bluuebunny/crossref_metadata_2025_split huggingface dataset:
First Hyperstatic-Riser Joint Field Tested for Deep Offshore Drilling
Authors: Poirette Y. , Guesnon J. , Dupuis D. 
Published: December 2008

Summary
The riser is one of the key elements for deep offshore drilling. However, the total weight of the system increases rapidly with the water depth in the same way as the required tensioning capacity. Static loads and fatigue may become critical and threaten riser integrity. Furthermore, the natural period of the riser in the disconnected mode may also reach the wave-energy window and may seem able to put the riser into a dangerous resonant state.
A new technology developed by the L'Institut Français du Pétrole (IFP) for integrating riser joints, presented in the paper, reduces the weight of the system by up to 30% and lowers the natural period significantly. It consists of joining together all the pipes constituting the riser (main pipe and peripheral lines) in such a manner as to share the axial tension between all of them. This so-called hyperstatic-working mode, which provides an axial-load sharing between all riser lines, may be used jointly with hybrids (steel/composite) previously developed for kill and choke lines (Guesnon et al. 2002).
After the first step of riser analysis and technical studies through extensive finite-element analyses (FEAs) and computer-assisted design (CAD), a field test was decided upon to obtain information on the capacity of the technology to work properly in the operational context of a drilling rig and its capacity to maintain the hyperstatic-working mode of the riser joint in that context. The Pride Angola drillship was chosen for the test.
This paper presents the basis of the technology, describes the three phases of the field test, and comments on the first results obtained from the rig. To conclude, the technology is then put in the context of deep-water drilling, and its benefits are discussed for conventional, slender, and dual-gradient risers.
Mitochondrial Reactive Oxygen Species Are Obligatory Signals for Glucose-Induced Insulin Secretion
Authors: Leloup Corinne , Tourrel-Cuzin Cécile , Magnan Christophe , Karaca Melis , Castel Julien , Carneiro Lionel , Colombani Anne-Laure , Ktorza Alain , Casteilla Louis , Pénicaud Luc 
Published: December 2008

OBJECTIVE—Insulin secretion involves complex events in which the mitochondria play a pivotal role in the generation of signals that couple glucose detection to insulin secretion. Studies on the mitochondrial generation of reactive oxygen species (ROS) generally focus on chronic nutrient exposure. Here, we investigate whether transient mitochondrial ROS production linked to glucose-induced increased respiration might act as a signal for monitoring insulin secretion.
RESEARCH DESIGN AND METHODS—ROS production in response to glucose was investigated in freshly isolated rat islets. ROS effects were studied using a pharmacological approach and calcium imaging.
RESULTS—Transient glucose increase from 5.5 to 16.7 mmol/l stimulated ROS generation, which was reversed by antioxidants. Insulin secretion was dose dependently blunted by antioxidants and highly correlated with ROS levels. The incapacity of β-cells to secrete insulin in response to glucose with antioxidants was associated with a decrease in ROS production and in contrast to the maintenance of high levels of ATP and NADH. Then, we investigated the mitochondrial origin of ROS (mROS) as the triggering signal. Insulin release was mimicked by the mitochondrial-complex blockers, antimycin and rotenone, that generate mROS. The adding of antioxidants to mitochondrial blockers or to glucose was used to lower mROS reversed insulin secretion. Finally, calcium imaging on perifused islets using glucose stimulation or mitochondrial blockers revealed that calcium mobilization was completely reversed using the antioxidant trolox and that it was of extracellular origin. No toxic effects were present using these pharmacological approaches.
CONCLUSIONS—Altogether, these complementary results demonstrate that mROS production is a necessary stimulus for glucose-induced insulin secretion.
Maternal Low-Protein Diet or Hypercholesterolemia Reduces Circulating Essential Amino Acids and Leads to Intrauterine Growth Restriction
Authors: Bhasin Kum Kum S. , van Nas Atila , Martin Lisa J. , Davis Richard C. , Devaskar Sherin U. , Lusis Aldons J. 
Published: December 2008

OBJECTIVE—We have examined maternal mechanisms for adult-onset glucose intolerance, increased adiposity, and atherosclerosis using two mouse models for intrauterine growth restriction (IUGR): maternal protein restriction and hypercholesterolemia.
RESEARCH DESIGN AND METHODS—For these studies, we measured the amino acid levels in dams from two mouse models for IUGR: 1) feeding C57BL/6J dams a protein-restricted diet and 2) feeding C57BL/6J LDL receptor–null (LDLR−/−) dams a high-fat (Western) diet.
RESULTS—Both protein-restricted and hypercholesterolemic dams exhibited significantly decreased concentrations of the essential amino acid phenylalanine and the essential branched chain amino acids leucine, isoleucine, and valine. The protein-restricted diet for pregnant dams resulted in litters with significant IUGR. Protein-restricted male offspring exhibited catch-up growth by 8 weeks of age and developed increased adiposity and glucose intolerance by 32 weeks of age. LDLR−/− pregnant dams on a Western diet also had litters with significant IUGR. Male and female LDLR−/− Western-diet offspring developed significantly larger atherosclerotic lesions by 90 days compared with chow-diet offspring.
CONCLUSIONS—In two mouse models of IUGR, we found reduced concentrations of essential amino acids in the experimental dams. This indicated that shared mechanisms may underlie the phenotypic effects of maternal hypercholesterolemia and maternal protein restriction on the offspring.
Gene Silencing of Phogrin Unveils Its Essential Role in Glucose-Responsive Pancreatic β-Cell Growth
Authors: Torii Seiji , Saito Naoya , Kawano Ayumi , Hou Ni , Ueki Kohjiro , Kulkarni Rohit N. , Takeuchi Toshiyuki 
Published: December 2008

OBJECTIVE—Phogrin and IA-2, autoantigens in insulin-dependent diabetes, have been shown to be involved in insulin secretion in pancreatic β-cells; however, implications at a molecular level are confusing from experiment to experiment. We analyzed biological functions of phogrin in β-cells by an RNA interference technique.
RESEARCH DESIGN AND METHODS—Adenovirus-mediated expression of short hairpin RNA specific for phogrin (shPhogrin) was conducted using cultured β-cell lines and mouse islets. Both glucose-stimulated insulin secretion and cell proliferation rate were determined in the phogrin-knockdown cells. Furthermore, protein expression was profiled in these cells. To see the binding partner of phogrin in β-cells, coimmunoprecipitation analysis was carried out.
RESULTS—Adenoviral expression of shPhogrin efficiently decreased its endogenous expression in pancreatic β-cells. Silencing of phogrin in β-cells abrogated the glucose-mediated mitogenic effect, which was accompanied by a reduction in the level of insulin receptor substrate 2 (IRS2) protein, without any changes in insulin secretion. Phogrin formed a complex with insulin receptor at the plasma membrane, and their interaction was promoted by high-glucose stimulation that in turn led to stabilization of IRS2 protein. Corroboratively, phogrin knockdown had no additional effect on the proliferation of β-cell line derived from the insulin receptor–knockout mouse.
CONCLUSIONS—Phogrin is involved in β-cell growth via regulating stability of IRS2 protein by the molecular interaction with insulin receptor. We propose that phogrin and IA-2 function as an essential regulator of autocrine insulin action in pancreatic β-cells.
Overexpression of Carnitine Palmitoyltransferase-1 in Skeletal Muscle Is Sufficient to Enhance Fatty Acid Oxidation and Improve High-Fat Diet–Induced Insulin Resistance
Authors: Bruce Clinton R. , Hoy Andrew J. , Turner Nigel , Watt Matthew J. , Allen Tamara L. , Carpenter Kevin , Cooney Gregory J. , Febbraio Mark A. , Kraegen Edward W. 
Published: December 2008

OBJECTIVE—Skeletal muscle insulin resistance is associated with lipid accumulation, but whether insulin resistance is due to reduced or enhanced flux of long-chain fatty acids into the mitochondria is both controversial and unclear. We hypothesized that skeletal muscle–specific overexpression of the muscle isoform of carnitine palmitoyltransferase 1 (CPT1), the enzyme that controls the entry of long-chain fatty acyl CoA into mitochondria, would enhance rates of fatty acid oxidation and improve insulin action in muscle in high-fat diet insulin-resistant rats.
RESEARCH DESIGN AND METHODS—Rats were fed a standard (chow) or high-fat diet for 4 weeks. After 3 weeks, in vivo electrotransfer was used to overexpress the muscle isoform of CPT1 in the distal hindlimb muscles (tibialis anterior and extensor digitorum longus [EDL]). Skeletal muscle insulin action was examined in vivo during a hyperinsulinemic-euglycemic clamp.
RESULTS—In vivo electrotransfer produced a physiologically relevant increase of ∼20% in enzyme activity; and although the high-fat diet produced insulin resistance in the sham-treated muscle, insulin action was improved in the CPT1-overexpressing muscle. This improvement was associated with a reduction in triacylglycerol content, the membrane-to-cytosolic ratio of diacylglycerol, and protein kinase C θ activity. Importantly, overexpression of CPT1 did not affect markers of mitochondrial capacity or function, nor did it alter skeletal muscle acylcarnitine profiles irrespective of diet.
CONCLUSIONS—Our data provide clear evidence that a physiological increase in the capacity of long-chain fatty acyl CoA entry into mitochondria is sufficient to ameliorate lipid-induced insulin resistance in muscle.
Dipeptidyl Peptidase IV Inhibition With MK0431 Improves Islet Graft Survival in Diabetic NOD Mice Partially via T-Cell Modulation
Authors: Kim Su-Jin , Nian Cuilan , Doudet Doris J. , McIntosh Christopher H.S. 
Published: December 2008

OBJECTIVE—The endopeptidase dipeptidyl peptidase-IV (DPP-IV) has been shown to NH2-terminally truncate incretin hormones, glucose-dependent insulinotropic polypeptide, and glucagon-like peptide-1, thus ablating their ability to potentiate glucose-stimulated insulin secretion. Increasing the circulating levels of incretins through administration of DPP-IV inhibitors has therefore been introduced as a therapeutic approach for the treatment of type 2 diabetes. DPP-IV inhibitor treatment has also been shown to preserve islet mass in rodent models of type 1 diabetes. The current study was initiated to define the effects of the DPP-IV inhibitor sitagliptin (MK0431) on transplanted islet survival in nonobese diabetic (NOD) mice, an autoimmune type 1 diabetes model.
RESEARCH DESIGN AND METHODS—Effects of MK0431 on islet graft survival in diabetic NOD mice were determined with metabolic studies and micropositron emission tomography imaging, and its underlying molecular mechanisms were assessed.
RESULTS—Treatment of NOD mice with MK0431 before and after islet transplantation resulted in prolongation of islet graft survival, whereas treatment after transplantation alone resulted in small beneficial effects compared with nontreated controls. Subsequent studies demonstrated that MK0431 pretreatment resulted in decreased insulitis in diabetic NOD mice and reduced in vitro migration of isolated splenic CD4+ T-cells. Furthermore, in vitro treatment of splenic CD4+ T-cells with DPP-IV resulted in increased migration and activation of protein kinase A (PKA) and Rac1.
CONCLUSIONS—Treatment with MK0431 therefore reduced the effect of autoimmunity on graft survival partially by decreasing the homing of CD4+ T-cells into pancreatic β-cells through a pathway involving cAMP/PKA/Rac1 activation.
Phenotypic Type 2 Diabetes in Obese Youth
Authors: Tfayli Hala , Bacha Fida , Gungor Neslihan , Arslanian Silva 
Published: December 2008

OBJECTIVE— Some obese youth with a clinical diagnosis of type 2 diabetes have evidence of islet cell autoimmunity with positive autoantibodies. In this study, we investigated the differences in insulin sensitivity and secretion between autoantibody-negative (Ab−) and -positive (Ab+) youth with clinically diagnosed type 2 diabetes in comparison with control subjects.
RESEARCH DESIGN AND METHODS— Sixteen Ab− and 26 Ab+ clinically diagnosed type 2 diabetic patients and 39 obese control youth underwent evaluation of insulin sensitivity (3-h hyperinsulinemic-euglycemic clamp), substrate oxidation (indirect calorimetry), first- and second-phase insulin secretion (2-h hyperglycemic clamp), body composition and abdominal adiposity (dual energy X-ray absorptiometry and computed tomography scan, respectively), and glucose disposition index (first-phase insulin secretion × insulin sensitivity).
RESULTS— Insulin-stimulated total, oxidative, and nonoxidative glucose disposal, and suppression of fat oxidation during hyperinsulinemia were significantly lower in Ab− compared with Ab+ clinically diagnosed type 2 diabetic and control subjects with no difference between the latter two. First- and second-phase insulin secretion and C-peptide were lower in Ab+ compared with Ab− type 2 diabetes. Glucose disposition index was not different between the Ab− and Ab+ clinically diagnosed type 2 diabetic patients, but both were significantly lower than that in control subjects. Systolic blood pressure and alanine aminotransferase were higher in Ab− versus Ab+ clinically diagnosed type 2 diabetic patients, whereas the frequency of ketonuria at diagnosis was higher in Ab+ versus Ab− patients.
CONCLUSIONS— Islet-cell Ab− clinically diagnosed type 2 diabetic youth are characterized by severe insulin resistance and relative insulin deficiency, whereas Ab+ youth have severe insulin deficiency and β-cell failure. The former group has additional features of insulin resistance. These important metabolic differences could influence the natural history of hyperglycemia, insulin dependence, and clinical outcomes in these youth.
Impact of Pay for Performance on Ethnic Disparities in Intermediate Outcomes for Diabetes: A Longitudinal Study
Authors: Millett Christopher , Netuveli Gopalakrishnan , Saxena Sonia , Majeed Azeem 
Published: December 2008

OBJECTIVE—The purpose of this study was to examine the impact of a major pay for performance incentive on trends in the quality of diabetes care in white, black, and South Asian ethnic groups in an urban setting in the U.K.
RESEARCH DESIGN AND METHODS—We developed longitudinal models examining the quality of diabetes care in a cohort of ethnically diverse patients in Southwest London using electronic family practice records. Outcome measures were mean blood pressure and A1C values between 2000 and 2005.
RESULTS—The introduction of pay for performance was associated with reductions in mean systolic and diastolic blood pressure, which were significantly greater than those predicted by the underlying trend in the white (−5.8 and −4.2 mmHg), black (−2.5 and −2.4 mmHg), and South Asian (−5.5 and −3.3 mmHg) groups. Reductions in A1C levels were significantly greater than those predicted by the underlying trend in the white group (−0.5%) but not in the black (−0.3%) or South Asian (−0.4%) groups. Ethnic group disparities in annual measurement of blood pressure and A1C were abolished before the introduction of pay for performance.
CONCLUSIONS—The introduction of a pay for performance incentive in U.K. primary care was associated with improvements in the intermediate outcomes of diabetes care for all ethnic groups. However, the magnitude of improvement appeared to differ between ethnic groups, thus potentially widening existing disparities in care. Policy makers should consider the potential impacts of pay for performance incentives on health disparities when designing and evaluating such programs.
Elevated Levels of the Anti-Inflammatory Interleukin-1 Receptor Antagonist Precede the Onset of Type 2 Diabetes
Authors: Herder Christian , Brunner Eric J. , Rathmann Wolfgang , Strassburger Klaus , Tabák Adam G. , Schloot Nanette C. , Witte Daniel R. 
Published: December 2008

OBJECTIVE—Interleukin-1 receptor antagonist (IL-1Ra), a natural inhibitor of interleukin-1β, has been shown to improve β-cell function and glycemic control in patients with type 2 diabetes. The aim of this study was to investigate whether baseline systemic levels of IL-1Ra are associated with incident type 2 diabetes during more than 10 years of follow-up.
RESEARCH DESIGN AND METHODS—We measured serum IL-1Ra concentrations in a nested case-control study (181 case and 376 age-, sex-, and BMI-matched normoglycemic control subjects) within the Whitehall II cohort (U.K.).
RESULTS—IL-1Ra concentrations were higher in case subjects (P = 0.0006) and associated with incident type 2 diabetes (odds ratio for a 1-SD increase of IL-1Ra 1.48 [95% CI 1.21–1.80]). This association remained significant after adjustment for multiple potential confounders but was attenuated by adjusting for 2-h glucose.
CONCLUSIONS—Our findings indicate that individuals who will develop type 2 diabetes are characterized by a complex immune activation that also includes upregulation of the anti-inflammatory cytokine IL-1Ra.
Pathology is alleviated by doxycycline in a laminin‐α2–null model of congenital muscular dystrophy
Authors: Girgenrath Mahasweta , Beermann Mary Lou , Vishnudas Vivek K. , Homma Sachiko , Miller Jeffrey Boone 
Published: December 2008

AbstractObjectiveCongenital muscular dystrophy type 1A is an autosomal recessive disease that is caused by loss‐of‐function mutations in the laminin‐α2 gene, and results in motor nerve and skeletal muscle dysfunction. In a previous study, we used genetic modifications to show that inappropriate induction of apoptosis was a significant contributor to pathogenesis in a laminin‐α2–deficient mouse model of congenital muscular dystrophy type 1A. To identify a possible pharmacological therapy for laminin‐α2 deficiency, we designed this study to determine whether treatment with minocycline or doxycycline, which are tetracycline derivatives reported to have antiapoptotic effects in mammals, would significantly increase lifespan and improve neuromuscular function in laminin‐α2–deficient mice.MethodsMice that were homozygous for a targeted, inactivating mutation of the laminin‐α2 gene were placed into control, minocycline‐treated, or doxycycline‐treated groups. Drug treatment began within 2 weeks of birth, and the progression of disease was followed over time using behavioral, growth, histological, and molecular assays.ResultsWe found that treatment with either minocycline or doxycycline increased the median lifespan of laminin‐α2–null mice from approximately 32 days to approximately 70 days. Furthermore, doxycycline improved postnatal growth rate and delayed the onset of hind‐limb paralysis. Doxycycline‐treated laminin‐α2–deficient muscles had increased Akt phosphorylation, decreased inflammation, and decreased levels of Bax protein, terminal deoxynucleotidyltransferase–mediated dUTP nick end labeling–positive myonuclei, and activated caspase‐3.InterpretationDoxycycline or other drugs with similar functional profiles may be a possible route to improving neuromuscular dysfunction caused by laminin‐α2‐deficiency. Ann Neurol 2008
An antitracking varnish for rated electrical application
Authors: Maiti Pravat Kumar 
Published: December 2008

AbstractWe report on a synthesis, characterization, and thermal evaluation of a pigmented and silicone‐modified medium oil alkyd insulating varnish for antitracking application in rated electrical machines such as traction motors, transformers, and large generators. The varnish is generally applied on the top surface of the main insulation of coils by spray or brush and then baked to remove solvent. The semiconducting pigments entrapped in solid polymer matrix reduces surface corona, flash‐over, and tracking of the main insulation by distributing uneven charges from polar or charged particles deposited on the surface after long time use of the machines. The varnish was thoroughly evaluated by means of electrical and mechanical properties over a temperature range. The temperature class of the antitracking varnish was 191.22°C determined by IEC 60216 methods on helical coil bond strength of the cured films. The dielectric strength, tracking, and arc resistance of the pigmented varnish were exceptionally high and it will save core insulation from the tracking, corona and short‐time flash‐over. © 2008 Wiley Periodicals, Inc. J Appl Polym Sci, 2009
Influence of electron beam sterilization on polymers when incubated in different media
Authors: Mrad O. , Saunier J. , Chodur C. Aymes , Agnely F. , Yagoubi N. 
Published: December 2008

AbstractPolyurethane catheters were irradiated with electron‐beam. We looked at the way the catheter is physically and chemically modified after incubation in different media. An extracting medium (methanol) was compared to other oxidative, enzymatic, and saline aqueous media, mimicking some aspects of biological fluids. Irradiation had a strong impact on the stability of polymer during incubation. For nonirradiated samples incubated in aqueous media, only a small diffusion of additives was observed; no oligomer release was put into evidence, and the polymer was almost not degraded. But the chain branching that occurred because of irradiation created some weaknesses in the polymer chains: irradiated samples were mostly sensitive to chain scission and oligomers released during incubation; this trend increased with the irradiation dose. © 2008 Wiley Periodicals, Inc. J Appl Polym Sci, 2009
Modification of electrospun poly(vinylidene fluoride‐co‐hexafluoropropylene) membranes through the introduction of poly(ethylene glycol) dimethacrylate
Authors: Zhao Liang , Zhang Hong , Li Xiaoran , Zhao Jin , Zhao Ci , Yuan Xiaoyan 
Published: December 2008

AbstractFor the modification of an electrospun poly (vinylidene fluoride‐co‐hexafluoropropylene) (PVDF–HFP) membrane for its potential use as an electrolyte or separator in lithium batteries, poly(ethylene glycol) dimethacrylate (PEGDMA) was introduced into a polymer solution for electrospinning. A post heat treatment of the as‐electrospun membrane at an elevated temperature was performed for PEGDMA polymerization, and this was verified by Fourier transform infrared spectroscopy. The results showed that no significant variations in the membrane morphology were detected when a small amount of PEGDMA (PVDF–HFP/PEGDMA mass ratio = 4/1) was incorporated. This electrospun membrane after heat treatment at 130°C for 2 h exhibited a significantly higher tensile strength (6.26 ± 0.22 MPa) than that of an electrospun PVDF–HFP membrane (3.28 ± 0.35 MPa) without PEGDMA. The porosity and liquid absorption of the electrospun PVDF–HFP/PEGDMA (4/1) membrane were 70.0 ± 1.6% and 267 ± 11%, respectively, lower than those of the electrospun PVDF–HFP membrane (76.5 ± 0.3% and 352 ± 15%) because of the introduction of PEGDMA. © 2008 Wiley Periodicals, Inc. J Appl Polym Sci, 2009