bluuebunny/crossref_metadata_2025_split huggingface dataset:
Environmental Patterns Associated with Active and Inactive Caribbean Hurricane Seasons
Authors: Jury Mark R. , Enfield David B. 
Published: November 2009

Abstract
This study of hurricanes passing through the Caribbean in the 1950–2005 period reveals that seasons with more intense hurricanes occur with the onset of Pacific La Niña events and when Atlantic SSTs west of Africa are above normal. Composites of NCEP reanalysis fields with regard to Caribbean hurricanes reveal development of an anomalous equatorial Atlantic zonal overturning circulation (upper easterly/lower westerly) that shifts toward the Caribbean coincident with a westward spread of the cold tongue in the east Pacific. Ocean–atmosphere coupling is promoted through interaction of the southern Hadley cell and the Atlantic ITCZ. A heat budget analysis suggests that evaporation governs SSTs in the major development region (MDR) and near Venezuela, but the signal is weak prior to May. Using the knowledge gained, statistical algorithms are developed to predict Caribbean hurricanes at seasonal lead times. These make use of equatorial Pacific SST, subtropical Atlantic SST, and the zonal Walker cell over the Atlantic.
Combined Effects of Wind-Driven Upwelling and Internal Tide on the Continental Shelf
Authors: Kurapov A. L. , Allen J. S. , Egbert G. D. 
Published: November 2009

Abstract
Internal tides on the continental shelf can be intermittent as a result of changing hydrographic conditions associated with wind-driven upwelling. In turn, the internal tide can affect transports associated with upwelling. To study these processes, simulations in an idealized, alongshore uniform setup are performed utilizing the hydrostatic Regional Ocean Modeling System (ROMS) with conditions corresponding, as closely as possible, to the central Oregon shelf. “Wind only” (WO), “tide only” (TO), and “tide and wind” (TW) solutions are compared, utilizing cases with constant upwelling-favorable wind stress as well as with time-variable observed stress. The tide is forced by applying cross-shore barotropic flow at the offshore boundary with intensity sufficient to generate an internal tide with horizontal velocity amplitudes near 0.15 m s−1, corresponding to observed levels. The internal tide affects the subinertial circulation, mostly through the changes in the bottom boundary layer variability, resulting in a larger bottom stress and a weaker depth-averaged alongshore current in the TW case compared to WO. The spatial variability of the cross-shore and vertical volume transport is also affected. Divergence in the Reynolds stress associated with the baroclinic tidal flow contributes to the tidally averaged cross-shore momentum balance. Internal waves cause high-frequency variability in the turbulent kinetic energy in both the bottom and surface boundary layers, causing periodic restratification of the inner shelf in the area of the upwelling front. Increased vertical shear in the horizontal velocity resulting from the superposition of the upwelling jet and the internal tide results in intermittent patches of intensified turbulence in the mid–water column. Variability in stratification associated with upwelling can affect not only the propagation of the internal tide on the shelf, but also the barotropic-to-baroclinic energy conversion on the continental slope, in this case changing the classification of the slope from nearly critical to supercritical such that less barotropic tidal energy is converted to baroclinic and a larger fraction of the baroclinic energy is radiated into the open ocean.
Congenic interval of CD45/Ly-5 congenic mice contains multiple genes that may influence hematopoietic stem cell engraftment
Authors: Waterstrat Amanda , Liang Ying , Swiderski Carol F. , Shelton Brent J. , Van Zant Gary 
Published: November 2009

AbstractThe B6.SJL-Ptprc(d)Pep3(b)/BoyJ (B6.SJL) congenic mouse strain, a valuable and widely used tool in murine bone marrow transplantation studies, has long been considered equivalent to the parental C57B/L6 (B6) strain with the exception of a small congenic interval on chromosome 1 harboring an alternative CD45/Ly-5 alloantigen (Ly-5.1). In this study we compared functional properties of stem and stromal cells between the strains, and delineated the boundary of the B6.SJL congenic interval. We identified a 25% reduction in homing efficiency, 3.8-fold reduction in transplantable long-term hematopoietic stem cells (LT-HSCs), a 5-fold reduction in LT-HSCs capable of 24-hour homing, and a cell-intrinsic engraftment defect of 30% to 50% in B6.SJL-derived bone marrow cells relative to B6-derived cells. These functional differences were independent of stem cell number, cycling, or apoptosis. Genotypic analysis revealed a 42.1-mbp congenic interval in B6.SJL including 306 genes, and at least 124 genetic polymorphisms. Moreover, expression profiling revealed 288 genes differentially expressed between nonhematopoietic stromal cells of the 2 strains. These results indicate that polymorphisms between the B6 and SJL genotype within the B6.SJL congenic interval influence HSC engraftment and result in transcriptional variation within bone marrow stroma.
The architectural pattern of FOXP3-positive T cells in follicular lymphoma is an independent predictor of survival and histologic transformation
Authors: Farinha Pedro , Al-Tourah Abdulwahab , Gill Karamjit , Klasa Richard , Connors Joseph M. , Gascoyne Randy D. 
Published: November 2009

AbstractPrevious studies of follicular lymphoma (FL) patients treated heterogeneously have suggested that decreased numbers of regulatory T cells correlates with improved survival. We studied advanced-stage FL patients from a single institution phase 2 trial. All patients were treated uniformly with multiagent chemotherapy and radiation. Tissue microarrays were constructed using diagnostic biopsies available in 105 patients and stained with CD4, CD8, CD25, and forkhead/winged helix transcription factor 3 (FOXP3) antibodies. Both cell content and cell distribution were evaluated. For all antibodies, there were cases with a predominant intrafollicular or perifollicular localization of cells (follicular pattern) while others displayed a diffuse pattern. The median follow-up of living patients was 17.1 years. The International Prognostic Index score predicted overall survival (OS; P = .004) but not risk of transformation (RT). Cell content did not impact survival, while immunoarchitectural patterns of CD4/CD8 were significant for progression-free survival (PFS; P = .056), CD25 for both PFS and OS (P = .002 and P = .024, respectively), and FOXP3+ predicted PFS, OS, and RT (P = .001, P < .001 and p = .002, respectively). A Cox multivariate model showed both International Prognostic Index score and FOXP3+ pattern were independent predictors of OS (P = .008 and P < .001, respectively), while only FOXP3+ pattern predicted RT (P = .004). We conclude that FOXP3+ cell distribution significantly predicts survival and RT in FL.
International Prognostic Scoring System–independent cytogenetic risk categorization in primary myelofibrosis
Authors: Hussein Kebede , Pardanani Animesh D. , Van Dyke Daniel L. , Hanson Curtis A. , Tefferi Ayalew 
Published: November 2009

Abstract
Among 200 patients with primary myelofibrosis, karyotype at diagnosis was abnormal in 83 (42%). To assess their individual prognostic impact, specific cytogenetic abnormalities with more than or equal to 5 informative cases were identified and the rest grouped separately as “other abnormalities.” Median survival in patients with sole +9 (n = 6), sole 20q− (n = 21), sole 13q− (n = 8), normal karyotype (n = 117), “other abnormalities” (n = 28), complex karyotype (n = 13), and sole +8 (n = 7) were “not reached,” 112, 105, 80, 46, 34, and 28 months, respectively (P = .01). Accordingly, 4 cytogenetic risk groups were considered: (1) favorable (sole +9, 20q−, or 13q−), (2) normal, (3) unfavorable (complex karyotype or sole +8), and (4) “other abnormalities.” Multivariable analysis confirmed the International Prognostic Scoring System (IPSS)–independent prognostic value of both 4-way and 2-way (ie, favorable/normal vs unfavorable/other abnormalities; IPSS-adjusted hazard ratio = 0.37; 95% confidence interval, 0.24-0.58) cytogenetic risk categorization (P < .01). The ability to prognostically dissect a specific IPSS category has major therapeutic implications.
DNA barcode analysis: a comparison of phylogenetic and statistical classification methods
Authors: Austerlitz Frederic , David Olivier , Schaeffer Brigitte , Bleakley Kevin , Olteanu Madalina , Leblois Raphael , Veuille Michel , Laredo Catherine 
Published: November 2009

Abstract

Background
DNA barcoding aims to assign individuals to given species according to their sequence at a small locus, generally part of the CO1 mitochondrial gene. Amongst other issues, this raises the question of how to deal with within-species genetic variability and potential transpecific polymorphism. In this context, we examine several assignation methods belonging to two main categories: (i) phylogenetic methods (neighbour-joining and PhyML) that attempt to account for the genealogical framework of DNA evolution and (ii) supervised classification methods (k-nearest neighbour, CART, random forest and kernel methods). These methods range from basic to elaborate. We investigated the ability of each method to correctly classify query sequences drawn from samples of related species using both simulated and real data. Simulated data sets were generated using coalescent simulations in which we varied the genealogical history, mutation parameter, sample size and number of species.

Results
No method was found to be the best in all cases. The simplest method of all, "one nearest neighbour", was found to be the most reliable with respect to changes in the parameters of the data sets. The parameter most influencing the performance of the various methods was molecular diversity of the data. Addition of genetically independent loci - nuclear genes - improved the predictive performance of most methods.

Conclusion
The study implies that taxonomists can influence the quality of their analyses either by choosing a method best-adapted to the configuration of their sample, or, given a certain method, increasing the sample size or altering the amount of molecular diversity. This can be achieved either by sequencing more mtDNA or by sequencing additional nuclear genes. In the latter case, they may also have to modify their data analysis method.
Endogenous control genes in complex vascular tissue samples
Authors: Folkersen Lasse , Kurtovic Sanela , Razuvaev Anton , Agardh Hanna E , Gabrielsen Anders , Paulsson-Berne Gabrielle 
Published: November 2009

Abstract

Background
Gene expression microarrays and real-time PCR are common methods used to measure mRNA levels. Each method has a fundamentally different approach of normalization between samples. Relative quantification of gene expression using real-time PCR is often done using the 2^(-ΔΔCt) method, in which the normalization is performed using one or more endogenous control genes. The choice of endogenous control gene is often arbitrary or bound by tradition. We here present an analysis of the differences in expression results obtained with microarray and real-time PCR, dependent on different choices of endogenous control genes.

Results
In complex tissue, microarray data and real-time PCR data show the best correlation when endogenous control genes are omitted and the normalization is done relative to total RNA mass, as measured before reverse transcription.

Conclusion
We have found that for real-time PCR in heterogeneous tissue samples, it may be a better choice to normalize real-time PCR Ct values to the carefully measured mass of total RNA than to use endogenous control genes. We base this conclusion on the fact that total RNA mass normalization of real-time PCR data shows better correlation to microarray data. Because microarray data use a different normalization approach based on a larger part of the transcriptome, we conclude that omitting endogenous control genes will give measurements more in accordance with actual concentrations.
Evaluation of routinely reported surgical site infections against microbiological culture results: a tool to identify patient groups where diagnosis and treatment may be improved
Authors: Krukerink Marco , Kievit Job , Marang-van de Mheen Perla J 
Published: November 2009

Abstract

Background
Surgeons may improve their decision making by assessing the extent to which their initial clinical diagnosis of a surgical site infection (SSI) was supported by culture results. Aim of the present study was to evaluate routinely reported SSI by surgeons against microbiological culture results, to identify patient groups with lower agreement where decision making may be improved.

Methods
701 admissions with SSI were reported by surgeons in a university medical centre in the period 1997-2005, which were retrospectively checked for microbiological culture results. Reporting a SSI was conditional on treatment being given (e.g. antibiotics) and was classified by severity. To identify specific patient groups, patients were classified according to the surgery group of the first operation during admission (e.g. trauma).

Results
Of all reported SSI, 523 (74.6%) had a positive culture result, 102 (14.6%) a negative culture result and 76 (10.8%) were classified as unknown culture result (due to no culture taken). Given a known culture result, reported SSI with positive culture results less often concerned trauma patients (16% versus 26%, X2 = 4.99 p = 0.03) and less severe SSI (49% versus 85%, X2 = 10.11 p < 0.01) suggesting that a more conservative approach may be warranted in these patients. The trauma surgeons themselves perceived to have become too liberal in administering antibiotics (and reporting SSI).

Conclusion
Routine reporting of SSI was mostly supported by culture results. However, this support was less often found in trauma patients and less severe SSI, thereby giving surgeons feedback that diagnosis and treatment may be improved in these cases.
Patterns of analgesic use, pain and self-efficacy: a cross-sectional study of patients attending a hospital rheumatology clinic
Authors: Blamey Ruth , Jolly Kate , Greenfield Sheila , Jobanputra Paresh 
Published: November 2009

Abstract

Background
Many people attending rheumatology clinics use analgesics and non-steroidal anti-inflammatories for persistent musculoskeletal pain. Guidelines for pain management recommend regular and pre-emptive use of analgesics to reduce the impact of pain. Clinical experience indicates that analgesics are often not used in this way. Studies exploring use of analgesics in arthritis have historically measured adherence to such medication. Here we examine patterns of analgesic use and their relationships to pain, self-efficacy and demographic factors.

Methods
Consecutive patients were approached in a hospital rheumatology out-patient clinic. Pattern of analgesic use was assessed by response to statements such as 'I always take my tablets every day.' Pain and self-efficacy (SE) were measured using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) and Arthritis Self-Efficacy Scale (ASES). Influence of factors on pain level and regularity of analgesic use were investigated using linear regression. Differences in pain between those agreeing and disagreeing with statements regarding analgesic use were assessed using t-tests.

Results
218 patients (85% of attendees) completed the study. Six (2.8%) patients reported no current pain, 26 (12.3%) slight, 100 (47.4%) moderate, 62 (29.4%) severe and 17 (8.1%) extreme pain. In multiple linear regression self efficacy and regularity of analgesic use were significant (p < 0.01) with lower self efficacy and more regular use of analgesics associated with more pain.
Low SE was associated with greater pain: 40 (41.7%) people with low SE reported severe pain versus 22 (18.3%) people with high SE, p < 0.001. Patients in greater pain were significantly more likely to take analgesics regularly; 13 (77%) of those in extreme pain reported always taking their analgesics every day, versus 9 (35%) in slight pain. Many patients, including 46% of those in severe pain, adjusted analgesic use to current pain level. In simple linear regression, pain was the only variable significantly associated with regularity of analgesic use: higher levels of pain corresponded to more regular analgesic use (p = 0.003).

Conclusion
Our study confirms that there is a strong inverse relationship between self-efficacy and pain severity. Analgesics are often used irregularly by people with arthritis, including some reporting severe pain.
PTEN inhibits BMI1 function independently of its phosphatase activity
Authors: Fan Catherine , He Lizhi , Kapoor Anil , Rybak Adrian P , De Melo Jason , Cutz Jean-Claude , Tang Damu 
Published: November 2009

Abstract

Background

PTEN is the second most mutated tumor suppressor gene other than p53. It suppresses tumorigenesis by dephosphorylating phosphatidylinositol (3,4,5)-triphosphate (PIP3) to phosphatidylinositol (4,5)-biphosphate (PIP2), thereby directly inhibiting phosphatidylinositol 3 kinase (PI3K)-mediated tumorigenic activities. Consistent with this model of action, cytosolic PTEN is recruited to the plasma membrane to dephosphorylate PIP3. While nuclear PTEN has been shown to suppress tumorigenesis by governing genome integrity, additional mechanisms may also contribute to nuclear PTEN-mediated tumor suppression. The nuclear protein BMI1 promotes stem cell self-renewal and tumorigenesis and PTEN inhibits these events, suggesting that PTEN may suppress BMI1 function.

Results
We investigated whether PTEN inhibits BMI1 function during prostate tumorigenesis. PTEN binds to BMI1 exclusively in the nucleus. This interaction does not require PTEN's phosphatase activity, as phosphatase-deficient PTEN mutants, PTEN/C124S (CS), PTEN/G129E (GE), and a C-terminal PTEN fragment (C-PTEN) excluding the catalytic domain, all associate with BMI1. Furthermore, the residues 186-286 of C-PTEN are sufficient for binding to BMI1. This interaction reduces BMI1's function. BMI1 enhances hTERT activity and reduces p16INK4A and p14ARF expression. These effects were attenuated by PTEN, PTEN(CS), PTEN(GE), and C-PTEN. Furthermore, knockdown of PTEN in DU145 cells increased hTERT promoter activity, which was reversed when BMI1 was concomitantly knocked-down, indicating that PTEN reduces hTERT promoter activity via inhibiting BMI1 function. Conversely, BMI1 reduces PTEN's ability to inhibit AKT activation, which can be attributed to its interaction with PTEN in the nucleus, making PTEN unavailable to dephosphorylate membrane-bound PIP3. Furthermore, BMI1 appears to co-localize with PTEN more frequently in clinical prostate tissue samples from patients diagnosed with PIN (prostatic intraepithelial neoplasia) and carcinoma compared to normal prostate epithelium. While PTEN co-localized with BMI1 in 2.4% of normal prostate epithelial cells, co-localization was observed in 37.6% and 18.5% of cells in PIN and carcinoma, respectively. Collectively, we demonstrate that PTEN inhibits BMI1 function via binding to BMI1 in a phosphatase independent manner.

Conclusion
We demonstrate that nuclear PTEN reduces BMI1 function independently of its phosphatase activity. It was recently observed that nuclear PTEN also suppresses tumorigenesis. Our results, therefore, provide a plausible mechanism by which nuclear PTEN prevents tumorigenesis.
Altered peptide ligands inhibit arthritis induced by glucose-6-phosphate isomerase peptide
Authors: Iwanami Keiichi , Matsumoto Isao , Yoshiga Yohei , Inoue Asuka , Kondo Yuya , Yamamoto Kayo , Tanaka Yoko , Minami Reiko , Hayashi Taichi , Goto Daisuke , Ito Satoshi , Nishimura Yasuharu , Sumida Takayuki 
Published: November 2009

Abstract
Introduction
Immunosuppressants, including anti-TNFα antibodies, have remarkable effects in rheumatoid arthritis; however, they increase infectious events. The present study was designed to examine the effects and immunological change of action of altered peptide ligands (APLs) on glucose-6-phosphate isomerase (GPI) peptide-induced arthritis.

Methods
DBA/1 mice were immunized with hGPI325-339, and cells of draining lymph node (DLN) were stimulated with hGPI325-339 to investigate the T-cell receptor (TCR) repertoire of antigen-specific CD4+ T cells by flow cytometry. Twenty types of APLs with one amino acid substitution at a TCR contact site of hGPI325-339 were synthesized. CD4+ T cells primed with human GPI and antigen-presenting cells were co-cultured with each APL and cytokine production was measured by ELISA to identify antagonistic APLs. Antagonistic APLs were co-immunized with hGPI325-339 to investigate whether arthritis could be antigen-specifically inhibited by APL. After co-immunization, DLN cells were stimulated with hGPI325-339 or APL to investigate Th17 and regulatory T-cell population by flow cytometry, and anti-mouse GPI antibodies were measured by ELISA.

Results
Human GPI325-339-specific Th17 cells showed predominant usage of TCRVβ8.1 8.2. Among the 20 synthesized APLs, four (APL 6; N329S, APL 7; N329T, APL 12; G332A, APL 13; G332V) significantly reduced IL-17 production by CD4+ T cells in the presence of hGPI325-339. Co-immunization with each antagonistic APL markedly prevented the development of arthritis, especially APL 13 (G332V). Although co-immunization with APL did not affect the population of Th17 and regulatory T cells, the titers of anti-mouse GPI antibodies in mice co-immunized with APL were significantly lower than in those without APL.

Conclusions
We prepared antagonistic APLs that antigen-specifically inhibited the development of experimental arthritis. Understanding the inhibitory mechanisms of APLs may pave the way for the development of novel therapies for arthritis induced by autoimmune responses to ubiquitous antigens.