bluuebunny/crossref_metadata_2025_split huggingface dataset:
Allogeneic hematopoietic stem cell transplantation as part of postremission therapy improves survival for adult patients with high‐risk acute lymphoblastic leukemia
Authors: Yanada Masamitsu , Matsuo Keitaro , Suzuki Takeshi , Naoe Tomoki 
Published: May 2006

AbstractBACKGROUNDThe prognosis for adult patients with acute lymphoblastic leukemia (ALL) remains unsatisfactory primarily because of the high incidence of recurrence. Therefore, optimal postremission therapy is a matter of vital concern. In particular, the clinical efficacy of allogeneic hematopoietic stem cell transplantation (HSCT) should be clarified.METHODSRigorous criteria were used to select 7 studies of adult ALL that prospectively assessed overall survival (OS) using natural randomization based on donor availability combined with intention‐to‐treat analyses. The authors then performed a metaanalysis to evaluate the role of allogeneic HSCT.RESULTSSeven studies that included 1274 patients were selected. A metaanalysis demonstrated that patients in the donor groups had significantly better survival than patients in the no‐donor groups (hazard ratio [HR], 1.29; 95% confidence interval [95% CI], 1.02–1.63 [P = .037]). When only high‐risk patients were included in the analysis, the superiority of the survival advantage was even greater (HR, 1.42; 95% CI, 1.06–1.90 [P = .019]). A meta‐regression analysis revealed that compliance with allogeneic HSCT showed a significant and positive correlation with survival (coefficient, 0.022; P<.01), suggesting that the greater the proportion of patients who actually received allogeneic HSCT, the better the survival of the donor group. No beneficial effects of autologous HSCT were observed.CONCLUSIONSThe current findings demonstrated that allogeneic HSCT improves the outcome of adult patients with high‐risk ALL. Although these analyses were based on abstracted data, the results indicated that allogeneic HSCT should be considered for such patients if a suitable donor is available. Cancer 2006. © 2006 American Cancer Society.
The influence of age and comorbidity on receiving radiotherapy as part of primary treatment for cancer in South Netherlands, 1995 to 2002
Authors: Vulto Ans J. C. M. , Lemmens Valery E. P. P. , Louwman Marieke W. J. , Janssen‐Heijnen Maryska L. G. , Poortmans Philip H. P. , Lybeert Marnix L. M. , Coebergh Jan Willem W. 
Published: May 2006

AbstractBACKGROUNDThe objective of this study was to study the influence of age and comorbidity on receiving radiotherapy (RT) in primary treatment of cancer.METHODSIn a population‐based setting, the authors calculated the proportion of irradiated patients within 6 months after they received a diagnosis of lung, rectal, breast, or prostate cancer or non‐Hodgkin lymphoma (n = 33,369 patients) according to age and comorbidity between 1995 and 2002. Logistic regression analysis was used to adjust for age, comorbidity, gender, and stage.RESULTSPatients with localized nonsmall cell lung cancer (NSCLC) ages 65 years to ≥80 years or with comorbid conditions received RT alone significantly more often compared with younger patients (ages 65‐79 years: odds ratio [OR], 3.4; age ≥80: OR, 12.0) and patients without comorbidities (1 comorbid condition: OR, 2.1; ≥2 comorbid conditions: OR, 2.4). This also applied to patients with nonlocalized NSCLC ages 65 years to 79 years compared with younger patients (OR, 1.4). RT was administered significantly less often to elderly patients with resected rectal cancers (ages 65‐79 years: OR, 0.7; age ≥80 years: OR, 0.4), patients age ≥80 years with breast cancer after undergoing conserving surgery (OR, 0.1), and patients age ≥80 years with clinical T1‐T3,N0,M0 prostate cancer age (OR, 0.1) compared with younger patients. Patients with breast cancer who underwent breast‐conserving surgery received RT significantly less often in the presence of comorbidities (1 comorbid condition: OR, 0.6; ≥2 comorbid conditions: OR, 0.4). Older patients with aggressive non‐Hodgkin lymphoma received only RT as treatment significantly more often compared with younger patients (OR, 3.4).CONCLUSIONSComorbidity and age did have influence over whether patients received RT, although, for most tumor types, age appeared to be a stronger predicting factor. Under treatment was observed among patients with breast cancer and rectal cancer. Cancer 2006. © 2006 American Cancer Society.
Effects of the dual 5 α‐reductase inhibitor dutasteride on apoptosis in primary cultures of prostate cancer epithelial cells and cell lines
Authors: Maria McCrohan Ann , Morrissey Colm , O'Keane Conor , Mulligan Niall , Watson Chanel , Smith James , Fitzpatrick John M. , Watson R. William G. 
Published: May 2006

AbstractBACKGROUNDThe profound reduction in serum dihydrotestosterone (DHT) observed with the dual 5 α‐reductase inhibitor (5ARI) dutasteride makes it an attractive agent for prostate cancer therapy. The objective of the current study was to determine whether dutasteride would induce apoptosis in a range of prostate epithelial cell lines and primary cultures.METHODSBoth human prostate androgen‐sensitive cell lines (PwR‐1E, PNT‐2, LNCaP, and PC3[AR2]) and an androgen‐independent cell line (PC‐3) were grown to confluence. Primary epithelial cells extracted from fresh prostate cancer radical prostatectomy specimens also were grown to confluence under optimal conditions. Total cellular protein was extracted to confirm cytokeratin 18 and antihuman α‐methylacyl‐CoA racemase (AMACR) expression of the primary cells. Apoptosis was assessed by propidium iodide DNA staining and flow cytometry after 24 hours of culture in from 0 μM to 10 μM of dutasteride.RESULTSDutasteride induced a dose‐dependent increase in apoptosis in the androgen‐sensitive prostate cell lines PwR‐1E, PNT‐2, and LNCaP and in the androgen receptor‐expressing PC3(AR2) cell line. However, there was no significant apoptosis noted in the parental PC‐3 cells. Of 16 primary epithelial cultures that were treated, 7 cultures were induced to undergo apoptosis, and 9 cultures were unresponsive. All primary cultures were positive for cytokeratin 18 expression, confirming their epithelial phenotype. Responder epithelial cells were positive for AMACR expression.CONCLUSIONSThe results of the current study confirmed that dutasteride differentially induced apoptosis in a subset of prostate cell lines and primary prostate epithelial cells. Understanding the cellular phenotype may indicate susceptible cells. Cancer 2006. © 2006 American Cancer Society.
Hartree–Fock Energy Partitioning in Terms of Hirshfeld Atoms
Authors: Mandado Marcos , Van Alsenoy Christian , Geerlings Paul , De Proft Frank , Mosquera Ricardo A. 
Published: May 2006

AbstractA Hirshfeld decomposition scheme of the Hartree–Fock total molecular energy into atomic energies is presented. The calculations are performed by direct numerical integration and the results are compared for a set of 28 molecules containing different kinds of atoms. The calculated atomic energies show a strong dependency on changes of atomic electron population and hybridization. Linear correlations are found between the energy and the population for H, these being related to the electronegativity of this atom and to the external potential created by the remaining atoms. The proposed energy partitioning scheme appears to be useful for studies such as proton acidity, the anomeric effect and group transferability, and allows atomic virial ratios to be obtained. Finally, the atomic potential energies are found to mimic trends based on exact expressions as well as trends displayed by molecular quantities, thus lending credibility to the partitioning scheme used.
Car–Parrinello Molecular Dynamics Study of the Blue‐Shifted F3CH⋅⋅⋅FCD3System in Liquid N2
Authors: Rodziewicz Pawel , Rutkowski Konstanty S. , Melikova Sonia M. , Koll Aleksander , Buda Francesco 
Published: May 2006

AbstractFluoroform, as confirmed by both experimental and theoretical studies, can participate in improper H‐bond formation, which is characterized by a noticeable increase in the fundamental stretching frequencyν(CH) (so‐called blue frequency shift), an irregular change of its integral intensity, and a CH bond contraction. A Car–Parrinello molecular dynamics simulation was performed for a complex formed by fluoroform (F3CH) and deuterated methyl fluoride (FCD3) in liquid nitrogen. Vibrational analysis based on the Fourier transform of the dipole moment autocorrelation function reproduces the blue shift of the fundamental stretching frequencyν(CH) and the decrease in the integral intensity. The dynamic contraction of the CH bond is also predicted. The stoichiometry of the solvated, blue‐shifted complexes and their residence times are examined.
Normal embryonic development and cardiac morphogenesis in mice with Wnt1‐Cre‐mediated deletion of connexin43
Authors: Kretz M. , Eckardt D. , Krüger O. , Kim J.S. , Maurer J. , Theis M. , van Rijen H.V. , Schorle H. , Willecke K. 
Published: May 2006

AbstractMice harboring a null mutation in the gap junction protein connexin43 (Cx43) die shortly after birth due to an obstruction of the right ventricular outflow tract of the heart. These hearts exhibit prominent pouches at the base of the pulmonary outlet, i.e., morphological abnormalities that were ascribed to Cx43‐deficiency in neural crest cells. In order to examine the Cx43 expression pattern in neural crest cells and derived tissues and to test whether neural crest‐specific deletion of Cx43 leads to the conotruncal defects seen in Cx43null mice, we ablated Cx43 using a Wnt1‐Cre transgene. Deletion of Cx43 was complete and occurred in neural crest cells as well as in neural crest‐derived tissues. Nevertheless, hearts of mice lacking Cx43 specifically in neural crest cells were indistinguishable from controls. Thus, the morphological heart abnormalities of Cx43 null mice are most likely not caused by lack of Cx43 in neural crest cells. genesis 44:269–276, 2006. © 2006 Wiley‐Liss, Inc.
Histamine modulates mast cell degranulation through an indirect mechanism in a model IgE‐mediated reaction
Authors: Carlos Daniela , Sá‐Nunes Anderson , de Paula Lúcia , Matias‐Peres Camila , Jamur Maria Célia , Oliver Constance , Serra Magda Fraguas , Martins Marco Aurélio , Faccioli Lúcia Helena 
Published: May 2006

AbstractHistamine is released in inflammatory reactions and exerts an immunoregulatory function on cells present in the microenvironment. In this study, we compared the effect of histamine on degranulation of mast cells derived from animals bearing a parasitic infection with those from uninfected animals. Peritoneal mast cells (PMC) were obtained 24 days after infection of Wistar rats withToxocara canis. The degree of degranulation was assessed either morphologically or by measuring the release of β‐hexosaminidase and TNF‐α. Non‐purified PMC or mast cells immunomagnetically purified with mAb AA4 were used. An increase in degranulation of non‐purified mast cells from infected animals was observed after incubation with histaminein vitroor when histamine was injected into the peritoneal cavity. When a purified mast cell population was used, this effect was no longer observed. Supernatants from spleen cells stimulated with histamine induced degranulation of purified mast cells, and again, this was potentiated with PMC from infected animals. However, when supernatants from peritoneal macrophages similarly stimulated were used, a reduction in the degranulation of PMC from infected animals was observed. Our results suggest that histamine may act as a regulator of mast cell degranulation, thus modulating inflammatory responses due to infection with certain parasites.
Sustained B7/CD28 interactions and resultant phosphatidylinositol 3‐kinase activity maintain G1→S phase transitions at an optimal rate
Authors: Bonnevier Jody L. , Yarke Cory A. , Mueller Daniel L. 
Published: May 2006

AbstractTwenty‐four hours of TCR engagement and CD28 costimulation was found sufficient to elicit an optimal rate of cell division over a 72‐h period only when a high concentration of IL‐2 was produced in the culture and remained readily available to the CD4+ T cells. The cell division response could be aborted following 24 h of stimulation by the simultaneous abrogation of IL‐2R signaling and the blockade of CD28 or TCR ligands. Biochemical and pharmacologic studies indicated that a phosphatidylinositol 3‐kinase‐Akt signaling cascade costimulated by the TCR and CD28 maintained the blasting cell division rate at a maximal level beyond 24 h even when IL‐2 was withdrawn, neutralized, or exhausted. These data show that CD4+ T cells remain sensitive to antigens (Ag) and costimulatory signals throughout the clonal expansion response. Furthermore, only those T cells that perceive the presence of a continued threat in the form of Ag/MHC complexes and B7 costimulatory ligands or a high concentration of a growth factor are directed to remain in cell cycle.
Revisiting the specificity of the MHC class II transactivator CIITA in vivo
Authors: Otten Luc A. , LeibundGut‐Landmann Salomé , Huarte Joachim , Kos‐Braun Isabelle C. , Lavanchy Christine , Barras Emmanuèle , Borisch Bettina , Steimle Viktor , Acha‐Orbea Hans , Reith Walter 
Published: May 2006

AbstractCIITA is a master regulatory factor for the expression of MHC class II (MHC‐II) and accessory genes involved in Ag presentation. It has recently been suggested that CIITA also regulates numerous other genes having diverse functions within and outside the immune system. To determine whether these genes are indeed relevant targets of CIITA in vivo, we studied their expression in CIITA‐transgenic and CIITA‐deficient mice. In contrast to the decisive control of MHC‐II and related genes by CIITA, nine putative non‐MHC target genes (Eif3s2, Kpna6, Tap1, Yars, Col1a2, Ctse, Ptprr, Tnfsf6 and Plxna1) were found to be CIITA independent in all cell types examined. Two other target genes, encoding IL‐4 and IFN‐γ, were indeed found to be up‐ and down‐regulated, respectively, in CIITA‐transgenic CD4+ T cells. However, there was no correlation between MHC‐II expression and this Th2 bias at the level of individual transgenic T cells, indicating an indirect control by CIITA. These results show that MHC‐II‐restricted Ag presentation, and its indirect influences on T cells, remains the only pathway under direct control by CIITA in vivo. They also imply that precisely regulated MHC‐II expression is essential for maintaining a proper Th1‐Th2 balance.
Macrophages require distinct arginine catabolism and transport systems for proliferation and for activation
Authors: Yeramian Andrée , Martin Lorena , Arpa Luis , Bertran Joan , Soler Concepció , McLeod Carol , Modolell Manuel , Palacín Manuel , Lloberas Jorge , Celada Antonio 
Published: May 2006

AbstractIn murine macrophages, as a result of arginine catabolism during activation, citruline is produced under the effect of IFN‐γ and LPS, and ornithine and polyamines by IL‐4 and IL‐10. For proliferation, arginine is required from the extracellular medium and is used for protein synthesis. During activation, most arginine (>95% in 6 h) was metabolized, while under proliferation only half was incorporated into proteins. Under basal conditions, this amino acid was preferentially transported by y+L activity. During activation, arginine transport increased drastically (4–5‐fold) through y+ cationic amino acid transporter (CAT) activity. By contrast, M‐CSF induced only a modest increase in uptake (0.5‐fold). The increase in arginine transport during activation, but not proliferation, was mediated by the SLC7A2/Cat2 gene. SLC7A1/Cat1 is constitutively expressed, and is not modified by proliferating or activating agents. M‐CSF‐dependent proliferation was not affected in the macrophages of SLC7A2 knockout mice; however, these cells showed a drastic reduction in the production of citruline or ornithine and polyamines during activation. The data show that a large increase in a specific transport system (CAT2) is necessary for activation‐induced arginine metabolism, while arginine is in excess for the requirements of proliferation and a modest increase in transport occurs.
An absence of reactive oxygen species improves the resolution of lung influenza infection
Authors: Snelgrove Robert J. , Edwards Lorna , Rae Aaron J. , Hussell Tracy 
Published: May 2006

AbstractThree influenza virus pandemics occurred in the last century, in 1918 killing 40–50 million people. In the absence of strain‐specific vaccines, with potential resistance to antivirals and the threat of an imminent pandemic, strategies that alleviate symptoms are a priority. Reactive oxygen species are potent antimicrobial agents but cause immunopathology when produced in excess. Mice lacking a functional phagocyte NADPH oxidase (Cybb tm1 mice) or treated with the metalloporphyrin antioxidant manganese (III) tetrakis (N‐ethyl pyridinium‐2‐yl) porpyhrin (MnTE‐2‐PyP) show heightened inflammatory infiltrates in their airways in response to pulmonary influenza infection, with augmented macrophage populations and a Th1‐skewed T cell infiltrate. Underlying this exuberant macrophage response was a significant reduction in apoptosis and down‐regulation of the myeloid inhibitory molecule CD200. Both, Cybb tm1 and MnTE‐2‐PyP‐treated mice exhibited a reduced influenza titer in the lung parenchyma. Inflammatory infiltrate into the lung parenchyma was markedly reduced and lung function significantly improved. Manipulation of the homeostatic control of myeloid cells by inflammatory mediators therefore represents a novel therapeutic strategy in the treatment of influenza virus infection.
TLR4, TLR9 and MyD88 are not requiredfor the positive selection of autoreactive B cells intothe primary repertoire
Authors: Silver Karlee , Ferry Helen , Crockford Tanya , Cornall Richard J. 
Published: May 2006

AbstractToll‐like receptors (TLR) have been shown to play an essential role in the generation of autoantibodies in mouse models of autoimmunity, but the timing and context of these effects are poorly understood. One hypothesis is that TLR ligands assist in the positive selection of self‐reactive B cells into the primary repertoire and, in this way, distinguish between immunogenic and tolerogenic forms of self‐antigen. To explore this idea we generated hen egg lysozyme‐specific immunoglobulin (IgHEL) and isotype class‐switching anti‐HEL mice deficient in MyD88, TLR4 or TLR9 signalling and studied B cell development and autoantibody secretion in the presence or absence of an intracellular form of self‐antigen HEL that positively selects B1 cells. Our findings show that TLR4, TLR9 and MyD88 are not required for the positive selection of autoreactive B cells in the primary B cell repertoire, nor is MyD88 required for the generation of isotype‐switched antibodies in the absence of antigen. These results suggest that the significant effects of TLR on autoimmunity occur in the established repertoire and not during B cell development.
Spatial‐temporal model for ambient air pollutants in the state of Kuwait
Authors: Al‐Awadhi Fahimah A. , Al‐Awadhi Shafiqah A. 
Published: May 2006

AbstractIn this paper we consider dynamic Bayesian models for four different pollutants: nitric oxide(NO), carbon monoxide(CO), sulphur dioxide(SO2) and non‐methane hydrocarbon (NCH4) recorded daily in six different stations in Kuwait from 1999 to 2002. The structure of the models depends on time, space and pollutants dependencies. The approach strives to incorporate the uncertainty of the covariance structure into simulated models and final inference; therefore, hierarchical Bayesian model is applied. Association between level of pollutants and different meteorological variables, such as wind speed, wind directions, temperature and humidity are considered. The models will decompose into two main components: a deterministic part to represent the observed components term and a stochastic term to represent the unobservable components. Our analysis will start with basic model and gradually increase its complexity. At each stage the efficiency of the model will be measured. The resulting models subsequently are tested by comparing the output terms and by comparing and the predictions with the real observations. Copyright © 2006 John Wiley & Sons, Ltd.
BglII‐based panhandle and reverse panhandle PCR approaches increase capability for cloning der(II) and der(other) genomic breakpoint junctions of MLL translocations
Authors: Robinson Blaine W. , Slater Diana J. , Felix Carolyn A. 
Published: May 2006

AbstractPanhandle PCR techniques to amplify known sequence flanked by unknown sequence have been useful for MLL genomic breakpoint junctions and fusion transcripts because MLL has a large number of partner genes. However, genomic panhandle PCR approaches are impeded when the restriction fragment that contains the breakpoint junction is too large to amplify. We devised new panhandle PCR approaches for MLL genomic breakpoint junctions that create the template from BglII restriction fragments by attaching MLL sequence to a BglII site in the partner gene. This leads to the annealing of MLL and its complement in the handle and creates an intrastrand loop containing the breakpoint junction sequence for amplification with primers all from MLL. BglII panhandle PCR for der(11) breakpoint junctions was accomplished by ligating a phosphorylated oligonucleotide containing a BglII overhang and sequence complementary to MLL exon 7 to the 3′ ends of BglII digested DNA, and forming the template from the sense strand of DNA. In BglII reverse panhandle PCR for der(other) breakpoint junctions, a phosphorylated oligonucleotide containing a BglII overhang and the complement of antisense sequence in MLL exon 10 was ligated to the 3′ ends of BglII digested DNA, and the template was formed from the antisense strand of DNA. These approaches amplified 5′‐MLL‐MLLT4‐3′ and 5′‐AFF1‐MLL‐3′ breakpoint junctions. The former is significant because few t(6;11) genomic breakpoint junctions have been sequenced. BglII panhandle PCR approaches increase the possibilities for cloning MLL genomic breakpoint junctions where there is heterogeneity in partner genes and breakpoint locations. © 2006 Wiley‐Liss, Inc.