bluuebunny/crossref_metadata_2025_split huggingface dataset:
Synthesis of soluble branched polyimides derived from an ABB′ monomer
Authors: Wang Kun‐Li , Jikei Mitsutoshi , Kakimoto Masa‐aki 
Published: May 2004

AbstractA novel ABB′ monomer, an isomeric mixture of 4‐[4‐(2,4‐diaminophenoxy)phenoxy]phthalic acid 2‐methyl ester, was successfully prepared. The direct polycondensation of the ABB′ monomer was carried out to form polyamic acid monomethyl ester as a precursor with an inherent viscosity of 0.30 dL/g and a number‐average molecular weight of 12,000. The degree of branching of the precursor, determined by 1H NMR, was 0.07. The low degree of branching was caused by the differences in the reactivities of the amino groups. The shape factor was calculated to be 0.72. End‐modified reactions with acetyl chloride, benzoyl chloride, and phthalic anhydride were carried out. After the chemical imidization of the end‐modified precursors, end‐modified polyimides were successfully prepared. The end‐modified polyimides were soluble in dimethyl sulfoxide, dimethylformamide (DMF), and N‐methyl‐2‐pyrrolidinone. On the basis of thermogravimetry and differential scanning calorimetry measurements of the polyimides, the 5 wt % thermal loss temperatures were determined to be 400–520 °C, and the glass‐transition temperatures were determined to be 200–258 °C. According to the X‐ray diffraction measurements, the end‐modified polyimides were amorphous. A strong but brittle film was prepared from an acetamide end‐modified polyimide solution, via casting from a DMF solution, with a tensile strength of 46 MPa, an elongation at break of 4%, and a modulus of 1.3 GPa. © 2004 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 42: 3200–3211, 2004
Self‐assembly and photovoltaic properties of multilayer films based on partially doped polyaniline and poly(4‐carboxyphenyl)acetylene
Authors: Guijun Yao , Boqiu Wang , Yuping Dong , Maofeng Zhang , Zhaohui Yang , Qiaoling Yao , Yip Lam Jacky Wing , Benzhong Tang 
Published: May 2004

AbstractMultilayer self‐assembled films, consisting of partially doped polyaniline (PAN) as a polycation and water‐soluble poly(4‐carboxyphenyl)acetylene (PCPA) as a polyanion, were fabricated through electrostatic attraction. These ultrathin PCPA/PAN films were relatively stable toward aqueous electrolyte solutions and polar organic solvents, and the photoelectric conversion properties of the self‐assembled PCPA/PAN films could be measured with traditional three‐electrode cells in 0.5 M KCl aqueous solutions. With an increase in the bilayer number, the photocurrent rose, and it reached its maximum at eight bilayers. A further increase led to a current drop due to an increase in the recombination probability and weak visible‐light transmission. When neutral PAN films were used, the photocurrent increased consecutively within 15 bilayers, and this indicated that the PAN molecules in the neutral state were stronger electron donors than those in the partially doped state. © 2004 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 42: 3224–3229, 2004
Synthesis, optical properties, and electroluminescence of conjugated poly(p‐phenylenevinylene) derivatives containing 1,3,4‐oxadiazole and pyridine rings in the main chain
Authors: Mikroyannidis John A. , Barberis Vasilios P. , Ding Liming , Karasz Frank E. 
Published: May 2004

AbstractThree new poly(p‐phenylenevinylene) derivatives—PO, POD, and POP—with oxadiazole and pyridine rings along the main chain were synthesized via Heck coupling. The polymers were amorphous and dissolved readily in common organic solvents. They showed relatively low glass‐transition temperatures (up to 42 °C) and satisfactory thermal stability. Solutions of the polymers emitted blue‐greenish light with photoluminescence (PL) emission maxima around 460 nm and PL quantum yields of 0.28–0.49. Thin films of the polymers displayed PL emission maxima at 461–521 nm, and their tendency to form aggregates was significantly influenced by the chemical structure. Light‐emitting diodes with polymers PO and POP, with an indium tin oxide/poly(ethylenedioxythiophene) (PEDOT)/polymer/Ca configuration, emitted yellow and green light, respectively, and this could be attributed to excimer emission. © 2004 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 42: 3212–3223, 2004
Cationic polymerization of styrene in a neutral ionic liquid
Authors: Biedroń Tadeusz , Kubisa Przemysław 
Published: May 2004

AbstractThe cationic polymerization of styrene in a neutral ionic liquid, 1‐butyl‐3‐methylimidazolium hexafluorophosphate, with a 1‐phenetyl chloride/TiCl4 initiating system is reported. The polymerization proceeds to a high conversion, but an analysis of the matrix‐assisted laser desorption/ionization time‐of‐flight spectra of the polymers indicates that chain transfer is significant, leading to a lack of control over the molecular weight and molecular weight distribution. © 2004 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 42: 3230–3235, 2004
pH‐Responsive ampholytic terpolymers of acrylamide, sodium 3‐acrylamido‐3‐methylbutanoate, and (3‐acrylamidopropyl)trimethylammonium chloride. I. Synthesis and characterization
Authors: Fevola Michael J. , Bridges J. Kasey , Kellum Matthew G. , Hester Roger D. , Mccormick Charles L. 
Published: May 2004

AbstractLow‐charge‐density ampholytic terpolymers composed of acrylamide, sodium 3‐acrylamido‐3‐methylbutanoate (NaAMB), and (3‐acrylamidopropyl)trimethylammonium chloride were prepared via free‐radical polymerization in 0.5 M NaCl to yield terpolymers with random charge distributions. NaOOCH was used as a chain‐transfer agent during the polymerization to eliminate the effects of the monomer feed composition on the degree of polymerization (DP) and to suppress gel effects and broadening of the molecular weight distribution. The terpolymer compositions were obtained via 13C NMR spectroscopy, and the residual counterion content was determined via elemental analysis for Na+ and Cl−. The molecular weights (MWs) and polydispersity indices (PDIs) were determined via size exclusion chromatography/multi‐angle laser light scattering (SEC–MALLS); the terpolymer MWs ranged from 1.3–1.6 × 106 g/mol, corresponding to DPs of 1.6–1.9 × 104 repeat units, with all terpolymers exhibiting PDIs of less than 2.0. Intrinsic viscosities determined from SEC–MALLS data and the Flory–Fox relationship were compared to intrinsic viscosities determined via low‐shear dilute‐solution viscometry and were found to agree rather well. Data from the SEC–MALLS analysis were used to analyze the radius of gyration/molecular weight (Rg–M) relationships and the Mark–Houwink–Sakurada intrinsic viscosity/molecular weight ([η]–M) relationships for the terpolymers. The Rg–M and [η]–M relationships revealed that most of the terpolymers exhibited little or no excluded volume effects under size exclusion chromatography conditions. Potentiometric titration of terpolymer solutions in deionized water showed that the apparent pKa value of the poly[acrylamide‐co‐sodium 3‐acrylamido‐3‐methylbutanoate‐co‐(3‐acrylamidopropyl)trimethylammonium chloride] terpolymers increased with increasing NaAMB content in the terpolymers and increasing ratios of anionic monomer to cationic monomer at a constant terpolymer charge density. © 2004 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 42: 3236–3251, 2004
Lineage relationship between LNCaP and LNCaP‐derived prostate cancer cell lines
Authors: Liu Alvin Y. , Brubaker Kristen D. , Goo Young Ah , Quinn Janna E. , Kral Sabine , Sorensen Carrie M. , Vessella Robert L. , Belldegrun Arie S. , Hood Leroy E. 
Published: May 2004

AbstractBACKGROUNDLNCaP and its derivative cell lines, which include C4‐2 (and the related C4‐2B) and CL1, are used as models of prostate cancer. Unlike LNCaP, the other cell lines show features of progressed disease such as metastatic capability and hormone independence. Analyses were done to determine if C4‐2 or CL1 cells were selected from pre‐existent subpopulations in LNCaP.METHODSProstate cancer cells were characterized by cluster designation (CD) phenotyping. Specific cell populations were sorted by flow cytometry. DNA array analysis was used to probe differential gene expression.RESULTSCD phenotyping showed that CL1 and C4‐2 (and C4‐2B) were very dissimilar, and C4‐2 was more similar to LNCaP. One common difference between LNCaP and its derivatives was CD26, in which virtually all C4‐2 or CL1 cells were CD26+ but only ∼10% of LNCaP cells were CD26+. The CD26+ subpopulation of LNCaP was isolated and cultured in vitro. After culture, a high percentage of the cells (descended from the sorted cells) were CD26+, in contrast to those sorted by CD13 or CD44. The cultured CD13 and CD44 populations did not show a high percentage of CD13+ and CD44+ cells, respectively. CD13 and CD44 are markers, in addition to CD26, for CL1 but not for C4‐2.CONCLUSIONSC4‐2 arose probably from CD26+ LNCaP cells, while CL1 arose de novo. © 2004 Wiley‐Liss, Inc.
Evidence of pluripotent human prostate stem cells in a human prostate primary xenograft model
Authors: Huss Wendy J. , Gray Danny R. , Werdin Eric S. , Funkhouser William K. , Smith Gary J. 
Published: May 2004

AbstractINTRODUCTIONThe phenotypic plasticity of the human prostate stem cell within human prostate tissue was examined to determine the response of the stem cell to changes in the androgenic environment.METHODSProstate xenografts were transplanted into athymic nu/nu mice implanted with testosterone pellets, allowed to establish for 1 month time point, the hosts were castrated and pellets removed, and following 1 month of androgen deprivation, the hosts were stimulated with androgen for 2 days to induce proliferation of the residual population of stem cells (2‐month time point).RESULTSGlands in benign xenografts harvested at the 1‐ and 2‐month time points contained basal cell layers that expressed p63 and high molecular weight cytokeratin, and in which essentially all of the cellular proliferation was localized, consistent with the proposed localization of the prostate stem cell. Benign glandular structures in the xenografts were populated by basal, secretory epithelial, neuroendocrine (NE), or squamous cells overlaying the basal cell layer, whereas, adenocarcinoma glands in the xenografts resembled the original prostate cancer (CaP) tissue.CONCLUSIONSIn this human prostate primary xenograft model, the residual stem cell population that survives transplantation, or androgen deprivation, maintains significant pluripotentiality as demonstrated by the capacity to generate progeny that differentiate along multiple lineages in response to microenvironmental signals, particularly along the secretory epithelial lineage in response to androgen, and along the NE cell lineage in response to androgen deprivation. © 2004 Wiley‐Liss, Inc.
Up‐regulation of cathepsin X in prostate cancer and prostatic intraepithelial neoplasia
Authors: Nägler Dorit K. , Krüger Sabine , Kellner Angela , Ziomek Edmund , Menard Robert , Buhtz Peter , Krams Matthias , Roessner Albert , Kellner Udo 
Published: May 2004

AbstractBACKGROUNDEvidence is accumulating that several proteases are involved in prostate cancer progression. A locus which is often amplified in prostate cancer is the chromosomal region 20q13. Interestingly, one of the genes encoding the cysteine protease cathepsin X maps to this region. The aim of this study was to assess the expression pattern of cathepsin X in malignant and non‐malignant prostatic tissue samples.METHODSMatched malignant and non‐malignant tissue specimens were obtained from 56 men after radical prostatectomy. Cathepsin X was quantified at both protein and mRNA levels using several detection methods: Western blotting, immunohistochemistry, quantitative RT‐PCR, and in situ hybridization. Furthermore, genomic DNA was analyzed by PCR for possible gene amplification.RESULTSImmunohistochemical analysis of formalin‐fixed, paraffin‐embedded sections of radical prostatectomy specimens was performed utilizing a polyclonal antibody against human procathepsin X and revealed staining of acinar basal cells in normal prostate glands. Prostatic intraepithelial neoplasias (PINs) and prostate carcinomas stained highly positive for cathepsin X, showing a significant difference to the staining of normal prostate glands. In contrast, relatively weak and heterogenous staining was observed for cathepsins F, B, and L. Up‐regulation of cathepsin X at the protein level was confirmed by Western blotting. No statistically significant difference was observed at the mRNA level. PCR of genomic DNA revealed that cathepsin X up‐regulation most likely occurs in the absence of genomic amplification.CONCLUSIONSThe high expression levels of cathepsin X both in PIN and invasive adenocarcinomas of the prostate suggest that cathepsin X may play a role in the early tumorigenesis of prostate cancer. Further studies are needed to define the utility of this cysteine protease as a diagnostic marker for the early detection of prostate cancer. © 2004 Wiley‐Liss, Inc.
High mobility group protein HMGI(Y) enhances tumor cell growth, invasion, and matrix metalloproteinase‐2 expression in prostate cancer cells
Authors: Takaha Natsuki , Resar Linda M.S. , Vindivich Don , Coffey Donald S. 
Published: May 2004

AbstractBACKGROUNDThe high mobility group protein HMGI(Y) has oncogenic properties and correlates with an aggressive phenotype in prostate cancer. The molecular mechanisms involved in transformation associated with HMGI(Y) overexpression remain unknown.METHODSThe HMG‐I isoform was transfected and overexpressed in nonmetastatic Dunning prostate cancer cells (G cells) without detectable HMGI(Y). The assays of cell proliferation, tumor formation, in vitro invasion, and cDNA microarray were performed to assess the effect of HMGI(Y) overexpression in the transfected G cells.RESULTSOverexpression of HMG‐I in G cells significantly increases cell proliferation and tumor growth and also modestly enhances in vitro invasion compared to mock transfectant. cDNA microarray revealed that expression of the matrix metalloproteinase‐2 (MMP‐2) proform was increased eightfold in G cells overexpressing HMG‐I.CONCLUSIONSOverexpression of HMG‐I in prostate cancer cells enhances cell growth, invasion, and expression of the proform of MMP‐2, which may initiate early steps involved in the metastatic cascade. © 2004 Wiley‐Liss, Inc.
Interleukin‐8 expression is increased in senescent prostatic epithelial cells and promotes the development of benign prostatic hyperplasia
Authors: Castro Patricia , Xia Chen , Gomez Lori , Lamb Dolores J. , Ittmann Michael 
Published: May 2004

AbstractBACKGROUNDBenign prostatic hyperplasia (BPH) is an extremely common disease of older men characterized by increased growth of prostatic epithelial and stromal cells. Previously we showed that senescent epithelial cells accumulate in the prostate of aging men and secrete interleukin‐1α (IL‐1α). IL‐8 is also present at increased levels in BPH tissues and induces expression of FGF2, a potent stromal growth factor. Therefore, we sought to determine if IL‐8 is also expressed at increased levels by senescent epithelial cells and if this secreted IL‐8 plays a role in the pathogenesis of BPH.METHODSExpression of IL‐8 in human BPH tissue and primary cultures of prostatic epithelial cells was analyzed using an enzyme‐linked immunoabsorption assay (ELISA). Tissue senescence was assessed by a quantitative assay for senescence‐associated β galactosidase (SA‐β gal). Proliferation of primary and immortalized prostatic epithelial cells in response to IL‐8 was determined by counting of cells at intervals after addition of IL‐8.RESULTSExpression of IL‐8 is significantly increased in vitro when cultured prostatic epithelial cells undergo senescence. Quantitative assay of BPH tissue extracts revealed that tissue IL‐8 levels are correlated with both SA‐β gal activity and prostate weight. IL‐8 promotes proliferation of primary and immortalized prostfatic epithelial cells in culture.CONCLUSIONSSenescence of prostatic epithelial cells results in increased expression of IL‐8, which can promote proliferation of non‐senescent epithelial and stromal cells by direct and indirect mechanisms, and in this manner contributes to the increased tissue growth seen in BPH. © 2004 Wiley‐Liss, Inc.
Translationally controlled tumor protein (TCTP) in the human prostate and prostate cancer cells: Expression, distribution, and calcium binding activity
Authors: Arcuri Felice , Papa Stefania , Carducci Antonietta , Romagnoli Roberta , Liberatori Sabrina , Riparbelli Maria Giovanna , Sanchez Jean‐Charles , Tosi Piero , del Vecchio Maria Teresa 
Published: May 2004

AbstractBACKGROUNDThe translationally controlled tumor protein (TCTP) is an abundantly expressed protein found in a wide range of organisms from both the animal and plant kingdom. Initially described as a growth‐related protein, knowledge of the biological actions of TCTP has been recently extended to include calcium binding, regulation of apoptosis, and microtubules stabilization. This report describes expression, distribution, and characterization of TCTP in human prostatic tissues and cell lines.METHODSSamples were analyzed by Western blot, RT‐PCR, immunohistochemistry, and confocal microscopy. Calcium binding activity of the recombinant human prostatic protein was evaluated on a calcium overlay assay. A public SAGE database was analyzed to determine TCTP expression levels in normal and cancer tissues.RESULTSTCTP protein and mRNA were detected in all the specimens and cell lines analyzed. The protein was mainly expressed by the secretory luminal epithelial and basal layer cells. A significant amount of protein was present in the prostatic fluids. Subcellular distribution studies in prostate epithelial cells detected the protein in the cytoplasm in interphase and colocalized with tubulin during mitosis. The calcium binding capacity of prostatic TCTP was shown in vitro. Finally, SAGE data indicated TCTP as the calcium binding protein with the highest expression levels among those examined.CONCLUSIONSThe results of the present study demonstrate, for the first time, the expression of TCTP in the human prostate and in prostate cancer cells, and suggest the involvement of the protein in key‐processes such as apoptosis, cellular differentiation, and in the control of sperm functions. © 2004 Wiley‐Liss, Inc.
Interleukin‐6 is responsible for drug resistance and anti‐apoptotic effects in prostatic cancer cells
Authors: Pu Yeong‐Shiau , Hour Tzyh‐Chyuan , Chuang Shuang‐En , Cheng Ann‐Lii , Lai Ming‐Kuen , Kuo Min‐Liang 
Published: May 2004

AbstractBACKGROUNDInterleukin (IL)‐6‐mediated anti‐apoptotic effects and drug‐resistance mechanisms in prostate cancer cells were investigated.METHODSIL‐6 levels of PC‐3 and LNCaP cells were studied by using ELISA. Protective effects of IL‐6 on cytotoxic agent‐induced apoptosis were studied by exogenous IL‐6 in serum‐starved PC‐3 cells and by anti‐sense IL‐6 strategy. Western blotting and reverse transcription‐polymerase chain reaction (RT‐PCR) were used to determine IL‐6 effects on Bcl‐2 family proteins. Tetracycline‐regulated Bcl‐xL expression system and dominant negative STAT3 transfectants were used to study IL‐6 signaling pathways and its anti‐apoptosis effects.RESULTSExogenous IL‐6 and anti‐sense IL‐6 oligonucleotide treatment conferred resistance to cytotoxic agent‐induced apoptosis. Among Bcl‐2 family proteins, only Bcl‐xL was evidently increased by IL‐6 stimulation. The anti‐apoptotic effect of IL‐6 can be significantly attenuated by anti‐sense bcl‐xL transfection and partially abrogated in dominant negative STAT3 transfectants.CONCLUSIONSIL‐6 is a survival factor against cytotoxic agent‐induced apoptosis through both STAT3 and bcl‐xL pathways in prostate cancer cells. © 2004 Wiley‐Liss, Inc.
Characterization of Lys‐698 to met substitution in human plasminogen catalytic domain
Authors: Terzyan Simon , Wakeham Nancy , Zhai Peng , Rodgers Karla , Zhang Xuejun C. 
Published: May 2004

AbstractStreptokinase (SK) is a human plasminogen (Pg) activator secreted by streptococci. The activation mechanism of SK differs from that of physiological Pg activators in that SK is not a protease and cannot proteolytically activate Pg. Instead, it forms a tight complex with Pg that proteolytically activates other Pg molecules. The residue Lys‐698 of human Pg was hypothesized to participate in triggering activation in the SK–Pg complex. Here, we report a study of the Lys‐698 to Met substitution in the catalytic domain of Pg (μPg) containing the proteolytic activation‐resistant background (R561A). While it remains competent in forming a complex with SK, maintaining a comparable equilibration dissociation constant (KD), the recombinant protein shows a nearly 60‐fold reduction in amidolytic activity relative to its R561A background when mixed with native SK. A 2.3 Å crystal structure of this mutant μPg confirmed the correct folding of this recombinant protein. Combined with other biochemical data, these results support the premise that Lys‐698 of human Pg plays a functional role in the so‐called N‐terminal insertion activation mechanism by SK. Proteins 2004. © 2004 Wiley‐Liss, Inc.
Molecular determinants of thapsigargin binding by SERCA Ca2+‐ATPase: A computational docking study
Authors: Paula Stefan , Ball William James 
Published: May 2004

AbstractThapsigargin (TG) is a potent and commonly used inhibitor of the ion transport activity of sarco/endoplasmic reticulum Ca2+‐ATPases (SERCA). Based on the recently published crystal structures of rabbit muscle SERCA1a in the Ca2+/E1 (E1) and TG/E2 (E2) conformations, we performed computational docking studies to characterize the molecular interactions that govern binding of TG and TG‐analogs by the enzyme. Using the program GOLD (genetic optimization for ligand docking) in combination with the scoring function ChemScore, TG was docked into the binding site of the E1 and E2 conformations of SERCA1a. The docking results revealed a consensus ligand‐binding mode consistent with the crystal structure and showed that hydrophobic interactions are the primary driving force of TG binding by SERCA. Moreover, it was shown that the conformational changes accompanying the E2 to E1 transition in the enzyme likely displace TG from its favored orientation in the binding site, thereby substantially reducing its binding affinity. This finding illustrates on the molecular level how TG may exert its inhibitory effect in binding tightly to the E2 form and preventing it from converting into its E1 form, a requirement for catalytic function. We also docked 9 TG analogs into the E2 conformation of the enzyme. Eight of the analogs adopted a binding mode very similar to that of TG, whereas one compound preferred a different orientation in the binding site. Analysis of the predicted binding affinities showed a good correlation with the experimentally observed inhibitory potencies of the analogs. Docking was also performed with several modeled mutants of SERCA1a, whose phenylalanine residue in position 256 (Phe256) had been modified. The experimentally observed declines in TG sensitivity in most of the Phe256 mutants was qualitatively accounted for and appears, at least in part, be due to a slightly altered TG‐binding mode. Proteins 2004. © 2004 Wiley‐Liss, Inc.