bluuebunny/crossref_metadata_2025_split huggingface dataset:
Towards sustainable chemical use through chemical leasing
Authors: Gilbert Y. M. , Downs J. D. 
Published: January 2011

Abstract
Reducing the environmental, health and safety impact of chemical operations is a recognised target for upstream Oil & Gas operations. Approaches include use of less hazardous products, optimisation of waste management and minimisation of discharges. This paper discusses a novel business model, Chemical Leasing (ChL) that promotes sustainable use of chemicals through linking the supplier's sales income to chemical performance. In this model chemical consumption becomes a cost instead of a revenue factor for the supplier. This in turn leads to: Operational impact: Concentrated efforts on behalf of the supplier to reduce losses to the environment and increase recycling and reuse leads to lower environmental impact and associated costs through reduced emissions, discharges and chemical waste. This also lowers the exposure of employees, communities and consumers.Life-cycle impact reduction: raw material, energy etc. invested in the chemical decreases as chemical use decreasesInnovation: linking revenue to life-cycle performance stimulates the suppliers R&D process towards products and process modifications that reduce overall HSE impact.
For the operator, ChL therefore provides a clear potential for a win-win situation with four key chemical management targets: better environmental performance, better operational cost efficiency, minimisation of chemical waste created and reduced exposure. For the supplier, there is a potential to increase profits and competitive edge.
ChL has been successfully used in a number of applications, including cooling, heating; cleaning, purification and biocides. The United Nations Industrial Development Organisation (UNIDO) promotes the use of ChL as a tool for sustainable chemical management. In 2010, UNIDO recognised two oilfield players for outstanding ChL performance: Ecopetrol SA, for oil dehydration and water clarification applications and Cabot Specialty Fluids for leasing formate brines as well construction fluids. The ChL model is reviewed through these two applications. Further potential product groups and applications for the oilfield where ChL could be a viable option are discussed.
Myths and Misconceptions about Behavior-Based Safety (BBS): BAPCO Experience
Authors: Ahmed Ismail Mohamed 
Published: January 2011

ABSTRACT
In mid-nineties there has been some indication that "behavior-based safety - BBS" is entering the mainstream vocabulary of safety professionals. Bapco has been one of the organizations in the region that implemented BBS during 2006 and is beginning to achieve its stated objectives.
There has been however many myths and misconceptions associated with BBS in the industry in general which hinders its potential impact in injury reduction.
This paper highlights Bapco's experience in addressing the six myths and misconceptions in implementing BBS system.
Ongoing β-Cell Turnover in Adult Nonhuman Primates Is Not Adaptively Increased in Streptozotocin-Induced Diabetes
Authors: Saisho Yoshifumi , Manesso Erica , Butler Alexandra E. , Galasso Ryan , Kavanagh Kylie , Flynn Mickey , Zhang Li , Clark Paige , Gurlo Tatyana , Toffolo Gianna M. , Cobelli Claudio , Wagner Janice D. , Butler Peter C. 
Published: January 2011

OBJECTIVE
β-Cell turnover and its potential to permit β-cell regeneration in adult primates are unknown. Our aims were 1) to measure β-cell turnover in adult nonhuman primates; 2) to establish the relative contribution of β-cell replication and formation of new β-cells from other precursors (defined thus as β-cell neogenesis); and 3) to establish whether there is an adaptive increase in β-cell formation (attempted regeneration) in streptozotocin (STZ)-induced diabetes in adult nonhuman primates.

RESEARCH DESIGN AND METHODS
Adult (aged 7 years) vervet monkeys were administered STZ (45–55 mg/kg, n = 7) or saline (n = 9). Pancreas was obtained from each animal twice, first by open surgical biopsy and then by euthanasia. β-Cell turnover was evaluated by applying a mathematic model to measured replication and apoptosis rates.

RESULTS
β-Cell turnover is present in adult nonhuman primates (3.3 ± 0.9 mg/month), mostly (∼80%) derived from β-cell neogenesis. β-Cell formation was minimal in STZ-induced diabetes. Despite marked hyperglycemia, β-cell apoptosis was not increased in monkeys administered STZ.

CONCLUSIONS
There is ongoing β-cell turnover in adult nonhuman primates that cannot be accounted for by β-cell replication. There is no evidence of β-cell regeneration in monkeys administered STZ. Hyperglycemia does not induce β-cell apoptosis in nonhuman primates in vivo.
Natural Killer Cells From Children With Type 1 Diabetes Have Defects in NKG2D-Dependent Function and Signaling
Authors: Qin Huilian , Lee I-Fang , Panagiotopoulos Constadina , Wang Xiaoxia , Chu Alvina D. , Utz Paul J. , Priatel John J. , Tan Rusung 
Published: January 2011

OBJECTIVENatural killer (NK) cells from NOD mice have numeric and functional abnormalities, and restoration of NK cell function prevents autoimmune diabetes in NOD mice. However, little is known about the number and function of NK cells in humans affected by type 1 diabetes. Therefore, we evaluated the phenotype and function of NK cells in a large cohort of type 1 diabetic children.RESEARCH DESIGN AND METHODSPeripheral blood mononuclear blood cells were obtained from subjects whose duration of disease was between 6 months and 2 years. NK cells were characterized by flow cytometry, enzyme-linked immunosorbent spot assays, and cytotoxicity assays. Signaling through the activating NK cell receptor, NKG2D, was assessed by immunoblotting and reverse-phase phosphoprotein lysate microarray.RESULTSNK cells from type 1 diabetic subjects were present at reduced cell numbers compared with age-matched, nondiabetic control subjects and had diminished responses to the cytokines interleukin (IL)-2 and IL-15. Analysis before and after IL-2 stimulation revealed that unlike NK cells from nondiabetic control subjects, NK cells from type 1 diabetic subjects failed to downregulate the NKG2D ligands, major histocompatibility complex class I–related chains A and B, upon activation. Moreover, type 1 diabetic NK cells also exhibited decreased NKG2D-dependent cytotoxicity and interferon-γ secretion. Finally, type 1 diabetic NK cells showed clear defects in NKG2D-mediated activation of the phosphoinositide 3-kinase–AKT pathway.CONCLUSIONSThese results are the first to demonstrate that type 1 diabetic subjects have aberrant signaling through the NKG2D receptor and suggest that NK cell dysfunction contributes to the autoimmune pathogenesis of type 1 diabetes.
Intracavernous Delivery of a Designed Angiopoietin-1 Variant Rescues Erectile Function by Enhancing Endothelial Regeneration in the Streptozotocin-Induced Diabetic Mouse
Authors: Jin Hai-Rong , Kim Woo Jean , Song Jae Sook , Piao Shuguang , Choi Min Ji , Tumurbaatar Munkhbayar , Shin Sun Hwa , Yin Guo Nan , Koh Gou Young , Ryu Ji-Kan , Suh Jun-Kyu 
Published: January 2011

OBJECTIVE
Patients with diabetic erectile dysfunction often have severe endothelial dysfunction and respond poorly to oral phosphodiesterase-5 inhibitors. We examined the effectiveness of the potent angiopoietin-1 (Ang1) variant, cartilage oligomeric matrix protein (COMP)-Ang1, in promoting cavernous endothelial regeneration and restoring erectile function in diabetic animals.

RESEARCH DESIGN AND METHODS
Four groups of mice were used: controls; streptozotocin (STZ)-induced diabetic mice; STZ-induced diabetic mice treated with repeated intracavernous injections of PBS; and STZ-induced diabetic mice treated with COMP-Ang1 protein (days −3 and 0). Two and 4 weeks after treatment, we measured erectile function by electrical stimulation of the cavernous nerve. The penis was harvested for histologic examinations, Western blot analysis, and cGMP quantification. We also performed a vascular permeability test.

RESULTS
Local delivery of the COMP-Ang1 protein significantly increased cavernous endothelial proliferation, endothelial nitric oxide (NO) synthase (NOS) phosphorylation, and cGMP expression compared with that in the untreated or PBS-treated STZ-induced diabetic group. The changes in the group that received COMP-Ang1 restored erectile function up to 4 weeks after treatment. Endothelial protective effects, such as marked decreases in the expression of p47phox and inducible NOS, in the generation of superoxide anion and nitrotyrosine, and in the number of apoptotic cells in the corpus cavernosum tissue, were noted in COMP-Ang1–treated STZ-induced diabetic mice. An intracavernous injection of COMP-Ang1 completely restored endothelial cell-cell junction proteins and decreased cavernous endothelial permeability. COMP-Ang1–induced promotion of cavernous angiogenesis and erectile function was abolished by the NOS inhibitor, N-nitro-L-arginine methyl ester, but not by the NADPH oxidase inhibitor, apocynin.

CONCLUSIONS
These findings support the concept of cavernous endothelial regeneration by use of the recombinant Ang1 protein as a curative therapy for diabetic erectile dysfunction.
An Allele of IKZF1 (Ikaros) Conferring Susceptibility to Childhood Acute Lymphoblastic Leukemia Protects Against Type 1 Diabetes
Authors: Swafford Austin D.-E. , Howson Joanna M.M. , Davison Lucy J. , Wallace Chris , Smyth Deborah J. , Schuilenburg Helen , Maisuria-Armer Meeta , Mistry Trupti , Lenardo Michael J. , Todd John A. 
Published: January 2011

OBJECTIVE
IKZF1 encoding Ikaros, an essential regulator of lymphopoiesis and immune homeostasis, has been implicated in the development of childhood acute lymphoblastic leukemia (C-ALL). Because recent genome-wide association (GWA) studies have linked a region of the 3′-UTR of IKZF1 with C-ALL susceptibility, we tested whether IKZF1 is associated with the autoimmune disease type 1 diabetes.

RESEARCH DESIGN AND METHODS
rs10272724 (T&gt;C) near IKZF1 at 7p12 was genotyped in 8,333 individuals with type 1 diabetes, 9,947 control subjects, and 3,997 families of European ancestry. Association was tested using logistic regression in the case-control data and by the transmission disequilibrium test in the families. Expression data for IKZF1 by rs10272724 genotype were obtained using quantitative PCR of mRNA/cDNA generated from peripheral blood mononuclear cells from 88 individuals, whereas expression data for five other neighboring genes were obtained from the online Genevar dataset.

RESULTS
The minor allele of rs10272724 (C) was found to be protective from type 1 diabetes (odds ratio 0.87 [95% CI 0.83–0.91]; P = 1.1 × 10−11). rs10272724 was not correlated with levels of two transcripts of IKZF1 in peripheral blood mononuclear cells.

CONCLUSIONS
The major susceptibility genotype for C-ALL confers protection from type 1 diabetes. Our finding strengthens the link between autoimmunity and lymphoid cancers. Further investigation is warranted for the genetic effect marked by rs10272724, its impact on IKZF1, and the role of Ikaros and other family members, Ailios (IKZF3) and Eos (IKZF4), in autoimmunity.
Genetic Defects in Human Pericentrin Are Associated With Severe Insulin Resistance and Diabetes
Authors: Huang-Doran Isabel , Bicknell Louise S. , Finucane Francis M. , Rocha Nuno , Porter Keith M. , Tung Y.C. Loraine , Szekeres Ferenc , Krook Anna , Nolan John J. , O’Driscoll Mark , Bober Michael , O’Rahilly Stephen , Jackson Andrew P. , Semple Robert K. ,   for the Majewski Osteodysplastic Primordial Dwarfism Study Group
Published: January 2011

OBJECTIVE
Genetic defects in human pericentrin (PCNT), encoding the centrosomal protein pericentrin, cause a form of osteodysplastic primordial dwarfism that is sometimes reported to be associated with diabetes. We thus set out to determine the prevalence of diabetes and insulin resistance among patients with PCNT defects and examined the effects of pericentrin depletion on insulin action using 3T3-L1 adipocytes as a model system.

RESEARCH DESIGN AND METHODS
A cross-sectional metabolic assessment of 21 patients with PCNT mutations was undertaken. Pericentrin expression in human tissues was profiled using quantitative real-time PCR. The effect of pericentrin knockdown on insulin action and adipogenesis in 3T3-L1 adipocytes was determined using Oil red O staining, gene-expression analysis, immunoblotting, and glucose uptake assays. Pericentrin expression and localization also was determined in skeletal muscle.

RESULTS
Of 21 patients with genetic defects in PCNT, 18 had insulin resistance, which was severe in the majority of subjects. Ten subjects had confirmed diabetes (mean age of onset 15 years [range 5–28]), and 13 had metabolic dyslipidemia. All patients without insulin resistance were younger than 4 years old. Knockdown of pericentrin in adipocytes had no effect on proximal insulin signaling but produced a twofold impairment in insulin-stimulated glucose uptake, approximately commensurate with an associated defect in cell proliferation and adipogenesis. Pericentrin was highly expressed in human skeletal muscle, where it showed a perinuclear distribution.

CONCLUSIONS
Severe insulin resistance and premature diabetes are common features of PCNT deficiency but are not congenital. Partial failure of adipocyte differentiation may contribute to this, but pericentrin deficiency does not impair proximal insulin action in adipocytes.
Sodium Phenylbutyrate, a Drug With Known Capacity to Reduce Endoplasmic Reticulum Stress, Partially Alleviates Lipid-Induced Insulin Resistance and β-Cell Dysfunction in Humans
Authors: Xiao Changting , Giacca Adria , Lewis Gary F. 
Published: January 2011

OBJECTIVE
Chronically elevated free fatty acids contribute to insulin resistance and pancreatic β-cell failure. Among numerous potential factors, the involvement of endoplasmic reticulum (ER) stress has been postulated to play a mechanistic role. Here we examined the efficacy of the chemical chaperone, sodium phenylbutyrate (PBA), a drug with known capacity to reduce ER stress in animal models and in vitro, on lipid-induced insulin resistance and β-cell dysfunction in humans.

RESEARCH DESIGN AND METHODS
Eight overweight or obese nondiabetic men underwent four studies each, in random order, 4 to 6 weeks apart. Two studies were preceded by 2 weeks of oral PBA (7.5 g/day), followed by a 48-h i.v. infusion of intralipid/heparin or saline, and two studies were preceded by placebo treatment, followed by similar infusions. Insulin secretion rates (ISRs) and sensitivity (SI) were assessed after the 48-h infusions by hyperglycemic and hyperinsulinemic-euglycemic clamps, respectively.

RESULTS
Lipid infusion reduced SI, which was significantly ameliorated by pretreatment with PBA. Absolute ISR was not affected by any treatment; however, PBA partially ameliorated the lipid-induced reduction in the disposition index (DI = ISR × SI), indicating that PBA prevented lipid-induced β-cell dysfunction.

CONCLUSIONS
These results suggest that PBA may provide benefits in humans by ameliorating the insulin resistance and β-cell dysfunction induced by prolonged elevation of free fatty acids.
Insulin Degludec in Type 1 Diabetes
Authors: Birkeland Kåre I. , Home Philip D. , Wendisch Ulrich , Ratner Robert E. , Johansen Thue , Endahl Lars A. , Lyby Karsten , Jendle Johan H. , Roberts Anthony P. , DeVries J. Hans , Meneghini Luigi F. 
Published: January 2011

OBJECTIVE
Insulin degludec (IDeg) is a basal insulin that forms soluble multihexamers after subcutaneous injection, resulting in an ultra-long action profile. We assessed the efficacy and safety of IDeg formulations administered once daily in combination with mealtime insulin aspart in people with type 1 diabetes.

RESEARCH DESIGN AND METHODS
In this 16-week, randomized, open-label trial, participants (mean: 45.8 years old, A1C 8.4%, fasting plasma glucose [FPG] 9.9 mmol/L, BMI 26.9 kg/m2) received subcutaneous injections of IDeg(A) (600 μmol/L; n = 59), IDeg(B) (900 μmol/L; n = 60), or insulin glargine (IGlar; n = 59), all given once daily in the evening. Insulin aspart was administered at mealtimes.

RESULTS
At 16 weeks, mean A1C was comparable for IDeg(A) (7.8 ± 0.8%), IDeg(B) (8.0 ± 1.0%), and IGlar (7.6 ± 0.8%), as was FPG (8.3 ± 4.0, 8.3 ± 2.8, and 8.9 ± 3.5 mmol/L, respectively). Estimated mean rates of confirmed hypoglycemia were 28% lower for IDeg(A) compared with IGlar (rate ratio [RR]: 0.72 [95% CI 0.52–1.00]) and 10% lower for IDeg(B) compared with IGlar (RR: 0.90 [0.65–1.24]); rates of nocturnal hypoglycemia were 58% lower for IDeg(A) (RR: 0.42 [0.25–0.69]) and 29% lower for IDeg(B) (RR: 0.71 [0.44–1.16]). Mean total daily insulin dose was similar to baseline. The frequency and pattern of adverse events was similar between insulin treatments.

CONCLUSIONS
In this clinical exploratory phase 2 trial in people with type 1 diabetes, IDeg is safe and well tolerated and provides comparable glycemic control to IGlar at similar doses, with reduced rates of hypoglycemia.
Cytomegalovirus chronic infection as a risk factor for stroke: a prospective study
Authors: Ķēniņa Viktorija , Auce Pauls , Priede Zanda , Irbe Inese , Vainšteina Lana , Smeltere Elvīra , Millers Andrejs 
Published: January 2011

Cytomegalovirus chronic infection as a risk factor for stroke: a prospective study
Stroke is the second most common cause of death in the world and a major cause of long-term disability. Chronic infection is an independent risk factor for ischemic stroke and related forms of atherosclerotic vascular disease. The aim of our study was to compare the plasma Cytomegalovirus (CMV) immunoglobulin G antibody level in a patient and control group, and to determine the association of CMV chronic infection with ischemic stroke, and with stroke subtype. The present study does not present a cogent demonstration that cytomegalovirus chronic infection is a risk factor of stroke. Further studies are necessary to clarify the effective prophylactic measures to determine other significant risk factors for stroke.
Comparative analysis of sweet cherry (P. avium) genetic diversity revealed by two methods of SSR marker detection
Authors: Lācis Gunārs , Rashal Isaak , Trajkovski Viktor 
Published: January 2011

Comparative analysis of sweet cherry (P. avium) genetic diversity revealed by two methods of SSR marker detectionThree previously described highly polymorphic SSR (microsatellite) primer pairs in 126 sweet cherry (Prunus aviumL.) accessions were tested using two microsatellite marker detection methods: ASCE (automated sequencer capillary electrophoresis) and PAGE (polyacrylamide gel electrophoresis) in screening of sweet cherry germplasm collections. It was determined that ASCE provided more precise genotyping. In the case of PAGE, due to possible manual scoring errors, a higher number of putative alleles was observed, which overestimated the level of polymorphism and hence the genetic diversity. This should be taken into account when comparing results obtained in different investigations. The ASCE detection method generally is considered as expensive, it requires more advanced and expensive equipment, and is available mostly in mid- to high-throughput laboratories. Nevertheless, the detection precision and possibility of complete unification of laboratory protocols among laboratories makes it a very useful tool in the identification and characterisation of sweet cherry breeding material, especially in large, diverse collecions.
Protective effects of mildronate in indinavir- and efavirenz-induced toxicity in mice
Authors: Pupure Jolanta , Isajevs Sergejs , Kalviņš Ivars , Kluša Vija 
Published: January 2011

Protective effects of mildronate in indinavir- and efavirenz-induced toxicity in micePreviously we showed that mildronate effectively protected mice heart tissue against the toxic influence of anti-HIV drugs azidothymidine, stavudine and lamivudine, which belong to nucleosideanalogue reverse transcriptase inhibitor (NRTI) class. Recently we also demonstrated that mildronate protected isolated rat liver mitochondria against mitochondrial damage caused by azidothymidine. The present study was devoted to examine the possible protective effectiveness of mildronate in cardio-, hepato- and neurotoxicity models caused by anti-HIV drugs of other classes: indinavir, a representative of protease inhibitor (PI) class, and efavirenz, a non-nucleoside-analogue reverse transcriptase inhibitor (NNRTI). Drugs were administered intraperitoneally for two weeks, at the dose of 50 mg/kg of anti-HIV drugs and 100 mg/kg for mildronate. Afterwards, mice heart, liver and brain tissue were examined morphologically and immunohistochemically. The results showed that indinavir in heart tissue caused inflammatory and degenerative changes, manifested as increased expression of nuclear factor kappaBp65 (NF-kBp65), as well as cardiomyocyte necrosis and cellular infiltration. Efavirenz did not cause pathological changes in mice heart tissue, whereas it induced marked expression of caspase-3 and glial fibrillary acidic protein (GFAP) in mice brain tissue and small degenerative alterations in mice liver tissue. The data obtained show mildronate's protective properties in indinavir-induced cardiotoxicity and efavirenz-induced neurotoxicity.
Renal anaemia: the role of haemoglobin control in patients with chronic kidney disease
Authors: Kuzema Viktorija , Pētersons Aivars , Čerņevskis Harijs , Lejnieks Aivars 
Published: January 2011

Renal anaemia: the role of haemoglobin control in patients with chronic kidney disease
Chronic kidney disease (CKD) is a significant and prevalent health problem in the world. Anaemia is one of the most common manifestations in patients with CKD. The correction of anaemia with erythropoietin normalises haemoglobin level and improves quality of life. Many aspects of the impact of anaemia treatment with erythropoiesis-stimulating agents on the progression of CKD remain unresolved and disputable. The present study is a retrospective chart review of 1654 outpatients with CKD. The data were collected from the Centre of Nephrology between 1 January 2002 and 31 December 2006. The aims of the study were to assess the causes of CKD; the prevalence of anaemia based on the current guidelines for anaemia management in CKD (Kidney Disease Dialysis Outcomes Quality Initiative; K/DOQI); to evaluate haemoglobin (Hb), systolic and diastolic blood pressure (SBP and DBP), glomerular filtration rate (GFR) at the first referral to a nephrologist and at the start of renal replacement therapy (RRT). The most common causes of CKD were arterial hypertension (17.2%), chronic glomerulonephritis (17.2%), chronic intersticial nephritis (13.3%), and diabetes (12.8%). Twenty-three percent of end-stage renal disease (ESRD) patients had diabetes mellitus. At the first visit in the renal department, 16% of the patients had an advanced degree of CKD (GFR <30 ml/min). The proportion of patients under an observation in the kidney centre for a period of six months and more was only 34% (554 of 1654). Hypertension was recorded in 72% of study subjects. The blood pressure (BP) values in patients at the first visit (n = 1633) vs. at the start of RRT (n = 154) were: mean SBP 147.4 ± 24.8 mm Hg vs. 152.2 ± 23.0 mm Hg (P < 0.05); mean DBP 88.8 ± 13.6 mm Hg vs. 88.4 ± 12.0 mm Hg (P 0.05). Anaemia was recorded in 41% of study subjects, estimated using K/DOQI recommendations. The prevalence of anaemia was increased from 30.2% to 44.8% of study patients with a rise of BP (from normal BP to hypertension; P < 0.05). The mean Hb level at the start of RRT was 9.8 ± 2.1 g/dl. Only 18% of patients with renal anaemia had used erythropoiesis-stimulating agents before RRT (28 of 155). Anaemia is the prevalent condition at moderate degrees of CKD. The severity of anaemia in the CKD population is determined by evidence of diabetes, cardiovascular disease, and renal function. Anaemia may often be unrecognised or untreated.