bluuebunny/crossref_metadata_2025_split huggingface dataset:
The association of hormonal contraceptive use and HPV prevalence
Authors: Marks Morgan , Gravitt Patti E. , Gupta Swati B. , Liaw Kai‐Li , Kim Esther , Tadesse Amha , Phongnarisorn Chailert , Wootipoom Virach , Yuenyao Pissamai , Vipupinyo Charoen , Rugpao Sungwal , Sriplienchan Somchai , Celentano David D. 
Published: August 2010

AbstractWomen diagnosed with cervical cancer report longer duration and more recent use of combined oral contraceptives (COCs). It is unclear whether COC use is associated with upstream events of human papillomavirus (HPV) infection prior to development of clinical disease. The objective of our study was to assess the association of contraceptive use on the risk for prevalent HPV infection in a cohort of long‐term hormonal contraceptive (HC) users. One thousand and seventy (n = 1,070) HIV‐negative women aged 20–37 from Thailand enrolled in a prospective study of the natural history of HPV. Baseline HPV genotype information, recency and duration of HC use, sexual behavior, other sexually transmitted infection (STI) information and cervical cytology and histology were assessed. At enrollment, 19.8% and 11.5% of women were infected with any HPV or any high‐risk (HR)‐HPV, respectively. After adjustment for age, current and past sexual risk behaviors, STI history and cytology, the use of COCs for >6 years was found to be associated with an increased risk of infection with any HPV [prevalence ratio (PR): 1.88 (1.21, 2.90)] and any HR‐HPV [PR: 2.68 (1.47, 4.88)] as compared to never users. Recent, long‐term COC use was associated with an increased risk for prevalent HPV infection independent of sexual behavior and cervical abnormalities. No similar association was observed for recent or long duration use of progestin‐only contraceptives (i.e., depomedroxyprogesterone acetate). These data suggest that COC use may impact early upstream events in the natural history of HPV infection.
Differential hypermethylation of genes in vulvar cancer and lichen sclerosus coexisting or not with vulvar cancer
Authors: Guerrero David , Guarch Rosa , Ojer Amaya , Casas Juan Manuel , Méndez‐Meca Carolina , Esteller Manel , Barba‐Ramos Edurne , Garcia‐Bragado Federico , Puras Ana 
Published: August 2010

AbstractSquamous cell carcinoma (SCC) of the vulva is a heterogeneous disease, associated or not with vulvar lichen sclerosus (LS). The precursor role of LS in vulvar cancer is unclear. We studied the epigenetic alterations of RASSF1A, RASSF2A, p16, TSP‐1 and MGMT genes in vulvar SCCs, LS associated with SCC, isolated LS and normal vulvar skin. Gene hypermethylation and human papillomavirus presence were evaluated by methylation‐specific PCR and PCR/reverse line blot, respectively. High‐risk human papillomavirus types were present in 16.7% of the patients with vulvar SCC. There were increasing percentages of hypermethylation of genes from isolated LS to LS associated with vulvar SCC and vulvar SCC. The genes were hypermethylated more frequently in vulvar SCC associated with LS than in those not associated with LS, MGMT and RASSF2A being unmethylated in LS not associated with vulvar SCC. TSP‐1 hypermethylation was related to recurrence in patients with vulvar cancer. Conclusions are as follows: (i) the epigenetic inactivation of genes is a common event in vulvar SCC and is also present in adjacent lesions, implying a possible precursor role for these alterations; (ii) MGMT and RASSF2A hypermethylation are present exclusively in vulvar SCC and LS associated with SCC, and absent from isolated LS; and (iii) TSP‐1 hypermethylation is a bad prognosis factor in vulvar SCC.
Predicting the progression of cervical precursor lesions by human papillomavirus genotyping: A prospective cohort study
Authors: Matsumoto Koji , Oki Akinori , Furuta Reiko , Maeda Hiroo , Yasugi Toshiharu , Takatsuka Naoyoshi , Mitsuhashi Akira , Fujii Takuma , Hirai Yasuo , Iwasaka Tsuyoshi , Yaegashi Nobuo , Watanabe Yoh , Nagai Yutaka , Kitagawa Tomoyuki , Yoshikawa Hiroyuki ,   for Japan HPV And Cervical Cancer (JHACC) Study Group
Published: August 2010

AbstractOnly a subset of cervical precursor lesions progress to cervical cancer and because of the lack of the predictive markers, it cannot be ascertained which lesions will progress or not. To estimate the risk of disease progression associated with human papillomavirus (HPV) genotypes, we followed 570 Japanese women with cytological LSIL (low‐grade squamous intraepithelial lesion) and histological CIN (cervical intraepithelial neoplasia) grade 1–2 lesions (479 CIN 1; 91 CIN 2) at 3 to 4 month intervals for a mean follow‐up period of 39.1 months. At entry, we detected HPV DNA in cervical samples by polymerase chain reaction‐based methodology. Over the period of follow‐up period, 46 lesions progressed to CIN 3 while 362 regressed to normal cytology. Women with multiple HPV infections were more likely to have persistent lesions (hazard ratio [HR] for regression, 0.65; 95% confidence interval [CI], 0.42–1.02; p = 0.07); however, multiple infections did not increase the risk of progression (HR for progression, 1.04; 95% CI, 0.37–2.94; p = 0.94). After adjusting for CIN grade and women's age, HRs for progression to CIN 3 (vs. women with low‐risk types or negative for HPV DNA) varied markedly by HPV genotype: type 16 (11.1, 95% CI: 1.39–88.3); 18 (14.1, 0.65–306); 31 (24.7, 2.51–243); 33 (20.3, 1.78–231); 35 (13.7, 0.75–251); 52 (11.6, 1.45–93.3); 58 (8.85, 1.01–77.6); other high‐risk types (4.04, 0.47–34.7). HPV 45 was not detected in our study subjects. The cumulative probability of CIN 3 within 5 years was 20.5% for HPV 16, 18, 31, 33, 35, 52 and 58; 6.0% for other high‐risk types; 1.7% for low‐risk types (p = 0.0001). In conclusion, type‐specific HPV testing for women with LSIL/CIN 1–2 lesions is useful for identifying populations at increased or decreased risk of disease progression.
Upregulation of TRAG3 gene in urothelial carcinoma of the bladder
Authors: Karam Jose A. , Huang Sandra , Fan Jinhai , Stanfield Jennifer , Schultz Roger A. , Pong Rey‐Chen , Sun Xiankai , Mason Ralph P. , Xie Xian‐Jin , Niu Gang , Chen Xiaoyuan , Frenkel Eugene P. , Sagalowsky Arthur I. , Hsieh Jer‐Tsong 
Published: August 2010

AbstractConventional chemotherapy is commonly used for advanced stages of bladder cancer with modest success and high morbidity. Identifying markers of resistance will allow clinicians to tailor treatment to a specific patient population. T24‐tumorigenic cell line was grown orthotopically in nude mice and monitored using bioluminescence imaging and microcomputed tomography until they developed metastases. Stable sublines were then developed from primary bladder (T24‐P), lung (T24‐L) and bone (T24‐B) tissues. Chromosomal analysis and DNA microarray were used to characterize these sublines. Real‐time quantitative polymerase chain reaction and immunohistochemistry were used for validation. Epigenetic modifiers were used to study gene regulation. The cell viability was quantified with MTT assay. Chromosomal analysis revealed multiple alterations in metastatic cell lines compared to T24‐P. DNA microarray analysis showed that taxol resistance‐associated gene (TRAG) 3 was the most upregulated gene. From real‐time quantitative polymerase chain reaction and immunohistochemistry, TRAG3 was significantly higher in T24‐L and T24‐B than T24‐P. TRAG3 gene expression is likely controlled by DNA methylation but not histone acetylation. Interestingly, T24‐B and T24‐L cells were more resistant than T24‐P to treatment with antimicrotubule agents such as docetaxel, paclitaxel and vinblastine. TRAG3 mRNA expression was higher in 20% of patients with ≤pT2 (n = 10) and 60% of patients with ≥pT3 (n = 20) compared to normal adjacent tissue (p = 0.05). In addition, the median TRAG3 expression was 6.7‐fold higher in ≥pT3 tumors compared to ≤pT2 tumors. Knowing the status of TRAG3 expression could help clinicians tailor treatment to a particular patient population that could benefit from treatment, while allocating patients with resistant tumors to new experimental therapies.
Antiapoptotic function of charged multivesicular body protein 5: A potentially relevant gene in acute myeloid leukemia
Authors: Shahmoradgoli Maria , Mannherz Otto , Engel Felix , Heck Stefanie , Krämer Alwin , Seiffert Martina , Pscherer Armin , Lichter Peter 
Published: August 2010

AbstractIn recent years, RNA interference (RNAi) has been widely used to uncover gene function or pathway context of novel genes. In our study, we describe a short‐hairpin RNA‐based RNAi screening of a set of functionally uncharacterized human genes for their possible capability to inhibit apoptosis. We thereby identified a new antiapoptotic function for CHMP5 (charged multivesicular body protein 5), which was confirmed by overexpression and rescue assays. Furthermore, caspase assays showed that CHMP5 silencing induced caspase cascade activation mainly through extrinsic apoptosis pathway. Based on genome‐wide expression array profiling, a possible regulatory role of CHMP5 on apoptosis‐associated genes and different signaling pathways including nuclear factor kappa B was revealed. In addition, we found significantly higher CHMP5 mRNA levels in acute myeloid leukemia patients. This observation together with the antiapoptotic feature of CHMP5 suggests a possible oncogenic function for this gene in leukemogenesis.
Role of p115RhoGEF in the regulation of extracellular Ca2+‐induced choline kinase activation and prostate cancer cell proliferation
Authors: Huang Chunfa , Liu Siguo , Miller R. Tyler 
Published: August 2010

AbstractCa2+ is a ubiquitous cellular signal which plays a central role in the regulation of cell function. To understand aberrant signaling through the Ca2+‐sensing receptor (CaR) in prostate cancer cells, we compared expression of CaR signaling components in human nonmalignant prostate epithelial cells and several prostate cancer cell lines, as well as normal human prostate and prostate tumor specimens. We found that levels of the CaR, Gα12 and p115RhoGEF expression are significantly up‐regulated in more tumorigenic prostate cancer cells and prostate tumor specimens. By silencing CaR, Gα12, p115RhoGEF or choline kinase (ChoK) expression, analyzing the change in lipid profiles, blocking signaling pathways using chemical inhibitors, and co‐immunoprecipitating the relevant signaling proteins, we demonstrate that p115RhoGEF, a regulator of G protein signaling (RGS) with GAP activity for Gα12/13 and with guanine nucleotide exchange activity for the small G protein Rho, plays an important role in the regulation of Ca‐induced ChoK activation and cell proliferation in more tumorigenic prostate cancer cell lines. The results demonstrate an important role of p115RhoGEF in prostate tumorigenesis and provide a potential target of cancer therapeutics.
Self‐Assembly of Nanostructures on Surfaces Using Metal–Organic Coordination
Authors: Rubinstein Israel , Vaskevich Alexander 
Published: August 2010

AbstractLayer‐by‐layer (LbL) assembly of multilayers is an established method for the construction of layered nanostructures on surfaces, affording control of the thickness, composition, and organization in the vertical direction. Binding between layers is accomplished using various types of interactions, including electrostatic binding, hydrogen bonding, covalent bonding, metal–organic coordination, host–guest interactions, biospecific interactions, and others. Here we focus on LbL assembly using metal–organic coordination, and specifically on layered nanostructures based on bishydroxamate–M4+ binding. The coordination approach offers attractive features, such as a simple reaction, a defined geometry, and reversibility under certain conditions. The basic scheme includes self‐assembly of a ligand (anchor) monolayer on the surface, followed by alternate binding of metal ions and multi‐functional ligand layers, to form a coordination multilayer. This approach is demonstrated by the construction of a variety of coordinated nanostructures, including bilayers, multilayers, dendrimers, and nanoparticle assemblies, prepared on gold and oxide substrates.
Electrochemistry at Ultramicroelectrode Arrays and Nanoelectrode Ensembles of Macro‐ and Ultramicroelectrode Dimensions
Authors: Zoski Cynthia G. , Wijesinghe Manjula 
Published: August 2010

AbstractRecent experiments on the development and characterization of nanoelectrode ensembles (NEEs) based on Au‐filled polycarbonate membranes and microfabricated addressable ultramicroelectrode (UME) arrays are described. Macro‐NEEs operate under primarily transient diffusion conditions while the more recently developed ultramicro‐NEEs operate under primarily steady‐state diffusion conditions due to the high rate of mass transport to the nanoelectrode sites and the overall ultramicro‐geometry; both types of NEEs are discussed. In addition to the traditional characterization methods of scanning electron microscopy (SEM) and cyclic voltammetry (CV) for arrays and ensembles, the use of scanning electrochemical microscopy (SECM) in assessing the viability of the insulated addressing tracks, as well as the electrochemical reactivity and conductivity of the individual UME sites, is discussed. The behavior of infinite (i. e., macro‐) arrays and ensembles of UME and NE sites is well understood, but this is not the case for finite (i. e., ultramicro‐) arrays and ensembles, where the perimeter sites now play a large role in the overall steady‐state behavior. A general theory and 3D simulations for these UME‐NEEs are described.
Formation, Characterization, and Applications of Organic and Inorganic Nanometric Films
Authors: Mandler Daniel 
Published: August 2010

AbstractThe formation of thin coatings based on either self‐assembled monolayers or polymeric films is discussed. These coatings are used to structure surfaces and control their physical and chemical properties. Different examples are given from our work emphasizing the advantages of monolayers and polymeric films. Finally, different approaches, which benefit from both monolayers and polymeric films, are presented.
Synergistic repression of estrogen receptor transcriptional activity by FHL2 and Smad4 in breast cancer cells
Authors: Xiong Zhihong , Ding Lihua , Sun Junzhong , Cao Jia , Lin Jing , Lu Zhaohui , Liu Yufei , Huang Cuifen , Ye Qinong 
Published: August 2010

AbstractFour and a half LIM domain protein 2 (FHL2) has been implicated in development and progression of various types of cancers. However, little is known about the biological function of FHL2 in breast cancer. Here, we report that FHL2 physically and functionally interacts with estrogen receptors (ERα and ERβ), important regulators of breast cancer development and progression. The N‐terminal half LIM domain or a single LIM domain of FHL2 was sufficient for its interaction with ERα and ERβ. Overexpression of FHL2 reduced ER transcriptional activity in breast cancer cells, whereas reduction of endogenous FHL2 with FHL2 small interfering RNA enhanced ER transactivation. Moreover, FHL2 cooperates with Smad4, a previously known corepressor for ERα, to inhibit ERα transcriptional activity as well as expression of the estrogen‐responsive gene cathepsin D. The synergistic inhibition of ERα transcriptional activity by FHL2 and Smad4 may be due to enhanced interaction of Smad4 with ERα by FHL2, because FHL2(1–156), the FHL2 deletion mutant, which showed no synergistic effect, failed to increase such interaction. These data suggested the cooperative regulation of estrogen signaling by FHL2 and Smad4 in breast cancer cells, and might provide a new regulation mechanism underlying breast cancer development and progression. © 2010 IUBMB IUBMB Life, 62(9): 669–676, 2010
In vitroeffect of nickel on bovine spermatozoa motility and annexin V‐labeled membrane changes
Authors: Lukac Norbert , Bardos Laszlo , Stawarz Robert , Roychoudhury Shubhadeep , Makarevich Alexander V. , Chrenek Peter , Danko Jan , Massanyi Peter 
Published: August 2010

AbstractIn this study the effect ofin vitroculture of bovine spermatozoa with nickel (NiCl2) on spermatozoa motility and membrane changes was analyzed. The spermatozoa motility significantly decreased after 120 min of culture at the concentration of 1000 μm Ni ml−1(P < 0.05) and after 240 min of culture at the concentration of 500 and 1000 μm Ni ml−1(P < 0.001) as compared with control. The progressive motility was the highest in the control group and in the groups with the lowest nickel concentrations (7.8 and 125 μm Ni ml−1). The progressive spermatozoa motility was significantly altered even after 30 min of culture in the group with the highest nickel concentration (1000 μm Ni ml−1). A significant decrease in progressive motility from the concentration of 250 μm Ni ml−1was detected after 240 min of culture. Concentrations from 125 μm Ni ml−1in various time periods of culture stimulated spermatozoa motility after 30 min (P < 0.001), but later an inhibitory effect was noted. After 240 min ofin vitrospermatozoa culture with 125 μm Ni ml−1a typical Annexin V fluorescence reaction was detected. Fluorescence was detected in mitochondrial segment of bovine spermatozoa. In spermatozoa exposed to higher nickel concentrations the Annexin V‐positive reaction was detected also on the spermatozoa head membrane. In the group with the highest concentration and the longest time of exposure (1000 μm Ni ml−1; 240 min) the apoptotic Annexin‐positive regions were detected not only in the mitochondrial part, but also in the spermatozoa head (acrosomal and postacrosomal part), showing significant alteration of spermatozoa membrane integrity. Copyright © 2010 John Wiley & Sons, Ltd.
Chemoprevention of a flavonoid fraction from Rhus verniciflua Stokes on aflatoxin B1‐induced hepatic damage in mice
Authors: Choi Ki‐Choon , Chung Wan‐Tae , Kwon Jung‐Kee , Jang Yong‐Suk , Yu Ji‐Yeon , Park Seung‐Moon , Lee Jeong‐Chae 
Published: August 2010

AbstractSince aflatoxin B1 (AFB1)‐mediated hepatic damage is related to the production of AFB1‐8,9‐epoxide and reactive oxygen species, bioactive compounds having antioxidant potentials are suggested to be capable of reducing AFB1‐induced toxicity. We previously purified a mixture of flavonoids that we named RCMF (Rhus verniciflua Stokes chloroform–methanol fraction), from a traditional Korean food additive and herbal medicine. RCMF exhibited various biological effects, including antioxidant and antitumor activities. In this study, we examined whether RCMF protects against AFB1‐induced liver injury using in vitro and in vivo systems. Pretreatment of HepG2 cells with RCMF significantly reduced AFB1‐stimulated production of ROS and malondialdehyde (MDA) to the control levels. RCMF also prevented the reduction in HepG2 cell viability caused by AFB1. Oral administration of RCMF to mice significantly suppressed an AFB1‐induced increase in serum levels of alanine aminotransferase, alkaline phosphatase and lactate dehydrogenase. It also prevented MDA formation and blocked decreases in glutathione levels and superoxide dismutase activities in the livers of AFB1‐treated mice. In addition, RCMF supplementation prevented an AFB1‐induced decrease in serum titers of IgA and IgG1. Collectively, these results suggest that RCMF attenuates AFB1‐mediated damage to the liver, and that this effect is at least partially related to the restoration of antioxidant defense systems and an increase in AFB1–GSH conjugate formation. Copyright © 2010 John Wiley & Sons, Ltd.
Developmental toxicity of dextromethorphan in zebrafish embryos/larvae
Authors: Xu Zheng , Williams Frederick E. , Liu Ming‐Cheh 
Published: August 2010

AbstractDextromethorphan is widely used in over‐the‐counter cough and cold medications. Its efficacy and safety for infants and young children remains to be clarified. The present study was designed to use zebrafish as a model to investigate the potential toxicity of dextromethorphan during embryonic and larval development. Three sets of zebrafish embryos/larvae were exposed to dextromethorphan at 24, 48 and 72 h post fertilization (hpf), respectively, during the embryonic/larval development. Compared with the 48 and 72 hpf exposure sets, the embryos/larvae in the 24 hpf exposure set showed much higher mortality rates which increased in a dose‐dependent manner. Bradycardia and reduced blood flow were observed for the embryos/larvae treated with increasing concentrations of dextromethorphan. Morphological effects of dextromethorphan exposure, including yolk sac and cardiac edema, craniofacial malformation, lordosis, non‐inflated swim bladder and missing gill, were also more frequent and severe among zebrafish embryos/larvae exposed to dextromethorphan at 24 hpf. Whether the more frequent and severe developmental toxicity of dextromethorphan observed among the embryos/larvae in the 24 hpf exposure set, as compared with the 48 and 72 hpf exposure sets, is due to the developmental expression of the phase I and phase II enzymes involved in the metabolism of dextromethorphan remains to be clarified. A reverse transcription‐polymerase chain reaction analysis, nevertheless, revealed developmental stage‐dependent expression of mRNAs encoding SULT3 ST1 and SULT3 ST3, two enzymes previously shown to be capable of sulfating dextrorphan, an active metabolite of dextromethorphan. Copyright © 2010 John Wiley & Sons, Ltd.
Does 2,2′,4,4′‐tetrabromodiphenyl ether interact directly with thyroid receptor?
Authors: Suvorov Alexander , Bissonnette Cyntia , Takser Larissa , Langlois Marie‐France 
Published: August 2010

Abstract2,2′,4,4′‐tetrabromodiphenyl Ether (BDE‐47) is a flame‐retardant chemical appearing at increasing concentrations and frequency in the environment and human samples. A number of health effects of exposure to BDE‐47 have been observed, thyroid disruption being the most sensitive. Our objective was to examine BDE‐47 interaction with thyroid receptor beta (TRβ). We used a variety of approaches, including in vitro binding assays, luciferase reporter‐gene transcriptional assays, and analysis of expression of thyroid responsive genes in rat offspring exposed perinatally to BDE‐47. We found that BDE‐47 alone or in mixture with 2,2′,4,4′,5‐pentabromodiphenyl ether (BDE‐99), 2,2′,4,4′,6‐pentabromodiphenyl ether (BDE‐100), and 2,2′,4,4′,5,5′‐hexabromodiphenyl ether (BDE‐153) does not compete with [125I]T3 for TRβ‐binding even at 4000 fold higher concentrations. Also, BDE‐47 does not affect thyroid responsive genes through TRβ in in vitro studies of transcription regulation. A subset of thyroid responsive genes were significantly differentially expressed in liver and frontal lobe brain samples of exposed pups, however, the action of BDE‐47 was neither agonistic or antagonistic to that of thyroid hormone. We conclude that BDE‐47 does not interact directly with TRβ1 nor does it influence its transcriptional activity. Developmental exposure of rats to BDE‐47 leads to differential expression of thyroid responsive genes in liver and brain due to unknown mechanism. Copyright © 2010 John Wiley & Sons, Ltd.