bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nonlinear dynamics and recurrence analysis of extreme precipitation for observed and general circulation model generated climates
Authors: Panagoulia Dionysia , Vlahogianni Eleni I. 
Published: March 2013

AbstractA statistical framework based on nonlinear dynamics theory and recurrence quantification analysis of dynamical systems is proposed to quantitatively identify the temporal characteristics of extreme (maximum) daily precipitation series. The methodology focuses on both observed and general circulation model (GCM) generated climates for present (1961–2000) and future (2061–2100) periods which correspond to 1xCO2 and 2xCO2 simulations. The daily precipitation has been modelled as a stochastic process coupled with atmospheric circulation. An automated and objective classification of daily circulation patterns (CPs) based on optimized fuzzy rules was used to classify both observed CPs and ECHAM4 GCM‐generated CPs for 1xCO2 and 2xCO2 climate simulations (scenarios). The coupled model ‘CP‐precipitation’ was suitable for precipitation downscaling. The overall methodology was applied to the medium‐sized mountainous Mesochora catchment in Central‐Western Greece. Results reveal substantial differences between the observed maximum daily precipitation statistical patterns and those produced by the two climate scenarios. A variable nonlinear deterministic behaviour characterizes all climate scenarios examined. Transitions’ patterns differ in terms of duration and intensity. The 2xCO2 scenario contains the strongest transitions highlighting an unusual shift between floods and droughts. The implications of the results to the predictability of the phenomenon are also discussed. Copyright © 2013 John Wiley & Sons, Ltd.
Comparison of three methods of hydrogeological parameter estimation in leaky aquifers using transient flow pumping tests
Authors: Li Peiyue , Qian Hui , Wu Jianhua 
Published: March 2013

AbstractAccurate knowledge of hydrogeological parameters is essential for groundwater modeling, protection and remediation. Three methods (type curve fitting method, inflection point method and global curve‐fitting method (GCFM)) which are frequently applied in the estimation of leaky aquifer parameters were compared using synthetic pumping tests. The results revealed GCFM could provide best parameter estimation among the three methods with fewer uncertainties associated with the processes of parameter estimation. GCFM was also found to be both time saving and of low cost and is thus more preferable for hydrogeological parameter estimation than the other two methods. Copyright © 2013 John Wiley & Sons, Ltd.
DRAINAGE PERFORMANCE ASSESSMENT IN A MODERNIZED OASIS SYSTEM
Authors: Ben Aissa I. , Bouarfa S. , Vincent B. , Chaumont C. , Perrier A. 
Published: March 2013

ABSTRACTSaharan oases are frequently subjected to waterlogging due to the presence of shallow and salty groundwater and poor irrigation and drainage conditions. To overcome this problem in Tunisia, in 2002 an official modernization programme was implemented based on two operations: (i) increasing irrigation efficiency by building concrete irrigation canals to limit losses due to water percolation and (ii) controlling waterlogging and salinity by installing a subsurface drainage system in place of the traditional open‐ditch system. In this study, a salinity balance was performed in Fatnassa, a representative Saharan oasis in Tunisia. Two spatial levels were monitored over a period of two years: an irrigated and drained field (0.8 ha) and the northern part of the oasis covering 114 ha. Results showed an equilibrated salinity balance at the field level, whereas, at the oasis level, the drainage system was unable to evacuate more than 30% of the salts in the first year and 15% in the second. We consider the clogging effect detected in several locations in the oasis as the main cause of this dysfunction. For the future, we recommend a more participatory approach to designing drainage systems, probably moving toward mixed systems with traditional open ditches and modern subsurface pipes, both easy to maintain by the farmers themselves. Adequate envelopes to prevent clogging in mineral soils have to be tested in situ before extension of subsurface drainage. Copyright © 2013 John Wiley & Sons, Ltd.
The neurobiology of tetrahydrobiopterin biosynthesis: A model for regulation of GTP cyclohydrolase I gene transcription within nigrostriatal dopamine neurons
Authors: Kapatos Gregory 
Published: March 2013

AbstractAbstractWithin the brain, the reduced pteridine cofactor 6R‐L‐erythro‐5,6,7,8‐tetrahydrobiopterin (BH4) is absolutely required for the synthesis of the monoamine (MA) neurotransmitters dopamine (DA), norepinephrine, epinephrine (E), and serotonin (5‐HT), the novel gaseous neurotransmitter nitric oxide and the production of yet to be identified 1‐O‐alkylglycerol‐derived lipids. GTP cyclohydrolase I (GTPCH) catalyzes the first and limiting step in the BH4 biosynthetic pathway, which is now thought to involve up to eight different proteins supporting six alternate de novo and two alternate salvage pathways. Gene expression analysis across different regions of the human brain shows the abundance of transcripts coding for all eight of these proteins to be highly correlated with each other and to be enriched within human MA neurons. The potential for multiple routes for BH4 synthesis therefore exists within the human brain. GTPCH expression is particularly heterogeneous across different populations of human and rodent MA‐containing neurons, with low expression levels and therefore BH4 being a characteristic of nigrostriatal DA (NSDA) neurons. Basic knowledge of how GCH1 gene transcription is controlled within NSDA neurons may explain the distinctive susceptibility of these neurons to human genetic mutations that result in BH4 deficiency. A model for cyclic adenosine monophosphate‐dependent GCH1 transcription is described that involves a unique combination of DNA regulatory sequences and transcription factors. This model proposes that low levels of GCH1 transcription within NSDA neurons are driven by their distinctive physiology, suggesting that pharmacological manipulation of GCH1 gene transcription can be used to modify BH4 levels and therefore DA synthesis in the basal ganglia. © 2013 IUBMB Life 65(4):323–333, 2013.
Phenylalanine hydroxylase: Function, structure, and regulation
Authors: Flydal Marte I. , Martinez Aurora 
Published: March 2013

AbstractMammalian phenylalanine hydroxylase (PAH) catalyzes the rate‐limiting step in the phenylalanine catabolism, consuming about 75% of the phenylalanine input from the diet and protein catabolism under physiological conditions. In humans, mutations in the PAH gene lead to phenylketonuria (PKU), and most mutations are mainly associated with PAH misfolding and instability. The established treatment for PKU is a phenylalanine‐restricted diet and, recently, supplementation with preparations of the natural tetrahydrobiopterin cofactor also shows effectiveness for some patients. Since 1997 there has been a significant increase in the understanding of the structure, catalytic mechanism, and regulation of PAH by its substrate and cofactor, in addition to improved correlations between genotype and phenotype in PKU. Importantly, there has also been an increased number of studies on the structure and function of PAH from bacteria and lower eukaryote organisms, revealing an additional anabolic role of the enzyme in the synthesis of melanin‐like pigments. In this review, we discuss these recent studies, which contribute to define the evolutionary adaptation of the PAH structure and function leading to sophisticated regulation for effective catabolic processing of phenylalanine in mammalian organisms. © 2013 IUBMB Life 65(4):341–349, 2013.
A distal forearm fracture in childhood is associated with an increased risk for future fragility fractures in adult men, but not women
Authors: Amin Shreyasee , Melton L Joseph , Achenbach Sara J , Atkinson Elizabeth J , Dekutoski Mark B , Kirmani Salman , Fischer Philip R , Khosla Sundeep 
Published: March 2013

ABSTRACT

Distal forearm fractures are among the most common fractures during childhood, but it remains unclear whether they predict an increased fracture risk later in life. We studied a population-based cohort of 1776 children ≤18 years of age, from Olmsted County, MN, USA, who had a distal forearm fracture in 1935–1992. Incident fractures occurring at age ≥35 years were identified through review of complete medical records using the linkage system of the Rochester Epidemiology Project. Observed nonpathologic fractures resulting from no more than moderate trauma (fragility fractures) were compared with expected numbers estimated from fracture site–specific incidence rates, based on age, sex, and calendar year, for Olmsted County (standardized incidence ratios [SIR]). In 1086 boys (mean ± SD age; 11 ± 4 years) and 690 girls (10 ± 4 years) followed for 27,292 person-years after the age of 35 years, subsequent fragility fractures were observed in 144 (13%) men and 74 (11%) women. There was an increased risk for future fragility fractures in boys who had a distal forearm fracture (SIR, 1.9; 95% CI, 1.6–2.3) but not girls (SIR, 1.0; 95% CI, 0.8–1.2). Fragility fractures at both major osteoporotic (hip, spine, wrist, and shoulder) sites (SIR, 2.6; 95% CI, 2.1–3.3) and remaining sites (SIR, 1.7; 95% CI, 1.3–2.0) were increased in men, irrespective of age at distal forearm fracture as boys. A distal forearm fracture in boys, but not girls, is associated with an increased risk for fragility fractures as older adults. It is necessary to determine whether the increased fractures observed in men is due to persistent deficits of bone strength, continued high fracture risk activity, or both. Until then, men should be asked about a childhood distal forearm fracture and, if so, warrant further screening and counseling on measures to optimize bone health and prevent fractures.
C-Reactive Protein, Bone Strength, and Nine-Year Fracture Risk: Data From the Study of Women's Health Across the Nation (SWAN)
Authors: Ishii Shinya , Cauley Jane A , Greendale Gail A , Crandall Carolyn J , Danielson Michelle E , Ouchi Yasuyoshi , Karlamangla Arun S 
Published: March 2013

ABSTRACT

Higher levels of C-reactive protein (CRP), an inflammatory marker, are associated with increased fracture risk, although previous studies on CRP and bone mineral density (BMD) have yielded conflicting results. We aimed to test the hypotheses that composite indices of femoral neck strength relative to load, which are inversely associated with fracture risk, would also be inversely associated with CRP, and would explain part of the association between CRP and fracture risk. We analyzed data from a multisite, multiethnic prospective cohort of 1872 community-dwelling women, premenopausal or early perimenopausal at baseline. Femoral neck composite strength indices in three failure modes were calculated using dual-energy X-ray absorptiometry (DXA)-derived femoral neck width (FNW), femoral neck axis length (FNAL), femoral neck BMD and body size at baseline, as BMD*FNW/weight for compression strength, BMD*(FNW)2/(FNAL*weight) for bending strength, and BMD*FNW*FNAL/(height*weight) for impact strength. Incident nondigital, noncraniofacial fractures were ascertained annually over a median follow-up of 9 years. In analyses adjusted for age, race/ethnicity, diabetes, menopause transition stage, body mass index, smoking, alcohol use, physical activity, medications, prior fracture, and study site, CRP was associated inversely with each composite strength index (0.035–0.041 SD decrement per doubling of CRP, all p &lt; 0.001), but not associated with femoral neck or lumbar spine BMD. During the follow-up, 194 women (10.4%) had fractures. In Cox proportional hazards analyses, fracture hazard increased linearly with loge(CRP), only for CRP levels ≥ 3 mg/L. Addition of femoral neck or lumbar spine BMD to the model did not attenuate the CRP-fracture association. However, addition of any of the composite strength indices attenuated the CRP-fracture association and made it statistically nonsignificant. We conclude that fracture risk increases with increasing CRP, only above the threshold of 3 mg/L. Unlike BMD, composite strength indices are inversely related to CRP levels, and partially explain the increased fracture risk associated with inflammation.
Serum IGF-1 Is Insufficient to Restore Skeletal Size in the Total Absence of the Growth Hormone Receptor
Authors: Wu Yingjie , Sun Hui , Basta-Pljakic Jelena , Cardoso Luis , Kennedy Oran D , Jasper Hector , Domené Horacio , Karabatas Liliana , Guida Clara , Schaffler Mitchell B , Rosen Clifford J , Yakar Shoshana 
Published: March 2013

ABSTRACT

States of growth hormone (GH) resistance, such those observed in Laron dwarf patients, are characterized by mutations in the GH receptor (GHR), decreased serum and tissue IGF-1 levels, impaired glucose tolerance, and impaired skeletal acquisition. IGF-1 replacement therapy in such patients increases growth velocity but does not normalize growth. Herein we combined the GH-resistant (GHR knockout [GHRKO]) mouse model with mice expressing the hepatic Igf-1 transgene (HIT) to generate the GHRKO-HIT mouse model. In GHRKO-HIT mice, serum IGF-1 levels were restored via transgenic expression of Igf-1, allowing us to study how endocrine IGF-1 affects growth, metabolic homeostasis, and skeletal integrity. We show that in a GH-resistant state, normalization of serum IGF-1 improved body adiposity and restored glucose tolerance but was insufficient to support normal skeletal growth, resulting in an osteopenic skeletal phenotype. The inability of serum IGF-1 to restore skeletal integrity in the total absence of GHR likely resulted from reduced skeletal Igf-1 gene expression, blunted GH-mediated effects on the skeleton that are independent of serum or tissue IGF-1, and poor delivery of IGF-1 to the tissues. These findings are consistent with clinical data showing that IGF-I replacement therapy in patients with Laron syndrome does not achieve full skeletal growth.
Novel role of VMP1 as modifier of the pancreatic tumor cell response to chemotherapeutic drugs
Authors: Gilabert Marine , Vaccaro Maria Inés , Fernandez‐Zapico Martin E. , Calvo Ezequiel L. , Turrini Olivier , Secq Véronique , Garcia Stéphane , Moutardier Vincent , Lomberk Gwen , Dusetti Nelson , Urrutia Raul , Iovanna Juan L. 
Published: March 2013

AbstractWe hypothesized that inhibiting molecules that mediate the adaptation response to cellular stress can antagonize the resistance of pancreatic cancer cells to chemotherapeutic drugs. Toward this end, here, we investigated how VMP1, a stress‐induced autophagy‐associated protein, modulate stress responses triggered by chemotherapeutic agents in PDAC. We find that VMP1 is particularly over‐expressed in poorly differentiated human pancreatic cancer. Pharmacological studies show that drugs that work, in part, via the endoplasmic reticulum stress response, induce VMP1 expression. Similarly, VMP1 is induced by known endoplasmic reticulum stress activators. Genetic inactivation of VMP1 using RNAi‐based antagonize the pancreatic cancer stress response to antitumoral agents. Functionally, we find that VMP1 regulates both autophagy and chemotherapeutic resistance even in the presence of chloroquin, ATG5 or Beclin 1 siRNAs, or a Beclin 1‐binding VMP1 mutant. In addition, VMP1 modulates endoplasmic reticulum stress independently of its coupling to the molecular and cellular autophagy machinery. Preclinical studies demonstrate that xenografts expressing an inducible and tractable form of VMP1 show increased resistance to the gemcitabine treatment. These results underscore a novel role for VMP1 as a potential therapeutic target for combinatorial therapies aimed at sensitizing pancreatic cancer cells to chemotherapeutic agents as well as provide novel molecular mechanisms to better understand this phenomenon. J. Cell. Physiol. 228: 1834–1843, 2013. © 2013 Wiley Periodicals, Inc.
GRK2 negatively regulates IGF‐1R signaling pathway and cyclins' expression in HepG2 cells
Authors: Wei Zhengyu , Hurtt Reginald , Gu Tina , Bodzin Adam S. , Koch Walter J. , Doria Cataldo 
Published: March 2013

AbstractG protein coupled receptor kinase 2 (GRK2) plays a central role in the regulation of a variety of important signaling pathways. Alternation of GRK2 protein level and activity casts profound effects on cell physiological functions and causes diseases such as heart failure, rheumatoid arthritis, and obesity. We have previously reported that overexpression of GRK2 has an inhibitory role in cancer cell growth. To further examine the role of GRK2 in cancer, in this study, we investigated the effects of reduced protein level of GRK2 on insulin‐like growth factor 1 receptor (IGF‐1R) signaling pathway in human hepatocellular carcinoma (HCC) HepG2 cells. We created a GRK2 knockdown cell line using a lentiviral vector mediated expression of GRK2 specific short hairpin RNA (shRNA). Under IGF‐1 stimulation, HepG2 cells with reduced level of GRK2 showed elevated total IGF‐1R protein expression as well as tyrosine phosphorylation of receptor. In addition, HepG2 cells with reduced level of GRK2 also demonstrated increased tyrosine phosphorylation of IRS1 at the residue 612 and increased phosphorylation of Akt, indicating a stronger activation of IGF‐1R signaling pathway. However, HepG2 cells with reduced level of GRK2 did not display any growth advantage in culture as compared with the scramble control cells. We further detected that reduced level of GRK2 induced a small cell cycle arrest at G2/M phase by enhancing the expression of cyclin A, B1, and E. Our results indicate that GRK2 has contrasting roles on HepG2 cell growth by negatively regulating the IGF‐1R signaling pathway and cyclins' expression. J. Cell. Physiol. 228: 1897–1901, 2013. © 2013 Wiley Periodicals, Inc.
Fibroblast cytoskeletal remodeling induced by tissue stretch involves ATP signaling
Authors: Langevin Helene M. , Fujita Takumi , Bouffard Nicole A. , Takano Takahiro , Koptiuch Cathryn , Badger Gary J. , Nedergaard Maiken 
Published: March 2013

AbstractFibroblasts in whole areolar connective tissue respond to static stretching of the tissue by expanding and remodeling their cytoskeleton within minutes both ex vivo and in vivo. This study tested the hypothesis that the mechanism of fibroblast expansion in response to tissue stretch involves extracellular ATP signaling. In response to tissue stretch ex vivo, ATP levels in the bath solution increased significantly, and this increase was sustained for 20 min, returning to baseline at 60 min. No increase in ATP was observed in tissue incubated without stretch or tissue stretched in the presence of the Rho kinase inhibitor Y27632. The increase in fibroblast cross sectional area in response to tissue stretch was blocked by both suramin (a purinergic receptor blocker) and apyrase (an enzyme that selectively degrades extracellular ATP). Furthermore, connexin channel blockers (octanol and carbenoxolone), but not VRAC (fluoxetine) or pannexin (probenecid) channel blockers, inhibited fibroblast expansion. Together, these results support a mechanism in which extracellular ATP signaling via connexin hemichannels mediate the active change in fibroblast shape that occurs in response to a static increase in tissue length. J. Cell. Physiol. 228: 1922–1926, 2013. © 2013 Wiley Periodicals, Inc.
EFFECTS OF REWARD BUNDLING ON MALE RATS' PREFERENCE FOR LARGER–LATER FOOD REWARDS
Authors: Stein Jeffrey S. , Smits Rochelle R. , Johnson Patrick S. , Liston Kennan J. , Madden Gregory J. 
Published: March 2013

AbstractIn both humans and nonhumans, prior research demonstrates increased preference for larger‐later over smaller‐sooner rewards when rewards are bundled together in a series (i.e., when an operant choice produces multiple discrete reward deliveries, as opposed to only a single delivery). These findings can be predicted using a traditional hyperbolic delay‐discounting model. The present study was designed to examine the parametric effects of the size of the reward bundle on larger‐later reward preference in male rats. During a reward‐bundling phase, rats were exposed to bundle‐sizes of either 1 (i.e., no bundling), 3, or 9 rewards. Rats in the Bundle‐size 9 group showed significantly greater larger‐later reward preference across a range of delays (0‐17.5 s) than rats in any other group, but no other significant differences in choice were observed between groups. In addition, when choice for unbundled rewards was assessed following the reward‐bundling phase, rats in the Bundle‐size 9 group showed a significant increase in larger‐later reward preference (compared to a pre‐test). Obtained data from the reward‐bundling phase are compared to model‐predicted data, and potential mechanisms of the observed increase in self‐control for unbundled rewards are discussed.
COMBINATIONS OF RESPONSE‐REINFORCER RELATIONS IN PERIODIC AND APERIODIC SCHEDULES
Authors: Kuroda Toshikazu , Cançado Carlos R. X. , Lattal Kennon A. , Elcoro Mirari , Dickson Chata A. , Cook James E. 
Published: March 2013

AbstractKey pecking of 4 pigeons was studied under a two‐component multiple schedule in which food deliveries were arranged according to a fixed and a variable interfood interval. The percentage of response‐dependent food in each component was varied, first in ascending (0, 10, 30, 70 and 100%) and then in descending orders, in successive conditions. The change in response rates was positively related to the percentage of response‐dependent food in each schedule component. Across conditions, positively accelerated and linear patterns of responding occurred consistently in the fixed and variable components, respectively. These results suggest that the response–food dependency determines response rates in periodic and aperiodic schedules, and that the temporal distribution of food determines response patterns independently of the response–food dependency. Running rates, but not postfood pauses, also were positively related to the percentage of dependent food in each condition, in both fixed and variable components. Thus, the relation between overall response rate and the percentage of dependent food was mediated by responding that occurred after postfood pausing. The findings together extend previous studies wherein the dependency was either always present or absent, and increase the generality of the effects of variations in the response–food dependency from aperiodic to periodic schedules.
COCAINE VERSUS FOOD CHOICE PROCEDURE IN RATS: ENVIRONMENTAL MANIPULATIONS AND EFFECTS OF AMPHETAMINE
Authors: Thomsen Morgane , Barrett Andrew C. , Negus S. Stevens , Caine S. Barak 
Published: March 2013

AbstractWe have adapted a nonhuman primate model of cocaine versus food choice to the rat species. To evaluate the procedure, we tested cocaine versus food choice under a variety of environmental manipulations as well as pharmacological pretreatments. Complete cocaine‐choice dose‐effect curves (0–1.0 mg/kg/infusion) were obtained for each condition under concurrent fixed ratio schedules of reinforcement. Percentage of responding emitted on the cocaine‐reinforced lever was not affected significantly by removal of cocaine‐associated visual or auditory cues, but it was decreased after removal of response‐contingent or response‐independent cocaine infusions. Cocaine choice was sensitive to the magnitude and fixed ratio requirement of both the cocaine and food reinforcers. We also tested the effects of acute (0.32, 0.56, 1.0, 1.8 mg/kg) and chronic (0.1, 0.32 mg/kg/hr) d‐amphetamine treatment on cocaine choice. Acute and chronic d‐amphetamine had opposite effects, with acute increasing and chronic decreasing cocaine choice, similar to observations in humans and in nonhuman primates. The results suggest feasibility and utility of the choice procedure in rats and support its comparability to similar procedures used in humans and monkeys.