bluuebunny/crossref_metadata_2025_split huggingface dataset:
Chemiluminescence ‐ A Novel Method in the Research of Degradation of Paper. I. The Effect of Light on Stacked Sheets of Paper
Authors: Matisová‐Rychlá Lyda , Bukovský Vladimír , Rychlý Jozef , Pleteníková Martina 
Published: February 2007

AbstractStatistical scission of cellulose macromolecules leading to the negative changes in mechanical properties of the paper has been quantified on irradiated stacks of newsprint papers. Attention has been paid to comparison of changes occurring in respective sheets of the stack. The correlation of the results of non‐isothermal chemiluminescence method from which the rate constant of paper oxidation has been determined for 105 °C with the changes of carbonyl groups concentration, pH and double folds has been outlined.
Filled Polysilsesquioxanes: A New Approach to Chemical Sensing
Authors: Castaldo Anna , Massera Ettore , Quercia Luigi , Di Francia Girolamo 
Published: February 2007

AbstractSummary: In an attempt to investigate new polymeric materials as constituents of an e‐nose we focus our attention on a new emerging class of versatile three‐dimensional polyhedral silicon polymers, called polysilsesquioxanes, containing nanosized inorganic cages. Such hybrid amphiphilic materials offer exceptional opportunities to create composites with singular properties. In particular we found that the polyhedral organosilsesquioxane (POSS) cages covalently attached to the polymer backbone as side‐chain act as an “internal” filler with a nanometric homogeneous dispersion. We show how it is possible to fabricate sensing devices based on selected POSS matrix and, by a suitable choice of other “external” home‐made fillers, (e.g. graphite, copper, silicon, zinc and their alloys) obtained by mechanical milling the response of the resulting composites towards different classes of compounds can be tuned. In particular we fabricated a new high sensitive relative humidity device, exhibiting a fivefold response change for relative humidity changing in the range 0% to 100%. This behaviour can not be modelled on the basis of the matrix swelling operating mechanism. Rather, the combined effect of the matrix and the filler has to be invoked in order to explain the formation of nanopores inside the material that are responsible of the porous behavior of our sensors.
Gas Sensor Devices Obtained by Ink‐jet Printing of Polyaniline Suspensions
Authors: Loffredo F. , Burrasca G. , Quercia L. , Sala D. Della 
Published: February 2007

AbstractWe report on the fabrication process of a sensing device obtained by ink‐jet printing of polyaniline suspension on alumina substrates. We optimized the inkjet parameters (amplitude and duration of jetting impulse, jetting frequency, substrate velocity) to obtain thin polyaniline lines as sensitive layers and we analyzed the morphology of PANI lines on substrate. Device response towards ammonia are also discussed and compared with reference device obtained by spin‐coating.
Halogen Free Flame Retardant Agents for Polypropylene in Wire Coating Process
Authors: Maio Luciano Di , Acierno Domenico , Martino Daniela Di 
Published: February 2007

Abstractthe processing behaviour and physical properties of polypropylene/flame retardant blends were investigated in order to evaluate their use in the wire‐coating process. In particular, the need of flame retardancy, suitable melt processability and good mechanical properties of blends was taken into account. Three types of halogen free flame retardants were chosen and were melt blended to the polypropylene matrix. Blends properties were analysed by rheological, mechanical, and thermal characterization including flame retardancy tests. The wire coating process was also performed by a laboratory wire coating apparatus. The results demonstrated that some of the blends are suitable for the purpose of flame retardancy of electrical household wires as an alternative to PVC.
Effect of Solvent (Plasticizers) on PVC Degradation
Authors: Zaikov G. E. , Artsis M. I. 
Published: February 2007

AbstractBoth plasticized (semi‐rigid and flexible) PVC materials as well as PVC in solutions, the rate of their thermal degradation and effective stabilization are caused by essentially different fundamental phenomena in comparison to aging of PVC in absence of the solvent. Both structure and macromolecular dynamics render the significant influence on its stability, i.e. chemical nature of the solvent (plasticizer), its basicity, specific and non‐specific solvation, degree of PVC in a solution (solubility), segmental mobility of macromolecules, thermodynamic properties of the solvent (plasticizer), formation of associates, aggregates, etc.The chemical stabilization of PVC plays a less significant role. The effect of above factors on stability (behavior) of semi‐rigid and flexible PVC will be done on quantitative level.It will be described effect of “echo”‐type of stabilization on the stability of PVC in the presence of plasticizers. If we would like to have stable material from PVC we should make stabilization of plasticizers as more reactive chemical compounds.
TGFα stimulates growth of skin papillomas by autocrine and paracrine mechanisms but does not cause neoplastic progression
Authors: Finzi Eric , Kilkenny Anne , Strickland James E. , Balaschak Mike , Bringman Timothy , Derynck Rik , Aaronson Stuart , Yuspa Stuart H. 
Published: February 2007

AbstractTo investigate the role of transforming growth factor α (TGFα) in tumor development, we introduced the human TGFα (hTGFα) cDNA into cultured primary mouse epidermal cells or papilloma cells using a replication‐defective retroviral vector and analyzed skin grafts constructed with such cells. Expression of the exogenous gene was confirmed by detection of hTGFα mRNA by northern RNA blot analysis, and the secreted hTGFα was measured by ELISA of culture supernatants. Tumor cells expressing hTGFα produced benign tumors (papillomas), which were 1.5‐ to 2‐fold larger than tumors of parental cells when tested as skin grafts on nude mice. Grafts of normal cells that expressed hTGFα produced normal skin. When mixtures of parental tumor cells and normal mouse keratinocytes were grafted to nude mice, papilloma formation was suppressed and tumors that did form were small. Grafts of hTGFα‐producing papilloma cells combined with either normal epidermal cells or hTGFα‐producing epidermal cells yielded large tumors. Mixed grafts containing keratinocytes expressing hTGFα and parental papilloma cells also produced large tumors. While the tumor size was substantially increased by hTGFα expression, the tumors that developed in all groups were histologically benign and reached a stable size 4–5 wk after grafting. These results indicate that expression of hTGFα by either tumor cells (autocrine) or adjoining normal cells (paracrine) can stimulate tumor growth, particularly when tumor growth is suppressed by normal tissue. However, expression of this growth factor did not appear to influence tumor progression directly.
Transforming activity of DNA from rat liver tumors induced by the carcinogen methyl(acetoxymethyl)nitrosamine
Authors: Goyette Michele , Dolan Maureen , Kaufmann William , Kaufman David , Shank Peter R. , Fausto Nelson 
Published: February 2007

AbstractAltered c‐Ha‐ras genes have been frequently detected in the DNA of spontaneous or chemically induced mouse liver tumors. To determine if ras gene mutation is a frequent event during liver carcinogenesis in rats, we examined the transforming activity of DNA from liver tumors that developed in rats injected with methyl(acetoxymethyl)nitrosamine (DMN‐OAc) after a partial hepatectomy. Three weeks after the injection of DMN‐OAc, rats were fed a diet contaiing phenobarbital. This carcinogen acts only on replicating liver cells. Six of eight tumor DNAs induced the transformation of NIH 3T3 cells. The transforming activity was stable upon a second round of transfection, and the transformants were tumorigenic in nude mice. Southern blot analysis of transformant DNAs showed that the transforming activity was not due to the acquisition of a ras (Ha, Ki, or N), neu, myc, A‐raf, v‐raf, erbA, or erbB gene of rat origin. Several transformants' restriction enzyme sensitivity was analyzed, and their activity indicated that similar transforming sequences were present in at least two tumors and that one tumor contained two different transforming sequences. These results suggest that during hepatocarcinogenesis induced in rats by DMN‐OAc, alterations in the ras gene family occur infrequently or not at all and that several different genes (which are not homologous to common oncogenes) become activated and are capable of transforming NIH 3T3 cells.
Comparison of P+ ‐active and ‐inactive pro‐1 homologues from human nasopharyngeal carcinoma cells
Authors: Dowjat W. Karol , Ya Cao , Nagashima Kunio , Sakai Ayako , Colburn Nancy H. 
Published: February 2007

AbstractEleven pro‐1 homologous clones from human nasopharyngeal carcinoma cell line CNE2 were studied with respect to their ability to transfer sensitivity to tumor promoter‐induced neoplastic transformation (P+ activity), their molecular structure, and their homology to both mouse pro‐1 and each other. Restriction mapping and Southern analysis of CNE2 pro‐1 homologous clones revealed three structural classes, all of which showed P+ activity. The approximate limits of mouse pro‐1 hybridizing sequences within CNE2 clones from each structural class were identified, and some of these minimum homologous sequences were tested for P+ activity by transfection into P+ cells. For all classes, a strong association between P+ activity and pro‐1 homology was observed. This finding implies that, for CNE2 clones to be P+‐active, structural homology to mouse pro‐1 is required. The minimum P+‐active sequence thus far identified was a 2.6‐kbp EcoRI‐Sstl fragment. One clone was inactive, even though it was indistinguishable from active clones of the same class by restriction mapping, Southern analysis, and electron microscope examination of heteroduplexes formed by an active and an inactive clone. This raises the possibility that discrete changes, involving a few nucleotides rather than gross rearrangement, may determine the P+ activation of these pro‐1‐homologous sequences.
Timing of proto‐oncogene replication: A possible determinant of early S phase sensitivity of C3H 10T1/2 cells to transformation by chemical carcinogens
Authors: Doggett Norman A. , Cordeiro‐Stone Marila , Chae Chi‐Bom , Kaufman David G. 
Published: February 2007

AbstractThe temporal order of replication of several genes was studied in 10T1/2 cells synchronized by release from confluence‐induced arrest of proliferation followed by treatment with 2 μg/mL aphidicolin for 24 h. DNA subjected to bromodeoxyuridine substitution for 1‐ or 2‐h intervals spanning the S phase was separated from the remaining DNA in cesium chloride gradients, filtered onto nitrocellulose in a slot‐blot apparatus, and hybridized with various 32P‐labeled probes. Ha‐ras was among the first genes replicated at the onset of the S phase. The myc proto‐oncogene replicated later but within the first hour of the S phase. The replication of Ki‐ras, raf, and mos was detected between hour 1 and 2 of the S phase. The dihydrofolate reductase gene replicated early (0–2 h) and the myb proto‐oncogene replicated in mid‐S phase (2–4 h). An immunoglobulin VH sequence and the β‐globin gene replicated late in 10T1/2 cells, 4–6 h after removal of aphidicolin. Replicating DNA is preferentially adducted by chemical carcinogens, and replication of damaged proto‐oncogenes before they are repaired may activate their transforming potential. Therefore, the observed replication of protooncogenes during the early S phase may underlie the enhanced sensitivity of 10T1/2 cells to chemically induced transformation at this point in the cell cycle.
Specific viral oncogenes cause differential effects on cell‐to‐cell communication, relevant to the suppression of the transformed phenotype by normal cells
Authors: Bignami Margherita , Rosa Silvia , Falcone Germana , Tató Franco , Katoh Fumitaka , Yamasaki Hiroshi 
Published: February 2007

AbstractWe have studied growth regulation in mixed cultures of normal and oncogene‐transformed 3T3 cells. The NIH 3T3 cells transformed by myc, src, and ras showed comparable cloning efficiency in semisolid medium. However, when they were plated on plastic with an excess of normal mouse embryo fibroblasts, BALB/c 3T3 CIA31–1–1, ras‐ and src‐transformed cells were able to form distinct foci on the layer of density‐arrested normal cells, whereas myc‐transformed cells lacked this ability. In order to determine whether suppression or expression of the transformed phenotype could be correlated with the ability of the different cell populations to communicate, gap‐junctional intercellular communication (IC) was measured by the Lucifer yellow dye transfer assay in coculture of normal and transformed cells. The dye was observed to spread from BALB/c 3T3 to myc‐NIH 3T3 cells, indicating the presence of IC between these two cell types. In contrast no passage of Lucifer yellow was observed between src‐NIH 3T3 or ras‐NIH 3T3 and BALB/c 3T3. Addition of a phorbol ester tumor promoter, phorbol‐12,13‐didecanoate, efficiently rescued proliferation and focus formation by myc‐transformed cells. The tumor promoter was able to inhibit IC in BALB/c 3T3 cells, although this response greatly varied among the different oncogene transformed clones. Tumorigenicity in nude mice strongly correlated with growth behavior in vitro: myc‐transformed cells were either nontumorigenic or slowly tumorigenic, and src‐ and ras‐transformed cells were highly tumorigenic. These data suggest an important role of IC in modulating abnormal growth behavior in vitro and in vivo.
Tumorigenic and molecular characterization of novel phorbol ester‐resistant and ‐sensitive lines of mice
Authors: Cope Frederick O. , Wagner Frederic J. , Conway Toni , Burns Pamela D. , Johnston Donna , Murphy Paula , Triggs Gloria , Wille John J. 
Published: February 2007

AbstractTwo outbred lines of CD‐1 mice were developed using males and females in an initiation (dimethyl‐benz[a]anthracene; DMBA), promotion (12‐O‐tetradecanoylphorbol‐13‐acetate; TPA) challenge, posttumorigenesis breeding protocol. Our results indicate that the phorbol ester‐resistive (PESTI) line developed tumors at a rate 4.1 times faster than the CD‐1 parental line, while the phorbol ester‐resistant (PERTI) line developed tumors at a rate 36 times slower than the CD‐1 parents. The average number of tumors per mouse reached levels of 27.5 at 12 wk in the PESTI line, 0.1 at 16 wk in the PERTI line, and 6.7 at 16 wk in the CD‐1 line. Biochemical tests showed that the PESTI line had both a high basal level and an enhanced epidermal ornithine decarboxylase (E.C. 4.1.1.17) response to TPA, the latter being nine times that of the PERTI line at their maximum dosages. An autoradiographic analysis of in vivo epidermal cell protein phosphorylation indicated marked differences in basal protein phosphorylation profiles (with high phosphate incorporation, PERTI, 112.7, 95.5, 64.4, 40.8, 18.6, 17.4, and 12.3 kDa; PESTI, 64.4, 40.8, 31.8, and 12.3 kDa) as well as TPA‐dependent changes in these profiles (difference from basal levels, PERTI, 31.8 and 12.8 kDa; PESTI, 139.6, 126.3, 37.2, and 18.6 kDa). These heterogeneous profiles indicate strong genetic segregation of these protein kinase C target substrates. This dermatologically based selection and breeding process also resulted in cosegregating genetic changes in TPA binding constants (Kd) for brain protein kinase C, which were reversed for cytosolic and plasma membrane fractions in the PESTI (cytosolic, 0.50 nM; plasma membrane, 1.89 nM) and PERTI (cytosolic, 2.02 nM; plasma membrane, 0.51 nM) mice. Moreover, TPA‐inducible phosphorylation of 43 and 110 kDa proteins in vivo in the brains of only the PERTI line mice suggests that the PESTI line has either high levels of endogenous phosphorylation or reduced expression of these proteins. In contrast, in vitro screening of brain cytosolic proteins indicated that both lines have a 120 kDa protein whose phosphorylation can be induced by TPA while the PESTI line has a 14 kDa protein whose phosphorylation regulatory controls differ from the PERTI line. Thus, these lines of mice provide experimental systems for defining the skin tumorigenesis process and possibly extending initiationpromotion observations and concepts to other tissues.
Malignant conversion of murine squamous papilloma cell lines by transfection with the fos oncogene
Authors: Greenhalgh David A. , Yuspa Stuart H. 
Published: February 2007

AbstractMurine papilloma cell lines 308 and SP‐1 have been used as recipients for transfected oncogenes to investigate malignant conversion. These cell lines express an activated crasHa gene with a codon 61 mutation and produce squamous papillomas when transplanted as skin grafts onto nude mice. They are not tumorigenic by subcutaneous injection. Both papilloma cell lines were stably transfected with plasmid DNA containing either a rearranged murine plasmacytoma‐derived c‐myc (minus exon 1), adenovirus 5 E1A, FBJ v‐fos or a human c‐fosl FBJ v‐fos chimera, using cotransfection with the neomycin resistance gene contained in pSV2neo to select for transformants. Southern and northern blotting analysis confirmed the uptake and expression of exogenous DNA in both G418‐selected cell lines and in the derived tumors. Unlike the E1A‐ and myc‐containing plasmids, both fos constructs caused malignant conversion in either cell line, as defined by the squamous cell carcinoma histology of tumors from grafted cells and the development of carcinomas after subcutaneous injection into athymic nude mice. Immunofluorescence analysis for specific keratin gene expression indicated that tumors derived by introduction of either of the fos oncogenes were devoid of staining for K1, a 67 kDa epidermal keratin that is expressed in papillomas but not in squamous carcinomas. Tumors from E1A, myc, or pSV2neo transfectants expressed K1, although in a focal distribution. The malignant phenotype induced by the fos oncogene constructs was not associated with the ability to form agar colonies in vitro or to express γ‐glutamyl transpeptidase in the tumors. Since both 308 and SP‐1 were sensitive to the fos oncogene for malignant conversion and insensitive to E1A or myc, it is possible that fos may cooperate with the endogenous‐activated c‐rasHa gene to convert these cells to malignancy. However, since γ‐glutamyl transpeptidase activity is found in the majority of chemically induced mouse skin carcinomas that possess an activated crasHa gene, fos activation may not be a common pathway for spontaneous malignant conversion.
Interaction of an ultimate carcinogen, benzo[a]pyrene diol epoxide, with nucleosomal core particles: Apparent lack of protection of DNA by histone proteins
Authors: Macleod Michael C. , Smith Bettye , Lew Linda Kao 
Published: February 2007

AbstractThe binding of chemical carcinogens to nuclear macromolecules, especially to DNA, is thought to be central to the initiation of carcinogenesis. Previous studies of the interactions of one such ultimate carcinogen, benzo[a]pyrene diol epoxide (BPDE‐I) with nuclei, chromatin and purified DNA, demonstrated that although some BPDE‐I‐DNA interactions were altered in chromatin, covalent binding to chromatin DNA at saturating chromatin concentrations was quantitatively the same as binding to purified DNA. We have now extended these studies to include the basic subunit of chromatin, the nucleosomal core particle. Association constants for BPDE‐I and a nonreactive analogue were determined by absorbance and fluorescence spectroscopy using either core particles or purified DNA and were found to be lower, by a factor of 30, for core particles. One of the major pathways of interaction of BPDE‐I with DNA is the catalysis of BPDE‐I hydrolysis by the exocyclic amino group of deoxyguanosine in native DNA. This detoxification reaction is inhibited about 30‐fold in core particles compared with DNA, consistent with the hypothesis that intercalation is important in this catalytic reaction. In contrast to these findings, at DNA concentrations that allow maximal binding, similar amounts of BPDE‐I are bound covalently to either free DNA or the DNA contained in core particles. This finding suggests that the interaction of DNA with histones to form the subunit structure of chromatin does not significantly protect DNA from damage by this ultimate carcinogen. The pattern of DNA adducts formed with core particle DNA shows a subtle shift toward the pattern seen with denatured DNA.
Chromatin structure and transcriptional regulation of human papillomavirus type 18 DNA in hela cells
Authors: Rösl Frank , Westphal Eva‐Maria , Hausen Harald Zur 
Published: February 2007

AbstractMapping analysis of the nucleosomal organization of integrated human papillomavirus type 18(HPV 18) DNA in HeLa cells reveals a very prominent nuclease‐hypersensitive site within the viral noncoding regulatory region that harbors transcriptional control sequences and coincides with most of the 5′ ends of the cytoplasmic early mRNAs. Moreover, it is shown that the conserved coamplified 5′ cellular flank, common to all HPV18 copies in HeLa cells and located close to the virus‐cell integration site, also contains several distinct hypersensitive sites, accessible not only to DNase I but also to restriction enzymes. Nuclear run‐on analysis in isolated HeLa nuclei demonstrates the occurrence of nascent transcripts covering the cellular flank (the late and the viral noncoding regulatory region), indicating that a cellular promoter, marked by the hypersensitive sites, cooperates with the viral control region in generating the HPV18 transcripts.Cycloheximide treatment of HeLa cells results in a reduction of the cytoplasmic steady‐state level of the 3.5‐kb mRNA corresponding to the viral E6, E7, and parts of the E1 open reading frames (ORFs), whereas the expression of the 1.6‐kb transcript corresponding only to the E6 and E7 ORFs is not influenced. Nuclear run‐on analysis carried out after the cycloheximide chase reveals that the distribution of nascent transcripts spanning the viral E6, E7, and parts of the E1 region is substantially decreased. In contrast to this finding, an even, pronounced increase of the elongation rate of those transcripts, which cover the cellular flank, the late and the viral noncoding regulatory region was noted indicating a different involvement of regulatory factors in the activity of both promoters.
Induction of metallothionein mRNA by tumor promoters in mouse skin and its constitutive expression in papillomas
Authors: Hashiba Hiroki , Hosoi Junichi , Karasawa Mika , Yamada Shuhei , Nose Kiyoshi , Kuroki Toshio 
Published: February 2007

AbstractA single topical application of 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) was found to induce mRNA of a metallothionein (MT) gene or genes in the skin of Sencar mice, and papillomas produced by repeated applications of TPA were shown to have elevated levels of MT mRNA. Induction of MT mRNA was maximal 4–8 h after application of TPA and returned to the control level 24 h later. A dose‐dependent increase of MT mRNA was observed with doses of TPA of 1–5 μg. Of the other promoters tested, phorbol‐12, 13‐didecanoate, mezerein, and the ionophore A23187 also induced MT mRNA, but 4‐O‐methyl‐TPA and benzoyl peroxide did not. Phorbol and 4α‐phorbol‐12, 13‐didecanoate, which are not promoters, also did not induce MT mRNA. Retinoic acid and 1α, 25‐dihydroxyvitamin D3, inhibitors of tumor promotion, did not induce MT mRNA themselves or inhibit the induction of MT mRNA by TPA. In C57BL/6 promotion‐resistant mice, TPA caused only slight induction of MT mRNA. These data suggest a correlation between induction of MT mRNA and epidermal hyperplasia. The constitutive elevation of MT mRNA levels in papillomas may be due to the loss, during the process of tumor promotion, of some mechanism regulating MT gene expression.