bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Geomechanics Of A Shale Play: What Makes A Shale Prospective!
Authors: Britt Larry K. , Schoeffler Jerry 
Published: October 2009

Abstract
Many shale plays are being successfully developed throughout North America. These shale plays are being evaluated based on a number of criteria, but primarily through typical unconventional and tight formation gas reservoir characteristics. Prospective shale plays share several interesting characteristics such as mineralogy, rock mechanics, and geomechanics. It is the intent of this paper to highlight and demonstrate the interrelationship of these characteristics, and to show their importance on completion and stimulation design and more importantly to the very prospectivity of an unconventional shale play.
This paper will first show, through an analysis of the mineralogy, that shale plays are made up of mostly silica and carbonate material and have few clay constituents. In other words, the prospective shales are actually fine-grained clastics and not shale!Second, prospective shales tend to be brittle, with the static Young’s Modulus generally in excess of 3.5 x 106 psi. Of course, this brittleness is related to the lack of clay constituents that make up these rocks. In addition, prospective shales tend to satisfy clastic correlations of dynamic to static Young’s Modulus. They do not behave like typical shales, but more like fine-grained isotropic (on a core scale) clastics!
Finally, gas can flow through induced fractures or natural fissures under effective stress conditions in these shale plays. As a result, water-frac treatments are the stimulation of choice! However, proppant is still necessary in at least the near wellbore vicinity to provide a conductive pathway to the wellbore. This paper focuses on three key elements (mineralogy, rock mechanics, and geomechanics) of prospective shale plays and benefits the petroleum industry by:Integrating the laboratory core work with multi-disciplinary data to develop a shale and unconventional reservoir prospectivity evaluation tool,Illustrating how this multi-disciplinary dataset influences completion and stimulation design, execution, and well performance, andDemonstrating how this multi-discipline dataset can be used to identify and mitigate well completion and stimulation risks in these unconventional reservoirs.
Horizontal Well Completion, Stimulation Optimization, and Risk Mitigation
Authors: Britt Larry K. , Smith Michael B. 
Published: October 2009

Abstract
Horizontal wells have become the industry standard for unconventional and tight formation gas reservoirs. Because these reservoirs have poorer quality pay, it takes a good, well-planned completion and fracture stimulation(s) to make an economic well. Even in a sweet spot in the unconventional and tight gas reservoir, good completion and stimulation practices are required; otherwise, a marginal or uneconomic well will result. But what are good completion and stimulation practices in horizontal wells? What are the objectives of horizontal wells and how do we relate the completion and stimulation(s) to achieving these goals? How many completions/stimulations do we need for best well performance and/or economics? How do we maximize the value from horizontal wells? When should a horizontal well be drilled longitudinally or transverse? These are just a few questions to be addressed in the subsequent paragraphs.
This paper focuses on some of the key elements of well completions and stimulation practices as they apply to horizontal wells. Optimization studies will be shown and used to highlight the importance of lateral length, number of fractures, inter-fracture distance, fracture half-length, and fracture conductivity. These results will be used to discuss the various completion choices such as cased and cemented, open hole with external casing packers, and open hole "pump and pray" techniques. This paper will also address key risks to horizontal wells and develop risk mitigation strategies so that project economics can be maximized. In addition, a field case study will be shown to illustrate the application of these design, optimization, and risk mitigation strategies for horizontal wells in tight and unconventional gas reservoirs.
This work provides insight for the completion and stimulation design engineers by: developing well performance and economic objectives for horizontal wells and highlighting the incremental benefits of various completion and stimulation strategies,establishing well performance and economic based criteria for drilling longitudinal or transverse horizontal wells,integrating the reservoir objectives and geomechanic limitations into a horizontal well completion and stimulation strategy, andidentifying horizontal well completion and stimulation risks and risk mitigation strategies for pre-horizontal well planning purposes.
Field Test of Wettability Alteration to Increase the Flow Rate from Aquifer Gas Storage Wells
Authors: Weiss William W. , Xie Xina , Weiss Jason W. 
Published: October 2009

Abstract
The St. Peter aquifer in northern Illinois is used to store natural gas during the summer months for the winter heating season. Since the fresh water aquifer is strongly water-wet, the capillary force promotes the retention of water in the pores to curtail the deliverability of gas to the wellbore during withdrawal. Similarly, the injection of gas during the filling cycle is also hampered. Laboratory work performed earlier demonstrated that the surfactant Tomadry N-4 could alter the wettability of the St. Peter core samples from strongly water-wet to neutral-wet, which in turn increased the gas deliverability. A field test was performed based on the laboratory results. The Waverly Storage Facility operated by Southern Union/Panhandle Energy was selected as the site for the field test of surfactant treatment. The storage reservoir is an 1800-ft sandstone aquifer located near Springfield, Illinois. Expansion and contraction of a spherical gas bubble provided pressure support as gas was injected and withdrawn from 37 individual wells. Three wells were selected for treatment with 1000 bbl of ~4% Tomadry N-4 solution. An additional three wells nearby were selected as control wells. The wells were treated at the end of the 2007 injection cycle, and the rate-pressure performance of the three treated wells and three control wells through the first month of 2009 was analyzed. Use of the productivity index technique was not as insightful as the conventional rate vs. cumulative production analysis technique. The Waverly test is belived to be the first field experiment of altering wettability to improve gas flow rates. Graphical presentation of the data suggests that at the beginning of the withdrawal cycle and injection period, the performance of the surfactant-treated wells was better than the control wells. The test results are encouraging, and further field tests should be developed. It appears that the gas withdrawal rate from two of the three treated wells was about 33% greater than prior to treatment.
Village Economies and the Structure of Extended Family Networks
Authors: Angelucci Manuela , De Giorgi Giacomo , Rangel Marcos , Rasul Imran 
Published: October 2009

Abstract
This paper documents how the structure of extended family networks in rural Mexico relates to the poverty and inequality of the village of residence. Using the Hispanic naming convention, we construct within-village extended family networks in 504 poor rural villages. Family networks are larger (both in the number of members and as a share of the village population) and out-migration is lower the poorer and the less unequal the village of residence. Our results are consistent with the extended family being a source of informal insurance to its members.
Carbohydrate-Responsive Element-Binding Protein (ChREBP) Is a Negative Regulator of ARNT/HIF-1β Gene Expression in Pancreatic Islet β-Cells
Authors: Noordeen Nafeesa A. , Khera Tarnjit K. , Sun Gao , Longbottom E. Rebecca , Pullen Timothy J. , da Silva Xavier Gabriela , Rutter Guy A. , Leclerc Isabelle 
Published: October 2009

OBJECTIVE
Carbohydrate-responsive element-binding protein (ChREBP) is a transcription factor that has been shown to regulate carbohydrate metabolism in the liver and pancreatic β-cells in response to elevated glucose concentrations. Because few genes have been identified so far as bona fide ChREBP-target genes, we have performed a genome-wide analysis of the ChREBP transcriptome in pancreatic β-cells.

RESEARCH DESIGN AND METHODS
Chromatin immunoprecipitation and high-density oligonucleotide tiling arrays (ChIP-chip; Agilent Technologies) using MIN6 pancreatic β-cell extracts were performed together with transcriptional and other analysis using standard techniques.

RESULTS
One of the genes identified by ChIP-chip and linked to glucose sensing and insulin secretion was aryl hydrocarbon receptor nuclear translocator (ARNT)/hypoxia-inducible factor-1β (HIF-1β), a transcription factor implicated in altered gene expression and pancreatic-islet dysfunction in type 2 diabetes. We first confirmed that elevated glucose concentrations decreased ARNT/HIF-1β levels in INS-1 (832/13) cells and primary mouse islets. Demonstrating a role for ChREBP in ARNT gene regulation, ChREBP silencing increased ARNT mRNA levels in INS-1 (832/13) cells, and ChREBP overexpression decreased ARNT mRNA in INS-1 (832/13) cells and primary mouse islets. We demonstrated that ChREBP and Max-like protein X (MLX) bind on the ARNT/HIF-1β promoter on the proximal region that also confers the negative glucose responsiveness.

CONCLUSIONS
These results demonstrate that ChREBP acts as a novel repressor of the ARNT/HIF-1β gene and might contribute to β-cell dysfunction induced by glucotoxicity.
Proteomics Analysis of Human Skeletal Muscle Reveals Novel Abnormalities in Obesity and Type 2 Diabetes
Authors: Hwang Hyonson , Bowen Benjamin P. , Lefort Natalie , Flynn Charles R. , De Filippis Elena A. , Roberts Christine , Smoke Christopher C. , Meyer Christian , Højlund Kurt , Yi Zhengping , Mandarino Lawrence J. 
Published: October 2009

OBJECTIVE
Insulin resistance in skeletal muscle is an early phenomenon in the pathogenesis of type 2 diabetes. Studies of insulin resistance usually are highly focused. However, approaches that give a more global picture of abnormalities in insulin resistance are useful in pointing out new directions for research. In previous studies, gene expression analyses show a coordinated pattern of reduction in nuclear-encoded mitochondrial gene expression in insulin resistance. However, changes in mRNA levels may not predict changes in protein abundance. An approach to identify global protein abundance changes involving the use of proteomics was used here.

RESEARCH DESIGN AND METHODS
Muscle biopsies were obtained basally from lean, obese, and type 2 diabetic volunteers (n = 8 each); glucose clamps were used to assess insulin sensitivity. Muscle protein was subjected to mass spectrometry–based quantification using normalized spectral abundance factors.

RESULTS
Of 1,218 proteins assigned, 400 were present in at least half of all subjects. Of these, 92 were altered by a factor of 2 in insulin resistance, and of those, 15 were significantly increased or decreased by ANOVA (P &lt; 0.05). Analysis of protein sets revealed patterns of decreased abundance in mitochondrial proteins and altered abundance of proteins involved with cytoskeletal structure (desmin and alpha actinin-2 both decreased), chaperone function (TCP-1 subunits increased), and proteasome subunits (increased).

CONCLUSIONS
The results confirm the reduction in mitochondrial proteins in insulin-resistant muscle and suggest that changes in muscle structure, protein degradation, and folding also characterize insulin resistance.
Age, Obesity, and Sex Effects on Insulin Sensitivity and Skeletal Muscle Mitochondrial Function
Authors: Karakelides Helen , Irving Brian A. , Short Kevin R. , O'Brien Peter , Nair K. Sreekumaran 
Published: October 2009

OBJECTIVE
Reductions in insulin sensitivity in conjunction with muscle mitochondrial dysfunction have been reported to occur in many conditions including aging. The objective was to determine whether insulin resistance and mitochondrial dysfunction are directly related to chronological age or are related to age-related changes in body composition.

RESEARCH DESIGN AND METHODS
Twelve young lean, 12 young obese, 12 elderly lean, and 12 elderly obese sedentary adults were studied. Insulin sensitivity was measured by a hyperinsulinemic-euglycemic clamp, and skeletal muscle mitochondrial ATP production rates (MAPRs) were measured in freshly isolated mitochondria obtained from vastus lateralis biopsy samples using the luciferase reaction.

RESULTS
Obese participants, independent of age, had reduced insulin sensitivity based on lower rates of glucose infusion during a hyperinsulinemic-euglycemic clamp. In contrast, age had no independent effect on insulin sensitivity. However, the elderly participants had lower muscle MAPRs than the young participants, independent of obesity. Elderly participants also had higher levels inflammatory cytokines and total adiponectin. In addition, higher muscle MAPRs were also noted in men than in women, whereas glucose infusion rates were higher in women.

CONCLUSIONS
The results demonstrate that age-related reductions in insulin sensitivity are likely due to an age-related increase in adiposity rather than a consequence of advanced chronological age. The results also indicate that an age-related decrease in muscle mitochondrial function is neither related to adiposity nor insulin sensitivity. Of interest, a higher mitochondrial ATP production capacity was noted in the men, whereas the women were more insulin sensitive, demonstrating further dissociation between insulin sensitivity and muscle mitochondrial function.
Idd9.1Locus Controls the Suppressive Activity of FoxP3+CD4+CD25+ Regulatory T-Cells
Authors: Yamanouchi Jun , Puertas Maria-Carmen , Verdaguer Joan , Lyons Paul A. , Rainbow Daniel B. , Chamberlain Giselle , Hunter Kara M. , Peterson Laurence B. , Wicker Linda S. , Santamaria Pere 
Published: October 2009

OBJECTIVEThe ∼45-cM insulin-dependent diabetes 9 (Idd9) region on mouse chromosome 4 harbors several different type 1 diabetes–associated loci. Nonobese diabetic (NOD) mice congenic for the Idd9 region of C57BL/10 (B10) mice, carrying antidiabetogenic alleles in three different Idd9 subregions (Idd9.1, Idd9.2, and Idd9.3), are strongly resistant to type 1 diabetes. However, the mechanisms remain unclear. This study aimed to define mechanisms underlying the type 1 diabetes resistance afforded by B10 Idd9.1, Idd9.2, and/or Idd9.3.RESEARCH DESIGN AND METHODSWe used a reductionist approach that involves comparing the fate of a type 1 diabetes–relevant autoreactive CD8+ T-cell population, specific for residues 206–214 of islet-specific glucose 6 phosphatase catalytic subunit–related protein (IGRP206–214), in noncongenic versus B10 Idd9–congenic (Idd9.1 + Idd9.2 + Idd9.3, Idd9.2 + Idd9.3, Idd9.1, Idd9.2, and Idd9.3) T-cell receptor (TCR)–transgenic (8.3) NOD mice.RESULTSMost of the protective effect of Idd9 against 8.3-CD8+ T-cell–enhanced type 1 diabetes was mediated by Idd9.1. Although Idd9.2 and Idd9.3 afforded some protection, the effects were small and did not enhance the greater protective effect of Idd9.1. B10 Idd9.1 afforded type 1 diabetes resistance without impairing the developmental biology or intrinsic diabetogenic potential of autoreactive CD8+ T-cells. Studies in T- and B-cell–deficient 8.3-NOD.B10 Idd9.1 mice revealed that this antidiabetogenic effect was mediated by endogenous, nontransgenic T-cells in a B-cell–independent manner. Consistent with this, B10 Idd9.1 increased the suppressive function and antidiabetogenic activity of the FoxP3+CD4+CD25+ T-cell subset in both TCR-transgenic and nontransgenic mice.CONCLUSIONSA gene(s) within Idd9.1 regulates the development and function of FoxP3+CD4+CD25+ regulatory T-cells and, in turn, the activation of CD8+ effector T-cells in the pancreatic draining lymph nodes, without affecting their development or intrinsic diabetogenic potential.
Complement Factor H Is Expressed in Adipose Tissue in Association With Insulin Resistance
Authors: Moreno-Navarrete José María , Martínez-Barricarte Rubén , Catalán Victoria , Sabater Mònica , Gómez-Ambrosi Javier , Ortega Francisco José , Ricart Wifredo , Blüher Mathias , Frühbeck Gema , Rodríguez de Cordoba Santiago , Fernández-Real José Manuel 
Published: October 2009

OBJECTIVE
Activation of the alternative pathway of the complement system, in which factor H (fH; complement fH [CFH]) is a key regulatory component, has been suggested as a link between obesity and metabolic disorders. Our objective was to study the associations between circulating and adipose tissue gene expressions of CFH and complement factor B (fB; CFB) with obesity and insulin resistance.

RESEARCH DESIGN AND METHODS
Circulating fH and fB were determined by enzyme-linked immunosorbent assay in 398 subjects. CFH and CFB gene expressions were evaluated in 76 adipose tissue samples, in isolated adipocytes, and in stromovascular cells (SVC) (n = 13). The effects of weight loss and rosiglitazone were investigated in independent cohorts.

RESULTS
Both circulating fH and fB were associated positively with BMI, waist circumference, triglycerides, and inflammatory parameters and negatively with insulin sensitivity and HDL cholesterol. For the first time, CFH gene expression was detected in human adipose tissue (significantly increased in subcutaneous compared with omental fat). CFH gene expression in omental fat was significantly associated with insulin resistance. In contrast, CFB gene expression was significantly increased in omental fat but also in association with fasting glucose and triglycerides. The SVC fraction was responsible for these differences, although isolated adipocytes also expressed fB and fH at low levels. Both weight loss and rosiglitazone led to significantly decreased circulating fB and fH levels.

CONCLUSIONS
Increased circulating fH and fB concentrations in subjects with altered glucose tolerance could reflect increased SVC-induced activation of the alternative pathway of complement in omental adipose tissue linked to insulin resistance and metabolic disturbances.
Prevalence of Loss-of-Function FTO Mutations in Lean and Obese Individuals
Authors: Meyre David , Proulx Karine , Kawagoe-Takaki Hiroko , Vatin Vincent , Gutiérrez-Aguilar Ruth , Lyon Debbie , Ma Marcella , Choquet Helene , Horber Fritz , Van Hul Wim , Van Gaal Luc , Balkau Beverley , Visvikis-Siest Sophie , Pattou François , Farooqi I. Sadaf , Saudek Vladimir , O'Rahilly Stephen , Froguel Philippe , Sedgwick Barbara , Yeo Giles S.H. 
Published: October 2009

OBJECTIVE
Single nucleotide polymorphisms (SNPs) in intron 1 of fat mass– and obesity-associated gene (FTO) are strongly associated with human adiposity, whereas Fto−/− mice are lean and Fto+/− mice are resistant to diet-induced obesity. We aimed to determine whether FTO mutations are disproportionately represented in lean or obese humans and to use these mutations to understand structure-function relationships within FTO.

RESEARCH DESIGN AND METHODS
We sequenced all coding exons of FTO in 1,433 severely obese and 1,433 lean individuals. We studied the enzymatic activity of selected nonsynonymous variants.

RESULTS
We identified 33 heterozygous nonsynonymous variants in lean (2.3%) and 35 in obese (2.4%) individuals, with 8 mutations unique to the obese and 11 unique to the lean. Two novel mutations replace absolutely conserved residues: R322Q in the catalytic domain and R96H in the predicted substrate recognition lid. R322Q was unable to catalyze the conversion of 2-oxoglutarate to succinate in the presence or absence of 3-methylthymidine. R96H retained some basal activity, which was not enhanced by 3-methylthymidine. However, both were found in lean and obese individuals.

CONCLUSIONS
Heterozygous, loss-of-function mutations in FTO exist but are found in both lean and obese subjects. Although intron 1 SNPs are unequivocally associated with obesity in multiple populations and murine studies strongly suggest that FTO has a role in energy balance, it appears that loss of one functional copy of FTO in humans is compatible with being either lean or obese. Functional analyses of FTO mutations have given novel insights into structure-function relationships in this enzyme.
Absence of p53-Dependent Apoptosis Combined With Nonhomologous End-Joining Deficiency Leads to a Severe Diabetic Phenotype in Mice
Authors: Tavana Omid , Puebla-Osorio Nahum , Sang Mei , Zhu Chengming 
Published: October 2009

OBJECTIVE
Regulation of pancreatic β-cell mass is essential to preserve sufficient insulin levels for the maintenance of glucose homeostasis. Previously, we reported that DNA double-strand breaks (DSBs) resulting from nonhomologous end-joining (NHEJ) deficiency induce apoptosis and, when combined with p53 deficiency, progressed rapidly into lymphomagenesis in mice. Combination of NHEJ deficiency with a hypomorphic mutation, p53R172P, leads to the abrogation of apoptosis, upregulation of p21, and senescence in precursor lymphocytes. This was sufficient to prevent tumorigenesis. However, these mutant mice succumb to severe diabetes and die at an early age. The aim of this study was to determine the pathogenesis of diabetes in these mutant mice.

RESEARCH DESIGN AND METHODS
We analyzed the morphology of the pancreatic islets and the function, proliferation rate, and senescence of β-cells. We also profiled DNA damage and p53 and p21 expression in the pancreas.

RESULTS
NHEJ-p53R172P mutant mice succumb to diabetes at 3–5 months of age. These mice show a progressive decrease in pancreatic islet mass that is independent of apoptosis and innate immunity. We observed an accumulation of DNA damage, accompanied with increased levels of p53 and p21, a significant decrease in β-cell proliferation, and cellular senescence in the mutant pancreatic islets.

CONCLUSIONS
Combined DSBs with an absence of p53-dependent apoptosis activate p53-dependent senescence, which leads to a diminished β-cell self-replication, massive depletion of the pancreatic islets, and severe diabetes. This is a model that connects impaired DNA repair and accumulative DNA damage, a common phenotype in aging individuals, to the onset of diabetes.