTL that was mapped on CFA01 (LOD score of 3.13 at 55 centimorgans) was located on the same chromosome reported to harbor a QTL for hip dysplasia in Portuguese Water Dogs and German Shepherd Dogs. In this study, CFAs 10, 20, 22, and 32 harbored QTL for hip dysplasia that have been identified in a Labrador Retriever–Greyhound pedigree and in German Shepherd Dogs.
Conclusions and Clinical Relevance—Multiple QTL were clearly involved with hip dysplasia. Identification of these QTL will enable fine-resolution mapping and subsequent assessment of candidate genes within the refined intervals to enable researchers to develop genetic screening tests and preventative and novel therapeutic regimens.
Comparison of clonal relatedness and antimicrobial susceptibility of fecal Escherichia coli from healthy dogs and their owners
Authors: Stenske Katherine A. , Bemis David A. , Gillespie Barbara E. , D'Souza Doris H. , Oliver Stephen P. , Draughon Francis A. , Matteson Karla J. , Bartges Joseph W. 
Published: September 2009

Abstract
Objective—To determine prevalence of within-household sharing of fecal Escherichia coli between dogs and their owners on the basis of pulsed-field gel electrophoresis (PFGE), compare antimicrobial susceptibility between isolates from dogs and their owners, and evaluate epidemiologic features of cross-species sharing by use of a questionnaire.
Sample Population—61 healthy dog-owner pairs and 30 healthy control humans.
Procedures—3 fecal E coli colonies were isolated from each participant; PFGE profiles were used to establish relatedness among bacterial isolates. Susceptibility to 17 antimicrobials was determined via disk diffusion. A questionnaire was used to evaluate signalment, previous antimicrobial therapy, hygiene, and relationship with dog.
Results—A wide array of PFGE profiles was observed in E coli isolates from all participants. Within-household sharing occurred with 9.8% prevalence, and across-household sharing occurred with 0.3% prevalence. No behaviors were associated with increased clonal sharing between dog and owner. No differences were found in susceptibility results between dog-owner pairs. Control isolates were more likely than canine isolates to be resistant to ampicillin and trimethoprim-sulfamethoxazole. Owners and control humans carried more multdrug-resistant E coli than did dogs.
Conclusions and Clinical Relevance—Within-household sharing of E coli was detected more commonly than across-household sharing, but both direct contact and environmental reservoirs may be routes of cross-species sharing of bacteria and genes for resistance. Cross-species bacterial sharing is a potential public health concern, and good hygiene is recommended.
Effect of the viral protein Npro on virulence of bovine viral diarrhea virus and induction of interferon type I in calves
Authors: Henningson Jamie N. , Topliff Christina L. , Gil Laura H. V. , Donis Ruben O. , Steffen David J. , Charleston Bryan , Eskridge Kent M. , Kelling Clayton L. 
Published: September 2009

Abstract
Objective—To characterize the influence of the viral protein Npro on virulence of bovine viral diarrhea virus (BVDV) and on type I interferon responses in calves.
Animals—10 calves, 4 to 6 months of age.
Procedures—BVDV virulence and type I interferon responses of calves (n = 5) infected with a noncytopathic BVDV with a deleted Npro were compared with those of calves (5) infected with a noncytopathic BVDV with a functional Npro. Rectal temperatures, clinical signs, platelet counts, and total and differential WBC counts were evaluted daily. Histologic examinations and immunohistochemical analyses of tissues were conducted to assess lesions and distribution of viral antigens, respectively. Serum type I interferon concentrations were determined.
Results—Calves infected with Npro-deleted BVDV developed leukopenia and lymphopenia, without developing increased rectal temperatures or lymphoid depletion of target lymphoid organs. There was minimal antigen deposition in lymphoid organs. Calves infected with Npro BVDV developed increased rectal temperatures, leukopenia, lymphopenia, and lymphoid depletion with marked BVDV antigen deposition in lymphatic tissues. Interferon type I responses were detected in both groups of calves.
Conclusions and Clinical Relevance—Deletion of Npro resulted in attenuation of BVDV as evidenced by reduced virulence in calves, compared with BVDV with a functional Npro. Deletion of Npro did not affect induction of type I interferon. The Npro-deleted BVDV mutant may represent a safe noncytopathic virus candidate for vaccine development.
Quantitative differences in activities of back and pelvic limb muscles during walking and trotting between chronically lame and nonlame horses
Authors: Zaneb Hafsa , Kaufmann Verena , Stanek Christian , Peham Christian , Licka Theresia F. 
Published: September 2009

Abstract
Objective—To assess differences in activities of back and pelvic limb muscles by use of surface electromyography (SEMG) in chronically lame and nonlame horses during walking and trotting.
Animals—12 nonlame horses and 12 horses with unilateral chronic mild to moderate pelvic limb lameness.
Procedures—On each horse, bipolar electrodes were attached to the skin over the midpoints of the right and left longissimus thoracis (Lot), semitendinosus (Set), biceps femoris (Bif), gluteus medius (Glm), and extensor digitorum longus (Edl) muscles. For each muscle, synchronous kinematic and SEMG recordings were made during walking and trotting on a treadmill; mean, maximum, and minimum muscle activities and maximum-to-mean and minimum-to-mean activity ratios were determined. For each lame or nonlame horse, data from both pelvic limbs were averaged; in lame horses, data from the nonlame and lame pelvic limbs were also examined separately (NL-L and L-L values, respectively). Comparisons were made among the 4 data sets and between gaits.
Results—During walking, the NL-L maximum-to-mean ratios for Bif and Glm muscles were significantly greater and in lame horses, L-L and NL-L minimum-to-mean ratios for Set, Bif, Glm, and Lot muscles were significantly less than those for nonlame horses. During trotting, minimum-to-mean ratios for Set, Glm, and Lot muscles in lame horses were significantly lower than those for nonlame horses. Activity of the Edl muscle was not affected by lameness.
Conclusions and Clinical Relevance—In lame horses, variation in muscle use was detectable via SEMG. In chronically lame horses, back and pelvic limb muscle activities were affected differently during walking and trotting.