bluuebunny/crossref_metadata_2025_split huggingface dataset:
Treatment of osteopenia and osteoporosis in anorexia nervosa: A systematic review of the literature
Authors: Mehler Philip S. , MacKenzie Thomas D. 
Published: October 2008

AbstractObjective:To systematically review the evidence supporting treatment of osteopenia and osteoporosis in patients with anorexia nervosa (AN).Data sources:We identified controlled clinical studies of interventions for low bone mass in AN via searches of MEDLINE; the Cochrane Library; EMBASE; PsycINFO; and cumulative index to nursing and allied health literature. Outcomes of interest were changes in bone mineral density and fracture incidence.Results:Six randomized controlled trials (RCTs) and two cohort trials examined five classes of medical therapy on bone mineral density outcomes. One RCT of bisphosphonates showed no benefit and a second flawed RCT showed some benefit; one RCT showed a benefit of insulin‐like growth factor‐I; none of the five trials evaluating estrogen therapy showed benefit.Discussion:Although patients with AN are often losing bone mass when they should be optimizing bone growth, there is no good evidence to guide medicinal interventions. Therefore, early detection and weight restoration are of utmost importance whereas ongoing trials define effective therapies. © 2008 by Wiley Periodicals, Inc. Int J Eat Disord 2009
Increasing the motivation for physical activity in obese patients
Authors: Schelling Simone , Munsch Simone , Meyer Andrea H. , Newark Patricia , Biedert Esther , Margraf Juergen 
Published: October 2008

AbstractObjective:In this randomized controlled study, a standardized motivation intervention was compared with a relaxation intervention with regard to its effectiveness in decreasing dropout rates and increasing physical activity in a sample of obese patients.Method:Thirty‐eight obese participants were randomly assigned to a one‐session motivation or relaxation intervention. Thereafter, both groups participated in an 8‐week aerobic program. Adherence, physical activity, motivational stage of change, and body mass index (BMI) were assessed during intervention and at 3‐ and 6‐month follow‐ups.Results:During the aerobic program, the motivation group showed significantly fewer dropouts but comparable adherence if only completers were considered. Moreover, their weekly minutes of physical activity increased over time before leveling off, whereas steady decreases were observed in the relaxation group. For motivational stage of change and BMI, no significant group differences were observed.Discussion:The importance and efficacy of motivational interventions in enhancing the high dropout rates in obesity treatment is underlined. © 2008 by Wiley Periodicals, Inc. Int J Eat Disord 2009
DSM‐IV psychiatric disorder comorbidity and its correlates in binge eating disorder
Authors: Grilo Carlos M. , White Marney A. , Masheb Robin M. 
Published: October 2008

AbstractObjective:To assess DSM‐IV lifetime and current psychiatric disorder comorbidity in patients with binge eating disorder (BED) and to examine associations of comorbidity with gender, selected historical obesity‐related variables, and current eating disorder psychopathology.Method:A consecutive series of 404 patients with BED (310 women, 94 men) were reliably administered semistructured diagnostic and clinical interviews to assess DSM‐IV psychiatric disorders and features of eating disorders.Results:Overall, 73.8% of patients with BED had at least one additional lifetime psychiatric disorder and 43.1% had at least one current psychiatric disorder. Lifetime‐wise, mood (54.2%), anxiety (37.1%), and substance use (24.8%) disorders were most common. In terms of current comorbidity, mood (26.0%) and anxiety (24.5%) were most common. Few gender differences were observed; men had higher lifetime rates of substance use disorders and current rates of obsessive compulsive disorder. Patients with BED with current psychiatric comorbidity reported earlier age at first diet and higher “lifetime‐high” BMI. Patients with current comorbidity also had significantly higher levels of current eating disorder psychopathology and negative affect and lower self‐esteem relative to patients with BED with either lifetime (noncurrent) or no psychiatric histories.Discussion:Among treatment‐seeking patients with BED, the presence of current psychiatric comorbidity is associated with greater eating disorder psychopathology and associated distress. © 2008 by Wiley Periodicals, Inc. Int J Eat Disord 2009
Multi‐round procurement auctions with secret reserve prices: theory and evidence
Authors: Ji Lu , Li Tong 
Published: October 2008

AbstractWhen a secret reserve price is used in an auction, the auctioneer cannot guarantee that the good can be sold out at the auction, and can reauction the unsold objects in the next round. Motivated by this interesting feature observed in the procurement auctions organized by the Indiana Department of Transportation, we construct a dynamic bidding model in multi‐round procurement auctions with secret reserve prices and evaluate how the release of the auctioneer's reserve price affects bidders' bidding behavior and the auctioneer's expected payment. Our theoretical model predicts that the equilibrium bids uniformly decline over stages, and the numerical analysis of our model indicates that hiding the reserve price may be better than announcing it for the auctioneer under some specifications of underlying distributions. We develop an empirical model with bidders' discount factor equal to zero to recover the unknown structural parameters and to conduct counterfactual analyses. Copyright © 2008 John Wiley & Sons, Ltd.
Evidence‐based algorithms for diagnosing and treating ventilator‐associated pneumonia
Authors: Wall Richard J. , Ely E. Wesley , Talbot Thomas R. , Weinger Matthew B. , Williams Mark V. , Reischel Joan , Burgess L. Hayley , Englebright Jane , Dittus Robert. S. , Speroff Theodore , Deshpande Jayant K. 
Published: October 2008

AbstractBACKGROUND:Ventilator‐associated pneumonia (VAP) is widely recognized as a serious and common complication associated with high morbidity and high costs. Given the complexity of caring for heterogeneous populations in the intensive care unit (ICU), however, there is still uncertainty regarding how to diagnose and manage VAP.OBJECTIVE:We recently conducted a national collaborative aimed at reducing health care–associated infections in ICUs of hospitals operated by the Hospital Corporation of America (HCA). As part of this collaborative, we developed algorithms for diagnosing and treating VAP in mechanically ventilated patients. In the current article, we (1) review the current evidence for diagnosing VAP, (2) describe our approach for developing these algorithms, and (3) illustrate the utility of the diagnostic algorithms using clinical teaching cases.DESIGN:This was a descriptive study, using data from a national collaborative focused on reducing VAP and catheter‐related bloodstream infections.SETTING:The setting of the study was 110 ICUs at 61 HCA hospitals.INTERVENTION:None.MEASUREMENTS AND RESULTS:We assembled an interdisciplinary team that included infectious disease specialists, intensivists, hospitalists, statisticians, critical care nurses, and pharmacists. After reviewing published studies and the Centers for Disease Control and Prevention VAP guidelines, the team iteratively discussed the evidence, achieved consensus, and ultimately developed these practical algorithms. The diagnostic algorithms address infant, pediatric, immunocompromised, and adult ICU patients.CONCLUSIONS:We present practical algorithms for diagnosing and managing VAP in mechanically ventilated patients. These algorithms may provide evidence‐based real‐time guidance to clinicians seeking a standardized approach to diagnosing and managing this challenging problem. Journal of Hospital Medicine 2008;3:409–422. © 2008 Society of Hospital Medicine.
Differences associated with age, transfer status, and insurance coverage in end‐of‐life hospital care for children
Authors: Caskey R. N. , Davis M. M. 
Published: October 2008

AbstractBACKGROUND:More than 40% of childhood mortality occurs while children are hospitalized. End‐of‐life health care utilization patterns for children have not been well characterized at the national level.OBJECTIVE:To describe patterns of length of stay, total charges, and principal diagnoses for children who die while admitted to a hospital, versus those who survive to discharge.METHODS:We conducted a cross‐sectional analysis of 3 years spanning a decade of the Nationwide Inpatient Sample (NIS), a nationally representative dataset of hospital discharges, to analyze sociodemographic characteristics and patterns of hospital resource use associated with in‐hospital mortality.RESULTS:Inpatient mortality rate was significantly higher for non‐newborn infants (<1 year old) than for all other age groups, and the overall number of deaths was greatest for newborns. Patients transferred between hospitals had significantly greater mortality rate, compared with patients admitted not on transfer. Insured children had lower mortality rates compared to uninsured, and decedents had significantly longer length of stay and higher charges compared with survivors. Uninsured decedents did not have longer lengths of stay than survivors, and hospital charges were significantly lower for uninsured children compared with insured children.CONCLUSION:As hospital staff strive to meet the needs of ill children and their families, they must be cognizant of the high burden of mortality among the youngest children and those transferred between hospitals, and the potential for less resource use and higher mortality risk for children without insurance, because these patients may require expanded services not readily available in most hospital settings. Journal of Hospital Medicine 2008;3:376–383. © 2008 Society of Hospital Medicine.
Just because you can, doesn't mean that you should: A call for the rational application of hospitalist comanagement
Authors: Siegal Eric M. 
Published: October 2008

AbstractMedical comanagement has become a mainstay of hospital medicine. Several studies, however, suggest that medical consultation and comanagement may not be as effective as originally anticipated. The expansion of comanagement services has helped fuel massive demand for hospitalists and with it a critical and potentially destabilizing hospitalist manpower shortage. Comanagement may also drive unanticipated consequences such as facilitating surgeon and specialist disengagement and hospitalist career dissatisfaction and burnout. Comanagement services should be developed carefully and methodically, paying close attention to consequences, intended and unintended. Journal of Hospital Medicine 2008;3:398–402. © 2008 Society of Hospital Medicine.
Progressive decrease in the level of YAPdeltaCs, prosurvival isoforms of YAP, in the spinal cord of transgenic mouse carrying a mutant SOD1 gene
Authors: Morimoto Nobutoshi , Nagai Makiko , Miyazaki Kazunori , Kurata Tomoko , Takehisa Yasushi , Ikeda Yoshio , Kamiya Tatsushi , Okazawa Hitoshi , Abe Koji 
Published: October 2008

AbstractAmyotrophic lateral sclerosis (ALS) is a progressive and fatal disease caused by the selective death of motor neurons. Between 5% and 10% of ALS patients have a genetically inherited form of the disease known as familial ALS (FALS), and approximately 20% of FALS patients have mutations in the SOD1 gene. Although the mechanism underlying motor neuron death has not yet been fully clarified, it is supposed to be not completely consistent with apoptosis, necrosis, or autophagic cell death. Recently, it was found that general transcriptional repression induces slowly progressive atypical cell death associated with the shift of balance between YAPdeltaCs as prosurvival factors and activated p73 promoting apoptosis. This type of neuronal death was named transcriptional repression–induced atypical death (TRIAD). Therefore, to investigate possible relationships between the mechanism of motor neuron death in ALS and TRIAD, G93ASOD1 transgenic mice (Tg) were examined as an ALS model. The levels of YAPdeltaCs in the spinal cords of Tg mice decreased with disease progression, even during the presymptomatic stage, whereas FL‐YAP, a p73 cofactor that promotes apoptosis, was preserved until the late symptomatic stage. Although the expression of total p73 also decreased with age in Tg mice, the ratio of phosphorylated p73 to total p73 increased during the late symptomatic stage in Tg mice. These results suggest that the progressive decrease in the levels of YAPdeltaCs and the relative increase in phosphorylation of p73 over the time course are correlated with disease progression in ALS model animals. © 2008 Wiley‐Liss, Inc.
Oxygen‐glucose deprivation activates 5‐lipoxygenase mediated by oxidative stress through the p38 mitogen‐activated protein kinase pathway in PC12 cells
Authors: Li Cheng‐Tan , Zhang Wei‐Ping , Lu Yun‐Bi , Fang San‐Hua , Yuan Yu‐Mei , Qi Ling‐Ling , Zhang Li‐Hui , Huang Xiao‐Jia , Zhang Lei , Chen Zhong , Wei Er‐Qing 
Published: October 2008

Abstract5‐Lipoxygenase (5‐LOX) is a key enzyme catalyzing arachidonic acid to form leukotrienes. We have reported that ischemic‐like injury activates 5‐LOX in PC12 cells; however, the mechanisms are unknown. To determine whether ischemic‐like injury activates 5‐LOX mediated by oxidative stress through the p38 MAPK pathway, we transfected GFP‐5‐LOX into PC12 cells and induced ischemic‐like injury by oxygen‐glucose deprivation (OGD). We found that the transfected GFP‐5‐LOX was localized primarily in the nuclei and translocated to the nuclear envelope after OGD/recovery reaching a maximum 2 hr after a 2‐hr exposure to OGD. The nonselective 5‐LOX inhibitor caffeic acid, 5‐LOX‐activating protein inhibitor MK886, and selective 5‐LOX inhibitor zileuton attenuated the cell injury and reduced the production of 5‐LOX products, cysteinyl leukotrienes, after OGD/recovery. However, only caffeic acid inhibited OGD/recovery‐induced 5‐LOX translocation. OGD/recovery also increased reactive oxygen species (ROS), which was inhibited by caffeic acid only. Hydrogen peroxide, an exogenous ROS, evoked similar cell injury and 5‐LOX translocation, and the inhibitors had effects on the changes after H2O2similar to those after OGD/recovery. Both OGD/recovery and H2O2increased the phosphorylated p38 MAPK level, which was inhibited by caffeic acid and the ROS scavenger edaravone, but not by MK886 or zileuton. Moreover, SB203580 (a p38 MAPK inhibitor) and edaravone inhibited the cell injury and 5‐LOX translocation induced by OGD/recovery and H2O2. Thus, we conclude that OGD/recovery‐induced ischemic‐like injury induces 5‐LOX activation, which is mediated by oxidative stress through activating the p38 MAPK pathway. © 2008 Wiley‐Liss, Inc.
Molecular consequences of altered neuronal cholesterol biosynthesis
Authors: Korade Željka , Kenworthy Anne K. , Mirnics Károly 
Published: October 2008

AbstractThe first dedicated step in de novo cholesterol biosynthesis begins with formation of squalene and ends with the reduction of 7‐dehydrocholesterol by 7‐dehydrocholesterol reductase (Dhcr7) into cholesterol, which is an essential structural and signaling molecule. Mutations in the Dhcr7 gene lead to Smith‐Lemli‐Opitz syndrome (SLOS), which is characterized by developmental deformities, incomplete myelination, and mental retardation. To understand better the molecular consequences of Dhcr7 deficiency in neuronal tissue, we analyzed the effect of cholesterol deficiency on the transcriptome in Neuro2a cells. Transient down‐regulation of Dhcr7 by siRNA led to altered expression of multiple molecules that play critical roles in intracellular signaling or vesicular transport or are inserted into membrane rafts (e.g. Egr1, Snx, and Adam19). A similar down‐regulation was also observed in stable Dhrc7‐shRNA‐transfected cell lines, and the findings were verified by qPCR. Furthermore, we investigated the Dhcr7‐deficient and control cells for the expression of several critical genes involved in lipid biosynthesis. Among these, fatty acid synthase, sterol‐regulatory element binding protein 2, SREBF chaperone, site‐1 protease, and squalene synthase showed a significant down‐regulation, suggesting that, in a neuronal cell line, Dhcr7 is a potent regulator of lipid biosynthesis. Importantly, the gene expression changes were present in both lipid‐containing and cholesterol‐deficient media, suggesting that intrinsic cholesterol biosynthesis is necessary for normal neuronal function and cannot be supplemented from extrinsic sources. © 2008 Wiley‐Liss, Inc.
Activation and reversal of lipotoxicity in PC12 and rat cortical cells following exposure to palmitic acid
Authors: Almaguel Frankis G. , Liu Jo‐Wen , Pacheco Fabio J. , Casiano Carlos A. , De Leon Marino 
Published: October 2008

AbstractLipotoxicity involves a series of pathological cellular responses after exposure to elevated levels of fatty acids. This process may be detrimental to normal cellular homeostasis and cell viability. The present study shows that nerve growth factor‐differentiated PC12 cells (NGFDPC12) and rat cortical cells (RCC) exposed to high levels of palmitic acid (PA) exhibit significant lipotoxicity and death linked to an “augmented state of cellular oxidative stress” (ASCOS). The ASCOS response includes generation of reactive oxygen species (ROS), alterations in the mitochondrial transmembrane potential, and increase in the mRNA levels of key cell death/survival regulatory genes. The observed cell death was apoptotic based on nuclear morphology, caspase‐3 activation, and cleavage of lamin B and PARP. Quantitative real‐time PCR measurements showed that cells undergoing lipotoxicity exhibited an increase in the expression of the mRNAs encoding the cell death‐associated proteins BNIP3 and FAS receptor. Cotreatment of NGFDPC12 and RCC cells undergoing lipotoxicity with docosahexaenoic acid (DHA) and bovine serum albumin (BSA) significantly reduced cell death within the first 2 hr following the initial exposure to PA. The data suggest that lipotoxicity in NGFDPC12 and cortical neurons triggers a strong cell death apoptotic response. Results with NGFDPC12 cells suggest a linkage between induction of ASCOS and the apoptotic process and exhibit a temporal window that is sensitive to DHA and BSA interventions. © 2008 Wiley‐Liss, Inc.
Protective function of taurine in glutamate‐induced apoptosis in cultured neurons
Authors: Leon Rebecca , Wu Heng , Jin Ying , Wei Jianning , Buddhala Chandana , Prentice Howard , Wu Jang‐Yen 
Published: October 2008

AbstractPreviously, we showed that taurine protects neurons against glutamate‐induced excitotoxicity by inhibiting the glutamate‐induced increase of [Ca2+]i. In this study, we report that taurine prevents glutamate‐induced chromosomal condensation, indicating that taurine inhibits glutamate‐induced apoptosis. We found that Bcl‐2 was down‐regulated while Bax was up‐regulated by glutamate treatment, and these changes were prevented in the presence of taurine. We have also shown that taurine inhibits glutamate‐induced activation of calpain. Furthermore, calpastatin, a specific calpain inhibitor, also prevented glutamate‐induced cell death. Here we propose the mechanisms underlying glutamate‐induced apoptosis and taurine's inhibition of glutamate‐induced apoptosis to be as follows: glutamate stimulation induces [Ca2+]ielevation, which in turn activates calpain; activation of calpain leads to a reduction of Bcl‐2:Bax ratios; with decreased Bcl‐2:Bax ratios Bax homodimers form, Bax homodimerization, and translocation to the mitochondria result in the release of cytochromec; released cytochromecin turn activates a downstream caspase cascade leading to apoptosis. The antiapoptotic function of taurine is due to its inhibition of glutamate‐induced membrane depolarization. © 2008 Wiley‐Liss, Inc.
Sporadic obstructive hydrocephalus in Aqp4 null mice
Authors: Feng Xuechao , Papadopoulos Marios C. , Liu Jun , Li Lihua , Zhang Di , Zhang Hongguo , Verkman A. S. , Ma Tonghui 
Published: October 2008

AbstractAquaporin‐4 (Aqp4) is a water transport protein expressed in glia and ependymocytes in brain. We report here the unexpected occurrence of severe obstructive hydrocephalus in a random subset of Aqp4 knockout mice. Of 612 Aqp4 knockout mice produced by heterozygote–heterozygote or knockout–knockout breedings, 9.6% of offspring manifested progressive encephalomegaly. Encephalomegaly was never seen in wild‐type or Aqp4 heterozygous mice. Examination of the subset encephalomegalic mice revealed marked triventricular hydrocephalus (lateral ventricle size ∼500 mm3), elevated intracranial pressure (19 ± 3 vs. 6.1 ± 0.6 mm Hg), and death by age 6 weeks, with a median survival of 28 days. Intraventricular dye injection studies revealed total obstruction of the cerebral aqueduct. Evans blue extravasation studies indicated an intact blood–brain barrier in the hydrocephalic mice. Brain histology revealed reduced ventricular size and ependymocyte disorganization in some nonhydrocephalic Aqp4 null mice. Our studies establish Aqp4 deletion as a predisposing factor for the development of congenital obstructive hydrocephalus in mice. We suggest that AQP4 polymorphisms might also contribute to the development of aqueduct stenosis in humans. © 2008 Wiley‐Liss, Inc.
Balancing exploration and exploitation in alternative work arrangements: a multiple case study in the professional and management services industry
Authors: Litrico Jean‐Baptiste , Lee Mary Dean 
Published: October 2008

AbstractIn this inductive study we investigate the local context surrounding professionals choosing to work on a reduced‐load basis. We analyze qualitative data collected from key individuals (spouse, boss, co‐worker, and HR manager) composing a network around several professionals working reduced load in the professional and management services industry. We describe the interactions in this network using the concepts of exploration and exploitation in four contexts (organization, workgroup, individual, and family). We also identify three emergent patterns of cross‐level distribution of exploration and exploitation across contexts, labeled Solo Performance, Organic Fluid Adjustment, and Orchestrated Cooperation. Each of these patterns illuminates a specific form of interaction between the dynamics of exploration and exploitation across contexts. We examine the different outcomes of each pattern for the organization, the individual, and the family. Implications of the findings for theories of work‐family interaction, organizational learning, and the organization of work in the professional and management services industry are discussed. Copyright © 2008 John Wiley & Sons, Ltd.