bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Evolution of Inert-Gas Systems on SBM FPSOs: The Problem of Venting and a Straightforward Solution
Authors: de Vos Dirk , Duddy Michael , Bronneburg Jos 
Published: July 2008

Summary
As a floating production, storage, and offloading vessel (FPSO) continually loads stabilized crude oil to the cargo tanks, the inert-gas (IG) blanket within the tanks is compressed. At a certain pressure, below that which could cause damage to the vessel structure, this mixture of now IG and volatile organic compounds (VOCs), emanated from the loaded crude, must be vented safely to atmosphere by some means.
From the very first FPSO that Single Buoy Moorings (SBM) operated, the FPSO II in 1980, errant gas (IG) has resulted in a number of emergency shutdowns (ESDs) while venting the cargo tanks during calm weather. With no wind to disperse the heavier-than-air gas, the result is the mixture falling onto the vessel main deck or the process modules, triggering the FPSO gas-detection system and subsequently causing an ESD. The cost can quickly become considerable because of loss or delay of production in this manner.
More importantly, while venting the cargo tanks, personnel are relocated to a safe area to ensure their safety, and any hot-work being undertaken is postponed. Crane and helicopter operations also are suspended. There is, of course, a cost associated with the loss of personnel productivity during these events.
To prevent reoccurrence of IG venting-related incidents, a number of operational measures are used. These usually consist of
Delaying venting during low-wind periods (&lt;2 ms) Employing the downstream vent mast (if two are fitted, one on either side of the vessel) Monitoring the gas concentration by way of the gas-detection system
As a high concentration is attained [usually approximately 40% of the lower-explosive limit (LEL)], venting is stopped until the gas has been dispersed. Typically, the alarm is activated at 20% LEL, and the executive action (in this case, an ESD) is set at 60% LEL.
With FPSOs becoming larger, and production rates correspondingly so (sometimes more than 300,000 B/D), the financial penalties resulting from an unplanned shutdown are even more significant. Although using operational means can be a successful way of mitigating both the safety and production risks associated with IG venting, a system that would obviate the need for such procedures has been sought by SBM since their first operating FPSO, more than 25 years ago.
This paper describes the evolution of the IG arrangements on board SBM's units, past and present systems that have been used with varying degrees of success and the recent (July 2005) retrofit of an IG eductor to 2 SBM FPSOs operating west of Africa. The details of the patented IG eductor, from conception, design, safety studies, construction, installation, and operational success, are also presented.
Economics of GTL Plants
Authors: Al-Saadoon Faleh T. 
Published: July 2008

Summary
A unique approach for assessing the economic viability of gas-to-liquid (GTL) plants is used. The capital expenditures (capex) are based on the production of 1 bbl of hydrocarbon liquid per day (BLPD), whereas the annual operating expenditures (opex) are expressed as percentages of capex. Both expenditures cover the range of costs envisioned by various vendors and investigators. It is assumed that the overall thermal efficiency of GTL plants is approximately 60% and that the plant operates 334 days per year. The capital expenditures used in this study are U.S. $20,000, $25,000, $30,000, $35,000, and $40,000 per BLPD. (Note: all expenditures in this paper are stated in U.S. dollars.) The annual operating expenditures used are 5, 6, and 7% of capex. Thus, the range of operating expenditures used is $3.03 to $8.48 per barrel of liquid hydrocarbon produced.
Two measures of profitability are used in assessing the economic viability of GTL plants, namely rate of return (ROR) and undis-counted payout time (POT). Rates of return used in this study are 10, 15, and 20%, whereas the payout times used are 4, 5, 6, 7, and 8 years. Construction periods of 3 and 4 years are considered in the analysis. A general survey of GTL processes is also included.
A Model To Predict Liquid Holdup and Pressure Gradient of Near-Horizontal Wet-Gas Pipelines
Authors: Fan Yongqian , Wang Qian , Zhang Hongquan , Danielson Thomas J. , Sarica Cem 
Published: July 2008

Summary
A mechanistic two-fluid model with new closure relationships is proposed to predict liquid holdup and pressure gradient of stratified flow. The proposed closure relationships include correlations of wetted-wall fraction factor, liquid-wall friction factor, and interfacial-friction factor. An iterative calculation procedure is implemented to solve for liquid holdup and pressure gradient for a given set of operating conditions, pipe geometry, and fluid properties.
Two sets of facilities, a small-scale facility with 51-mm internal diameter (ID) and a large-scale facility with 150-mm-ID test sections, were used to tune the model. Superficial gas and liquid velocities were varied from 5 to 25 m/s and 0.00025 to 0.03 m/s, respectively, in the small-scale facility while they were varied from 7.5 to 21 m/s and 0.005 to 0.05 m/s, respectively, in the large-scale facility. The pipe inclination angle varied from −2 to 2°. The liquid holdup was ranged between 0.003 and 0.12, emphasizing the low-liquid-loading two-phase flow.
The tuned model performance was then benchmarked against the high-pressure (up to 90 bar) SINTEF-stratified flow data. The model predictions agreed well with measured values of liquid holdup and pressure gradient. The comparison between the present model and OLGA® (a commercial transient multiphaseflow simulator by Scandpower Petroleum) performance was also presented.
Muscle-Specific IRS-1 Ser→Ala Transgenic Mice Are Protected From Fat-Induced Insulin Resistance in Skeletal Muscle
Authors: Morino Katsutaro , Neschen Susanne , Bilz Stefan , Sono Saki , Tsirigotis Dimitrios , Reznick Richard M. , Moore Irene , Nagai Yoshio , Samuel Varman , Sebastian David , White Morris , Philbrick William , Shulman Gerald I. 
Published: July 2008

OBJECTIVE—Insulin resistance in skeletal muscle plays a critical role in the pathogenesis of type 2 diabetes, yet the cellular mechanisms responsible for insulin resistance are poorly understood. In this study, we examine the role of serine phosphorylation of insulin receptor substrate (IRS)-1 in mediating fat-induced insulin resistance in skeletal muscle in vivo.
RESEARCH DESIGN AND METHODS—To directly assess the role of serine phosphorylation in mediating fat-induced insulin resistance in skeletal muscle, we generated muscle-specific IRS-1 Ser302, Ser307, and Ser612 mutated to alanine (Tg IRS-1 Ser→Ala) and IRS-1 wild-type (Tg IRS-1 WT) transgenic mice and examined insulin signaling and insulin action in skeletal muscle in vivo.
RESULTS—Tg IRS-1 Ser→Ala mice were protected from fat-induced insulin resistance, as reflected by lower plasma glucose concentrations during a glucose tolerance test and increased insulin-stimulated muscle glucose uptake during a hyperinsulinemic-euglycemic clamp. In contrast, Tg IRS-1 WT mice exhibited no improvement in glucose tolerance after high-fat feeding. Furthermore, Tg IRS-1 Ser→Ala mice displayed a significant increase in insulin-stimulated IRS-1–associated phosphatidylinositol 3-kinase activity and Akt phosphorylation in skeletal muscle in vivo compared with WT control littermates.
CONCLUSIONS—These data demonstrate that serine phosphorylation of IRS-1 plays an important role in mediating fat-induced insulin resistance in skeletal muscle in vivo.
Activation of NF-E2–Related Factor-2 Reverses Biochemical Dysfunction of Endothelial Cells Induced by Hyperglycemia Linked to Vascular Disease
Authors: Xue Mingzhan , Qian Qingwen , Adaikalakoteswari Antonysunil , Rabbani Naila , Babaei-Jadidi Roya , Thornalley Paul J. 
Published: July 2008

OBJECTIVE—Sulforaphane is an activator of transcription factor NF-E2–related factor-2 (nrf2) that regulates gene expression through the promoter antioxidant response element (ARE). Nrf2 regulates the transcription of a battery of protective and metabolic enzymes. The aim of this study was to assess whether activation of nrf2 by sulforaphane in human microvascular endothelial cells prevents metabolic dysfunction in hyperglycemia.
RESEARCH DESIGN AND METHODS—Human microvascular HMEC-1 endothelial cells were incubated in low and high glucose concentrations (5 and 30 mmol/l, respectively), and activation of nrf2 was assessed by nuclear translocation. The effects of sulforaphane on multiple pathways of biochemical dysfunction, increased reactive oxygen species (ROS) formation, hexosamine pathway, protein kinase C (PKC) pathway, and increased formation of methylglyoxal were assessed.
RESULTS—Activation of nrf2 by sulforaphane induced nuclear translocation of nrf2 and increased ARE-linked gene expression, for example, three- to fivefold increased expression of transketolase and glutathione reductase. Hyperglycemia increased the formation of ROS—an effect linked to mitochondrial dysfunction and prevented by sulforaphane. ROS formation was increased further by knockdown of nrf2 and transketolase expression. This also abolished the counteracting effect of sulforaphane, suggesting mediation by nrf2 and related increase of transketolase expression. Sulforaphane also prevented hyperglycemia-induced activation of the hexosamine and PKC pathways and prevented increased cellular accumulation and excretion of the glycating agent methylglyoxal.
CONCLUSIONS—We conclude that activation of nrf2 may prevent biochemical dysfunction and related functional responses of endothelial cells induced by hyperglycemia in which increased expression of transketolase has a pivotal role.
Spontaneous Diabetes in Hemizygous Human Amylin Transgenic Mice That Developed Neither Islet Amyloid nor Peripheral Insulin Resistance
Authors: Wong Winifred P.S. , Scott David W. , Chuang Chia-Lin , Zhang Shaoping , Liu Hong , Ferreira Athena , Saafi Etuate L. , Choong Yee Soon , Cooper Garth J.S. 
Published: July 2008

OBJECTIVES—We sought to 1) Determine whether soluble-misfolded amylin or insoluble-fibrillar amylin may cause or result from diabetes in human amylin transgenic mice and 2) determine the role, if any, that insulin resistance might play in these processes.
RESEARCH DESIGN AND METHODS—We characterized the phenotypes of independent transgenic mouse lines that display pancreas-specific expression of human amylin or a nonaggregating homolog, [25,28,29Pro]human amylin, in an FVB/n background.
RESULTS—Diabetes occurred in hemizygous human amylin transgenic mice from 6 weeks after birth. Glucose tolerance was impaired during the mid- and end-diabetic phases, in which progressive β-cell loss paralleled decreasing pancreatic and plasma insulin and amylin. Peripheral insulin resistance was absent because glucose uptake rates were equivalent in isolated soleus muscles from transgenic and control animals. Even in advanced diabetes, islets lacked amyloid deposits. In islets from nontransgenic mice, glucagon and somatostatin cells were present mainly at the periphery and insulin cells were mainly in the core; in contrast, all three cell types were distributed throughout the islet in transgenic animals. [25,28,29Pro]human amylin transgenic mice developed neither β-cell degeneration nor glucose intolerance.
CONCLUSIONS—Overexpression of fibrillogenic human amylin in these human amylin transgenic mice caused β-cell degeneration and diabetes through mechanisms independent from both peripheral insulin resistance and islet amyloid. These findings are consistent with β-cell death evoked by misfolded but soluble cytotoxic species, such as those formed by human amylin in vitro.
Hepatocyte Growth Factor Enhances Engraftment and Function of Nonhuman Primate Islets
Authors: Fiaschi-Taesch Nathalie M. , Berman Dora M. , Sicari Brian M. , Takane Karen K. , Garcia-Ocaña Adolfo , Ricordi Camillo , Kenyon Norma S. , Stewart Andrew F. 
Published: July 2008

OBJECTIVE—Adenoviral delivery of hepatocyte growth factor (HGF) to rodent islets improves islet graft survival and function, markedly reducing the number of islets required to achieve glucose control. Here, we asked whether these prior observations in rodent models extend to nonhuman primate (NHP) islets.
RESEARCH DESIGN AND METHODS—NHP islets were transduced with murine (Ad.mHGF) or human (Ad.hHGF) adenoviral HGF (Ad.HGF) at low multiplicity of infection and studied in vitro. To study the function of Ad.HGF-transduced NHP islets in vivo, a renal subcapsular marginal mass islet transplant model was developed in streptozotocin-induced diabetic NOD-SCID mice.
RESULTS—Baseline glucose values were 454.7 ± 11.3 mg/dl (n = 7). Transplant of 500 NHP islet equivalents (IE) had only a marginal effect on blood glucose (369.1 ± 9.7 mg/dl, n = 5). In striking contrast, 500 NHP IE transduced with Ad.mHGF promptly and continuously corrected blood glucose (142.0 ± 6.2 mg/dl, n = 7) for the 6-week duration of the experiment. Unilateral nephrectomy resulted in an immediate return of glucose to baseline diabetic levels. Interestingly, adenoviral DNA, as well as mouse HGF (mHGF) mRNA derived from the adenovirus, were present for 42 days posttransplantation. Surprisingly, transplant of 500 IE with Ad.hHGF, as compared with Ad.mHGF, resulted in only marginal correction of blood glucose, suggesting that human HGF is less efficient than mHGF in this system.
CONCLUSIONS—These studies demonstrate that mHGF markedly improves islet transplant outcomes in the highest preclinical species examined to date. HGF has promise as an agent that can improve islet mass and function in transplant models and likely in other models of types 1 and 2 diabetes.
Sulfasalazine Blocks the Development of Tactile Allodynia in Diabetic Rats
Authors: Berti-Mattera Liliana N. , Kern Timothy S. , Siegel Ruth E. , Nemet Ina , Mitchell Rochanda 
Published: July 2008

OBJECTIVE—Diabetic neuropathy is manifested either by loss of nociception (painless syndrome) or by mechanical hyperalgesia and tactile allodynia (pain in response to nonpainful stimuli). While therapies with vasodilators or neurotrophins reverse some functional and metabolic abnormalities in diabetic nerves, they only partially ameliorate neuropathic pain. The reported link between nociception and targets of the anti-inflammatory drug sulfasalazine prompted us to investigate its effect on neuropathic pain in diabetes.RESEARCH DESIGN AND METHODS—We examined the effects of sulfasalazine, salicylates, and the poly(ADP-ribose) polymerase-1 inhibitor PJ34 on altered nociception in streptozotocin-induced diabetic rats. We also evaluated the levels of sulfasalazine targets in sciatic nerves and dorsal root ganglia (DRG) of treated animals. Finally, we analyzed the development of tactile allodynia in diabetic mice lacking expression of the sulfasalazine target nuclear factor-κB (NF-κB) p50.RESULTS—Sulfasalazine completely blocked the development of tactile allodynia in diabetic rats, whereas relatively minor effects were observed with other salicylates and PJ34. Along with the behavioral findings, sciatic nerves and DRG from sulfasalazine-treated diabetic rats displayed a decrease in NF-κB p50 expression compared with untreated diabetic animals. Importantly, the absence of tactile allodynia in diabetic NF-κB p50−/− mice supported a role for NF-κB in diabetic neuropathy. Sulfasalazine treatment also increased inosine levels in sciatic nerves of diabetic rats.CONCLUSIONS—The complete inhibition of tactile allodynia in experimental diabetes by sulfasalazine may stem from its ability to regulate both NF-κB and inosine. Sulfasalazine might be useful in the treatment of nociceptive alterations in diabetic patients.
Common Variants in CDKAL1, CDKN2A/B, IGF2BP2, SLC30A8, and HHEX/IDE Genes Are Associated With Type 2 Diabetes and Impaired Fasting Glucose in a Chinese Han Population
Authors: Wu Ying , Li Huaixing , Loos Ruth J.F. , Yu Zhijie , Ye Xingwang , Chen Lihua , Pan An , Hu Frank B. , Lin Xu 
Published: July 2008

OBJECTIVE— Genome-wide association studies have identified common variants in CDKAL1, CDKN2A/B, IGF2BP2, SLC30A8, HHEX/IDE, EXT2, and LOC387761 loci that significantly increase the risk of type 2 diabetes. We aimed to replicate these observations in a population-based cohort of Chinese Hans and examine the associations of these variants with type 2 diabetes and diabetes-related phenotypes.
RESEARCH DESIGN AND METHODS— We genotyped 17 single nucleotide polymorhisms (SNPs) in 3,210 unrelated Chinese Hans, including 424 participants with type 2 diabetes, 878 with impaired fasting glucose (IFG), and 1,908 with normal fasting glucose.
RESULTS— We confirmed the associations between type 2 diabetes and variants near CDKAL1 (odds ratio 1.49 [95% CI 1.27–1.75]; P = 8.91 × 10−7) and CDKN2A/B (1.31 [1.12–1.54]; P = 1.0 × 10−3). We observed significant association of SNPs in IGF2BP2 (1.17 [1.03–1.32]; P = 0.014) and SLC30A8 (1.12 [1.01–1.25]; P = 0.033) with combined IFG/type 2 diabetes. The SNPs in CDKAL1, IGF2BP2, and SLC30A8 were also associated with impaired β-cell function estimated by homeostasis model assessment of β-cell function. When combined, each additional risk allele from CDKAL1-rs9465871, CDKN2A/B-rs10811661, IGF2BP2-rs4402960, and SLC30A8-rs13266634 increased the risk for type 2 diabetes by 1.24-fold (P = 2.85 × 10−7) or for combined IFG/type 2 diabetes by 1.21-fold (P = 6.31 × 10−11). None of the SNPs in EXT2 or LOC387761 exhibited significant association with type 2 diabetes or IFG. Significant association was observed between the HHEX/IDE SNPs and type 2 diabetes in individuals from Shanghai only (P &lt; 0.013) but not in those from Beijing (P &gt; 0.33).
CONCLUSIONS— Our results indicate that in Chinese Hans, common variants in CDKAL1, CDKN2A/B, IGF2BP2, and SLC30A8 loci independently or additively contribute to type 2 diabetes risk, likely mediated through β-cell dysfunction.
Impaired Collateral Recruitment and Outward Remodeling in Experimental Diabetes
Authors: van Golde Jolanda M. , Ruiter Matthijs S. , Schaper Nicolaas C. , Vöö Stefan , Waltenberger Johannes , Backes Walter H. , Post Mark J. , Huijberts Maya S. 
Published: July 2008

OBJECTIVE—In this study, the effect of chronic hyperglycemia on acute ligation-induced collateral vasodilation, on monocyte chemotaxis, and on structural outward remodeling of collaterals was investigated.
RESEARCH DESIGN AND METHODS—Femoral artery ligation was performed 8 weeks after alloxan or saline treatment in New Zealand White rabbits. Angiography was performed directly, 1 and 3 weeks after ligation. These angiographic recordings were used to quantify number of collaterals, lumen, and blood volume index. Reactive hyperemia response was tested by intramuscular laser Doppler measurements. Subsequently, blood was sampled from the aorta for monocyte chemotaxis.
RESULTS—Ligation resulted in markedly lower acute collateral vasodilation in diabetic compared with control rabbits. Also, hyperemic vasodilatory response to local ischemia was impaired in diabetic rabbits. This difference persisted at 1 and 3 weeks after ligation, with a lower number of visible collaterals. In addition, the collateral lumen was markedly lower in diabetic rabbits after the maturation phase. Likewise, a reduced blood volume index in the region of growing collaterals was observed in diabetic animals. The monocyte migration toward vascular endothelial growth factor-A and monocyte chemotactic protein-1 was strongly reduced in diabetic rabbits.
CONCLUSIONS—This study demonstrates that chronic hyperglycemia negatively affects the different phases of arteriogenesis: 1) impaired shear induced vasodilatation; 2) impaired outward collateral growth, reflected in the number of collaterals and blood volume index; and 3) inhibition of monocyte chemotaxis. Impairments were most evident in the acute phase of arteriogenesis. Therapies aimed at restoring acute collateral recruitment, such as vasodilators, may be of interest to improve collateral function in diabetes.
Simultaneous Islet and Kidney Transplantation in Seven Patients With Type 1 Diabetes and End-Stage Renal Disease Using a Glucocorticoid-Free Immunosuppressive Regimen With Alemtuzumab Induction
Authors: Tan Jianming , Yang Shunliang , Cai Jinquan , Guo Junqi , Huang Lianghu , Wu Zhixian , Chen Jin , Liao Lianming 
Published: July 2008

OBJECTIVE—The aim of this study was to evaluate the efficiency and safety of simultaneous islet and kidney transplantation in patients with type 1 diabetes and end-stage renal disease using a glucocorticoid-free immunosuppressive regimen with alemtuzumab induction.
RESEARCH DESIGN AND METHODS—Seven patients with type 1 diabetes and end-stage renal failure were transplanted with allogenic islets and kidneys procured from brain-dead donors. To prevent organ rejection, patients received alemtuzumab for induction immunosuppression, followed by sirolimus and tacrolimus. No glucocorticoids were given at any time.
RESULTS—The median duration of follow-up was 18.3 months (range 13–31). Kidney survival was 100%. Four patients became insulin independent at 1 year. The other three reduced insulin use to less than 25% of the amount required before transplantation. Serum C-peptide levels were significantly greater posttransplant in all patients, indicating continued islet function. No major procedure-related complications were observed.
CONCLUSIONS—Our results demonstrate that a steroid-free immunosuppressive regimen consisting of alemtuzumab, sirolimus, and tacrolimus is feasible for simultaneous islet and kidney transplantation. The question of whether this induction regimen is superior to more standard induction deserves large studies.
Plasma Fetuin-A Levels and the Risk of Type 2 Diabetes
Authors: Stefan Norbert , Fritsche Andreas , Weikert Cornelia , Boeing Heiner , Joost Hans-Georg , Häring Hans-Ulrich , Schulze Matthias B. 
Published: July 2008

OBJECTIVE—The liver-secreted protein fetuin-A induces insulin resistance in animals, and circulating fetuin-A is elevated in insulin resistance and fatty liver in humans. We investigated whether plasma fetuin-A levels predict the incidence of type 2 diabetes in a large prospective, population-based study.
RESEARCH DESIGN AND METHODS—A case-cohort study within the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam study comprising 27,548 subjects was designed. We randomly selected a subcohort of 2,500 individuals of whom 2,164 were diabetes free at baseline and had anamnestic, anthropometrical, and metabolic data for analysis. Of the 849 incident diabetic case subjects identified in the full cohort during 7 years of follow-up, 703 remained for analyses after similar exclusions.
RESULTS—Plasma fetuin-A levels were positively associated with diabetes risk after adjustment for age (relative risk [RR] for extreme quintiles 1.75 [95% CI 1.32–2.31]; RR for 10 μg/ml 1.04 [1.03–1.06]). The association remained significant after adjustment for sex, BMI, waist circumference, and lifestyle risk factors (RR for 10 μg/ml 1.03 [1.01–1.06]). Adjustment for glucose, triglycerides, HDL cholesterol, A1C, γ-glutamyltransferase, or high-sensitivity C-reactive protein or mutual adjustment for these biomarkers did not appreciably change this result (RR for 10 μg/ml full adjusted model 1.05 [1.02–1.07]). Furthermore, fetuin-A was associated with increased diabetes risk particularly in individuals with elevated plasma glucose.
CONCLUSIONS—Our data suggest that fetuin-A is an independent risk factor of type 2 diabetes.