bluuebunny/crossref_metadata_2025_split huggingface dataset:
Workers' Compensation Claims for Needlestick Injuries Among Healthcare Workers in Washington State, 1996-2000
Authors: Shah Syed M. , Bonauto David , Silverstein Barbara , Foley Michael 
Published: April 2006

AbstractObjectives:To characterize accepted workers' compensation claims for needlestick injuries filed by healthcare workers (HCWs) in non-hospital compared with hospital settings in Washington State.Design:Descriptive study of all accepted workers' compensation claims filed between 1996 and 2000 for needlestick injuries.Participants:All Washington State HCWs eligible to file a state fund workers' compensation claim and those who filed a workers' compensation claim for a needlestick injury.Results:There were 3,303 accepted state fund HCW needlestick injury claims. The incidence of needlestick injury claims per 10,000 full-time-equivalent HCWs in hospitals was 158.6; in dental offices, 104.7; in physicians' offices, 87.0; and in skilled nursing facilities, 80.8. The most common mechanisms of needlestick injury by work location were as follows: for hospitals, suturing and other surgical procedures (16.7%), administering an injection (12.7%), and drawing blood (10%); for dentists' offices, recapping (21.3%) and cleaning trays and instruments (18.2%); for physicians' offices, disposal (22.2%) and administering an injection (10.2%); and for skilled nursing facilities, disposal (23.7%) and administering an injection (14.9%). Nurses accounted for the largest (29%) proportion of HCWs involved, followed by dental assistants (17%) and laboratory technicians and phlebotomists (12%) in non-hospital settings. Rates of needlestick injury claims increased for non-hospital settings by 7.5% annually (95% confidence interval [CI95], 4.89% to 10.22%; P < .0001). Rates decreased for hospital settings by 5.8% annually, but the decline was not statistically significant (CI95, -12.50% to 1.34%; P < .1088). HCWs were exposed to hepatitis B, hepatitis C, and human immunodeficiency viruses in non-hospital settings.Conclusion:There was a difference in the incidence rate and mechanisms of needlestick injuries on review of workers' compensation claim records for HCWs in non-hospital and hospital settings.
Antiretroviral Drug Resistance Among Patients With Human Immunodeficiency Virus Who Act as Sources or Potential Sources in Occupational Accidents Involving Healthcare Workers
Authors: El-Far Fabiane , Medeiros Eduardo Alexandrino Servolo , Gasparoto Carlos Teodoro , Diaz Ricardo Sobhie 
Published: April 2006

AbstractObjective:To determine human immunodeficiency virus (HIV) type 1 genotypic antiretroviral drug resistance profiles of patients presenting a risk or potential risk for occupational exposure of healthcare workers.Design:Observational survey involving HIV-infected patients. Blood samples collected from source-patients and potential source-patients underwent HIV-1 genotypic antiretroviral resistance testing and determination of CD4 counts and viral load. Affected healthcare workers were monitored for 6 months after exposure.Setting:The survey was conducted in a tertiary-care hospital located in Sao Paulo, Brazil. Sao Paulo is considered the epicenter of the HIV-acquired immunodeficiency (AIDS) virus epidemic in Brazil.Participants:Source-patients, potential source-patients, and affected healthcare workers.Results:A total of 371 occupational exposures to biological materials were reported, 46 (12.3%) of which were from HIV-seropositive source-patients. Samples from 18 source-patients and 26 patients considered “potential sources for accidents” were analyzed. Of these 44 samples, 18 (41%) presented resistance-related mutations in reverse transcriptase, protease, or both. Of these 18 samples, 16 (89%) had resistance to drugs included in the prophylactic schedule recommended by the Brazilian Ministry of Health.Conclusions:Use of the Centers for Disease Control and Prevention-Brazilian post-exposure prophylaxis regimen will result in the administration of antiretroviral agents to which the source HIV-1 isolate will often be resistant. Therefore, it would be advisable to carefully investigate the history of use of antiretroviral agents by source-patients and adjust the prophylactic therapy based on those data and, subsequently, the results of resistance testing.
Placenta Growth Factor Overexpression Inhibits Tumor Growth, Angiogenesis, and Metastasis by Depleting Vascular Endothelial Growth Factor Homodimers in Orthotopic Mouse Models
Authors: Xu Lei , Cochran David M. , Tong Ricky T. , Winkler Frank , Kashiwagi Satoshi , Jain Rakesh K. , Fukumura Dai 
Published: April 2006

Abstract
The role of placenta growth factor (PlGF) in pathologic angiogenesis is controversial. The effects of PlGF on growth, angiogenesis, and metastasis from orthotopic tumors are not known. To this end, we stably transfected three human cancer cell lines (A549 lung, HCT116 colon, and U87-MG glioblastoma) with human plgf-2 full-length cDNA. Overexpression of PlGF did not affect tumor cell proliferation or migration in vitro. The growth of PlGF-overexpressing tumors grown orthotopically or ectopically was impaired in all three tumor models. This decrease in tumor growth correlated with a decrease in tumor angiogenesis. The PlGF-overexpressing tumors had decreased vessel density and increased vessel diameter, but vessel permeability was not different from the parental tumors. Tumors overexpressing PlGF exhibited higher levels of PlGF homodimers and PlGF/vascular endothelial growth factor (VEGF) heterodimers but decreased levels of VEGF homodimers. Our study shows that PlGF overexpression decreases VEGF homodimer formation and inhibits tumor progression. (Cancer Res 2006; 66(8): 3971-7)
Complete Elimination of Colorectal Tumor Xenograft by Combined Manganese Superoxide Dismutase with Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand Gene Virotherapy
Authors: Zhang Yanhong , Gu Jinfa , Zhao Lili , He Lingfeng , Qian Wenbin , Wang Jinhui , Wang Yigang , Qian Qijun , Qian Cheng , Wu Jian , Liu Xin Yuan 
Published: April 2006

Abstract
Manganese superoxide dismutase (MnSOD) is a latent tumor suppressor gene. To investigate the therapeutic effect of MnSOD and its mechanisms, a replication-competent recombinant adenovirus with E1B 55-kDa gene deletion (ZD55) was constructed, and human MnSOD and tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) genes were inserted to form ZD55-MnSOD and ZD55-TRAIL. ZD55-MnSOD exhibited an inhibition in tumor cell growth ∼1,000-fold greater than Ad-MnSOD. ZD55-TRAIL was shown to induce the MnSOD expression in SW620 cells. Accordingly, by the combined use of ZD55-MnSOD with ZD55-TRAIL (i.e., “dual gene virotherapy”), all established colorectal tumor xenografts were completely eliminated in nude mice. The evidence exists that the MnSOD overexpression led to a slower tumor cell growth both in vitro and in vivo as a result of apoptosis caused by MnSOD and TRAIL overexpression after adenoviral transduction. Our results showed that the production of hydrogen peroxide derived from MnSOD dismutation activated caspase-8, which might down-regulate Bcl-2 expression and induce Bax translocation to mitochondria. Subsequently, Bax translocation enhanced the release of apoptosis-initiating factor and cytochrome c. Cytochrome c finally triggered apoptosis by activating caspase-9 and caspase-3 in apoptotic cascade. Bax-mediated apoptosis seems to be dependent on caspase-8 activation because the inhibition of caspase-8 prevented Bid processing and Bax translocation. In conclusion, our dual gene virotherapy completely eliminated colorectal tumor xenografts via enhanced apoptosis, and this novel strategy points toward a new direction of cancer treatment. (Cancer Res 2006; 66(8): 4291-8)
Related to Testes-Specific, Vespid, and Pathogenesis Protein-1 (RTVP-1) Is Overexpressed in Gliomas and Regulates the Growth, Survival, and Invasion of Glioma Cells
Authors: Rosenzweig Tovit , Ziv-Av Amotz , Xiang Cunli , Lu Wei , Cazacu Simona , Taler Dvir , Miller Cathie G. , Reich Reuven , Shoshan Yigal , Anikster Yair , Kazimirsky Gila , Sarid Ronit , Brodie Chaya 
Published: April 2006

AbstractIn this study, we examined the expression and functions of related to testes-specific, vespid, and pathogenesis protein 1 (RTVP-1) in glioma cells. RTVP-1 was expressed in high levels in glioblastomas, whereas its expression in low-grade astrocytomas and normal brains was very low. Transfection of glioma cells with small interfering RNAs targeting RTVP-1 decreased cell proliferation in all the cell lines examined and induced cell apoptosis in some of them. Overexpression of RTVP-1 increased astrocyte and glioma cell proliferation and the anchorage-independent growth of the cells. In addition, overexpression of RTVP-1 rendered glioma cells more resistant to the apoptotic effect of tumor necrosis factor–related apoptosis-inducing ligand and serum deprivation. To delineate the molecular mechanisms involved in the survival effects of RTVP-1, we examined the expression and phosphorylation of various apoptosis-related proteins. We found that overexpression of RTVP-1 decreased the phosphorylation of c-Jun-NH2-kinase and increased the expression of Bcl2 and that the protective effect of RTVP-1 was partially mediated by Bcl2. Finally, we found that RTVP-1 regulated the invasion of glioma cells as was evident by their enhanced migration through Matrigel and by their increased invasion in a spheroid confrontation assay. The increased invasive potential of the RTVP-1 overexpressors was also shown by the increased activity of matrix metalloproteinase 2 in these cells. Our results suggest that the expression of RTVP-1 is correlated with the degree of malignancy of astrocytic tumors and that RTVP-1 is involved in the regulation of the growth, survival, and invasion of glioma cells. Collectively, these findings suggest that RTVP-1 is a potential therapeutic target in gliomas. (Cancer Res 2006; 66(8): 4139-48)
Characterization of the Mouse IFN-λ Ligand-Receptor System: IFN-λs Exhibit Antitumor Activity against B16 Melanoma
Authors: Lasfar Ahmed , Lewis-Antes Anita , Smirnov Sergey V. , Anantha Shubha , Abushahba Walid , Tian Bin , Reuhl Kenneth , Dickensheets Harold , Sheikh Faruk , Donnelly Raymond P. , Raveche Elizabeth , Kotenko Sergei V. 
Published: April 2006

AbstractRecently discovered type III IFNs (IFN-λ) exert their antiviral and immunomodulatory activities through a unique receptor complex composed of IFN-λR1 and interleukin-10 receptor 2. To further study type III IFNs, we cloned and characterized mouse IFN-λ ligand-receptor system. We showed that, similar to their human orthologues, mIFN-λ2 and mIFN-λ3 signal through the IFN-λ receptor complex, activate IFN stimulated gene factor 3, and are capable of inducing antiviral protection and MHC class I antigen expression in several cell types including B16 melanoma cells. We then used the murine B16 melanoma model to investigate the potential antitumor activities of IFN-λs. We developed B16 cells constitutively expressing murine IFN-λ2 (B16.IFN-λ2 cells) and evaluated their tumorigenicity in syngeneic C57BL/6 mice. Although constitutive expression of mIFN-λ2 in melanoma cells did not affect their proliferation in vitro, the growth of B16.IFN-λ2 cells, when injected s.c. into mice, was either retarded or completely prevented. We found that rejection of the modified tumor cells correlated with their level of IFN-λ2 expression. We then developed IFN-λ-resistant B16.IFN-λ2 cells (B16.IFN-λ2Res cells) and showed that their tumorigenicity was also highly impaired or completely abolished similar to B16.IFN-λ2 cells, suggesting that IFN-λs engage host mechanisms to inhibit melanoma growth. These in vivo experiments show the antitumor activities of IFN-λs and suggest their strong therapeutic potential. (Cancer Res 2006; 66(8): 4468-77)
High Expression of Ligands for Chemokine Receptor CXCR2 in Alveolar Epithelial Neoplasia Induced by Oncogenic Kras
Authors: Wislez Marie , Fujimoto Nobukazu , Izzo Julie G. , Hanna Amy E. , Cody Dianna D. , Langley Robert R. , Tang Hongli , Burdick Marie D. , Sato Mitsuo , Minna John D. , Mao Li , Wistuba Ignacio , Strieter Robert M. , Kurie Jonathan M. 
Published: April 2006

AbstractCXCL8, a ligand for the chemokine receptor CXCR2, was recently reported to be a transcriptional target of Ras signaling, but its role in Ras-induced tumorigenesis has not been fully defined. Here, we investigated the role of KC and MIP-2, the murine homologues of CXCL8, in KrasLA1 mice, which develop lung adenocarcinoma owing to somatic activation of the KRAS oncogene. We first investigated biological evidence of CXCR2 ligands in KrasLA1 mice. Malignant progression of normal alveolar epithelial cells to adenocarcinoma in KrasLA1 mice was associated with enhanced intralesional vascularity and neutrophilic inflammation, which are hallmarks of chemoattraction by CXCR2 ligands. In in vitro migration assays, supernatants of bronchoalveolar lavage samples from KrasLA1 mice chemoattracted murine endothelial cells, alveolar inflammatory cells, and the LKR-13 lung adenocarcinoma cell line derived from KrasLA1 mice, an effect that was abrogated by pretreatment of the cells with a CXCR2-neutralizing antibody. CXCR2 and its ligands were highly expressed in LKR-13 cells and premalignant alveolar lesions in KrasLA1 mice. Treatment of KrasLA1 mice with a CXCR2-neutralizing antibody inhibited the progression of premalignant alveolar lesions and induced apoptosis of vascular endothelial cells within alveolar lesions. Whereas the proliferation of LKR-13 cells in vitro was resistant to treatment with the antibody, LKR-13 cells established as syngeneic tumors were sensitive, supporting a role for the tumor microenvironment in the activity of CXCR2. Thus, high expression of CXCR2 ligands may contribute to the expansion of early alveolar neoplastic lesions induced by oncogenic KRAS. (Cancer Res 2006; 66(8): 4198-207)
Ligand Activation of Peroxisome Proliferator–Activated Receptor β Inhibits Colon Carcinogenesis
Authors: Marin Holly E. , Peraza Marjorie A. , Billin Andrew N. , Willson Timothy M. , Ward Jerrold M. , Kennett Mary J. , Gonzalez Frank J. , Peters Jeffrey M. 
Published: April 2006

Abstract
There is considerable debate whether peroxisome proliferator–activated receptor β/δ (PPARβ/δ) ligands potentiate or suppress colon carcinogenesis. Whereas administration of a PPARβ ligand causes increased small intestinal tumorigenesis in Apcmin/+ mice, PPARβ-null (Pparb−/−) mice exhibit increased colon polyp multiplicity in colon cancer bioassays, suggesting that ligand activation of this receptor will inhibit colon carcinogenesis. This hypothesis was examined by treating wild-type (Pparb+/+) and Pparb−/− with azoxymethane, coupled with a highly specific PPARβ ligand, GW0742. Ligand activation of PPARβ in Pparb+/+ mice caused an increase in the expression of mRNA encoding adipocyte differentiation–related protein, fatty acid–binding protein, and cathepsin E. These findings are indicative of colonocyte differentiation, which was confirmed by immunohistochemical analysis. No PPARβ-dependent differences in replicative DNA synthesis or expression of phosphatase and tensin homologue, phosphoinositide-dependent kinase, integrin-linked kinase, or phospho-Akt were detected in ligand-treated mouse colonic epithelial cells although increased apoptosis was found in GW0742-treated Pparb+/+ mice. Consistent with increased colonocyte differentiation and apoptosis, inhibition of colon polyp multiplicity was also found in ligand-treated Pparb+/+ mice, and all of these effects were not found in Pparb−/− mice. In contrast to previous reports suggesting that activation of PPARβ potentiates intestinal tumorigenesis, here we show that ligand activation of PPARβ attenuates chemically induced colon carcinogenesis and that PPARβ-dependent induction of cathepsin E could explain the reported disparity in the literature about the effect of ligand activation of PPARβ in the intestine. (Cancer Res 2006; 66(8): 4394-401)
Identification of Domains of BRCA1 Critical for the Ubiquitin-Dependent Inhibition of Centrosome Function
Authors: Sankaran Satish , Starita Lea M. , Simons Amanda M. , Parvin Jeffrey D. 
Published: April 2006

Abstract
The breast and ovarian cancer specific tumor suppressor BRCA1, bound to BARD1, has multiple functions aimed at maintaining genomic stability in the cell. We have shown earlier that the BRCA1/BARD1 E3 ubiquitin ligase activity regulates centrosome-dependent microtubule nucleation. In this study, we tested which domains of BRCA1 and BARD1 were required to control the centrosome function. In the present study, (a) we confirmed that the ubiquitination activity of BRCA1 regulates centrosome number and function in Hs578T breast cancer cells; (b) we observed that both the amino and carboxyl termini of BRCA1 are required for regulation of centrosome function in vitro; (c) an internal domain (770-1,290) is dispensable for centrosome regulation; (d) BARD1 is required for regulation of centrosome function and protein sequences within the terminal 485 amino acids are necessary for activity; and (e) BARD1 is localized at the centrosome throughout the cell cycle. We conclude that the BRCA1-dependent E3 ubiquitin ligase functions to restrain centrosomes in mammary cells, and loss of BRCA1 in the precancerous breast cell leads to centrosomal hypertrophy, a phenotype commonly observed in incipient breast cancer. (Cancer Res 2006; 66(8): 4100-7)
Akt Signaling and Cancer: Surviving but not Moving On
Authors: Toker Alex , Yoeli-Lerner Merav 
Published: April 2006

Abstract
The frequent deregulation of the phosphoinositide 3-kinase/Akt survival signaling pathway in cancer has prompted significant interest in blocking this pathway to treat cancer. Recently, however, two studies have shown that the Akt isoform Akt1 limits the invasive migration of breast cancer cells. These studies suggest that Akt1 may have a dual role in tumorigenesis, acting not only pro-oncogenically by suppressing apoptosis but also anti-oncogenically by suppressing invasion and metastasis. We discuss the possible implications of these findings for therapeutic development of Akt inhibitors to treat cancer. (Cancer Res 2006; 66(8): 3963-6)
Salinity Assimilation Using S(T): Covariance Relationships
Authors: Haines K. , Blower J. D. , Drecourt J-P. , Liu C. , Vidard A. , Astin I. , Zhou X. 
Published: April 2006

Abstract
Assimilation of salinity into ocean and climate general circulation models is a very important problem. Argo data now provide far more salinity observations than ever before. In addition, a good analysis of salinity over time in ocean reanalyses can give important results for understanding climate change. Here it is shown from the historical ocean database that over large regions of the globe (mainly midlatitudes and lower latitudes) variance of salinity on an isotherm S(T) is often less than variance measured at a particular depth S(z). It is also shown that the dominant temporal variations in S(T) occur more slowly than variations in S(z), based on power spectra from the Bermuda time series. From ocean models it is shown that the horizontal spatial covariance of S(T) often has larger scales than S(z). These observations suggest an assimilation method based on analyzing S(T). An algorithm for assimilating salinity data on isotherms is then presented, and it is shown how this algorithm produces orthogonal salinity increments to those produced during the assimilation of temperature profiles. It is argued that the larger space and time scales can be used for the S(T) assimilation, leading to better use of scarce salinity observations. Results of applying the salinity assimilation algorithm to a single analysis time within the ECMWF seasonal forecasting ocean model are also shown. The separate salinity increments coming from temperature and salinity data are identified, and the independence of these increments is demonstrated. Results of an ocean reanalysis with this method will appear in a future paper.
A Methodology for the Regional-Scale-Decomposed Atmospheric Water Budget: Application to a Simulation of the Canadian Regional Climate Model Nested by NCEP–NCAR Reanalyses over North America
Authors: Bielli Soline , Laprise René 
Published: April 2006

Abstract
The purpose of this work is to study the added value of a regional climate model with respect to the global analyses used to drive the regional simulation, with a special emphasis on the nonlinear interactions between different spatial scales, focusing on the moisture flux divergence. The atmospheric water budget is used to apply the spatial-scale decomposition approach, as it is a key factor in the energetics of the climate. A Fourier analysis is performed individually for each field on pressure levels. Each field involved in the computation of moisture flux divergence is separated into three components that represent selected scale bands, using the discrete cosine transform. The divergence of the moisture flux is computed from the filtered fields. Instantaneous and monthly mean fields from a simulation performed with the Canadian Regional Climate Model are decomposed and allowed to separate the added value of the model to the total fields.
Results show that the added value resides in the nonlinear interactions between large (greater than 1000 km) and small (smaller than 600 km) scales. The main small-scale forcing of the wind is topographic, whereas the humidity tends to show more small scales over the ocean. The time-mean divergence of moisture flux is also decomposed into contributions from stationary eddies and transient eddies. Both stationary and transient eddies are decomposed into different spatial scales and show very different patterns. The time-mean divergence due to transient eddies is dominated by large-scale (synoptic scale) features with little small scales. The divergence due to stationary eddies is a combination of small- and large-scale terms, and the main small-scale contribution occurs over the topography.
The same decomposition has been applied to the NCEP–NCAR reanalyses used to drive the regional simulation; the results show that the model best reproduces the time-fluctuation component of the moisture flux divergence, with a correlation between the model simulation and the NCEP–NCAR reanalyses above 0.90.
Chloropropyl-modified MCM-41 as Gas Chromatography Matrix for the Separation of Water–Alcohol Mixtures
Authors: Guan Lianxiu , Li Junping , Cao Hu , Zhao Ning , Wang Xiuzhi , Wei Wei , Sun Yuhan 
Published: April 2006

Abstract
In the present work, chloropropyl-functionlized MCM-41 were prepared by a simple synthetic pathway and firstly studied as gas chromatography matrix for the separation of water–alcohol mixtures.
A Novel Method to Identify Illegal Diesel Fuel, II: the Use of [1-D] n-Alkane with Stable Hydrogen Isotope Analysis
Authors: Suzuki Yaeko , Korenaga Takashi , Chikaraishi Yoshito 
Published: April 2006

Abstract
We demonstrated a novel identification method of illegal diesel fuel by using a deuterium (D) labeled n-alkane ([1-D] n-alkane) as a new chemical marker instead of coumarin. In a mixing system of diesel fuel with marker-labeled kerosene, kerosene content is quantitatively determined by D-enrichment of a target n-alkane in a mixed oil using compound-specific stable hydrogen isotope analysis. Thus, [1-D] n-alkane will become a high potential chemical marker instead of coumarin.