bluuebunny/crossref_metadata_2025_split huggingface dataset:
HRQoL changes, mood disorders and satisfaction after treatment in an unselected population of patients with lung cancer
Authors: Rolke Heidi Berg , Bakke Per Sigvald , Gallefoss Frode 
Published: November 2009

AbstractObjectives:  This study intended to explore the impact of the first treatment modality on health‐related quality of life (HRQoL), mood disorders and mastery in an unselected population of patients with primary lung cancer and to judge patient satisfaction with treatment.Materials and Methods:  An unselected group of 479 patients with newly diagnosed lung cancer in Southern Norway (Agder counties) were included prospectively from June 2002 to June 2005, collecting data on histology, treatment options, HRQoL, mood disorders and mastery at baseline as well as satisfaction with treatment, and changes in HRQoL and mood disorders after finishing the first treatment modality.Results:  After finishing the first treatment modality, patients experienced a worsening of nine HRQoL parameters and an improvement in one. Patients in good performance status experienced reduced physical and role function, and if in reduced performance, improved emotional and role function. Patients with mood disorders experienced reduced anxiety and depression, anxious patients experienced reduced neuropathies, and depressed patients experienced improved social functioning and appetite. Half of the patients treated actively were definitely positive to repeat the same treatment again compared with only 15% in the best supportive care group.Surgery was associated with reduced role function and increased dyspnoea, radiation was associated with increased fatigue, and chemotherapy in small cell lung cancer (SCLC), to a larger extent, was associated with alopecia than in non‐SCLC (NSCLC).Conclusion:  The development of many HRQoL parameters after the first treatment modality in an unselected population of patients with primary lung cancer seemed, at large, well correlated to general disease progression and to well‐known treatment side effects. However, reduced role function after lung surgery, and reduced anxiety and depression in patients with mood disorders at baseline might be surprising. Patient satisfaction with treatment was surprisingly good. Several findings in this study may help clinicians to improve their handling of patients with lung cancer.Please cite this paper as: Rolke HB, Bakke PS and Gallefoss F. HRQoL changes, mood disorders and satisfaction after treatment in an unselected population of patients with lung cancer. The Clinical Respiratory Journal 2010; 4: 168–175.
Neural contrast sensitivity calculated from measured total contrast sensitivity and modulation transfer function
Authors: Michael Ralph , Guevara Osvaldo , de la Paz Maria , Alvarez de Toledo Juan , Barraquer Rafael I. 
Published: November 2009

Abstract.Purpose:  To test the feasibility of calculating neural contrast sensitivity function (neural CSF) from conventionally measured total contrast sensitivity function (total CSF) and measured modulation transfer function (MTF). Neural CSF considers the retina and the brain, whereas total CSF considers the optical eye media, the retina and the brain together.Methods:  We studied three groups comprising nine eyes each: one group with normal ocular optics but retinal alterations (mild diabetic retinopathy), one with altered ocular optics and normal retina (keratoconus), and a normal control group.Results:  Total CSF in the keratoconus and retinopathy groups was significantly lower compared to the control group. Modulation transfer function for keratoconus was lower, and in the retinopathy group was similar to that of the control group. Calculated neural CSF in the diabetes mellitus group was lower than in the control group whereas in the keratoconus group it was similar to that of the control group, with overestimations for some keratoconus cases.Conclusion:  It is possible to calculate a meaningful neural CSF from measured total CSF and MTF data. The neural CSF represents a CSF adjusted for optical aberrations. This would allow comparison of the neural component of visual function in eyes with different optical aberrations.
Placebo Effect in Canine Epilepsy Trials
Authors: Muñana K.R. , Zhang D. , Patterson E.E. 
Published: November 2009

Background:The placebo effect is a well‐recognized phenomenon in human medicine; in contrast, little information exists on the effect of placebo administration in veterinary patients.Hypothesis:Nonpharmacologic therapeutic effects play a role in response rates identified in canine epilepsy trials.Animals:Thirty‐four dogs with epilepsy.Methods:Meta‐analysis of the 3 known prospective, placebo‐controlled canine epilepsy trials. The number of seizures per week was compiled for each dog throughout their participation in the trial. Log‐linear models were developed to evaluate seizure frequency during treatment and placebo relative to baseline.Results:Twenty‐two of 28 (79%) dogs in the study that received placebo demonstrated a decrease in seizure frequency compared with baseline, and 8 (29%) could be considered responders, with a 50% or greater reduction in seizures. For the 3 trials evaluated, the average reduction in seizures during placebo administration relative to baseline was 26% (P= .0018), 29% (P= .17), and 46% (P= .01).Conclusions and Clinical Importance:A positive response to placebo administration, manifesting as a decrease in seizure frequency, can be observed in epileptic dogs. This is of importance when evaluating open label studies in dogs that aim to assess efficacy of antiepileptic drugs, as the reported results might be overstated. Findings from this study highlight the need for more placebo‐controlled trials in veterinary medicine.
Whole Blood Manganese Concentrations in Dogs with Congenital Portosystemic Shunts
Authors: Gow A.G. , Marques A.I.C. , Yool D.A. , Duncan A. , Mellanby R.J. 
Published: November 2009

Background: Manganese (Mn) is an essential mineral that is a cofactor for many enzymes required in the synthesis of proteins, carbohydrates, and lipids. Because hepatic clearance is essential in Mn homeostasis, conditions in humans resulting in hepatic insufficiency including cirrhosis and both acquired and congenital portosystemic shunting have been reported to result in increased blood Mn concentrations and increased Mn content in the central nervous system. Because Mn toxicity causes neurologic disturbances, increased Mn concentrations have been implicated in the pathogenesis of hepatic encephalopathy.Hypotheses: Dogs with congenital portosystemic shunts (cPSS) have significantly higher whole blood Mn concentrations than do healthy dogs or those with nonhepatic illnesses.Animals: Eighteen dogs with cPSS, 26 dogs with nonhepatic illnesses, and 14 healthy dogs.Methods: Whole blood Mn was measured by graphite furnace atomic absorption spectrometry. The diagnosis of cPSS was made by ultrasonography or during celiotomy either by visual inspection of a shunting vessel or portovenography.Results: Dogs with a cPSS had significantly higher whole blood Mn concentrations than did healthy dogs and dogs with nonhepatic illnesses. Whole blood Mn concentrations were not significantly different between healthy dogs and dogs with nonhepatic illnesses.Conclusion and Clinical Importance: Dogs with a cPSS have significantly increased whole blood Mn concentrations. Additional studies are warranted to investigate the role of Mn in cPSS‐associated hepatic encephalopathy.
Antithrombotic Effect of Enoxaparin in Clinically Healthy Cats: A Venous Stasis Model
Authors: Van De Wiele C.M. , Hogan D.F. , Green H.W. , Sederquist K.D. 
Published: November 2009

Background:Systemic arterial thromboembolic events are a serious complication of cardiac disease in cats.Objectives:To determine if enoxaparin induces an antithrombotic effect in cats at a dosage of 1 mg/kg SC q12h and if this antithrombotic effect is predicted by anti‐Xa activity.Animals:Fourteen clinically healthy cats were divided into 3 groups: control (4 cats), treated and assessed at 4 hours (5 cats), and treated and assessed at 12 hours (5 cats).Methods:A venous stasis model was used and the extent of thrombus formation estimated by measuring thrombus weight and accretion of125I‐fibrinogen. Plasma anti‐Xa activity was measured in treated cats.Results:There was a significant reduction in thrombus formation in the 4 h group compared with control (median weight, 0.000 versus 0.565 mg/mm,P< .01; median %125I‐fibrinogen accretion, 0.0 versus 42.0%,P< .01). There was a reduction in thrombus formation in the 12 h group (median weight, 0.006 mg/mm,P= .09; median %125I‐fibrinogen accretion, 3.83%,P= .09) but this reduction was not significant. The median percent thrombus inhibition for treated cats was 100.0% at 4 hours and 91.4% at 12 hours. Plasma anti‐Xa activity was not significantly correlated with thrombus formation.Conclusions and Clinical Importance:This pilot study demonstrates that enoxaparin, when administered at a dosage of 1 mg/kg SC q12h, produces an antithrombotic effect in a venous statsis model in clinically healthy cats. Furthermore, this study demonstrates that anti‐Xa activity is a poor predictor of enoxaparin's antithrombotic effect.
Performance Analysis of an Air Drier for a Liquid Dehumidifier Solar
Air Conditioning System
Authors: Queiroz A. G. , Orlando A. F. , Saboya F. E. M. 
Published: November 2009

Abstract
A model was developed for calculating the operating conditions of a non-adiabatic liquid dehumidifier used in solar air conditioning systems. In the experimental facility used for obtaining the data, air and triethylene glycol circulate countercurrently outside staggered copper tubes which are the filling of an absorption tower. Water flows inside the copper tubes, thus cooling the whole system and increasing the mass transfer potential for drying air. The methodology for calculating the mass transfer coefficient is based on the Merkel integral approach, taking into account the lowering of the water vapor pressure in equilibrium with the water glycol solution.
Influence of Reynolds Number on Performance Modeling of Horizontal
Axis Wind Rotors
Authors: Musial W. D. , Cromack D. E. 
Published: November 2009

Abstract
This paper investigates the influence of Reynolds number on performance modeling of horizontal axis wind rotors. A procedure for accounting for Reynolds number effects on airfoil section models was developed and implemented for NACA 0012 and NACA 4415 profiles; both of these models is valid through angles of attack up to 90 deg and for Reynolds numbers ranging from 4 × 104 to 3 × 106. These models were incorporated into both a lifting line computer code, LL200R, adapted for this report. This enabled greater certainty to be obtained in evaluating theoretical performance codes with respect to actual data, as well as providing a means by which a parametric analysis of the relative effects of Re changes on rotor performance to be performed. The use of low Reynolds number section data was found to significantly lower the predicted values of power coefficient, particularly at off-design tip-speed-ratios. For symmetrical airfoils, this effect on performance was only significant for low tip-speed-ratios, while cambered airfoils were affected more uniformly at all operating conditions. Changes in performance were induced by parametric variations of wind speed, rotor scale, and rotor generating mode using the Reynolds number dependent section models. Results show that wind speed variations are more significant for smaller rotors at lower wind-speeds, and section models represented at only a single Reynolds number are more suitable for the analysis of constant RPM rotors.
Fixed Points for Pseudocontractive Mappings on Unbounded Domains
Authors: García-Falset Jesús , Llorens-Fuster E 
Published: November 2009

AbstractWe give some fixed point results for pseudocontractive mappings on nonbounded domains which allow us to obtain generalizations of recent fixed point theorems of Penot, Isac, and Németh. An application to integral equations is given.
Autophagy Is Activated by TGF-β and Potentiates TGF-β–Mediated Growth Inhibition in Human Hepatocellular Carcinoma Cells
Authors: Kiyono Kunihiko , Suzuki Hiroshi I. , Matsuyama Hironori , Morishita Yasuyuki , Komuro Akiyoshi , Kano Mitsunobu R. , Sugimoto Koichi , Miyazono Kohei 
Published: November 2009

Abstract
Transforming growth factor-β (TGF-β) is a multifunctional cytokine that regulates cell growth, differentiation, and apoptosis of various types of cells. Autophagy is emerging as a critical response of normal and cancer cells to environmental changes, but the relationship between TGF-β signaling and autophagy has been poorly understood. Here, we showed that TGF-β activates autophagy in human hepatocellular carcinoma cell lines. TGF-β induced accumulation of autophagosomes and conversion of microtubule-associated protein 1 light chain 3 and enhanced the degradation rate of long-lived proteins. TGF-β increased the mRNA expression levels of BECLIN1, ATG5, ATG7, and death-associated protein kinase (DAPK). Knockdown of Smad2/3, Smad4, or DAPK, or inhibition of c-Jun NH2-terminal kinase, attenuated TGF-β–induced autophagy, indicating the involvement of both Smad and non-Smad pathway(s). TGF-β activated autophagy earlier than execution of apoptosis (6-12 versus 48 h), and reduction of autophagy genes by small interfering RNA attenuated TGF-β–mediated growth inhibition and induction of proapoptotic genes Bim and Bmf, suggesting the contribution of autophagy pathway to the growth-inhibitory effect of TGF-β. Additionally, TGF-β also induced autophagy in some mammary carcinoma cells, including MDA-MB-231 cells. These findings show that TGF-β signaling pathway activates autophagy in certain human cancer cells and that induction of autophagy is a novel aspect of biological functions of TGF-β. [Cancer Res 2009;69(23):8844–52]
Dynamic Gene Expression Analysis Links Melanocyte Growth Arrest with Nevogenesis
Authors: Yang Guang , Thieu Khanh , Tsai Kenneth Y. , Piris Adriano , Udayakumar Durga , Njauw Ching-Ni Jenny , Ramoni Marco F. , Tsao Hensin 
Published: November 2009

Abstract
Like all primary cells in vitro, normal human melanocytes exhibit a physiologic decay in proliferative potential as it transitions to a growth-arrested state. The underlying transcriptional program(s) that regulate this phenotypic change is largely unknown. To identify molecular determinants of this process, we performed a Bayesian-based dynamic gene expression analysis on primary melanocytes undergoing proliferative arrest. This analysis revealed several related clusters whose expression behavior correlated with the melanocyte growth kinetics; we designated these clusters the melanocyte growth arrest program (MGAP). These MGAP genes were preferentially represented in benign melanocytic nevi over melanomas and selectively mapped to the hepatocyte fibrosis pathway. This transcriptional relationship between melanocyte growth stasis, nevus biology, and fibrogenic signaling was further validated in vivo by the demonstration of strong pericellular collagen deposition within benign nevi but not melanomas. Taken together, our study provides a novel view of fibroplasia in both melanocyte biology and nevogenesis. [Cancer Res 2009;69(23):9029–37]
De-N-acetyl GM3 Promotes Melanoma Cell Migration and Invasion through Urokinase Plasminogen Activator Receptor Signaling–Dependent MMP-2 Activation
Authors: Liu Ji-Wei , Sun Ping , Yan Qiu , Paller Amy S. , Gerami Pedram , Ho Nancy , Vashi Neelam , Le Poole I. Caroline , Wang Xiao-qi 
Published: November 2009

Abstract
We have recently discovered that de-N-acetyl GM3 [NeuNH2LacCer, d-GM3], a derivative of ganglioside GM3, is specifically expressed in metastatic tumor cells and that its expression correlates with an enhanced metastatic phenotype. Although the classic N-acetylated form of GM3 (NeuAcLacCer, c-GM3) is found in both normal and tumor cells, metastatic tumor cells (but not other cells) predominantly express d-GM3 (82–95% of total GM3). d-GM3 expression is mainly found in metastatic melanomas, but not in benign nevi or the majority of primary melanomas. Using metastatic (d-GM3–positive) and poorly invasive (d-GM3–negative) human melanoma cell lines, we found that d-GM3 stimulates cell migration and invasion by increasing the expression and activation of urokinase-like plasminogen activator (uPA). Further studies showed that d-GM3 activates matrix metalloproteinase-2 (MMP-2), but not MMP-9, when uPA receptor signaling is activated. These results implicate d-GM3 as a specific marker for metastatic melanoma and a novel therapeutic target for neoplastic diseases. [Cancer Res 2009;69(22):8662–9]
Targeted Disruption of theS1P2Sphingosine 1-Phosphate Receptor Gene Leads to Diffuse Large B-Cell Lymphoma Formation
Authors: Cattoretti Giorgio , Mandelbaum Jonathan , Lee Nancy , Chaves Alicia H. , Mahler Ashley M. , Chadburn Amy , Dalla-Favera Riccardo , Pasqualucci Laura , MacLennan A. John 
Published: November 2009

AbstractS1P2 sphingosine 1-phosphate receptor signaling can regulate proliferation, survival, morphology, and migration in many cell types in vitro. Here, we report that S1P2−/− mice develop clonal B-cell lymphomas with age, such that approximately half of the animals display this neoplasm by 1.5 to 2 years of age. Histologic, immunophenotypic, and molecular analyses revealed a uniform tumor phenotype with features of germinal center (GC)–derived diffuse large B-cell lymphoma (DLBCL). Tumor formation was preceded by increases in GC B cells and CD69+ T cells, as well as an increased formation of spontaneous GCs, suggesting that S1P2 loss may promote lymphomagenesis in part by disrupting GC B-cells homeostasis. With the sole exception of rare lung tumors, the effect of S1P2 gene disruption is remarkably restricted to DLBCL. In humans, 28 of 106 (26%) DLBCL samples were found to harbor multiple somatic mutations in the 5′ sequences of the S1P2 gene. Mutations displayed features resembling those generated by the IgV-associated somatic hypermutation mechanism, but were not detected at significant levels in normal GC B cells, indicating a tumor-associated aberrant function. Collectively, our data suggest that S1P2 signaling may play a critical role in suppressing DLBCL formation in vivo. The high incidence of DLBCL in S1P2−/− mice, its onset at old age, and the relative lack of other neoplasms identify these mice as a novel, and potentially valuable, model for this highly prevalent and aggressive human malignancy. [Cancer Res 2009;69(22):8686–92]
Persistence of Betapapillomavirus Infections as a Risk Factor for Actinic Keratoses, Precursor to Cutaneous Squamous Cell Carcinoma
Authors: Plasmeijer Elsemieke I. , Neale Rachel E. , de Koning Maurits N.C. , Quint Wim G.V. , McBride Penelope , Feltkamp Mariet C.W. , Green Adele C. 
Published: November 2009

Abstract
Human papillomaviruses from the β genus (βPV) are a possible cause of cutaneous squamous cell carcinoma (SCC). We assessed the extent to which βPV infections persisted long-term in a subtropical Australian community and whether βPV persistence is positively associated with actinic keratoses, precursor for SCC. Eyebrow hairs were collected from 171 participants of the community-based Nambour Skin Cancer Study in 1996 and 2003. Hair samples were tested for the presence of DNA from 25 different βPV types and assessed in relation to actinic keratosis presence in 2007. In 1996, a total of 413 βPV infections were found in 73% of participants, increasing to 490 infections among 85% in 2003. Of the total βPV infections detected, 211 (30%) were found to persist. Age was significantly associated with βPV persistence: those ages &gt;60 years had 1.5-fold (95% confidence interval, 1.1-1.9) increased risk of type-specific viral persistence than those ages &lt;40 years. After accounting for actinic keratoses at baseline, persistence of βPV DNA resulted in a 1.4-fold (95% confidence interval, 1.0-1.9) increase in risk of having actinic keratoses on the face in 2007. In conclusion, persistent βPV infections in this population were associated with an increased occurrence of actinic keratosis. Additional studies are needed to determine the possible association of βPV persistence with SCC. [Cancer Res 2009;69(23):8926–31]
Calcineurin Inhibitors Activate the Proto-Oncogene Ras and Promote Protumorigenic Signals in Renal Cancer Cells
Authors: Datta Dipak , Contreras Alan G. , Basu Aninda , Dormond Olivier , Flynn Evelyn , Briscoe David M. , Pal Soumitro 
Published: November 2009

Abstract
The development of cancer is a major problem in immunosuppressed patients, particularly after solid organ transplantation. We have recently shown that calcineurin inhibitors (CNI) used to treat transplant patients may play a critical role in the rapid progression of renal cancer. To examine the intracellular signaling events for CNI-mediated direct tumorigenic pathway(s), we studied the effect of CNI on the activation of proto-oncogenic Ras in human normal renal epithelial cells (REC) and renal cancer cells (786-0 and Caki-1). We found that CNI treatment significantly increased the level of activated GTP-bound form of Ras in these cells. In addition, CNI induced the association of Ras with one of its effector molecules, Raf, but not with Rho and phosphatidylinositol 3-kinase; CNI treatment also promoted the phosphorylation of the Raf kinase inhibitory protein and the downregulation of carabin, all of which may lead to the activation of the Ras-Raf pathway. Blockade of this pathway through either pharmacologic inhibitors or gene-specific small interfering RNA significantly inhibited CNI-mediated augmented proliferation of renal cancer cells. Finally, it was observed that CNI treatment increased the growth of human renal tumors in vivo, and the Ras-Raf pathway is significantly activated in the tumor tissues of CNI-treated mice. Together, targeting the Ras-Raf pathway may prevent the development/progression of renal cancer in CNI-treated patients. [Cancer Res 2009;69(23):8902–9]
Improved Expression and Reactivity of Transduced Tumor-Specific TCRs in Human Lymphocytes by Specific Silencing of Endogenous TCR
Authors: Okamoto Sachiko , Mineno Junichi , Ikeda Hiroaki , Fujiwara Hiroshi , Yasukawa Masaki , Shiku Hiroshi , Kato Ikunoshin 
Published: November 2009

Abstract
Adoptive T-cell therapy using lymphocytes genetically engineered to express tumor antigen-specific TCRs is an attractive strategy for treating patients with malignancies. However, there are potential drawbacks to this strategy: mispairing of the introduced TCR α/β chains with the endogenous TCR subunits and competition of CD3 molecules between the introduced and endogenous TCRs can impair cell surface expression of the transduced TCR, resulting in insufficient function and potential generation of autoreactive T cells. In addition, the risk of tumor development following the infusion of cells with aberrant vector insertion sites increases with the vector copy number in the transduced cells. In this study, we developed retroviral vectors encoding both small interfering RNA constructs that specifically down-regulate endogenous TCR and a codon-optimized, small interfering RNA–resistant TCR specific for the human tumor antigens MAGE-A4 or WT1. At low copy numbers of the integrated vector, the transduced human lymphocytes exhibited high surface expression of the introduced tumor-specific TCR and reduced expression of endogenous TCRs. In consequence, the vector-transduced lymphocytes showed enhanced cytotoxic activity against antigen-expressing tumor cells. Therefore, our novel TCR gene therapy may open a new gate for effective immunotherapy in cancer patients. [Cancer Res 2009;69(23):9003–11]