bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dynamics of Atomic Ordering in Bulk and Thin Film Intermetallic Alloys: A Complementary Approach to Atomic Migration
Authors: Pfeiler Wolfgang , Püschl Wolfgang , Issro Chaisak , Kozubski Rafal , Pierron-Bohnes Veronique 
Published: February 2009

AbstractOne of the foremost challenges in today's materials science is the design and development of materials with physical properties customized for technical application. Due to their excellent corrosion resistance and their advantageous mechanical and in many cases also magnetic properties, intermetallic alloys are among the most important materials of the 21st century. Most of their outstanding qualities are linked to long-range order, the fact that unlike atoms are preferred as neighbours, which then segregate to different sublattices. In most intermetallics atomic order persists up to rather high temperatures, if not up to melting. However, connected with the entropy gain, the degree of order depends on temperature and thereby the stability of the designed beneficial materials properties is affected. By monitoring changes in the degree of atomic order an access to atom migration is gained, which is complementary to the usual diffusion experiments, where the degree of order is not changed on average. It is shown in this review on some selected examples how an adequate thermal treatment of the samples in combination with the experimental approach gives detailed information on atom jump mechanisms and structural changes, especially if experiment is combined with up-to-date kinetic Monte Carlo simulations.
First-principles Investigations of Point Defect Behavior and Elastic Properties of TiNi Based Alloys
Authors: Lu Jian-min , Hu Qing-miao , Yang Rui 
Published: February 2009

AbstractFirst-principles calculations by the use of a plane-wave pseudopotential method are performed to investigate intrinsic point defect behavior in TiNi. The results show that TiNi is an antisite type intermetallic compound. The calculated interaction energies between the point defects demonstrate that Ti antisites are attractive to each other whereas Ni antisites are mutually repulsive. The attraction between Ti antisites indicates that excess Ti in TiNi may agglomerate so that a Ti-rich phase can easily precipitate. The repulsion between Ni antisites implies that the excess Ni is of certain solubility in TiNi. This result explains well the asymmetric feature of TiNi field on the binary phase diagram. In order to understand the correlation between the composition dependent elastic modulus and martensitic transformation (MT) temperature, the elastic moduli critical to MT, i.e., c′ and c44, are calculated as a function of the composition of the off-stoichiometric TiNi and a series of ternary TiNi-X alloys, by the use of exact muffin-tin orbital method in combination with coherent potential approximation. It turns out that, generally speaking, the early transition metal (TM) alloying elements in the periodic table increase c′ but decrease c44; the middle ones increase both c′ and c44, whereas the late ones decrease c′ but increase c44. An examination of the theoretical composition dependent elastic modulus and the experimental MT temperature shows that the MT temperature is more sensitive to the variation of c44 than to that of c′.
Do Binucleate Cardiomyocytes Have A Role in Myocardial Repair? Insights Using Isolated Rodent Myocytes and Cell Culture
Authors: Stephen Michael J , Poindexter Brian J , Moolman Johan A , Sheikh-Hamad David , Bick Roger J 
Published: February 2009

Neonatal and adult cardiomyocytes were isolated from rat hearts. Some of the adult myocytes were cultured to allow for cell dedifferentiation, a phenomenon thought to mimic cell changes that occur in stressed myocardium, with myocytes regressing to a fetal pattern of metabolism and stellate neonatal shape.
Using fluorescence deconvolution microscopy, cells were probed with fluorescent markers and scanned for a number of proteins associated with ion control, calcium movements and cardiac function. Image analysis of deconvoluted image stacks and sequential real-time image recordings of calcium transients of cells were made.
All three myocyte groups were predominantly comprised of binucleate cells. Clustering of proteins to a single nucleus was a common observation, suggesting that one nucleus is active in protein synthesis pathways, while the other nucleus assumes a ‘dormant’ or different role and that cardiomyocytes might be mitotically active even in late development, or specific protein syntheses could be targeted and regulated for reintroduction into the cell cycle.
Such possibilities would extend cardiac disease associated stem cell research and therapy options, while producing valuable insights into developmental and death pathways of binucleate cardiomyocytes (word count 183).
Dynamic Changes in Pancreatic Endocrine Cell Abundance, Distribution, and Function in Antigen-Induced and Spontaneous Autoimmune Diabetes
Authors: Pechhold Klaus , Zhu Xiaolong , Harrison Victor S. , Lee Janet , Chakrabarty Sagarika , Koczwara Kerstin , Gavrilova Oksana , Harlan David M. 
Published: February 2009

OBJECTIVE
Insulin deficiency in type 1 diabetes and in rodent autoimmune diabetes models is caused by β-cell–specific killing by autoreactive T-cells. Less is known about β-cell numbers and phenotype remaining at diabetes onset and the fate of other pancreatic endocrine cellular constituents.

RESEARCH DESIGN AND METHODS
We applied multicolor flow cytometry, confocal microscopy, and immunohistochemistry, supported by quantitative RT-PCR, to simultaneously track pancreatic endocrine cell frequencies and phenotypes during a T-cell–mediated β-cell–destructive process using two independent autoimmune diabetes models, an inducible autoantigen-specific model and the spontaneously diabetic NOD mouse.

RESULTS
The proportion of pancreatic insulin-positive β-cells to glucagon-positive α-cells was about 4:1 in nondiabetic mice. Islets isolated from newly diabetic mice exhibited the expected severe β-cell depletion accompanied by phenotypic β-cell changes (i.e., hypertrophy and degranulation), but they also revealed a substantial loss of α-cells, which was further confirmed by quantitative immunohistochemisty. While maintaining normal randomly timed serum glucagon levels, newly diabetic mice displayed an impaired glucagon secretory response to non–insulin-induced hypoglycemia.

CONCLUSIONS
Systematically applying multicolor flow cytometry and immunohistochemistry to track declining β-cell numbers in recently diabetic mice revealed an altered endocrine cell composition that is consistent with a prominent and unexpected islet α-cell loss. These alterations were observed in induced and spontaneous autoimmune diabetes models, became apparent at diabetes onset, and differed markedly within islets compared with sub–islet-sized endocrine cell clusters and among pancreatic lobes. We propose that these changes are adaptive in nature, possibly fueled by worsening glycemia and regenerative processes.
Age-Dependent Decline in β-Cell Proliferation Restricts the Capacity of β-Cell Regeneration in Mice
Authors: Tschen Shuen-Ing , Dhawan Sangeeta , Gurlo Tatyana , Bhushan Anil 
Published: February 2009

OBJECTIVE
The aim of this study was to elucidate whether age plays a role in the expansion or regeneration of β-cell mass.

RESEARCH DESIGN AND METHODS
We analyzed the capacity of β-cell expansion in 1.5- and 8-month-old mice in response to a high-fat diet, after short-term treatment with the glucagon-like peptide 1 (GLP-1) analog exendin-4, or after streptozotocin (STZ) administration.

RESULTS
Young mice responded to high-fat diet by increasing β-cell mass and β-cell proliferation and maintaining normoglycemia. Old mice, by contrast, did not display any increases in β-cell mass or β-cell proliferation in response to high-fat diet and became diabetic. To further assess the plasticity of β-cell mass with respect to age, young and old mice were injected with a single dose of STZ, and β-cell proliferation was analyzed to assess the regeneration of β-cells. We observed a fourfold increase in β-cell proliferation in young mice after STZ administration, whereas no changes in β-cell proliferation were observed in older mice. The capacity to expand β-cell mass in response to short-term treatment with the GLP-1 analog exendin-4 also declined with age. The ability of β-cell mass to expand was correlated with higher levels of Bmi1, a polycomb group protein that is known to regulate the Ink4a locus, and decreased levels of p16Ink4aexpression in the β-cells. Young Bmi1−/− mice that prematurely upregulate p16Ink4afailed to expand β-cell mass in response to exendin-4, indicating that p16Ink4alevels are a critical determinant of β-cell mass expansion.

CONCLUSIONS
β-Cell proliferation and the capacity of β-cells to regenerate declines with age and is regulated by the Bmi1/p16Ink4apathway.
Type 2 Diabetes Risk Alleles Are Associated With Reduced Size at Birth
Authors: Freathy Rachel M. , Bennett Amanda J. , Ring Susan M. , Shields Beverley , Groves Christopher J. , Timpson Nicholas J. , Weedon Michael N. , Zeggini Eleftheria , Lindgren Cecilia M. , Lango Hana , Perry John R.B. , Pouta Anneli , Ruokonen Aimo , Hyppönen Elina , Power Chris , Elliott Paul , Strachan David P. , Järvelin Marjo-Riitta , Smith George Davey , McCarthy Mark I. , Frayling Timothy M. , Hattersley Andrew T. 
Published: February 2009

OBJECTIVE
Low birth weight is associated with an increased risk of type 2 diabetes. The mechanisms underlying this association are unknown and may represent intrauterine programming or two phenotypes of one genotype. The fetal insulin hypothesis proposes that common genetic variants that reduce insulin secretion or action may predispose to type 2 diabetes and also reduce birth weight, since insulin is a key fetal growth factor. We tested whether common genetic variants that predispose to type 2 diabetes also reduce birth weight.

RESEARCH DESIGN AND METHODS
We genotyped single-nucleotide polymorphisms (SNPs) at five recently identified type 2 diabetes loci (CDKAL1, CDKN2A/B, HHEX-IDE, IGF2BP2, and SLC30A8) in 7,986 mothers and 19,200 offspring from four studies of white Europeans. We tested the association between maternal or fetal genotype at each locus and birth weight of the offspring.

RESULTS
We found that type 2 diabetes risk alleles at the CDKAL1 and HHEX-IDE loci were associated with reduced birth weight when inherited by the fetus (21 g [95% CI 11–31], P = 2 × 10−5, and 14 g [4–23], P = 0.004, lower birth weight per risk allele, respectively). The 4% of offspring carrying four risk alleles at these two loci were 80 g (95% CI 39–120) lighter at birth than the 8% carrying none (Ptrend = 5 × 10−7). There were no associations between birth weight and fetal genotypes at the three other loci or maternal genotypes at any locus.

CONCLUSIONS
Our results are in keeping with the fetal insulin hypothesis and provide robust evidence that common disease-associated variants can alter size at birth directly through the fetal genotype.
Association Between Increased Platelet P-Selectin Expression and Obesity in Patients With Type 2 Diabetes
Authors: Schneider David J. , Hardison Regina M. , Lopes Neuza , Sobel Burton E. , Brooks Maria Mori ,   the Pro-Thrombosis Ancillary Study Group
Published: February 2009

OBJECTIVE
To determine whether obesity increases platelet reactivity and thrombin activity in patients with type 2 diabetes plus stable coronary artery disease.

RESEARCH DESIGN AND METHODS
We assessed platelet reactivity and markers of thrombin generation and activity in 193 patients from nine clinical sites of the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D). Blood taken at the time of enrollment was used for assay of the concentration of prothrombin fragment 1.2 (PT1.2, released when prothrombin is activated) and fibrinopeptide A (FPA, released when fibrinogen is cleaved). Platelet activation was identified with the use of flow cytometry in response to 0, 0.2, and 1 μmol/l adenosine diphosphate (ADP).

RESULTS
Concentrations of FPA, PT1.2, and platelet activation in the absence of agonist were low. Greater BMI was associated with higher platelet reactivity in response to 1 μm ADP as assessed by surface expression of P-selectin (r = 0.29, P &lt; 0.0001) but not reflected by the binding of fibrinogen to activated glycoprotein IIb-IIIa. BMI was not associated with concentrations of FPA or PT1.2. Platelet reactivity correlated negatively with A1C (P &lt; 0.04), was not related to the concentration of triglycerides in blood, and did not correlate with the concentration of C-reactive peptide.

CONCLUSIONS
Among patients enrolled in this substudy of BARI 2D, a greater BMI was associated with higher platelet reactivity at the time of enrollment. Our results suggest that obesity and insulin resistance that accompanies obesity may influence platelet reactivity in patients with type 2 diabetes.
Coenzyme Q10 Improves Endothelial Dysfunction in Statin-Treated Type 2 Diabetic Patients
Authors: Hamilton Sandra J. , Chew Gerard T. , Watts Gerald F. 
Published: February 2009

OBJECTIVE
The vascular benefits of statins might be attenuated by inhibition of coenzyme Q10 (CoQ10) synthesis. We investigated whether oral CoQ10 supplementation improves endothelial dysfunction in statin-treated type 2 diabetic patients.

RESEARCH DESIGN AND METHODS
In a double-blind crossover study, 23 statin-treated type 2 diabetic patients with LDL cholesterol &lt;2.5mmol/l and endothelial dysfunction (brachial artery flow-mediated dilatation [FMD] &lt;5.5%) were randomized to oral CoQ10 (200 mg/day) or placebo for 12 weeks. We measured brachial artery FMD and nitrate-mediated dilatation (NMD) by ultrasonography. Plasma F2-isoprostane and 24-h urinary 20-hydroxyeicosatetraenoic acid (HETE) levels were measured as systemic oxidative stress markers.

RESULTS
Compared with placebo, CoQ10 supplementation increased brachial artery FMD by 1.0 ± 0.5% (P = 0.04), but did not alter NMD (P = 0.66). CoQ10 supplementation also did not alter plasma F2-isoprostane (P = 0.58) or urinary 20-HETE levels (P = 0.28).

CONCLUSIONS
CoQ10 supplementation improved endothelial dysfunction in statin-treated type 2 diabetic patients, possibly by altering local vascular oxidative stress.
Cerebrovascular Reactivity, Intima-Media Thickness, and Nephropathy Presence in Patients With Type 1 Diabetes
Authors: Kozera Grzegorz M. , Wolnik Bogumił , Kunicka Katarzyna B. , Szczyrba Sebastian , Wojczal Joanna , Schminke Ulf , Nyka Walenty M. , Bieniaszewski Leszek 
Published: February 2009

OBJECTIVE
Cerebrovascular reactivity impairment was reported as a marker of cerebral microangiopathy in long-term type 1 diabetes. Intima-media complex thickening reflects early stages of macroangiopathy in type 1 diabetes. The analysis of the relationship between these variables and other microangiopathic complications might serve as a beneficial indicator for early prophylaxis in these patients.

RESEARCH DESIGN AND METHODS
Vasomotor reactivity reserve (VMRr) and breath-holding index (BHI) of the middle cerebral artery were measured with transcranial Doppler in 59 patients (median age 32.0 years, range 20–51, 36 females) with type 1 diabetes, without history of cerebrovascular events, and 30 healthy control subjects (median age 31.5 years, range 25–39, 15 females). The relationships between the presence of selected vascular complications of type 1 diabetes and biochemical parameters, intima-media thickness (IMT), and VMRr and BHI in patients were analyzed.

RESULTS
VMRr and BHI were lower in patients with type 1 diabetes when compared with healthy subjects (81.5 vs. 100%, P &lt; 0.01, and 1.6 vs. 2.2, P = 0.04, respectively), whereas IMT was significantly higher in patients then in healthy control subjects (0.36 vs. 0.30 mm, P = 0.001). However, no association of IMT with VMRr was found. We found a significant reduction of VMRr and BHI in patients with diabetic nephropathy.

CONCLUSIONS
The presence of diabetic nephropathy, but not IMT, can be regarded as an indicator of cerebral microangiopathy severity in patients with type 1 diabetes.
Childhood Predictors of Adult Acute Insulin Response and Insulin Action
Authors: Thearle Marie S. , Bunt Joy C. , Knowler William C. , Krakoff Jonathan 
Published: February 2009

OBJECTIVE
Because declines in acute insulin response (AIR) and insulin action (M) predict development of type 2 diabetes, we sought to determine childhood factors that predict insulin action and AIR using longitudinal data from young Pima Indian adults with normal glucose regulation.

RESEARCH DESIGN AND METHODS
Predictors of adult M, measured by the euglycemic-hyperinsulinemic clamp, and AIR, measured after a 25-g glucose bolus, were assessed in 76 individuals from a set of childhood data (BMI, systolic blood pressure [sBP] and diastolic blood pressure, cholesterol, fasting and 2-h insulin, and glucose levels during an oral glucose tolerance test).

RESULTS
After adjustment for sex, adult percent body fat, adult and childhood age, childhood BMI, and sBP were negative and independent predictors of adult M. A 5 kg/m2 increase in childhood BMI was associated with a 7.4% decrease in adult insulin action (95% CI −12.7 to −1.8%, P = 0.01) and a 10-mmHg increase in childhood sBP with a 5.0% decrease in adult M (95% CI −8.4 to −1.4%, P = 0.007). After a similar adjustment with M as an additional covariate, childhood 2-h insulin was a positive predictor of adult AIR such that a 25% increase predicted a 7.3% increase in adult AIR (95% CI 1.5–13.5%, P = 0.014).

CONCLUSIONS
Childhood insulin response during an oral glucose challenge predicts adult AIR, indicating that β-cell capacity may be set early in life. Childhood measures related to adiposity predict adult insulin action, which may reflect common underlying mechanisms that may be amenable to modification through programs targeting prevention or treatment of childhood obesity.
Relation of Abdominal Fat Depots to Systemic Markers of Inflammation in Type 2 Diabetes
Authors: Sam Susan , Haffner Steven , Davidson Michael H. , D'Agostino Ralph B. , Feinstein Steven , Kondos George , Perez Alfonso , Mazzone Theodore 
Published: February 2009

OBJECTIVE
Both visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) have been linked to systemic inflammation in nondiabetic cohorts. We examined the relationships between VAT and SAT and systemic inflammatory markers in a large well-characterized cohort of subjects with type 2 diabetes.

RESEARCH DESIGN AND METHODS
Three hundred eighty-two subjects with type 2 diabetes in the CHICAGO (Carotid Intima-Media Thickness in Atherosclerosis Using Pioglitazone) study cohort underwent abdominal computed tomography to determine SAT and VAT distribution. Fasting blood was obtained for measurement of inflammatory markers. The relationships between inflammatory markers and BMI, SAT, and VAT were examined using regression models adjusted for age, sex, diabetes treatment, duration of diabetes, smoking, statin use, and A1C.

RESULTS
VAT was positively related to CRP, monocyte chemoattractant protein (MCP), intracellular adhesion molecule (ICAM)-1, and plasminogen activator inhibitor type 1 (PAI-1) antigen before adjustment for BMI. After adjustment for BMI, the relationship to CRP was lost but positive associations with MCP (P &lt; 0.01), PAI-1 (P &lt; 0.0001), ICAM-1 (P &lt; 0.01), and vascular cell adhesion molecule (P = 0.01) were evident. BMI was positively related to CRP (P &lt; 0.0001) and IL-6 (P &lt; 0.01) even after adjustment for VAT and SAT. SAT was not related to any inflammatory marker after adjustment for BMI.

CONCLUSIONS
In this large group of subjects with type 2 diabetes, BMI was most strongly associated with CRP and IL-6 levels. SAT was not associated with markers of systemic inflammation. The size of the VAT depot provided information additional to that provided by BMI regarding inflammatory markers that are strongly related to vascular wall remodeling and coagulation. Our findings suggest that adipose tissue distribution remains an important determinant of systemic inflammation in type 2 diabetes.
Predictors and Impact of Intensification of Antihyperglycemic Therapy in Type 2 Diabetes
Authors: McEwen Laura N. , Bilik Dori , Johnson Susan L. , Halter Jeffrey B. , Karter Andrew J. , Mangione Carol M. , Subramanian Usha , Waitzfelder Beth , Crosson Jesse C. , Herman William H. 
Published: February 2009

OBJECTIVE
The purpose of this study was to examine the predictors of intensification of antihyperglycemic therapy in patients with type 2 diabetes; its impact on A1C, body weight, symptoms of anxiety/depression, and health status; and patient characteristics associated with improvement in A1C.

RESEARCH DESIGN AND METHODS
We analyzed survey, medical record, and health plan administrative data collected in Translating Research into Action for Diabetes (TRIAD). We examined patients who were using diet/exercise or oral antihyperglycemic medications at baseline, had A1C &gt;7.2%, and stayed with the same therapy or intensified therapy (initiated or increased the number of classes of oral antihyperglycemic medications or began insulin) over 18 months.

RESULTS
Of 1,093 patients, 520 intensified therapy with oral medications or insulin. Patients intensifying therapy were aged 58 ± 12 years, had diabetes duration of 11 ± 9 years, and had A1C of 9.1 ± 1.5%. Younger age and higher A1C were associated with therapy intensification. Compared with patients who did not intensify therapy, those who intensified therapy experienced a 0.49% reduction in A1C (P &lt; 0.0001), a 3-pound increase in weight (P = 0.003), and no change in anxiety/depression (P = 0.5) or health status (P = 0.2). Among those who intensified therapy, improvement in A1C was associated with higher baseline A1C, older age, black race/ethnicity, lower income, and more physician visits.

CONCLUSIONS
Treatment intensification improved glycemic control with no worsening of anxiety/depression or health status, especially in elderly, lower-income, and minority patients with type 2 diabetes. Interventions are needed to overcome clinical inertia when patients might benefit from treatment intensification and improved glycemic control.
Predictors of Overweight During Childhood in Offspring of Parents With Type 1 Diabetes
Authors: Hummel Sandra , Pflüger Maren , Kreichauf Susanne , Hummel Michael , Ziegler Anette-G. 
Published: February 2009

OBJECTIVE
To study which perinatal factors affect the risk of childhood overweight in offspring with a first-degree relative (FDR) with type 1 diabetes and to determine whether maternal diabetes is an independent contributor to overweight risk.

RESEARCH DESIGN AND METHODS
Data on a child's weight and height were collected at age 2, 5, and 8 years from 1,214 children participating in the prospective BABYDIAB study. All children had an FDR with type 1 diabetes, including 783 whose mothers had type 1 diabetes. Overweight was defined as BMI percentile ≥90. Data on birth size, breast-feeding, maternal age, and smoking during pregnancy were collected by questionnaires. Risk estimates were calculated by logistic regression analyses.

RESULTS
Breastfeeding duration and birth size both contributed significantly to overweight risk at all age intervals. Full breast-feeding &gt;4 months or any breast-feeding &gt;6 months reduced risk of overweight (aged 8 years: odds ratio 0.3 [95% CI 0.2–0.7], P = 0.004; and 0.3 [0.1–0.6], P = 0.001). Large-for-gestational-age status increased risk of overweight (aged 8 years: 2.4 [1.4–4.3], P = 0.002). Importantly, no evidence was found for an independent contribution of maternal type 1 diabetes to childhood overweight.

CONCLUSIONS
Our findings indicate that maternal type 1 diabetes is not an independent risk factor for overweight during childhood in offspring of type 1 diabetic mothers but that factors associated with maternal type 1 diabetes, such as short breast-feeding duration and high birth size, predispose children to overweight during childhood.