bluuebunny/crossref_metadata_2025_split huggingface dataset:
Discrepancy of Interdecadal Changes in the Asian Region among the NCEP–NCAR Reanalysis, Objective Analyses, and Observations
Authors: Wu Renguang , Kinter J. L. , Kirtman B. P. 
Published: September 2005

Abstract
This study compares decadal means and interdecadal changes of surface and sea level pressures, tropospheric heights, and winds in the National Centers for Environmental Prediction–National Center for Atmospheric Research (NCEP–NCAR) reanalysis with objective analyses and observations. It is found that over Asia the NCEP–NCAR reanalysis pressures and heights are systematically lower than objective analyses and observations before the late 1970s. The magnitude of the differences changes from one decade to another and shows obvious seasonal dependence. The nonuniform spatial distribution of pressure and height differences is consistent with the discrepancy in lower-level meridional winds along the east Asian coast. The seasonal dependence of pressure differences affects the strength of the seasonal cycle over Asia. More importantly, large changes in the discrepancies from one decade to another lead to inconsistent interdecadal changes between the reanalysis and objective analyses or observations in the Asian region. While the reanalysis displays a large increase of pressure around 1977 and in the mid-1960s and an obvious decrease in the late 1950s, the changes are small in objective analyses and observations. Inconsistent interdecadal changes are also present in tropospheric heights and winds. The results indicate that the reanalysis may overestimate interdecadal changes over Asia. This calls for caution in utilizing the reanalysis output to study the interdecadal variability or the interannual variability without removal of interdecadal variations in the Asian region.
Total body irradiation selectively induces murine hematopoietic stem cell senescence
Authors: Wang Yong , Schulte Bradley A. , LaRue Amanda C. , Ogawa Makio , Zhou Daohong 
Published: September 2005

Abstract
Exposure to ionizing radiation (IR) and certain chemotherapeutic agents not only causes acute bone marrow (BM) suppression but also leads to long-term residual hematopoietic injury. This latter effect has been attributed to damage to hematopoietic stem cell (HSC) self-renewal. Using a mouse model, we investigated whether IR induces senescence in HSCs, as induction of HSC senescence can lead to the defect in HSC self-renewal. It was found that exposure of C57BL/6 mice to a sublethal dose (6.5 Gy) of total body irradiation (TBI) resulted in a sustained quantitative and qualitative reduction of LKS+ HSCs. In addition, LKS+ HSCs from irradiated mice exhibited an increased expression of the 2 commonly used biomarkers of cellular senescence, p16Ink4a and SA-β-gal. In contrast, no such changes were observed in irradiated LKS- hematopoietic progenitor cells. These results provide the first direct evidence demonstrating that IR exposure can selectively induce HSC senescence. Of interest, the induction of HSC senescence was associated with a prolonged elevation of p21Cip1/Waf1, p19Arf, and p16Ink4a mRNA expression, while the expression of p27Kip1 and p18Ink4c mRNA was not increased following TBI. This suggests that p21Cip1/Waf1, p19Arf, and p16Ink4a may play an important role in IR-induced senescence in HSCs.
FDG-PET after two cycles of chemotherapy predicts treatment failure and progression-free survival in Hodgkin lymphoma
Authors: Hutchings Martin , Loft Annika , Hansen Mads , Pedersen Lars Møller , Buhl Thora , Jurlander Jesper , Buus Simon , Keiding Susanne , D'Amore Francesco , Boesen Anne-Marie , Berthelsen Anne Kiil , Specht Lena 
Published: September 2005

Abstract
Risk-adapted lymphoma treatment requires early and accurate assessment of prognosis. This investigation prospectively assessed the value of positron emission tomography with 2-[18F]fluoro-2-deoxy-D-glucose (FDG-PET) after two cycles of chemotherapy for prediction of progression-free survival (PFS) and overall survival (OS) in Hodgkin lymphoma (HL). Seventy-seven consecutive, newly diagnosed patients underwent FDG-PET at staging, after two and four cycles of chemotherapy, and after completion of chemotherapy. Median follow-up was 23 months. After two cycles of chemotherapy, 61 patients had negative FDG-PET scans and 16 patients had positive scans. Eleven of 16 FDG-PET–positive patients progressed and 2 died. Three of 61 FDG-PET–negative patients progressed; all were alive at latest follow-up. Survival analyses showed strong associations between early FDG-PET after two cycles and PFS (P < .001) and OS (P < .01). For prediction of PFS, interim FDG-PET was as accurate after two cycles as later during treatment and superior to computerized tomography (CT) at all times. In regression analyses, early interim FDG-PET was stronger than established prognostic factors. Other significant prognostic factors were stage and extranodal disease. Early interim FDG-PET is a strong and independent predictor of PFS in HL. A positive early interim FDG-PET is highly predictive of progression in patients with advanced-stage or extranodal disease.
XPD Lys751Gln polymorphism in the etiology and outcome of childhood acute myeloid leukemia: a Children's Oncology Group report
Authors: Mehta Parinda A. , Alonzo Todd A. , Gerbing Robert B. , Elliott James S. , Wilke Tiffany A. , Kennedy Rebekah J. , Ross Julie A. , Perentesis John P. , Lange Beverly J. , Davies Stella M. 
Published: September 2005

AbstractGenetic polymorphisms result in interindividual variation in DNA repair capacity and may, in part, account for susceptibility of a cell to genotoxic agents and to malignancy. Polymorphisms in XPD, a member of the nucleotide excision repair pathway, have been associated with development of treatment-related acute myeloid leukemia (AML) and with poor outcome of AML in elderly patients. We hypothesized that XPD Lys751Gln polymorphism may play a role in causation of AML in children and, as shown in adults, may affect the outcome of childhood AML therapy. Genotyping of 456 children treated for de novo AML was performed at XPD exon 23. Genotype frequencies in patients were compared with healthy control subject frequencies, and patient outcomes were analyzed according to genotype. Gene frequencies in AML patients and healthy controls were similar. There were no significant differences in overall survival (P = .82), event-free survival (P = .78), treatment-related mortality (P = .43), or relapse rate (RR) (P = .92) between patients with XPD751AA versus 751AC versus 751CC genotypes, in contrast to reports in adult AML. These data, representing the only data in pediatric AML, suggest that XPD genotype does not affect the etiology or outcome of childhood AML.
KSHV G protein-coupled receptor inhibits lytic gene transcription in primary-effusion lymphoma cells via p21-mediated inhibition of Cdk2
Authors: Cannon Mark , Cesarman Ethel , Boshoff Chris 
Published: September 2005

AbstractKaposi sarcoma (KS) remains the most common AIDS-associated malignancy worldwide. In sub-Saharan Africa especially, this aggressive endothelial-cell tumor is a cause of widespread morbidity and mortality. Infection with Kaposi sarcoma-associated herpesvirus (KSHV) is now known to be an etiologic force behind KS and primary-effusion lymphoma (PEL). Over time, KSHV has pirated many human genes whose products regulate angiogenesis, inflammation, and the cell cycle. One of these, the KSHV vGPCR, is a lytic product that is a constitutively active homolog of the IL-8 receptor. Although it is considered a viral oncogene and causes KS-like lesions in mice, vGPCR expression results in cell-cycle arrest of KSHV-infected PEL cells. In the present study, we show that this arrest is mediated by p21 in a p53-independent manner; the resulting Cdk2 inhibition decreases the efficiency of chemical induction of KSHV lytic transcripts ORF 50 and 26. Importantly, Cdk2 activity is also essential for replication in other human herpesviruses. The ability of vGPCR to delay or abort KSHV replication may explain how despite being a lytic product, this potent signaling molecule has a vital role in tumor formation via its induction of various KS-associated cytokines.
Fetal tolerance to maternal antigens improves the outcome of allogeneic bone marrow transplantation by a CD4+CD25+ T-cell–dependent mechanism
Authors: Matsuoka Ken-ichi , Ichinohe Tatsuo , Hashimoto Daigo , Asakura Shoji , Tanimoto Mitsune , Teshima Takanori 
Published: September 2005

Abstract
The lack of donor availability is a major limitation to the widespread use of allogeneic hematopoietic stem cell transplantation, and therefore it would be beneficial to identify less immunogenic HLA mismatches. The maternal and fetal antigens that are transmitted through the bidirectional transplacental passage during pregnancy may induce tolerance to noninherited maternal antigens (NIMAs) in offspring and to inherited paternal antigens (IPAs) in the mother. Using mouse models of bone marrow transplantation (BMT), we found that a “child-to-mother” BMT from a NIMA-exposed donor reduced the morbidity and mortality of graft-versus-host disease in an antigen-specific manner; however, a “mother-to-child” BMT from an IPA-exposed donor did not. The NIMA-complementary BMT preserved the graft-versus-leukemia effects and favored the immune reconstitution, thus resulting in a marked improvement of the outcome after BMT. These tolerogenic NIMA effects were completely abolished by the depletion of CD4+CD25+ cells from the donor inocula, thus suggesting the involvement of CD4+CD25+ regulatory T cells in the tolerogenic NIMA effects. Our findings may therefore have profound implications on the performance of clinical BMT while also potentially helping to develop new strategies for using a NIMA-mismatched donor in the absence of an HLA-identical donor.
Micro-Mar: a database for dynamic representation of marine microbial biodiversity
Authors: Pushker Ravindra , D'Auria Giuseppe , Alba-Casado Jose Carlos , Rodríguez-Valera Francisco 
Published: September 2005

Abstract
Background
The cataloging of marine prokaryotic DNA sequences is a fundamental aspect for bioprospecting and also for the development of evolutionary and speciation models. However, large amount of DNA sequences used to quantify prokaryotic biodiversity requires proper tools for storing, managing and analyzing these data for research purposes.

Description
The Micro-Mar database has been created to collect DNA diversity information from marine prokaryotes for biogeographical and ecological analyses. The database currently includes 11874 sequences corresponding to high resolution taxonomic genes (16S rRNA, ITS and 23S rRNA) and many other genes including CDS of marine prokaryotes together with available biogeographical and ecological information.

Conclusion
The database aims to integrate molecular data and taxonomic affiliation with biogeographical and ecological features that will allow to have a dynamic representation of the marine microbial diversity embedded in a user friendly web interface. It is available online at http://egg.umh.es/micromar/.
Comprehensive search for intra- and inter-specific sequence polymorphisms among coding envelope genes of retroviral origin found in the human genome: genes and pseudogenes
Authors: de Parseval Nathalie , Diop Gora , Blaise Sandra , Helle François , Vasilescu Alexandre , Matsuda Fumihiko , Heidmann Thierry 
Published: September 2005

Abstract

Background
The human genome carries a high load of proviral-like sequences, called Human Endogenous Retroviruses (HERVs), which are the genomic traces of ancient infections by active retroviruses. These elements are in most cases defective, but open reading frames can still be found for the retroviral envelope gene, with sixteen such genes identified so far. Several of them are conserved during primate evolution, having possibly been co-opted by their host for a physiological role.

Results
To characterize further their status, we presently sequenced 12 of these genes from a panel of 91 Caucasian individuals. Genomic analyses reveal strong sequence conservation (only two non synonymous Single Nucleotide Polymorphisms [SNPs]) for the two HERV-W and HERV-FRD envelope genes, i.e. for the two genes specifically expressed in the placenta and possibly involved in syncytiotrophoblast formation. We further show – using an ex vivo fusion assay for each allelic form – that none of these SNPs impairs the fusogenic function. The other envelope proteins disclose variable polymorphisms, with the occurrence of a stop codon and/or frameshift for most – but not all – of them. Moreover, the sequence conservation analysis of the orthologous genes that can be found in primates shows that three env genes have been maintained in a fully coding state throughout evolution including env W and env FRD.

Conclusion
Altogether, the present study strongly suggests that some but not all envelope encoding sequences are bona fide genes. It also provides new tools to elucidate the possible role of endogenous envelope proteins as susceptibility factors in a number of pathologies where HERVs have been suspected to be involved.
The use of end-quintile comparisons to identify under-servicing of the poor and over-servicing of the rich: A longitudinal study describing the effect of socioeconomic status on healthcare
Authors: Brameld Kate J , Holman C D'Arcy J 
Published: September 2005

Abstract

Background
To demonstrate the use of end-quintile comparisons in assessing the effect of socio-economic status on hospital utilisation and outcomes in Western Australia.

Methods
Hospital morbidity records were extracted from the WA Data Linkage System for the period 1994–99, with follow-up to the end of 2000. Multivariate modelling was used to estimate the effect of socio-economic status on hospital admission rates, average and total length of stay (LOS), cumulative incidence of readmission at 30 days and one year, and case fatality at one year.

Results
The study demonstrated higher rate ratios of hospital admission in the more disadvantaged quintiles: rate ratios were 1.31 (95% CI 1.25–1.37) and 1.32 (1.26–1.38) in the first quintile (most disadvantaged) and the second quintile respectively, compared with the fifth quintile (most advantaged). There was a longer total LOS in the most disadvantaged quintile compared with quintile 5 (LOS ratio 1.24; 1.23–1.26). The risk of readmission at 30 days and one year and the risk of death at one year were also greater in those with greater disadvantage: the hazard ratios for quintiles 1:quintile 5 were 1.07 (1.05–1.09), 1.17 (1.16–1.18) and 1.10 (1.07–1.13) respectively. In contradiction to the trends towards higher hospital utilisation and poorer outcomes with increasing social disadvantage, in some MDC's the rate ratio of quintile 1:quintile 2 was less than 1, and quintile 4:quintile 5 was greater than 1. For all surgical admissions the most disadvantaged had a significantly lower admission rate than the second quintile.

Conclusion
This study has shown that the disadvantaged within Western Australia are more intensive users of hospital services but their outcomes following hospitalisation are worse, consistent with their health status. Instances of overuse in the least disadvantaged and under use in the most disadvantaged have also been identified.
hZIP1 zinc uptake transporter down regulation and zinc depletion in prostate cancer
Authors: Franklin Renty B , Feng Pei , Milon B , Desouki Mohamed M , Singh Keshav K , Kajdacsy-Balla André , Bagasra Omar , Costello Leslie C 
Published: September 2005

Abstract

Background
The genetic and molecular mechanisms responsible for and associated with the development and progression of prostate malignancy are largely unidentified. The peripheral zone is the major region of the human prostate gland where malignancy develops. The normal peripheral zone glandular epithelium has the unique function of accumulating high levels of zinc. In contrast, the ability to accumulate zinc is lost in the malignant cells. The lost ability of the neoplastic epithelial cells to accumulate zinc is a consistent factor in their development of malignancy. Recent studies identified ZIP1 (SLC39A1) as an important zinc transporter involved in zinc accumulation in prostate cells. Therefore, we investigated the possibility that down-regulation of hZIP1 gene expression might be involved in the inability of malignant prostate cells to accumulate zinc. To address this issue, the expression of hZIP1 and the depletion of zinc in malignant versus non-malignant prostate glands of prostate cancer tissue sections were analyzed. hZIP1 expression was also determined in malignant prostate cell lines.

Results

hZIP1 gene expression, ZIP1 transporter protein, and cellular zinc were prominent in normal peripheral zone glandular epithelium and in benign hyperplastic glands (also zinc accumulating glands). In contrast, hZIP1 gene expression and transporter protein were markedly down-regulated and zinc was depleted in adenocarcinomatous glands and in prostate intra-epithelial neoplastic foci (PIN). These changes occur early in malignancy and are sustained during its progression in the peripheral zone. hZIP1 is also expressed in the malignant cell lines LNCaP, PC-3, DU-145; and in the nonmalignant cell lines HPr-1 and BPH-1.

Conclusion
The studies clearly establish that hZIP1 gene expression is down regulated and zinc is depleted in adenocarcinomatous glands. The fact that all the malignant cell lines express hZIP1 indicates that the down-regulation in adenocarcinomatous glands is likely due to in situ gene silencing. These observations, coupled with the numerous and consistent reports of loss of zinc accumulation in malignant cells in prostate cancer, lead to the plausible proposal that down regulation of hZIP1 is a critical early event in the development prostate cancer.
Augmented cell survival in eutopic endometrium from women with endometriosis: Expression of c-myc, TGF-beta1 and bax genes
Authors: Johnson M Cecilia , Torres Marisa , Alves Alessandra , Bacallao Ketty , Fuentes Ariel , Vega Margarita , Boric M Angélica 
Published: September 2005

Abstract

Background
Endometriosis is a common gynaecological disorder characterized by the presence of endometrial tissue outside of the uterus. The fragments in normal menstruation are composed of necrotic and living cells, which do not survive in ectopic locations because of programmed cell death. The aim of this study was to evaluate if the balance between cell proliferation and apoptosis is changed in eutopic endometrium from women with endometriosis throughout the menstrual cycle by studying bax (pro-apoptotic), c-myc (regulator of cell cycle) and TGF-beta1 (involved in cell differentiation) genes.

Methods
Eutopic endometrium was obtained from: 30 women with endometriosis (32.8 +/- 5 years) and 34 fertile eumenorrheic women (36 +/- 5.3 years). We analyzed apoptosis (TUNEL: DNA fragmentation); cell proliferation (immunohistochemistry (IHC) for Ki67); c-myc, bax and TGF-beta1 mRNA abundance (RT-PCR) and TGF-beta1 protein (IHC) in endometrial explants.

Results
Cell proliferation strongly decreased from proliferative to late secretory phases in glands, but not in stroma, in both endometria. Positive staining in glands and stroma from proliferative endometrium with endometriosis was 1.9- and 2.2-fold higher than control endometrium, respectively (p < 0.05). Abundance of c-myc mRNA was 65% higher in proliferative endometrium from endometriosis than normal tissue (p < 0.05). TGF-beta1 (mRNA and protein) augmented during mid secretory phase in normal endometrium, effect not observed in endometrium with endometriosis. In normal endometrium, the percentage of apoptotic epithelial and stromal cells increased more than 30-fold during late secretory phase. In contrast, in endometrium from endometriosis, not only this increase was not observed, besides bax mRNA decreased 63% versus normal endometrium (p < 0.05). At once, in early secretory phase, apoptotic stromal cells increased 10-fold with a concomitant augment of bax mRNA abundance (42%) in endometria from endometriosis (p < 0.05).

Conclusion
An altered expression of c-myc, TGF-beta1 and bax was observed in eutopic endometrium from endometriosis, suggesting its participation in the regulation of cell survival in this disease. The augmented cell viability in eutopic endometrium from these patients as a consequence of a reduction in cell death by apoptosis, and also an increase in cell proliferation indicates that this condition may facilitate the invasive feature of the endometrium.
Sensitivity of the anterior lateral line to natural stimuli in the oyster toadfish,Opsanus tau(Linnaeus)
Authors: Palmer Lucy M. , Deffenbaugh Max , Mensinger Allen F. 
Published: September 2005

SUMMARYInductive neural telemetry was used to record from microwire electrodes chronically implanted into the anterior lateral line nerve of the oyster toadfish, Opsanus tau (L.). The lateral lines of free-ranging toadfish were stimulated by the swimming movements of a prey fish(Fundulus heteroclitus), and the corresponding neural activity was quantified. Both spontaneously active and silent afferent fibers experienced an increase in neural firing as the prey approached the lateral line. Activity was evoked when the prey fish approached to within 8-12 cm of the neuromast,with increases in nerve firing rates directly correlated with diminishing distance. Thus, adult toadfish (28 cm standard length; 33 cm total length)were only able to detect mobile prey that approached within approximately 40%of their body length. Both spontaneously active and silent afferent fibers also experienced a dramatic increase in firing during predatory strikes,indicating that the fibers were not inhibited during rapid body movement. This study investigates, for the first time, the neural response of the anterior lateral line to prey stimuli in free-ranging fish.
Adaptive bone formation in acellular vertebrae of sea bass(Dicentrarchus labrax L.)
Authors: Kranenbarg Sander , van Cleynenbreugel Tim , Schipper Henk , van Leeuwen Johan 
Published: September 2005

SUMMARY
Mammalian bone is an active tissue in which osteoblasts and osteoclasts balance bone mass. This process of adaptive modelling and remodelling is probably regulated by strain-sensing osteocytes. Bone of advanced teleosts is acellular yet, despite the lack of osteocytes, it is capable of an adaptive response to physical stimuli. Strenuous exercise is known to induce lordosis. Lordosis is a ventrad curvature of the vertebral column, and the affected vertebrae show an increase in bone formation.
The effects of lordosis on the strain distribution in sea bass(Dicentrarchus labrax L.) vertebrae are assessed using finite element modelling. The response of the local tissue is analyzed spatially and ontogenetically in terms of bone volume.
Lordotic vertebrae show a significantly increased strain energy due to the increased load compared with normal vertebrae when loaded in compression. High strain regions are found in the vertebral centrum and parasagittal ridges. The increase in strain energy is attenuated by a change in architecture due to the increased bone formation. The increased bone formation is seen mainly at the articular surfaces of the vertebrae, although some extra bone is formed in the vertebral centrum.
Regions in which the highest strains are found do not spatially correlate with regions in which the most extensive bone apposition occurs in lordotic vertebrae of sea bass. Mammalian-like strain-regulated bone modelling is probably not the guiding mechanism in adaptive bone modelling of acellular sea bass vertebrae. Chondroidal ossification is found at the articular surfaces where it mediates a rapid adaptive response, potentially attenuating high stresses on the dorsal zygapophyses.