bluuebunny/crossref_metadata_2025_split huggingface dataset:
Human papillomavirus genotype in cervical intraepithelial neoplasia grades 2 and 3 of Taiwanese women
Authors: Chao Angel , Jao Mei‐Shan , Huang Chu‐Chun , Huang Huei‐Jean , Cheng Hui‐Hsin , Yang Jung‐Erh , Hsueh Swei , Chen Tse‐Ching , Qiu Jian‐Tai , Lin Cheng‐Tao , Fu Chang‐Jui , Chou Hung‐Hsueh , Lai Chyong‐Huey 
Published: April 2010

AbstractWe aimed to assess the distribution of human papillomavirus (HPV) genotypes in high‐grade cervical lesions in Taiwan. The study included 1,086 paraffin‐embedded, formaldehyde‐fixed cervical intraepithelial neoplasia (CIN) 2/3 specimens. HPV genotyping was performed using polymerase chain reaction (PCR)‐based methods. Multiple HPV types were validated by E6 type‐specific PCR, direct sequencing and/or real‐time PCR. HPV DNA was detected in 995 (91.6%) specimens, and multiple HPV types were identified in 192 (19.3%) samples. The leading HPV types were HPV16 (24%), HPV52 (20%), HPV58 (20%), HPV33 (13%), HPV31 (8%) and HPV18 (4.6%). Although the leading six types consisted of 87.6%, HPV16 or 18 comprised only 30.9%. The prevalence of different HPV types showed a significant association with age. In women older than 50 yr, HPV16 and 18 comprised 21.3% (83/389), while HPV52, 58 and 33 represented 55.5% (216/389). In women aged less than 50 yr, HPV16 and 18 comprised 32.1% (224/697, p < 0.0001), while HPV 52, 58 and 33 represented 47.9% (334/697, p = 0.02). The distribution of HPV genotypes was compared with previously reported findings for Taiwanese women with cervical cancer (CC). The overall HPV16 positivity rate was significantly higher in CC than in CIN 2/3 (odds ratio: 2.14, 95% CI: 1.91–2.40). In addition, HPV18, 39 and 45 were significantly overrepresented in CC, whereas HPV52, 58, 33, 31, 35, 51 and 53 were underrepresented. We concluded that an effective vaccine against the most common HPV types could prevent a significant proportion of cervical cancer cases that occur in Taiwan.
Association of haplotypes of inflammation‐related genes with gastric preneoplastic lesions in African Americans and Caucasians
Authors: Zabaleta Jovanny , Camargo Maria C. , Ritchie Marylyn D. , Piazuelo Maria B. , Sierra Rosa A. , Turner Stephen D. , Delgado Alberto , Fontham Elizabeth T.H. , Schneider Barbara G. , Correa Pelayo , Ochoa Augusto C. 
Published: April 2010

AbstractIdentification of biomarkers is needed for development of screening programs to prevent gastric cancer. Because racial differences exist in cancer rates, we aimed to evaluate the association between polymorphisms in inflammation‐related genes and gastric preneoplastic lesions in African Americans and Caucasians from Louisiana, USA. Gastric biopsies from 569 adults (361 African Americans and 208 Caucasians) undergoing diagnostic endoscopy were used for histological diagnosis and genomic DNA extraction. Polymorphisms within eight genes (IL1B, IL8, IL6, TNF, PTGS2, ARG1, IL10 and TGFB1) were investigated by TaqMan. The cagA status of Helicobacter pylori infection was assessed by PCR. Haplotype logistic regression models were used to identify variables associated with intestinal metaplasia or dysplasia. African Americans carrying the haplotype IL1B‐511T/−31C/+3954T, which includes the three risk‐associated alleles at the IL1B locus, were more likely to being diagnosed with intestinal metaplasia or dysplasia than those carrying the most common haplotype T‐C‐C (adjusted OR: 2.51, 95% CI: 1.1–5.5). None of the polymorphisms were associated with intestinal metaplasia and dysplasia in Caucasians. Age and cagA‐positive status were independent factors associated with these lesions. Haplotypes at the IL1B locus may participate in mediating the susceptibility to gastric carcinogenesis and might be useful as markers of advanced premalignant lesions in African Americans. Interestingly, carriage of IL1B+3954T allele seems to be the key factor, even though the role played by other polymorphisms cannot be excluded.
Higher susceptibility to aflatoxin B1‐related hepatocellular carcinoma in glycine N‐methyltransferase knockout mice
Authors: Liu Shih‐Ping , Li Ying‐Shiuan , Lee Cheng‐Ming , Yen Chia‐Hung , Liao Yi‐Jen , Huang Shiu‐Feng , Chien Chau‐Heng , Chen Yi‐Ming Arthur 
Published: April 2010

AbstractIn both humans and rodents, males are known to be more susceptible than females to hepatocarcinogenesis. We have previously reported that glycine N‐methyltransferase (GNMT) interacts with aflatoxin B1 (AFB1) and reduces both AFB1‐DNA adduct formation and hepatocellular carcinoma (HCC) in mice. We also reported that 50% of the males and 100% of the females in a small group of Gnmt null (Gnmt−/−) mice developed HCC, with first dysplastic hepatocellular nodules detected at mean ages of 17 and 16.5 months, respectively. In our study, we tested our hypothesis that male and female Gnmt−/− mice are susceptible to AFB1 carcinogenesis, and that the absence of Gnmt expression may accelerate AFB1‐induced liver tumorigenesis. We inoculated Gnmt−/− and wild‐type mice intraperitoneally with AFB1 at 7 days and 9 weeks of age and periodically examined them using ultrasound. Dysplastic hepatocellular nodules were detected in six of eight males and five of five females at 12.7 and 12 months of ages, respectively. Dysplastic hepatocellular nodules from 5/8 (62.5%) male and 4/5 (80%) female Gnmt−/− mice were diagnosed as having HCC, ∼6 months earlier than AFB1‐treated wild‐type mice. Results from microarray and real‐time PCR analyses indicate that five detoxification pathway‐related genes were downregulated in AFB1‐treated Gnmt−/− mice: Cyp1a2, Cyp3a44, Cyp2d22, Gsta4 and Abca8a. In summary, we observed overall higher susceptibility to AFB1‐related HCC in Gnmt−/− mice, further evidence that GNMT overexpression is an important contributing factor to liver cancer resistance.
Enhancement of DNA vaccine potency by antigen linkage to IFN‐γ‐inducible protein‐10
Authors: Kang Tae Heung , Kim Keon Woo , Bae Hyun Cheol , Seong Seung‐Yong , Kim Tae Woo 
Published: April 2010

AbstractDNA vaccines have emerged as an attractive approach to generate antigen‐specific T‐cell immune response. Nevertheless, the potency of DNA vaccines still needs to be improved for cancer immunotherapy. In this study, we explored whether functional linkage of a Th1‐polarizing chemokine, IP‐10, to a model tumor antigen, human papillomavirus type 16 (HPV‐16) E7, enhanced DNA vaccine potency. IP‐10 linkage changed the location of E7 from the nucleus to the endoplasmic reticulum and led to the secretion of functionally chemoattractive chimeric IP‐10/E7 protein. In addition, this linkage drastically enhanced the endogenous processing of E7 antigen through MHC class I. More importantly, we found that C57BL/6 mice intradermally vaccinated with IP‐10/E7 DNA exhibited a dramatic increase in the number of E7‐specific CD4+ Th1 T‐cells and CD8+ T‐cells and, consequently, were strongly resistant over the long term to E7‐expressing tumors compared to mice vaccinated with wild‐type E7 DNA. Thus, because of the increase in tumor antigen‐specific T‐cell immune responses obtained through both enhanced antigen presentation and chemoattraction, vaccination with DNA encoding IP‐10 linked to a tumor antigen holds great promise for treating tumors.
Role of mesenchymal stem cells in tissue engineering of meniscus
Authors: Zellner Johannes , Mueller Michael , Berner Arne , Dienstknecht Thomas , Kujat Richard , Nerlich Michael , Hennemann Burkhard , Koller Michael , Prantl Lukas , Angele Martin , Angele Peter 
Published: April 2010

AbstractTissue engineering is a promising approach for the treatment of tissue defects. Mesenchymal stem cells are of potential use as a source of repair cells or of important growth factors for tissue engineering. The purpose of this study was to examine the role of mesenchymal stem cells in meniscal tissue repair. This was tested using several cell and biomaterial‐based treatment options for repair of defects in the avascular zone of rabbit menisci. Circular meniscal punch defects (2 mm) were created in the avascular zone of rabbit menisci and left empty or filled with hyaluronan‐collagen composite matrices without cells, loaded with platelet‐rich plasma, autologous bone marrow, or autologous mesenchymal stem cells. In some experiments, matrices with stem cells were precultured in chondrogenic medium for 14 days before implantation. Rabbits were then allowed free cage movement after surgery for up to 12 weeks. Untreated defects and defects treated with cell‐free implants had muted fibrous healing responses. Neither bone marrow nor platelet‐rich plasma loaded in matrices produced improvement in healing compared with cell‐free implants. The implantation of 14 days precultured chondrogenic stem cell‐matrix constructs resulted in fibrocartilage‐like repair tissue, which was only partially integrated with the native meniscus. Non‐precultured mesenchymal stem cells in hyaluronan‐collagen composite matrices stimulated the development of completely integrated meniscus‐like repair tissue. The study shows the necessity of mesenchymal stem cells for the repair of meniscal defects in the avascular zone. Mesenchymal stem cells seem to fulfill additional repair qualities besides the delivery of growth factors. © 2010 Wiley Periodicals, Inc. J Biomed Mater Res Part A, 2010.
Epidermal and dermal integration into sphere‐templated porous poly(2‐hydroxyethyl methacrylate) implants in mice
Authors: Fukano Y. , Usui M. L. , Underwood R. A. , Isenhath S. , Marshall A. J. , Hauch K. D. , Ratner B. D. , Olerud J. E. , Fleckman P. 
Published: April 2010

AbstractPercutaneous medical devices remain susceptible to infection and failure. We hypothesize that healing of the skin into the percutaneous device will provide a seal, preventing bacterial attachment, biofilm formation, and subsequent device failure. Porous poly(2‐hydroxyethyl methacrylate) [poly(HEMA)] with sphere‐templated pores (40 μm) and interconnecting throats (16 μm) were implanted in normal C57BL/6 mice for 7, 14, and 28 days. Poly(HEMA) was either untreated, keeping the surface nonadhesive for cells and proteins, or modified with carbonyldiimidazole (CDI) or CDI reacted with laminin 332 to enhance adhesion. No clinical signs of infection were observed. Epidermal and dermal response within the poly(HEMA) pores was evaluated using light and transmission electron microscopy. Cells (keratinocytes, fibroblasts, endothelial cells, inflammatory cells) and basement membrane proteins (laminin 332, β4 integrin, type VII collagen) could be demonstrated within the poly(HEMA) pores of all implants. Blood vessels and dermal collagen bundles were evident in all of the 14‐ and 28‐day implants. Fibrous capsule formation and permigration were not observed. Sphere‐templated polymers with 40 μm pores demonstrate an ability to recapitulate key elements of both the dermal and the epidermal layers of skin. Our morphological findings indicate that the implant model can be used to study the effects of biomaterial pore size, pore interconnect (throat) size, and surface treatments on cutaneous biointegration. Further, this model may be used for bacterial challenge studies. © 2010 Wiley Periodicals, Inc. J Biomed Mater Res Part A, 2010.
Isolation and characterization of a novel copper‐inducible metallothionein gene of a ciliate, Tetrahymena tropicalis lahorensis
Authors: Chaudhry Raheela , Shakoori Abdul Rauf 
Published: April 2010

AbstractThe two isoforms of copper metallothionein (CuMT) gene of a copper resistant ciliate, Tetrahymena tropicalis lahorensis (Ttl), have been isolated and characterized. The molecular cloning and nucleotide sequencing of cDNAs coding for the two CuMT isoforms revealed that TtlCuMT1 gene has 300, while TtlCuMT2 has 327 nucleotides, both with ATG as the initiation codon and TGA as the translational termination codon. TAG codes for glutamine in TtlCuMT2 gene which is peculiar to Tetrahymena. The deduced or translated TtlCuMT1 and TtlCuMT2 peptide sequences contain 100 and 108 amino acid residues including 28 and 32 cysteine residues, respectively. The amino acid sequences of TtlCuMT1 and TtlCuMT2 have special features of two and three CXCXXCXCXXCXC intragenic tandem repeats with a conserved structural pattern of cysteine, respectively. The predicted tertiary structures of these two isoforms indicate two domains. Domain I and the initial part of domain II showed >98% homology with other Tetrahymena CuMT. On the basis of the differences in the domain II, the metallothionein subfamily 7b can be divided into two groups, one (TtlCuMT1) comprising >100 amino acids and the other (TtlCuMT2) comprising <100 amino acids. This is a novel finding of the present study as no such report on this type of classification exists at the moment. TtlCuMT1 has 95%, while TtlCuMT2 has 97% resemblance with the previously reported CuMT genes of Tetrahymena spp. SDS‐PAGE analysis using fluorescent probe as well as coomassie brilliant blue staining also confirmed the presence of metallothionein. J. Cell. Biochem. 110: 630–644, 2010. © 2010 Wiley‐Liss, Inc.
Carboxylated N‐glycans on RAGE promote S100A12 binding and signaling
Authors: Srikrishna Geetha , Nayak Jonamani , Weigle Bernd , Temme Achim , Foell Dirk , Hazelwood Larnele , Olsson Anna , Volkmann Niels , Hanein Dorit , Freeze Hudson H. 
Published: April 2010

AbstractThe receptor for advanced glycation end products (RAGE) is a signaling receptor protein of the immunoglobulin superfamily implicated in multiple pathologies. It binds a diverse repertoire of ligands, but the structural basis for the interaction of different ligands is not well understood. We earlier showed that carboxylated glycans on the V‐domain of RAGE promote the binding of HMGB1 and S100A8/A9. Here we study the role of these glycans on the binding and intracellular signaling mediated by another RAGE ligand, S100A12. S100A12 binds carboxylated glycans, and a subpopulation of RAGE enriched for carboxylated glycans shows more than 10‐fold higher binding potential for S100A12 than total RAGE. When expressed in mammalian cells, RAGE is modified by complex glycans predominantly at the first glycosylation site (N25IT) that retains S100A12 binding. Glycosylation of RAGE and maximum binding sites for S100A12 on RAGE are also cell type dependent. Carboxylated glycan‐enriched population of RAGE forms higher order multimeric complexes with S100A12, and this ability to multimerize is reduced upon deglycosylation or by using non‐glycosylated sRAGE expressed in E. coli. mAbGB3.1, an antibody against carboxylated glycans, blocks S100A12‐mediated NF‐κB signaling in HeLa cells expressing full‐length RAGE. These results demonstrate that carboxylated N‐glycans on RAGE enhance binding potential and promote receptor clustering and subsequent signaling events following oligomeric S100A12 binding. J. Cell. Biochem. 110: 645–659, 2010. © 2010 Wiley‐Liss, Inc.
Controlled delivery of the heparan sulfate/FGF‐2 complex by a polyelectrolyte scaffold promotes maximal hMSC proliferation and differentiation
Authors: Calarco Anna , Petillo Orsolina , Bosetti Michela , Torpedine Angela , Cannas Mario , Perrone Lorena , Galderisi Umberto , Melone Mariarosa A.B. , Peluso Gianfranco 
Published: April 2010

AbstractGrowth factors and other regulatory molecules are required to direct differentiation of bone marrow‐derived human mesenchymal stem cells (hMSC) along specific lineages. However, the therapeutic use of growth factors is limited by their susceptibility to degradation, and the need to maintain prolonged local release of growth factor at levels sufficient to stimulate hMSC. The aim of this study was to investigate whether a device containing heparan sulfate (HS), which is a co‐factor in growth factor‐mediated cell proliferation and differentiation, could potentiate and prolong the delivery of fibroblast growth factor‐2 (FGF‐2) and thus enhance hMSC stimulation. To this aim, we synthesized cationic polyelectrolyte polymers covalently and non‐covalently anchored to HS and evaluated their effect on hMSC proliferation. Polymers non‐covalently bound to HS resulted in the release of an HS/FGF‐2 complex rather than FGF‐2 alone. The release of this complex significantly restored hMSC proliferation, which was abolished in serum‐free medium and only partially restored by the release of FGF‐2 alone as occurred with polymer covalently bound to HS. We also demonstrate that exposure to HS/FGF‐2 during early growth but not during post‐confluence is essential for hMSC differentiation down the fibroblast lineage, which suggests that both factors are required to establish the correct stem cell commitment that is necessary to support subsequent differentiation. In conclusion, the delivery platform described here is a step towards the development of a new class of biomaterial that enables the prolonged, non‐covalent binding and controlled delivery of growth factors and cofactors without altering their potency. J. Cell. Biochem. 110: ??–??, 2010. © 2010 Wiley‐Liss, Inc.
Biology and pathology of Rho GTPase, PI‐3 kinase‐Akt, and MAP kinase signaling pathways in chondrocytes
Authors: Beier Frank , Loeser Richard F. 
Published: April 2010

AbstractChondrocytes provide the framework for the developing skeleton and regulate long‐bone growth through the activity of the growth plate. Chondrocytes in the articular cartilage, found at the ends of bones in diarthroidial joints, are responsible for maintenance of the tissue through synthesis and degradation of the extracellular matrix. The processes of growth, differentiation, cell death and matrix remodeling are regulated by a network of cell signaling pathways in response to a variety of extracellular stimuli. These stimuli consist of soluble ligands, including growth factors and cytokines, extracellular matrix proteins, and mechanical factors that act in concert to regulate chondrocyte function through a variety of canonical and non‐canonical signaling pathways. Key chondrocyte signaling pathways include, but are not limited to, the p38, JNK and ERK MAP kinases, the PI‐3 kinase‐Akt pathway, the Jak‐STAT pathway, Rho GTPases and Wnt‐β‐catenin and Smad pathways. Modulation of the activity of any of these pathways has been associated with various pathological states in cartilage. This review focuses on the Rho GTPases, the PI‐3 kinase‐Akt pathway, and some selected aspects of MAP kinase signaling. Most studies to date have examined these pathways in isolation but it is becoming clear that there is significant cross‐talk among the pathways and that the overall effects on chondrocyte function depend on the balance in activity of multiple signaling proteins. J. Cell. Biochem. 110: 573–580, 2010. © 2010 Wiley‐Liss, Inc.
The development of the conditionally replication‐competent adenovirus: replacement of E4 orf1‐4 region by exogenous gene
Authors: Nam Jae‐Kook , Lee Mi‐Hyang , Seo Hae‐Hyun , Kim Seok‐Ki , Lee Kang‐Huyn , Kim In‐Hoo , Lee Sang‐Jin 
Published: April 2010

AbstractBackgroundTumor or tissue specific replicative adenovirus armed with a therapeutic gene has shown a promising anti‐cancer therapeutic modality. However, because the genomic packaging capacity is constrained, only a few places inside it are available for transgene insertion. In the present study, we introduce a novel strategy utilizing the early E4 region for the insertion of therapeutic gene(s).MethodsWe constructed the conditionally replication‐competent adenovirus (CRAd), Ad5E4(mRFP) by: (i) replacing the E4/E1a promoter by the prostate‐specific enhancer element; (ii) inserting mRFP inside the E4orf1‐4 deletion region; and (iii) sub‐cloning enhanced green fluorescent protein controlled by cytomegalovirus promoter in the left end of the viral genome. Subsequently, we evaluated its replication abilities and killing activities in vitro, as well as its in vivo anti‐tumor efficacy in CWR22rv xenografts.ResultsWhen infected with Ad5E4(mRFP), the number and intensity of the mRFP gene products increased in a prostate cancer cell‐specific manner as designed, suggesting that the mRFP gene and E4orfs other than E4orf1‐4 were well synthesized from one transcript via alternative splicing as the recombinant adenovirus replicated. As expected from the confirmed virus replication capability, Ad5E4(mRFP) induced cell lysis as potent as the wild‐type adenovirus and effectively suppressed tumor growth when tested in the CWR22rv xenografts in nude mice. Furthermore, Ad5E4(endo/angio) harboring an endostatin‐angiostatin gene in E4orf1‐4 was able to enhance CRAd by replacing mRFP with a therapeutic gene.ConclusionsThe approach employed in the present study for the insertion of a therapeutic transgene in CRAd should facilitate the construction of CRAd containing multiple therapeutic genes in the viral genome that may have the potential to serve as highly potent cancer therapeutic reagents. Copyright © 2010 John Wiley & Sons, Ltd.
Synthesis of new 4‐oxo‐thiazolidine‐5‐ylidenes of antitumor and antioxidant activities
Authors: Aly Ashraf A. , Brown Alan B. , Abdel‐Aziz Mohamed , Abuo‐Rahma Gamal El‐Din A. A. , Radwan Mohamed F. , Ramadan Mohamed , Gamal‐Eldeen Amira M. 
Published: April 2010

Abstract
magnified image Reaction of diacyl thiocarbohydrazides with dimethyl but‐2‐ynedioate in refluxing ethanol led to 4‐oxa‐thiazolidine‐5‐ylidene‐acetates in good yields. Reaction of the newly prepared N‐(2‐(propan‐2‐ylidene) hydrazine‐carbonothioyl)arylhydrazides with dimethyl but‐2‐ynedioate gave the corresponding (Z)‐methyl‐2‐arylhydrazide‐4‐oxo‐3‐(propan‐2‐ylideneamino)thiazolidine‐5‐ylidene)‐acetates. The mechanism is discussed. Antitumor and antioxidant activities have been also investigated. J. Heterocyclic Chem., (2010).
Flux measurements in Cairo. Part 1: in situ measurements and their applicability for comparison with satellite data
Authors: Frey Corinne M. , Parlow Eberhard , Vogt Roland , Harhash Maha , Abdel Wahab Mohammad M. 
Published: April 2010

AbstractCairo Air Pollution and Climate (CAPAC) is dedicated to the understanding of the urban energy balance in Cairo, Egypt, through measurements from space and at ground stations. The in situ measurements will provide a focussed insight into three carefully chosen microclimates (urban, suburban‐agriculture, and suburban‐desert) and provide at the same time ground‐truth data for satellite image analysis, which will expand the acquired knowledge into the spatial domain. In situ measurements were made during a field campaign in Greater Cairo from November 2007 to February 2008. In this study, the dataset of the CAPAC measurement campaign will be presented and analysed in terms of use for a remote sensing study. Measured variables complied with our expectations. The urban area featured a distinct nocturnal heat island. During the day the choice of reference station was responsible for the magnitude of the heat island. The diurnal cycle of radiative temperature at the suburban‐desert station clearly exceeded the one at the urban station, thus the urban setting seemed to have a better heat storage than the suburban‐desert. The stations also determined the partitioning of the turbulent heat fluxes. While in Cairo and at the suburban‐desert station most of the available energy was partitioned into the sensible heat flux, the suburban‐agricultural station maintained a high latent heat flux. The radiation and soil heat flux measurements proved to be applicable for comparison with remotely sensed data. However, the analysis of the turbulent heat fluxes showed that several constraints exist: measured fluxes tend to underestimate the actual flux and directional effects complicate the interpretation. An energy balance closure and footprint modelling is necessary to compare measured fluxes with satellite image retrieved products. Finally, turbulent fluxes are time averages, which is contrary to the remote sensing principle. Consequently, a direct use is problematic. Copyright © 2010 Royal Meteorological Society