bluuebunny/crossref_metadata_2025_split huggingface dataset:
Triple Gene Block Protein Interactions Involved in Movement of
Barley Stripe Mosaic Virus
Authors: Lim Hyoun-Sub , Bragg Jennifer N. , Ganesan Uma , Lawrence Diane M. , Yu Jialin , Isogai Masimachi , Hammond John , Jackson Andrew O. 
Published: March 2008

ABSTRACT

Barley stripe mosaic virus
(BSMV) encodes three movement proteins in an overlapping triple gene block (TGB), but little is known about the physical interactions of these proteins. We have characterized a ribonucleoprotein (RNP) complex consisting of the TGB1 protein and plus-sense BSMV RNAs from infected barley plants and have identified TGB1 complexes in planta and in vitro. Homologous TGB1 binding was disrupted by site-specific mutations in each of the first two N-terminal helicase motifs but not by mutations in two C-terminal helicase motifs. The TGB2 and TGB3 proteins were not detected in the RNP, but affinity chromatography and yeast two-hybrid experiments demonstrated that TGB1 binds to TGB3 and that TGB2 and TGB3 form heterologous interactions. These interactions required the TGB2 glycine 40 and the TGB3 isoleucine 108 residues, and BSMV mutants containing these amino acid substitution were unable to move from cell to cell. Infectivity experiments indicated that TGB1 separated on a different genomic RNA from TGB2 and TGB3 could function in limited cell-to-cell movement but that the rates of movement depended on the levels of expression of the proteins and the contexts in which they are expressed. Moreover, elevated expression of the wild-type TGB3 protein interfered with cell-to-cell movement but movement was not affected by the similar expression of a TGB3 mutant that fails to interact with TGB2. These experiments suggest that BSMV movement requires physical interactions of TGB2 and TGB3 and that substantial deviation from the TGB protein ratios expressed by the wild-type virus compromises movement.
Inhibition of Transcription and DNA Replication by the Papillomavirus E8⁁E2C Protein Is Mediated by Interaction with Corepressor Molecules
Authors: Ammermann Ingo , Bruckner Markus , Matthes Frank , Iftner Thomas , Stubenrauch Frank 
Published: March 2008

ABSTRACT
Papillomavirus genomes replicate as nuclear plasmids at a low copy number in undifferentiated keratinocytes. Papillomaviruses encode the E1 and E2 proteins that bind to the origin of replication and are required for the activation of replication. In addition to E2, several papillomaviruses express an E8⁁E2C protein, which is generated by alternative splicing and functions as a transcriptional repressor and inhibitor of the E1/E2-dependent replication of the viral origin. Previous analyses suggested that the E8 domain functions as a transferable repression domain. In this report we present evidence that the E8 domain is responsible for the interaction with cellular corepressor molecules such as histone deacetylases, the histone methyltransferase SETDB1, and the TRIM28/KAP-1/TIF1β/KRIP-1 protein. Whereas the interaction with histone deacetylases is involved only in transcriptional repression, the interaction with TRIM28/KAP-1/TIF1β/KRIP-1 contributes to the inhibition of E1/E2-dependent replication. The corepressor TRIM28/KAP-1/TIF1β/KRIP-1 has been described to be part of multicomponent complexes involved in transcriptional regulation and functions as a scaffold protein. Since neither histone deacetylases nor the histone methyltransferase SETDB1 appears to be involved in the inhibition of E1/E2-dependent replication, most likely the modification of non-histone proteins contributes to the replication repression activity of E8⁁E2C.
Genetic structure of wild emmer wheat populations as reflected by transcribed versus anonymous SSR markers
Authors: Peleg Zvi , Fahima Tzion , Abbo Shahal , Krugman Tamar , Saranga Yehoshua 
Published: March 2008

Simple sequence repeat (SSR) markers have become a major tool in population genetic analyses. The anonymous genomic SSRs (gSSRs) have been recently supplemented with expressed sequence tag (EST) derived SSRs (eSSRs), which represent the transcribed regions of the genome. In the present study, we used 8 populations of wild emmer wheat ( Triticum turgidum subsp. dicoccoides ) to compare the usefulness of the two types of SSR markers in assessing allelic diversity and population structure. gSSRs revealed significantly higher diversity than eSSRs in terms of average number of alleles (14.92 vs. 7.4, respectively), polymorphic information content (0.87 vs. 0.68, respectively), and gene diversity (He; 0.55 vs. 0.38, respectively). Despite the overall differences in the level of diversity, Mantel tests for correlations between eSSR and gSSR pairwise genetic distances were found to be significant for each population as well as for all accessions jointly (RM= 0.54, p = 0.01). Various genetic structure analyses (AMOVA, PCoA, STRUCTURE, unrooted UPGMA tree) revealed a better capacity of eSSRs to distinguish between populations, while gSSRs showed a higher proportion of intrapopulation (among accessions) diversity. We conclude that eSSR and gSSR markers should be employed in conjunction to obtain a high inter- and intra-specific (or inter- and intra-varietal) distinctness.
FACTORIZATIONS OF THE THOMPSON–HIGMAN GROUPS, AND CIRCUIT COMPLEXITY
Authors: BIRGET JEAN-CAMILLE 
Published: March 2008

We consider the subgroup lpGk,1of length preserving elements of the Thompson–Higman group Gk,1and we show that all elements of Gk,1have a unique lpGk,1· Fk,1factorization. This applies to the Thompson–Higman group Tk,1as well. We show that lpGk,1is a "diagonal" direct limit of finite symmetric groups, and that lpTk,1is a k∞Prüfer group. We find an infinite generating set of lpGk,1which is related to reversible boolean circuits.We further investigate connections between the Thompson–Higman groups, circuits, and complexity. We show that elements of Fk,1cannot be one-way functions. We show that describing an element of Gk,1by a generalized bijective circuit is equivalent to describing the element by a word over a certain infinite generating set of Gk,1; word length over these generators is equivalent to generalized bijective circuit size.We give some coNP-completeness results for Gk,1(e.g., the word problem when elements are given by circuits), and [Formula: see text]-completeness results (e.g., finding the lpGk,1· Fk,1factorization of an element of Gk,1given by a circuit).
Decreased Expression of UK114 Is Related to the Differentiation Status of Human Hepatocellular Carcinoma
Authors: Chong Chin-Liew , Huang Shiu-Feng , Hu Cheng-po , Chen Ya-Ling , Chou Hsin-Ying , Chau Gar-Yang , Shew Jin-Yuh , Tsai Yue-Lin , Chen Chiung-Tong , Chang Chungming , Chen Mong-Liang 
Published: March 2008

Abstract
Previous studies have identified that the expression of UK114 is tissue specific and the protein has been found to be most abundant in liver and kidney. However, the expression of UK114 in human hepatocellular carcinoma and its relationship to differentiation and transformation of hepatocellular carcinoma have not been studied. In this study, the expression of UK114 in human hepatocellular carcinoma was examined by Northern and Western blot analyses. We found that UK114 was significantly down-regulated in most of hepatocellular carcinoma tissues compared with adjacent nontumor tissues (72.7%) at both mRNA and protein levels. We looked into the possibility that this decreased expression of UK114 in the hepatocellular carcinoma tissues may play a role in the differentiation or tumorigenicity of hepatocellular carcinoma. Immunohistochemical staining showed that the reduced expression of UK114 in hepatocellular carcinoma tissues was correlated with the tumor differentiation status as graded by the Edmondson-Steiner classification. On the other hand, overexpression of UK114 was not able to suppress the proliferation of human hepatoma cells and tumorigenicity in nude mice. These results suggest that UK114 does not seem to act as a tumor suppressor gene; however, it may useful as a biomarker that will assist in the grading of the differentiation status of hepatocellular carcinoma samples. (Cancer Epidemiol Biomarkers Prev 2008;17(3):535–42)
Is Mammography Adequate for Screening Women with Inherited BRCA Mutations and Low Breast Density?
Authors: Bigenwald Rachel Z. , Warner Ellen , Gunasekara Anoma , Hill Kimberley A. , Causer Petrina A. , Messner Sandra J. , Eisen Andrea , Plewes Donald B. , Narod Steven A. , Zhang Liying , Yaffe Martin J. 
Published: March 2008

Abstract
Background: Several observational studies have shown that magnetic resonance imaging (MRI) is significantly more sensitive than mammography for screening women over age 25 at high risk for hereditary breast cancer; however, MRI is more costly and less specific than mammography. We sought to determine the extent to which the low sensitivity of mammography is due to greater breast density.
Methods: Breast density was evaluated for all patients on a high-risk screening study who were diagnosed with breast cancer between November 1997 and July 2006. Density was measured in two ways: qualitatively using the four categories characterized by the Breast Imaging Reporting and Data System and quantitatively using a computer-aided technique and classified as (a) ≤10%, (b) 11% to 25%, (c) 26% to 50%, and (d) &gt;50% density. Comparison of sensitivity of mammography (and MRI) for each individual density category and after combining the highest two and lowest two density categories was done using Fisher's exact test.
Results: A total of 46 breast cancers [15 ductal carcinoma in situ (DCIS) and 31 invasive] were diagnosed in 45 women (42 with BRCA mutations). Mean age was 48.3 (range, 32-68) years. Overall, sensitivity of mammography versus MRI was 20% versus 87% for DCIS and 26% versus 90% for invasive cancer. There was a trend towards greater mammographic sensitivity for invasive cancer in women with fattier breasts compared with those with greater breast density (37-43% versus 8-12%; P = 0.1), but this trend was not seen for DCIS.
Conclusion: It is necessary to add MRI to mammography for screening women with BRCA mutations even if their breast density is low. (Cancer Epidemiol Biomarkers Prev 2008;17(3):706–11)
Comparative Bioavailability of Sulindac in Capsule and Tablet Formulations
Authors: Reid Joel M. , Mandrekar Sumithra J. , Carlson Elsa C. , Harmsen W. Scott , Green Erin M. , McGovern Renee M. , Szabo Eva , Ames Matthew M. , Boring Daniel , Limburg Paul J. ,   for the Cancer Prevention Network
Published: March 2008

Abstract
The cyclooxygenase (COX)-2 enzyme appears to be an important target for cancer chemoprevention. Given the recent emergence of potentially serious cardiovascular toxicity associated with selective COX-2 inhibitors, nonsteroidal antiinflammatory drugs (NSAIDs), which inhibit both COX-1 and COX-2, have received renewed attention as candidate chemoprevention agents. Sulindac has shown consistent chemopreventive potential in preclinical studies as well as in a limited number of clinical trials reported to date. For the current pharmacokinetic study, sulindac capsules were prepared to facilitate ample agent supplies for future intervention studies. Encapsulation of the parent compound (sulindac sulfoxide) can be readily accomplished, but the effects of alternate formulations on bioavailability have not been rigorously examined. In the present single-dose, two-period crossover trial, we conducted pharmacokinetic analyses of sulindac in capsule (test) versus tablet (reference) formulations. Overall, bioavailability appeared to be higher for the capsule compared with the tablet formulation based on test-to-reference pharmacokinetic variable ratios for the parent compound alone. However, additional analyses based on the sulfide and sulfone metabolites of sulindac with the same pharmacokinetic variables indicated similar chemopreventive exposures between the capsule and tablet formulations. These data support the use of sulindac capsules, which can be readily prepared with matching placebos, in future blinded chemoprevention trials. (Cancer Epidemiol Biomarkers Prev 2008;17(3):674–9)
Fetal MouseCyp1b1and Transplacental Carcinogenesis from Maternal Exposure to Dibenzo(a,l)pyrene
Authors: Castro David J. , Baird William M. , Pereira Clifford B. , Giovanini Jack , Löhr Christiane V. , Fischer Kay A. , Yu Zhen , Gonzalez Frank J. , Krueger Sharon K. , Williams David E. 
Published: March 2008

AbstractDibenzo(a,l)pyrene (DBP) is among the most potent carcinogenic polycyclic aromatic hydrocarbons. Previously, we showed that DBP administration to pregnant mice resulted in high mortality of offspring from an aggressive T-cell lymphoma. All mice that survive to 10 months of age exhibit lung tumors with high multiplicity. Recombinant cytochrome P450 (cyp) 1b1 from mice and the homologue 1B1 in humans exhibit high activity toward the metabolic activation of DBP. Targeted disruption of the cyp1b1 gene protects against most DBP-dependent cancers. Mice heterozygous for the disrupted cyp1b1 allele were used to examine the effect of cyp1b1 gene dosage on DBP transplacental carcinogenesis. Dams were treated with 1 or 15 mg/kg of DBP or 50 mg/kg of benzo(a)pyrene. Cyp1b1-null offspring did not develop lymphoma, whereas wild-type and heterozygous siblings, born to dams given the high dose of DBP, exhibited significant mortalities between 10 and 30 weeks of age. At 10 months, all groups had lung adenomas or carcinomas [9.5%, 40.3%, 25.6%, and 100% incidences for controls, benzo(a)pyrene, 1 and 15 mg/kg DBP, respectively]. Cyp1b1 status did not alter benzo(a)pyrene-dependent carcinogenesis. At 1 mg/kg DBP, cyp1b1 status altered the incidence of lung tumors (19.0, 27.8, and 28.6% for nulls, heterozygous, and wild-type, respectively). At 15 mg/kg, tumor multiplicities in cyp1b1 wild-type (9.3) and heterozygous (9.5) offspring were nearly twice that of cyp1b1-null siblings (5.0). These data confirm that cyp1b1 bioactivation of DBP occurs in fetal target tissues, following transplacental exposure, with the thymus and lung as primary and secondary targets, respectively.
Regulation of Prostaglandin Transporters in Colorectal Neoplasia
Authors: Holla Vijaykumar R. , Backlund Michael G. , Yang Peying , Newman Robert A. , DuBois Raymond N. 
Published: March 2008

Abstract
Prostaglandin E2 (PGE2) promotes cancer progression by affecting cell proliferation, apoptosis, angiogenesis, and the immune response. It has been reported that PGE2 is transported or passes through the cell membrane via prostaglandin-specific transporters including the prostaglandin transporter (PGT, an influx transporter) and the multidrug resistance-associated protein 4 (an efflux transporter). PGT can facilitate the removal of PGE2 from the extracellular milieu by transporting it into the cell, where 15-hydroxyprostaglandin dehydrogenase (15-PGDH) then oxidizes PGE2 into 15-keto PGE2. We previously reported that 15-PGDH expression is reduced in most colorectal cancers, indicating the tumor suppressor role of this gene. In the present study, we show that PGT expression is also decreased (whereas multidrug resistance-associated protein 4 expression is elevated) in human colorectal cancer specimens (compared with expression in normal mucosa) and in colorectal cancer cell lines. Furthermore, we found that PGT expression decreased in premalignant adenomas in APCmin mice and was partially restored (in human colorectal cancer cell lines) by treatment with a DNA demethylating agent or histone deacetylase inhibitor. Forced PGT overexpression in vitro dose dependently reduced extracellular PGE2 levels and increased intracellular levels of its catabolic product 15-keto PGE2. Our collective data suggest that the existing model to explain increased PGE2 in colorectal neoplasia should be modified to include the novel mechanism of coordinated up- and down-regulation of genes involved in PGE2 transport.
High-dose erythropoietin alters platelet reactivity and bleeding time in rodents in contrast to the neuroprotective variant carbamyl-erythropoietin (CEPO)
Authors: Torup Lars , Bochsen Louise , Kjalke Marianne , Abel Kristin , Theilgaard-Monch Kim , Johansson Pär , Bjørn Søren , Kirkeby Agnete , Gerwien Jens , Leist Marcel 
Published: March 2008

SummaryThe haematopoietic hormone erythropoietin (EPO) has neuroprotective properties and is currently being explored for treatment of stroke and other neurological disorders. Short-term, high-dose treatment with EPO seems to improve neurological function of stroke patients but may be associated with increased thrombotic risk, whereas alternative non-erythropoietic neuroprotective derivatives of EPO, such as carbamylated EPO (CEPO), may be devoid of such side-effects. We investigated the effects of short-term, high-dose treatment with EPO and CEPO on platelet function and haemostasis in healthy mice and rats. Animals received three daily doses of EPO or CEPO (50 μg/kg), and blood was compared with respect to alterations in haematology and platelet reactivity. In rats, treatment with EPO increased the haematocrit to >50% and the mean platelet volume by 37%,while CEPO had no effect on these parameters. Platelets from EPO-treated rats showed an increased sensitivity to thrombin receptor agonist peptides and elevated plasma levels of soluble P-selectin (sP-selectin) were found in treated mice. Further indicators of platelet hyperreactivity in EPO, but not CEPO-treated animals, were significantly increased aggregatory responses to collagen in whole blood and platelet-rich plasma (PRP).The increased platelet reactivity was paralleled by a decreased bleeding time after tail transection in rats. Samples from EPO-treated rats showed an attenuated response to ADP in whole blood aggregometry and thrombelastography (TEG) platelet mapping but not in apyrase-treated PRP, suggesting involvement of ADP receptor desensitization. These findings suggest that while EPO affects various aspects of platelet function, CEPO is devoid of such effects.
Time course of prothrombotic and proinflammatory substance release after intracoronary stent implantation
Authors: Jordanova Nelli , Strehblow Christoph , Syeda Bonni , Meyer Brigitte , Charvat Silvia , Zorn Gerlinde , Scheinig Daniela , Wojta Johann , Huber Kurt , Glogar Dietmar , Gyöngyösi Mariann , Wexberg Paul 
Published: March 2008

SummaryWe hypothesized that restenosis after coronary stenting is predicted by elevated levels of markers of thrombus formation and inflammation. Plasma levels of representative markers of inflammation, the thrombin and plasmin activation systems and adhesion molecules were measured in 59 patients with stable angina pectoris before, immediately after and 6 hours (h), 12 h, 24 h, one month and six months after elective stent implantation (radioactive phosphorus-32 stents /RSs/ n=16,bare-metal stents /BMSs/ n=43). All patients underwent clinical and angiographic follow-up (FUP) six months after stenting. RSs had significantly higher angiographic severity of restenosis than BMSs (47.1 ± 20.1% vs. 27.6 ± 22.0%, p=0.003). Repeated measures ANOVA revealed significant differences between the BMS and RS groups as regards the increases in plasma levels of vascular cell adhesion molecule-1 (VCAM-1, p=0.022), plasminogen activator inhibitor-1 (PAI-1, p=0.047), tissue-type plasminogen activator (tPA, p=0.047) and CD40 ligand (CD40L, p=0.038). tPA levels tended to increase immediately after stenting in both groups, whereas the PAI-1 level one month after stenting was elevated significantly only in the RS group. In the RS group, the plasma levels of CD40L were increased at 24 h and six months after stenting, and the VCAM-1 level rose immediately after stenting and remained high during the FUP. Multivariate analysis on pooled laboratory data of both groups revealed elevated levels of VCAM-1 at 12 h and at six months as significant predictors of the severity of stent restenosis. In conclusion, the process of inflammation and thrombosis occurring after coronary interventions seems to be prolonged and enhanced in patients with highgrade restenosis at the follow up.
Prediction of the outcome of preoperative chemotherapy in breast cancer using DNA probes that provide information on both complete and incomplete responses
Authors: Natowicz René , Incitti Roberto , Horta Euler Guimarães , Charles Benoît , Guinot Philippe , Yan Kai , Coutant Charles , Andre Fabrice , Pusztai Lajos , Rouzier Roman 
Published: March 2008

Abstract

Background
DNA microarray technology has emerged as a major tool for exploring cancer biology and solving clinical issues. Predicting a patient's response to chemotherapy is one such issue; successful prediction would make it possible to give patients the most appropriate chemotherapy regimen. Patient response can be classified as either a pathologic complete response (PCR) or residual disease (NoPCR), and these strongly correlate with patient outcome. Microarrays can be used as multigenic predictors of patient response, but probe selection remains problematic. In this study, each probe set was considered as an elementary predictor of the response and was ranked on its ability to predict a high number of PCR and NoPCR cases in a ratio similar to that seen in the learning set. We defined a valuation function that assigned high values to probe sets according to how different the expression of the genes was and to how closely the relative proportions of PCR and NoPCR predictions to the proportions observed in the learning set was. Multigenic predictors were designed by selecting probe sets highly ranked in their predictions and tested using several validation sets.

Results
Our method defined three types of probe sets: 71% were mono-informative probe sets (59% predicted only NoPCR, and 12% predicted only PCR), 25% were bi-informative, and 4% were non-informative. Using a valuation function to rank the probe sets allowed us to select those that correctly predicted the response of a high number of patient cases in the training set and that predicted a PCR/NoPCR ratio for validation sets that was similar to that of the whole learning set. Based on DLDA and the nearest centroid method, bi-informative probes proved more successful predictors than probes selected using a t test.

Conclusion
Prediction of the response to breast cancer preoperative chemotherapy was significantly improved by selecting DNA probe sets that were successful in predicting outcomes for the entire learning set, both in terms of accurately predicting a high number of cases and in correctly predicting the ratio of PCR to NoPCR cases.
Using RNase sequence specificity to refine the identification of RNA-protein binding regions
Authors: Wang Xin , Wang Guohua , Shen Changyu , Li Lang , Wang Xinguo , Mooney Sean D , Edenberg Howard J , Sanford Jeremy R , Liu Yunlong 
Published: March 2008

Abstract
Massively parallel pyrosequencing is a high-throughput technology that can sequence hundreds of thousands of DNA/RNA fragments in a single experiment. Combining it with immunoprecipitation-based biochemical assays, such as cross-linking immunoprecipitation (CLIP), provides a genome-wide method to detect the sites at which proteins bind DNA or RNA. In a CLIP-pyrosequencing experiment, the resolutions of the detected protein binding regions are partially determined by the length of the detected RNA fragments (CLIP amplicons) after trimming by RNase digestion. The lengths of these fragments usually range from 50-70 nucleotides. Many genomic regions are marked by multiple RNA fragments. In this paper, we report an empirical approach to refine the localization of protein binding regions by using the distribution pattern of the detected RNA fragments and the sequence specificity of RNase digestion. We present two regions to which multiple amplicons map as examples to demonstrate this approach.