bluuebunny/crossref_metadata_2025_split huggingface dataset:
Testicular germ cell tumors exhibit evidence of hormone dependence
Authors: Douglas Meaghan L. , Richardson Michelle M. , Nicol David L. 
Published: July 2005

AbstractThe aim of this investigation was to test the hypothesis that testicular germ cell tumors (TGCTs) are hormone‐dependent cancers. Human TGCT cells were implanted in the left testis of male severe combined immunodeficient mice receiving either no treatment or hormone manipulation treatment [blockade of gonadotropin‐releasing hormone secretion and/or signaling using leuprolide or leuprolide plus exogenous testosterone]. Real‐time RT‐PCR analysis was used to determine the expression profiles of hormone pathway‐associated genes. Tumor burden was significantly smaller in mice receiving both leuprolide and testosterone. Real‐time RT‐PCR analysis of follicle‐stimulating hormone (FSH) receptor, luteinizing hormone (LH) receptor and P450 aromatase revealed changes in expression in normal testis tissue related to presence of xenograft tumors and manipulation of hormone levels but a complete absence of expression of these genes in tumor cells themselves. This was confirmed in human specimens of TGCT. Reduced TGCT growth in vivo was associated with significant downregulation of LH receptor and P450 aromatase expression in normal testes. In conclusion, manipulation of hormone levels influenced the growth of TGCT in vivo, while the presence of xenografted tumors influenced the expression of hormone‐related genes in otherwise untreated animals. Human TGCTs, both in the animal model and in clinical specimens, appear not to express receptors for FSH or LH. Similarly, expression of the P450 aromatase gene is absent in TGCTs. Impaired estrogen synthesis and/or signaling may be at least partly responsible for inhibition of TGCT growth in the animal model. © 2005 Wiley‐Liss, Inc.
Association between serum pepsinogens and polymorphismof PTPN11 encoding SHP‐2 among Helicobacter pylori seropositive Japanese
Authors: Goto Yasuyuki , Ando Takafumi , Yamamoto Kazuhito , Tamakoshi Akiko , El‐Omar Emad , Goto Hidemi , Hamajima Nobuyuki 
Published: July 2005

AbstractHelicobacter pylori (H. pylori) plays a crucial role in the development of gastric atrophy and cancer, and cagA‐positive strains, which are universal in Japan, increase the risk of these outcomes substantially. The CagA protein is injected from attached H. pylori into gastric epithelial cells and undergoes Src‐dependent tyrosine phosphorylation and activation of the eukaryotic phosphatase SHP‐2. The CagA/SHP‐2 interactions elicit cellular changes that increase the risk of carcinogenesis. We investigated the association of a frequent single nucleotide polymorphism (SNP; JST057927; G‐to‐A) in the PTPN11 gene that encodes SHP‐2 with gastric atrophy and gastric cancer in Japan. Gastric atrophy was assessed by measuring serum pepsinogen I and II levels. The subjects comprised 454 healthy controls (126 males; mean age, 58.4) and 202 gastric cancer cases (134 males and 68 females; mean age, 66.7). All gastric cancer cases and 250 (55%) controls were H. pylori seropositive; 179 (89%) of the gastric cancer cases had gastric atrophy compared to 137 (55%) of the H. pylori seropositive controls (p < 0.001). Among HP seropositive controls compared to the common PTPN11 G/G genotype, the odds ratio of atrophy was nonsignificantly reduced with the G/A genotype (0.70; 95% CI = 0.39–1.25) and significantly reduced with the A/A genotype (0.09; 95% CI = 0.01–0.72). Lower risk for gastric atrophy had a gene‐dose association with the A allele (p = 0.01, trend test). There was a clear deficiency of the A/A genotype in those with atrophy compared to those without (1 subject in the gastric atrophy group vs. 8 in the group without). Cancer cases differed from controls in frequencies of PTPN11 G/A genotype only because of a higher prevalence of atrophy among the cancer cases. The G/A SNP in the PTPN11 gene appears to be a risk factor for gastric atrophy in subjects infected with cagA‐positive H. pylori. This may explain why only a proportion of CagA‐positive individuals develop gastric atrophy and gastric cancer, even though infection with cagA strains is universal in Asian countries such as Japan. The functional consequences of the G/A polymorphism remain to be elucidated. © 2005 Wiley‐Liss, Inc.
Application research of plasma‐enhanced electrochemical surface ceramic‐coating technology on titanium implants
Authors: Nan Kaihui , Wang Yingjun , Chen Xiaofeng , Ning Chengyun , Wang lingyu , Zhao Naru 
Published: July 2005

AbstractPlasma electrochemical surface ceramic coating (PECC) is an enhanced electrochemistry technique accomplished by means of plasma arc discharge in an electrolyte medium obtain coating structures on valve‐metal surfaces. Oxide films of titanium obtained by PECC in the electrolyte of sodium phosphate were investigated. The film was composed mainly of TiO2 in the form of anatase and rutile and enriched with Na and P elements on their surfaces. Their apatite‐inducing ability was also evaluated in a simulated body fluid (SBF). When immersed in SBF for over 30 days, an oriented hydroxy‐carbonate‐apatite was induced on the surface of the films, which suggests the PECC‐treated titanium has the promising positive biological response. © 2005 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2005
Initial adhesion of glass‐fiber–reinforced composite to the surface of porcine calvarial bone
Authors: Tuusa S. M. R. , Lassila L. V. J. , Matinlinna J. P. , Peltola M. J. , Vallittu P. K. 
Published: July 2005

AbstractThe aim of this preliminary study was to compare the initial bond strength of the glass‐fiber–reinforced composite veil to the surface of the porcine calvarial compact bone using different adhesives. Fiber‐reinforced composite (FRC) made of E‐glass fiber veil with the BisGMA‐PMMA resin system was used in the study. For the shear bond strength test, porcine calvarial bone cubes were mounted into resin matrix. FRC‐veil discs were bonded to compact bone with different types of adhesives: (A) BisGMA‐HEMA based (3M‐ESPE Scotchbond Multi‐Purpose Adhesive), (B) 4‐META/UDMA/BisGMA based (Unifil Bond Bonding Agent) and MDP based (Clearfil Se Bond adhesive), (C) UDMA/BisGMA/PMMA‐based experimental adhesive, and (D) silane‐based (APS, ICS, MPS) experimental adhesives. The surface of the bone was mechanically roughened and was either used as such, treated with dental primers (Unifil Bond Self‐etching Primer, Clearfil Se Bond Primer), or treated with an experimental silane mixture (APS, ICS, MPS), or with a mixture of the experimental silane liquid and Clearfil Se Bond Primer. The 3M‐ESPE Scotchbond Multi‐Purpose Adhesive and UDMA/BisGMA/PMMA experimental adhesive gave poor results in the shear bond test (0.58 and 0.40 MPa, respectively). Unifil Bond Bonding Agent and Clearfil Se Bond adhesive with respective primers markedly improved the shear bond strength; with Unifil the result was 3.40 MPa, and with Clearfil it was 6.19 MPa. When the bone surface was primed with a mixture of Clearfil Se Bond Primer and Clearfil Porcelain Bond Activator, the Clearfil Se Bond adhesive‐impregnated FRC veil gave the best adhesion to the bone surface in this test: 9.50 MPa. The addition of bioactive glass granules between the veil and the bone lowered the shear bond strength in the test system described above to 6.72 MPa. The test systems with the silane mixture were also promising. In the SEM study, it was found that the mechanical treatment reveals the pores of the bone surface. Chemical treatments of the bone surface improved the adhesion of the FRC veil to the bone. The results showed that the adhesion of the FRC to the surface of the bone can be significantly improved with mechanical roughening and with special chemical treatments of the bone surface. © 2005 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2005
In vitro evaluation of caries inhibition promoted by self‐etching adhesive systems containing antibacterial agents
Authors: Lobo Maristela M. , Gonçalves Reginaldo B. , Pimenta Luiz André F. , Bedran‐Russo Ana Karina B. , Pereira Patrícia N. R. 
Published: July 2005

AbstractThis study evaluated the cariostatic effect of antibacterial self‐etching adhesive systems, by means of an in vitro bacterial caries model. Seventy‐five prepared bovine slabs were randomly divided into groups (n = 15): (1) unbonded composite, no carious challenge (UNB‐NC); (2) unbonded composite, carious challenge (UNB‐C); (3) Clearfil SE Bond, no antibacterial agent (CSE); (4) Protect Bond, containing MDPB and fluoride (PB); and (5) Reactmer Bond, fluoride‐releasing (RB). All preparations were restored with Filtek™ Z‐250. Groups (2)–(5) were submitted to a medium containing Streptococcus mutans (ATCC ‐ 25175) for 5 days, and Group (1) was kept in a noninoculated medium. Insoluble polysaccharides present in tooth biofilms were quantified, Knoop hardness (KHN) was measured on the enamel adjacent to restorations, and standard 35‐mm polarized light photomicrographs were taken as illustrations. Polysaccharide and Knoop hardness results were analyzed with the use of ANOVA, with a split‐split–plot statistical design for KHN. Except for Group (1), all groups showed similar caries formation. Biofilm over PB restorations showed the smallest amounts of polysaccharides (14.37 μg/mg), and CSE showed the highest amounts (20.87 μg/mg). All self‐etching systems tested were unable to inhibit secondary caries in a bacterial model simulating a high caries challenge, even though there was reduced glucan synthesis provided by the adhesive system containing MDPB and fluoride. © 2005 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2005
Serum albumin enhances polyethylenimine‐mediated gene delivery to human respiratory epithelial cells
Authors: Carrabino Salvatore , Di Gioia Sante , Copreni Elena , Conese Massimo 
Published: July 2005

AbstractBackgroundThe interaction of polyethylenimine (PEI) polyplexes with proteins in cystic fibrosis (CF) airway secretions poses a significant hurdle to this nonviral delivery system. The aim of this study was to evaluate whether albumin may increase the efficiency of PEI complexes in mediating gene transfer into respiratory epithelial cells in the presence of CF mucus.MethodsPEI (25 kDa) was complexed to DNA in the presence of human serum albumin (HSA) and used to transfect confluent A549 and 9HTEo‐ cells. Alternatively, albumin was added to preformed PEI‐DNA complexes. The cytotoxicity of complexes was analysed by the LDH (lactate dehydrogenase) assay. CF CFT1‐C2 cells were allowed to polarise and were transfected either with luciferase‐ or CFTR‐expressing plasmids. To evaluate the effect of CF respiratory secretions on transfection efficiency, confluent cells were transfected in the presence of sputum obtained from two CF patients.ResultsThe ternary PEI‐HSA complexes increased luciferase expression in confluent cultures in a dose‐dependent fashion up to 100 times as compared to PEI‐DNA. The number of GFP‐expressing cells, as evaluated by epifluorescence, was augmented several‐fold. When HSA was added to preformed PEI‐DNA complexes, a further 5–10‐fold increase in gene expression was observed. No significant cytotoxicity was observed with either PEI or PEI‐HSA polyplexes. The ternary complexes determined detectable CFTR gene transfer and expression at the apical membrane in polarised CFT1‐C2 cells, as evaluated by confocal microscopy. CF sputum inhibited PEI‐mediated gene transfer by 7–186‐fold. Although luciferase expression mediated by PEI‐HSA was still inhibited by CF sputum, these levels were 18–83.8‐fold higher than with PEI.ConclusionsOur results demonstrate that albumin increases PEI gene transfer efficiency in confluent and polarised respiratory epithelial cells and can allow CFTR gene expression in the appropriate cellular compartment. PEI‐HSA complexes display a higher efficiency than PEI also in the presence of CF sputum, indicating that albumin‐containing polyplexes may help overcome barriers imposed by CF airway secretions. Copyright © 2005 John Wiley & Sons, Ltd.
Impact of drug resistance genotypes on CD4+ counts and plasma viremia in heavily antiretroviral‐experienced HIV‐infected patients
Authors: Rodes Berta , García Federico , Gutierrez Carolina , Martinez‐Picado Javier , Aguilera Antonio , Saumoy Maria , Vallejo Alex , Domingo Pere , Dalmau David , Ribas Maria Angels , Blanco José Luis , Pedreira José , Perez‐Elias Maria Jesús , Leal Manuel , de Mendoza Carmen , Soriano Vincent 
Published: July 2005

AbstractThe number of HIV‐infected individuals with prior multiple treatment failures is increasing as time passes by. The success of antiretroviral therapy in these patients is often compromised by the selection of drug‐resistant viruses. Despite initial concerns, a rebound in AIDS cases among heavily treatment‐experienced patients failing virologically their antiretroviral therapy has not occurred yet. In a multicenter study conducted in Spain, HIV‐infected patients were assessed with prior failure to antiretrovirals from the three main drug families who presented during the last semester of the year 2003 with plasma HIV‐RNA values above 1,000 copies/ml, despite good treatment adherence. The relationships between CD4+ T cell counts, viral loads and drug‐resistant genotypes were examined. A total of 273 patients were identified in 12 centers (78% male, median age: 41 years). The mean viral load was 50,438 copies/ml and the mean CD4+ count was 328 cells/μl. Only 19.5% had less than 200 CD4+ T cells/μl. Most patients (95%) were receiving nucleoside reverse transcriptase inhibitors (NRTI) in their last antiretroviral regimen, while 63% were treated with protease inhibitors (PI) and 27% on non‐nucleoside reverse transcriptase inhibitors (NNRTI). Overall, 97.4% had at least one drug resistance mutation (87.2% for NRTI, 68.5% for NNRTI, and 92.7% for PI). Using the virtual phenotype, resistance to three or more drugs within each class was recognized in 45.8% for NRTI, 40.7% for NNRTI, and 44.7% for PI. Moreover, cross‐resistance to compounds from two or three drug families was recognized in 41% and 19.4% of patients, respectively. Nearly half of the patients had plasma HIV‐RNA below 10,000 copies/ml and they showed significantly higher CD4 + counts than those with greater viremia (408 versus 259 cells/μl; P < 0.001). Patients with higher plasma viremia had significantly more drug resistance mutations than those with lower viremia. No favorable effect on viral load could be recognized for individual drug resistance mutations known to reduce viral fitness in vitro (i.e., rtM184V, rtL74V, rtK65R, proD30N, or proI50L). In summary, a large proportion of treatment‐experienced patients failing their current antiretroviral regimen carry viruses with broad cross‐resistant genotypes. Nearly half of the patients with these multi‐drug resistant viruses had < 10,000 HIV‐RNA copies/ml and 80% have more than 200 CD4 + T cells/μl. Thus, maintaining treatment HIV‐infected individuals failing virologically and harboring drug‐resistant viruses might ameliorate immunological deterioration until new drugs became available. J. Med. Virol. 77:23–28, 2005. © 2005 Wiley‐Liss, Inc.
Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)‐associated coronavirus infection
Authors: Yang Yao‐Hsu , Huang Yu‐Hui , Chuang Ya‐Hui , Peng Chung‐Min , Wang Li‐Chieh , Lin Yu‐Tsan , Chiang Bor‐Luen 
Published: July 2005

AbstractThe severe acute respiratory syndrome (SARS) is caused by infection with the SARS‐associated coronavirus (SARS‐CoV) and characterized by severe pulmonary inflammation and fibrosis. In this study, the development of autoantibodies against human epithelial cells and endothelial cells in patients with SARS at different time periods (the first week: phase I, 1 month after the disease onset: phase II/phase III) were investigated. Antibodies in sera of patients and healthy controls against: (1) A549 human pulmonary epithelial cell‐line, (2) human umbilical venous endothelial cells (HUVEC), (3) primary human pulmonary endothelial cells (HPEC) were detected by cell‐based ELISA and indirect immunofluorescence staining. The results revealed that serum levels of IgG anti‐A549 cells antibodies, IgG anti‐HUVEC antibodies, and IgM anti‐HPEC antibodies were significantly higher in SARS patients at phase II/phase III than those in healthy controls. Sera from SARS patients at phase II/phase III could mediate complement dependent cytotoxicity against some A549 cells and HPEC. It is concluded that some autoantibodies against human epithelial cells and endothelial cells would be developed after SARS‐CoV infection and this phenomenon may indicate post‐infectious cellular injury and also induce SARS‐induced immunopathology. J. Med. Virol. 77:1–7, 2005. © 2005 Wiley‐Liss, Inc.
Genetic analysis of human immunodeficiency virus type 1 nef in portugal: Subtyping, identification of mosaic genes, and amino acid sequence variability
Authors: Parreira Ricardo , Pádua Elizabeth , Piedade João , Venenno Teresa , Paixão Maria Teresa , Esteves Aida 
Published: July 2005

AbstractExtending our previous genetic characterization of human immunodeficiency virus type 1 (HIV‐1) strains circulating in Portugal, we here report the first phylogenetic and putative amino acid sequence variability analyses of nef accessory gene. Viral sequences (n = 53) were amplified by nested PCR from proviral DNA purified from peripheral blood mononuclear cells of HIV‐1 infected individuals (n = 49). Phylogenetic inference analysis demonstrated a distribution of the viral sequences between subtypes A (sub‐subtype A1), B, D, F (sub‐subtype F1), G, H, and J, with subtypes G and B accounting altogether for more than half of the genotypes found. A significant number of the proviral DNA sequences analyzed (18.4%) were shown to correspond to intragenic nef recombinants, with the majority having the typical CRF02_AG nef structure. In addition, three novel intragenic recombinant structures were found (B/G/B, CRF02_AG/H, and D/G). From phylogenetic analysis, it was concluded that part of the non‐recombinant nef genes might have actually been amplified from mosaic viruses: CRF06_cpx, CRF14_BG, and a new envA/nefJ recombinant. While comparing all the putative Nef sequences, significant amino acid sequence variability was observed. However, most of the described nef functional motifs were relatively well conserved in the majority of the sequences analyzed and numerous amino acid changes fell outside these regions. The results presented unambiguously endorse the high level of complexity of HIV‐1 epidemics in Portugal. J. Med. Virol. 77:8–16, 2005. © 2005 Wiley‐Liss, Inc.
Distinct geographic distributions of hepatitis B virus genotypes in patients with acute infection in Japan
Authors: Yotsuyanagi Hiroshi , Okuse Chiaki , Yasuda Kiyomi , Orito Etsuro , Nishiguchi Shuhei , Toyoda Joji , Tomita Eiichi , Hino Keisuke , Okita Kiwamu , Murashima Shiro , Sata Michio , Hoshino Hiromi , Miyakawa Yuzo , Iino Shiro 
Published: July 2005

AbstractGenotypes of hepatitis B virus (HBV) were determined in 145 patients with acute hepatitis B from various districts in Japan to establish their geographic distribution and evaluating the influence on the clinical illness and outcome. Genotypes were A in 27 (19%) patients, B in 8 (5%), C in 109 (75%) and mixed with B and C in the remaining one (1%). Genotype A was more frequent in metropolitan than the other areas (21/69 (30%) vs. 6/76 (8%), P < 0.001). On phylogenetic analysis, seven of the nine (78%) HBV/A isolates selected at random clustered with those from Europe and the United States, while the remaining two with those of subgroup A' prevalent in Asia and Africa. Maximum ALT levels were lower (2069 ± 1075 vs. 2889 ± 1867 IU/L, P = 0.03) and baseline HBV DNA titers were higher (5.90 ± 1.45 vs. 5.13 ± 1.36 log genome equivalents (LGE)/ml, P = 0.002) in patients infected with genotype A than C. Hepatitis B surface antigen persisted longer in patients infected with genotype A than C (1.95 ± 1.09 vs. 1.28 ± 1.42 months, P = 0.02). HBV infection became chronic in one (4%) patient with genotype A and one (1%) with genotype C infection. Fulminant hepatic failure developed in none of the patients with genotype A, one (13%) with genotype B and five (5%) with genotype C. The point mutation in the precore region (A1896) or the double mutations in the basic core promoter (BCP) region (T1762/A1764) were detected in none of the patients with genotype A, two (25%) with genotype B and 27 (26%) with genotype C. In conclusion, genotype A is frequent in patients with acute hepatitis B in metropolitan areas of Japan, probably reflecting particular transmission routes, and associated with longer and milder clinical course than genotype C. J. Med. Virol. 77:39–46, 2005. © 2005 Wiley‐Liss, Inc.
Full genome analysis of hepatitis B virus genotype E strains from South‐Western Africa and madagascar reveals low genetic variability
Authors: Kramvis Anna , Restorp Karin , Norder Heléne , Botha Johan F. , Magnius Lars O. , Kew Michael C. 
Published: July 2005

AbstractThe eight genotypes of hepatitis B virus (HBV), A–H, have a characteristic geographical distribution. The high prevalence of genotype E within a wide expanse of Africa makes it important to characterize this genotype. Although the preS/S region of a large number of genotype E isolates has been sequenced, to date only eight complete genotype E genomes have been published. The aim of this study, therefore, was to sequence and characterize the complete genome of genotype E isolates obtained from geographically distinct regions in Africa, including Namibia, Angola, and Madagascar. The nine newly sequenced genotype E isolates were closely related with an intra‐group nucleotide divergence of 1.2%, reflecting their close geographical origin. All genotype E strains have the same characteristics, an in‐frame deletion of three nucleotides (one amino acid) in the 5′ pre‐S1, a signature pattern of amino acids in the pre‐S1 region and the serological subtype ayw4. In addition, we have identified another unique attribute of genotype E strains, the introduction of another start codon Met83 in the pre‐S1 region that may result in the translation of an elongated middle hepatitis B surface protein (MHBs). J. Med. Virol. 77:47–52, 2005. © 2005 Wiley‐Liss, Inc.
Oral fluid as a medium for the detection of hepatitis B surface antigen
Authors: Hutse Veronik , Verhaegen Els , De Cock Liesbet , Quoilin Sophie , Vandenberghe Hans , Horsmans Yves , Michielsen Peter , Damme Pierre Van , Vlierberghe Hans Van , Claeys Françoise , Vranckx Robert , Oyen Herman Van 
Published: July 2005

AbstractCurrently viral antigens and antibodies are detected by traditional serological tests. However, the introduction of oral fluid as an alternative medium would allow other alternatives. The collection of oral fluid is, in comparison with venepuncture, less invasive, less painful, less expensive (i.e., no trained personal required), and safe (prevention of needle stick injuries). Also large numbers of samples can be collected easily for epidemiological purposes. Forty‐three HBsAg positive and seventy‐three HBsAg negative paired serum/oral fluid samples were tested. They were collected from patients attending university hospitals. The oral fluid samples were collected using the Oracol collection device and they were subjected to an IgG quantification assay to ensure their quality and quantity. The detection of HBsAg in oral fluid was carried out using a modified ETI‐MAK‐4 ELISA. The validation of this oral fluid test gave a sensitivity and specificity of 90.7% and 100%, respectively. The modified ETI‐MAK‐4 ELISA is a suitable test for oral fluid samples collected by the Oracol collection device for epidemiological purposes. J. Med. Virol. 77:53–56, 2005. © 2005 Wiley‐Liss, Inc.