bluuebunny/crossref_metadata_2025_split huggingface dataset:
A soluble CAR‐SCF fusion protein improves adenoviral vector‐mediated gene transferto c‐Kit‐positive hematopoietic cells
Authors: Itoh Akira , Okada Takashi , Mizuguchi Hiroyuki , Hayakawa Takao , Mizukami Hiroaki , Kume Akihiro , Takatoku Masaaki , Komatsu Norio , Hanazono Yutaka , Ozawa Keiya 
Published: October 2003

AbstractBackgroundAlthough adenoviral vectors primarily derived from the adenovirus serotype 5 (Ad5) are widely used for many gene transfer applications, they cannot efficiently infect hematopoietic cells, since these cells do not express the coxsackie‐adenoviral receptor (CAR).MethodsWe have developed a soluble fusion protein that bridges adenoviral fibers and the c‐Kit receptor to alter Ad5 tropism to immature hematopoietic cells. The CAR‐SCF fusion protein consists of the extracellular domains of CAR and stem cell factor (SCF). The human megakaryoblastic leukemia cell lines UT‐7 and M07e, human chronic myelogenous leukemia cell line K‐562, and erythroleukemia cell line TF‐1 were used to assess CAR‐SCF‐assisted Ad5‐mediated gene transfer. Hematopoietic cell lines were infected with an Ad5 vector (Ad5‐eGFP) or a fiber‐mutant Ad5/F35 (Ad5/F35‐eGFP) expressing the enhanced green fluorescent protein gene in the presence or absence of CAR‐SCF.ResultsTwenty‐four hours after infection, more than 80% of M07e cells infected in the presence of CAR‐SCF were eGFP‐positive, compared with very few eGFP‐positive cells following Ad5‐eGFP infection in the absence of CAR‐SCF. The enhancement of Ad5‐eGFP infection by CAR‐SCF was greater than that caused by Ad5/F35‐eGFP (50%). The ability of CAR‐SCF to enhance Ad5‐eGFP infectivity was highly dependent on cellular c‐Kit expression levels. Furthermore, CAR‐SCF also enhanced Ad5‐mediated gene transfer into human primary CD34+ cells.ConclusionsThe CAR‐SCF fusion protein assists Ad5‐mediated transduction to c‐Kit+ CAR− hematopoietic cells. The use of this fusion protein would enhance a utility of Ad5‐mediated hematopoietic cell transduction strategies. Copyright © 2003 John Wiley & Sons, Ltd.
Efficient gene transfer of a simian immuno‐deficiency viral vector into cardiomyocytes derived from primate embryonic stem cells
Authors: Nagata Mihoko , Takahashi Masafumi , Muramatsu Shin‐ichi , Ueda Yasuji , Hanazono Yutaka , Takeuchi Koichi , Okada Koji , Suzuki Yutaka , Kondo Yasushi , Suemori Masafumi , Ikeda Uichi , Nakano Imaharu , Kobayashi Eiji , Hasegawa Mamoru , Ozawa Keiya , Nakatsuji Norio , Shimada Kazuyuki 
Published: October 2003

AbstractBackgroundEmbryonic stem (ES) cells continually proliferate and can generate large numbers of differentiated cells. Genetic manipulation of transplantable cells derived from primate ES cells offers considerable potential for development research and regenerative cell therapy. However, protocols for efficient gene transfer into primate ES‐cell‐derived cells have not yet been established.MethodsSpontaneously contracting areas were derived from cynomolgus monkey ES cells. Features of cardiomyocytes in the area were analyzed according to gene expression (RT‐PCR), morphology (immunostaining and electron microscopy), and function (intracellular calcium transience). Beating cells were transduced using a simian immunodeficiency virus (SIV) vector expressing enhanced green fluorescence protein (EGFP), then transplanted into ischemic rat myocardium.ResultsBeating cells derived from monkey ES cells displayed gene expression, ultrastructural and functional properties of early‐stage cardiomyocytes. Highly efficient (97% cardiac phenotype) and stable transduction of these ES‐cell‐derived cardiomyocytes was achieved using SIV vector without altering contractile function. In addition, transduced cardiomyocytes survived in the myocardium of a rat myocardial infarction model.ConclusionsA lentiviral vector system based on SIV represents a useful vehicle for genetic modification of cardiomyocytes derived from primate ES cells, and can extend the application of primate ES cells to gene therapy. Copyright © 2003 John Wiley & Sons, Ltd.
Mice body weight gain is prevented after naked human leptin cDNA transfer into skeletal muscle by electroporation
Authors: Wang Xue‐Dong , Liu Jian , Yang Ji‐Chun , Chen Wei‐Qiang , Tang Jian‐Guo 
Published: October 2003

AbstractBackgroundIn this investigation, the feasibility of gene therapy for obesity by electroporational transfer of naked plasmid with leptin cDNA into skeletal muscle was tested. Both young and adult mice were studied.MethodsHuman leptin cDNA was attached to the human insulin precursor secretion signal peptide gene. The fused gene was then inserted into the mammalian expression vector pcDNA3.1(−) and transferred into skeletal muscle of normal female mice using electroporation.ResultsDuring the time of exogenic gene expression, daily food intake of leptin cDNA‐treated mice was observed to be lower than the control. The body weight gain was prevented efficaciously regardless of if they were young or adult. At the 7th week after gene transfer, the body weight of both young and adult leptin cDNA‐treated mice was about 20% lighter than the control. Although the body weight of pair fed controlled adult mice was close to the leptin cDNA‐treated mice at the 8th week, they were always heavier than the leptin cDNA‐treated mice before this time. The levels of retroperitoneal fats and serum TG of leptin cDNA‐treated mice were markedly lower than that of the control. The relative serum hyperleptinemic level could last for about 2 months. The expression of leptin cDNA in muscle cells was also detected by RT‐PCR. The levels of serum insulin and glucose of leptin cDNA‐treated mice decreased slightly. Our data also showed that the hyperleptinmia resulted in uterus expansion in young mice, but not in the adults.ConclusionThe present study provides evidence of successful electroporation of naked plasmid DNA transfer for prevention or treatment of mice obesity. Copyright © 2003 John Wiley & Sons, Ltd.
Study of the metal dusting behaviour of high‐temperature alloys
Authors: Di Gabriele F. , Bernstein J. R. , Al‐Qhatani M. M. , Liu Z. , Jordan M. P. , Richardson J. A. , Stott F. H. 
Published: October 2003

AbstractThe corrosion phenomenon named metal dusting has been observed in many high‐temperature industrial plants. An experimental research programme is being carried out into the degradation resistance of wrought and cast commercial and development high‐temperature alloys in H2/CO gas mixtures at temperatures of 550°C to 750°C. Emphasis is placed on very high carbon activities, consistent with the next generation of steam‐reforming and similar plants that are susceptible to metal dusting. The overall programme is concerned with the mechanisms of initiation and propagation of dusting and the sensitivity to damage of the more resistant alloys, as a function of environmental parameters.Initial tests have been carried out on a number of commercial alloys: Alloy 600, 693, 602CA, 601, 603 XL, 671, 617, 690 (wrought), and H46M (cast). The specimens were exposed to a gas mixture of high carbon activity at 650°C for a total of 1000 hours. Many of the alloys showed at least the initial stages of metal dusting. Preliminary analysis using electron microscopy revealed that initiation of metal dusting is influenced by microstructure, stress state and composition. In some cases, attack was enhanced at stress points, such as corners and edges. Sample holders were found to influence strongly the length of the initiation period for the onset of the corrosion phenomenon. The reaction layers in the alloy beneath areas of damage were analysed by EDX and EPMA. Mechanical characterisation of such areas has been carried out using nanoindentation methods. These early results are discussed in terms of the effectiveness of oxide scales in inhibiting the onset of damage and presence of impurities in the ceramic holder in initiating the onset of damage.
The influence of carbonyl sulphide on the inhibition of filamentary carbon deposition on stainless steel
Authors: Millward G. R. , Evans H. E. , Jones I. P. , Eley C. D. , Mowforth C. W. 
Published: October 2003

AbstractThis paper examines the role that COS plays in the inhibition of carbon deposition onto a Si‐free 20Cr‐25Ni‐Nb‐stabilized austenitic stainless steel. We have shown that the addition of just 240 vppb of COS to a standard gas deposit mixture of high carbon activity (1000 vppm C2H4, 1% CO, balance CO2) yields a dramatic fall in the amount of filamentous carbon deposited. The inhibitive effect persists when treatment is continued after COS has been subsequently removed from the treatment gas. Clearly, in these experiments the phenomenon is a result of substrate surface modification by the COS rather than changes in gas phase kinetics. Deposition onto surfaces where filamentous carbon has already been laid down is similarly inhibited.
Electron spin resonance studies of anisotropy in semiconducting polymeric films
Authors: Breiby Dag W. , Sato Shuichi , Samuelsen Emil J. , Mizoguchi Kenji 
Published: October 2003

AbstractX‐band electron spin resonance was employed to study the structural anisotropy in several polythiophene derivatives. Because of the dominating homogeneous width, the obtained absorption spectra were Lorentzian‐shaped. Information about the structural anisotropy was obtained from the position and width of the absorption peak. Qualitatively, the anisotropy was in full agreement with earlier results from X‐ray diffraction, including a flip in molecular orientation with respect to the film substrate between solution‐cast and spin‐cast films. With the Monte Carlo technique, the spectra were fitted with a biaxial g tensor, an anisotropy parameter S, and an intrinsic width σ. The simulations showed that g could be treated as pseudo‐uniaxial, with the unique axis along the side chains rather than along the ring normal. Closed‐form analytical expressions relating g to the anisotropy were obtained and used for a quantitative assessment of the molecular anisotropy. Because the molecular g tensor for these materials was not known, a known value of S for one of the samples obtained by X‐ray diffraction was used for normalization. Fairly consistent values were obtained for both g and S. © 2003 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 41: 3011–3025, 2003
Self‐assembled supramolecular microgels: Fractal structure and aggregation mechanism
Authors: Gu Zhenyu , Patterson Gary , Cao Rong , Armitage Bruce 
Published: October 2003

AbstractMultifunctional molecules were designed to produce microgels with specific structures. Both static light scattering and dynamic light scattering were employed to determine the fractal dimension of the microgels. The protein, avidin, was strongly bound to four biotin moieties. Biotin was attached covalently to specifically engineered peptide nucleic acid (PNA) oligomers. Three designed DNA oligomers self‐assembled to produce a trifunctional three‐way junction (TWJ) with single‐stranded ends that were complementary to the PNA sequence. The sizes of the supramolecular aggregates were characterized by dynamic light scattering. The fractal dimension was obtained from the angular dependence of the scattered intensity when the microgels were large enough. When the microgels were formed via cooling from a temperature above the melting point of the PNA–DNA helices, reversible structures with a fractal dimension of approximately 1.86 were formed, which is consistent with a cluster–cluster aggregation mechanism. When the microgels were formed by the slow addition of biotinylated PNA bound to the TWJ to a solution of avidin at room temperature, the observed fractal dimension approached 2.6, which is consistent with a point–cluster aggregation mechanism. © 2003 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 41: 3037–3046, 2003
Electric, dielectric, and dynamic mechanical behavior of carbon black/styrene‐butadiene‐styrene composites
Authors: Leyva María Elena , Barra Guilherme M. O. , Moreira Ana C. F. , Soares Bluma G. , Khastgir Dipak 
Published: October 2003

AbstractThe conductivity of styrene‐butadiene‐styrene block copolymers containing different amounts of extraconductive carbon black (CB) was investigated as a function of the mold temperature. The composites exhibited reduced percolation thresholds (between 1.0 and 2.0 vol % CB). The dynamic mechanical analysis characterization revealed that the glass‐rubber‐transition temperatures of both segments were not affected by the CB addition, although the damping of the polybutadiene phase displayed a progressive drop with an increase in the CB concentration. The normalized curves of tan δ/tan δmax (where tan δ represents the value of the loss tangent at any measurement temperature and tan δmax represents the loss tangent peak value at the corresponding temperature Tmax) versus T/Tmax (where T is the temperature and Tmax is the maximum temperature), corresponding to both polystyrene and polybutadiene phases as well as the activation energy related to the glass‐rubber‐transition process, did not present any significant change with the addition of CB. The dielectric analysis revealed the presence of two relaxation peaks in the composite containing 1.5 vol % CB, the magnitude of which was strongly influenced by the frequency, being attributed to interfacial Maxwell‐Wagner‐Sillars relaxations caused by the presence of different interfaces in the composite. The mechanical properties were not affected by the presence of CB at concentrations of up to 2.5 vol %. © 2003 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 41: 2983–2997, 2003
Interactions of glucose and polyacrylamide in solutions and gels
Authors: Livney Yoav D. , Portnaya Irina , Faupin Benjamin , Fahoum Lulu , Ramon Ory , Cohen Yachin , Mizrahi Shimon , Cogan Uri 
Published: October 2003

AbstractThe swelling of polyacrylamide (PAAm) gels increased with rising glucose concentrations, and so did the osmotic pressure of the soluble polymer and its intrinsic viscosity. A Flory–Huggins‐based model for the osmotic pressure of a nonionic hydrophilic polymer in a ternary solution consisting of a main solvent, a polymer, and a nondissociating low‐molecular‐weight cosolute was developed and examined. The model‐calculated values were in reasonably good agreement with experimental results for the water–PAAm–glucose system studied when PAAm–water and glucose–water interaction coefficients from the binary systems were used, and only the PAAm–glucose interaction coefficient was adjusted. Its negative value suggested a favorable interaction of glucose and PAAm, supporting the notion of glucose being a good cosolvent for PAAm. Isothermal titration microcalorimetry results showed no evidence for the binding of glucose to PAAm, but an exothermic interaction was indicated between glucose and PAAm. Microcalorimetrically determined enthalpic contributions to the Flory–Huggins interaction coefficients showed enthalpically favorable binary interactions, particularly the enthalpic component of the PAAm–glucose interaction coefficient (χH23), which was slightly negative. The enthalpically favorable interaction between glucose and PAAm may explain the increased osmotic pressure of PAAm in glucose solutions. © 2003 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 41: 3053–3063, 2003
Where are the prostate cancer genes?—A summary of eight genome wide searches
Authors: Easton Douglas F. , Schaid Daniel J. , Whittemore Alice S. , Isaacs William J. 
Published: October 2003

AbstractBACKGROUNDThere is strong evidence for genetic susceptibility to prostate cancer, but most of the genes underlying this susceptibility remain to be identified.METHODSWe reviewed the results of eight genome‐wide linkage searches based on 1,293 families with multiple cases of prostate cancer.RESULTSAcross these studies, 11 linkage peaks with LOD scores in excess of 2 were identified. However, no chromosomal region was reported as significant at this level by more than one study and only one corresponded to a peak previously suggested by another group.CONCLUSIONSThese results indicate that prostate cancer is genetically complex, and that combined analyses of large family sets will be required to evaluate reliably the linkage evidence. Prostate 57: 261–269, 2003. © 2003 Wiley‐Liss, Inc.
Genome‐wide scan for linkage in finnish hereditary prostate cancer (HPC) families identifies novel susceptibility loci at 11q14 and 3p25‐26
Authors: Schleutker Johanna , Baffoe‐Bonnie Agnes B. , Gillanders Elizabeth , Kainu Tommi , Jones Mary‐Pat , Freas‐Lutz Diana , Markey Carol , Gildea Derek , Riedesel Erica , Albertus Julie , Gibbs Kenneth D. , Matikainen Mika , Koivisto Pasi A. , Tammela Teuvo , Bailey‐Wilson Joan E. , Trent Jeffrey M. , Kallioniemi Olli‐P. 
Published: October 2003

AbstractBACKGROUNDIn order to identify predisposition loci to hereditary prostate cancer (HPC), we performed a genome‐wide linkage analysis using samples from a genetically homogeneous population, with 13 Finnish multiplex prostate cancer families.METHODSAltogether 87 DNA samples were genotyped from 13 families. Logarithm‐of‐odds (LOD) scores were calculated for all autosomes using FASTLINK and GENEHUNTER designating all unaffected men and all women as unknown.RESULTSThe highest LOD scores in the affected‐only analyses were found at 11q14, where the two‐point LOD score was 2.97 (θ = 0.0 at D11S901), GENEHUNTER heterogeneity LOD (HLOD) of 3.36, and a non‐parametric‐linkage (NPL) score of 2.67 (P = 0.008). A second positive site was at 3p25‐26, with a two‐point LOD score of 2.57 (θ = 0.01 at D3S1297), HLOD of 2.15, and NPL score of 2.27 (P = 0.02).CONCLUSIONSThe results suggest two HPC regions in the Finnish population, which have not been reported previously and warrant further study. Prostate 57: 280–289, 2003. © 2003 Wiley‐Liss, Inc.
Genome‐wide scan of Swedish families with hereditary prostate cancer: Suggestive evidence of linkage at 5q11.2 and 19p13.3
Authors: Wiklund Fredrik , Gillanders Elizabeth M. , Albertus Julie A. , Bergh Anders , Damber Jan‐Erik , Emanuelsson Monica , Freas‐Lutz Diana L. , Gildea Derek E. , Göransson Ingela , Jones MaryPat S. , Jonsson Björn‐Anders , Lindmark Fredrik , Markey Carol J. , Riedesel Erica L. , Stenman Elisabeth , Trent Jeffry M. , Grönberg Henrik 
Published: October 2003

AbstractBACKGROUNDProstate cancer (CaP) is a common disorder with multiple genetic and environmental factors contributing to the disease. CaP susceptibility loci can be identified through genome‐wide scans of high‐risk families.METHODSAllele sharing at 405 markers, distributed across the genome, among 50 families with hereditary prostate cancer, ascertained throughout Sweden, was evaluated through linkage analyses. Genotype data were analyzed utilizing multipoint parametric and non‐parametric methods.RESULTSTwo regions provided suggestive evidence for linkage: 19p13.3 (marker D19S209, LOD = 2.91, P = 0.0001) and 5q11.2 (marker D5S407, LOD = 2.24, P = 0.0007). Additional regions with moderate evidence for linkage in the complete set of families, or stratified subsets, were observed on chromosome 1, 4, 6, 7, 8, and X.CONCLUSIONSOur results provide strong confirmatory evidence of linkage at 19q13.3 and 5q11.2. The lack of confirmation of linkage at several loci identified in other genome‐wide scans emphasizes the need to combine linkage data between research groups. Prostate 57: 290–297, 2003. © 2003 Wiley‐Liss, Inc.
Genome‐wide scan of brothers: Replication and fine mapping of prostate cancer susceptibility and aggressiveness loci
Authors: Witte John S. , Suarez Brian K. , Thiel Bonnie , Lin Jennifer , Yu Adong , Banerjee Tarit K. , Burmester James K. , Casey Graham , Catalona William J. 
Published: October 2003

AbstractBACKGROUNDSubstantial evidence suggests that genetic factors play an important role in both the risk of prostate cancer and its biologic aggressiveness. Here we investigate prostate cancer susceptibility and aggressiveness with genome‐wide linkage analyses of affected brothers.METHODSWe first undertook a new genome‐wide linkage study of 259 brothers with prostate cancer. Our analyses tested whether the proportion of marker alleles shared by brothers was correlated with disease status or Gleason score. To further clarify 11 linkage regions observed here or previously, we genotyped and analyzed an additional 101 finely spaced markers in the 259 men, and in 594 previously studied brothers, allowing for a pooled genome‐wide analysis of 853 affected brothers.RESULTSIn the new study, we detected linkage to prostate cancer on chromosome 16q23 (P = 0.009), replicating previous results, and to chromosome 11q24 (P = 0.001). In the pooled analysis, the 16q23 linkage was strengthened (P = 0.0005), as was our previous linkage to chromosome 16p (P = 0.0001), and we detected linkage to chromosome 2q32 (P = 0.009). When evaluating Gleason score, our new study detected linkage to chromosome 7q32 (P = 0.0009), again replicating previous results, and to chromosomes 5p15 (P = 0.003), 9q34 (P = 0.009), 10q26 (P = 0.03), and 18p11 (P = 0.02). In the pooled analysis of Gleason score, we observed stronger linkage to chromosome 7q32 (P = 0.0002), but slightly weaker linkage to chromosomes 5q33 (P = 0.005) and 19q13 (P = 0.009) than previously reported. In addition, the new linkages to chromosomes 10q26 and 18p11 were strengthened (P = 0.0002 and P = 0.002, respectively).CONCLUSIONSOur results provide compelling evidence for loci harboring prostate cancer susceptibility and tumor aggressiveness genes, especially on chromosomes 16q23 and 7q32. Prostate 57: 298–308, 2003. © 2003 Wiley‐Liss, Inc.
Genomic scan of 254 hereditary prostate cancer families
Authors: Janer Marta , Friedrichsen Danielle M. , Stanford Janet L. , Badzioch Michael D. , Kolb Suzanne , Deutsch Kerry , Peters Mette A. , Goode Ellen L. , Welti Russ , DeFrance Hawkins B. , Iwasaki Lori , Li Sarah , Hood Leroy , Ostrander Elaine A. , Jarvik Gail P. 
Published: October 2003

AbstractHereditary prostate cancer (HPC) is a genetically heterogeneous disease, complicating efforts to map and clone susceptibility loci. We have used stratification of a large dataset of 254 HPC families in an effort to improve power to detect HPC loci and to understand what types of family features may improve locus identification. The strongest result is that of a dominant locus at 6p22.3 (heterogeneity LOD (HLOD) = 2.51), the evidence for which is increased by consideration of the age of PC onset (HLOD = 3.43 in 214 families with median age‐of‐onset 56–72 years) and co‐occurrence of primary brain cancer (HLOD = 2.34 in 21 families) in the families. Additional regions for which we observe modest evidence for linkage include chromosome 7q and 17p. Only weak evidence of several previously implicated HPC regions is detected. These analyses support the existence of multiple HPC loci, whose presence may be best identified by analyses of large, including pooled, datasets which consider locus heterogeneity. Prostate 57: 308–319, 2003. © 2003 Wiley‐Liss, Inc.