bluuebunny/crossref_metadata_2025_split huggingface dataset:
Temperature Changes in Silorane‐, Ormocer‐, and Dimethacrylate‐Based Composites and Pulp Chamber Roof during Light‐Curing
Authors: MILETIC VESNA , IVANOVIC VLADIMIR , DZELETOVIC BOJAN , LEZAJA MAJA 
Published: April 2009

ABSTRACTStatement of the Problem:  Light‐curing of resin‐based composites (RBCs) is associated with temperature increase in the pulp chamber, which may have a detrimental effect on the vital pulp.Purpose:  The purpose of the study was to evaluate temperature changes of silorane‐, ormocer‐, and dimethacrylate‐based RBCs at the bottom surface of the RBC and in the pulp chamber roof dentin (PCRD) during curing.Materials and Methods:  In part A, temperatures were measured for Filtek LS (3M ESPE, St. Paul, MN, USA), Admira (Voco GmbH, Cuxhaven, Germany), and Herculite XRV (Kerr Corp., Orange, CA, USA) with a high‐power light‐emitting diode (LED) unit by placing thermocouples in contact with the bottom surface of the material in standardized acrylic molds. In part B, temperature changes in PCRD were measured in extracted molars during light‐curing of adhesives and RBCs in 2‐mm‐deep cavities with a remaining dentin thickness (RDT) of 1 mm.Results:  Filtek LS showed a different temperature curve compared with Admira and Herculite XRV. Significantly higher temperatures were recorded for Filtek LS (p < 0.001) than for Admira and Herculite XRV in acrylic molds. Temperature rises recorded in PCRD for adhesives and RBCs were between 4.1 and 6.4°C. No significant differences in PCRD temperatures were found between the three groups during adhesive curing and RBC curing (p > 0.05).Conclusions:  Filtek LS showed a different heat‐generation pattern from and significantly higher temperatures than Admira and Herculite XRV when the materials were tested in acrylic molds. Similar temperatures were recorded in the PCRD during curing of adhesives and RBCs.CLINICAL SIGNIFICANCEAlthough a substantial temperature rise in the bulk material occurred during light‐curing of the three resin‐based composites, a remaining dentin thickness of 1 mm caused a significant reduction in pulp chamber roof dentin temperatures. Temperatures measured in the pulp chamber roof dentin corresponding to the zone occupied by the postmitotic odontoblast layer were not statistically different for the three types of resin‐based composites.
Shakespeare and the Senses
Authors: Dugan Holly 
Published: April 2009

AbstractThis article examines recent critical approaches to Shakespeare and the senses. Historicizing the senses has posed certain methodological challenges: what is the relationship between subjective sensory perceptions and broader cultural understandings of sensation? Does the sensate have a history? Recent work on each of the five senses demonstrates that the answer is yes. And, surprisingly, Shakespeare and his literary works are at the center of the field. As an important figure of the English literary canon, yet one about whom we know so very little, Shakespeare's sensory archive is both omnipresent and illusive. Shakespearean sensations thus provide a way of grappling with the larger methodological stakes of this field. This article examines a wide range of critical approaches to Shakespeare's sensory archive and ends by considering possible paths for further research.
Development and characterization of 30 polymorphic microsatellite markers for the Atlantic surfclam, Spisula solidissima (Dillwyn, 1817)
Authors: WANG YAN , WANG AIMIN , GUO XIMING 
Published: April 2009

AbstractThirty polymorphic microsatellite markers were developed for the Atlantic surfclam, Spisula solidissima, from an enriched library and characterized in 24 clams from a wild population. The number of alleles ranged from 3 to 16 per locus. The expected and observed heterozygosities ranged from 0.1942 to 0.9238 and 0.0833 to 0.875 respectively. Six loci showed significant (P < 0.05 after Bonferroni correction) deviation from Hardy–Weinberg equilibrium, probably because of the presence of null alleles. Three primer pairs amplified duplicated loci with two involving tandem mini‐satellite repeats. Most of the microsatellite markers developed here should be useful for genetic studies in this species.
Treatment of nonalcoholic steatohepatitis with colestimide
Authors: Taniai Makiko , Hashimoto Etsuko , Tobari Maki , Yatsuji Satoru , Haruta Ikuko , Tokushige Katsutoshi , Shiratori Keiko 
Published: April 2009

Aim:  To clarify the usefulness of colestimide in patients with nonalcoholic steatohepatitis (NASH) with hyperlipidemia.Methods:  In an open‐label randomized controlled trial, 17 NASH patients with hyperlipidemia received colestimide (3 g/day) for 24 weeks. There were 21 control patients. All patients received lifestyle modification therapy. Efficacy was assessed based on metabolic profile, insulin resistance, transaminases, serum hepatic fibrosis markers, adipokine levels, visceral fat on computed tomography (CT), and the fatty liver grade on CT. NASH patients with moderate to severe steatosis by histology were also evaluated separately.Results:  Baseline clinical characteristics of the two groups were similar. Both groups experienced a significant decrease of BMI with no difference between them. However, visceral fat decreased significantly more in the colestimide group (P = 0.046). Aspartate aminotransferase (AST) showed a significantly greater decrease in the colestimide group compared with the control group (P = 0.042). In patients with moderate to severe histological steatosis, there were significant differences between the two groups regard to HbA1c, transaminases, and hyaluronic acid (P = 0.018 for HbA1c, P = 0.003 for AST, P = 0.042 for alanine aminotransferase, and P = 0.042 for hyaluronic acid). Steatosis significantly improved in patients in the colestimide group who had fatty liver on CT (P = 0.049). In the colestimide group, abdominal distension and/or constipation were seen, but mostly tolerable, no other clinical or laboratory adverse events associated with the use of this medicine were not observed.Conclusions:  Colestimide seems to increase the efficacy of lifestyle modification in NASH patients with hyperlipidemia. Its beneficial effects were more prominent in NASH patients with moderate to severe histological steatosis.
Is There a Role for Acupuncture in Endometriosis Pain, Or ‘endometrialgia’?
Authors: Lundeberg Thomas , Lund Iréne 
Published: April 2009

Endometriosis is a common cause of pelvic pain in women, many of whom suffer a progression of symptoms over their menstrual life. Symptoms may include combinations of abnormal visceral sensations and emotional distress. Endometriosis pain, or ‘endometrialgia’ often has a negative influence on the ability to work, on family relationships and sense of worth.Endometrialgia is often considered to be a homogeneous sensory entity, mediated by a specialised high threshold sensory system, which extends from the periphery through the spinal cord, brain stem and thalamus to the cerebral cortex. However, multiple mechanisms have been detected in the nervous system responsible for the pain including peripheral sensitisation, phenotypic switches, central sensitisation, ectopic excitability, structural reorganisation, decreased inhibition and increased facilitation, all of which may contribute to the pain.Although the causes of endometrialgia can differ (eg inflammatory, neuropathic and functional), they share some characteristics. Endometrialgia may be evoked by a low intensity, normally innocuous stimulus (allodynia), or it may be an exaggerated and prolonged response to a noxious stimulus (hyperalgesia). The pain may also be spontaneous in the absence of any apparent peripheral stimulus.Oestrogens and prostaglandins probably play key modulatory roles in endometriosis and endometrialgia. Consequently many of the current medical treatments for the condition include oral drugs, like non-steroid anti-inflammatory drugs, contraceptives, progestogens, androgenic agents, gonadotrophin releasing hormone analogues, as well as laparoscopic surgical excision of the endometriosis lesions. However, management of pain in women with endometriosis is currently inadequate for many. Possibly acupuncture and cognitive therapy may be used as an adjunct.
Src-Induced Cisplatin Resistance Mediated by Cell-to-Cell Communication
Authors: Peterson-Roth Elizabeth , Brdlik Cathleen M. , Glazer Peter M. 
Published: April 2009

Abstract
Cisplatin-induced cell death can be triggered by cell-to-cell communication through gap junctions. Here, we show that activated src produces tyrosine phosphorylation of the gap junction protein connexin 43, decreases gap junction communication, and increases cell survival in response to cisplatin. Experiments with mixed cell populations show that src activity in one cell can confer increased cisplatin survival on neighboring cells, even when the neighboring cells lack such src activity. This work is the first demonstration that expression of an oncogene in one cell can affect the survival of a neighboring cell not expressing the oncogene in response to a chemotherapeutic drug. The trans-acting effect of activated src on neighboring cells can be blocked by inhibitors of src kinase or by siRNA-mediated knockdown of src expression, and it can be counteracted by forced up-regulation of connexin 43, via either gene transfer or proteasome inhibition. These results identify a novel pathway of cisplatin resistance that may be amenable to therapeutic intervention. [Cancer Res 2009;69(8):3619–24]
Combined Integrin Phosphoproteomic Analyses and Small Interfering RNA–Based Functional Screening Identify Key Regulators for Cancer Cell Adhesion and Migration
Authors: Chen Yanling , Lu Bingwen , Yang Qingkai , Fearns Colleen , Yates John R. , Lee Jiing-Dwan 
Published: April 2009

Abstract
Integrins interact with extracellular matrix (ECM) and deliver intracellular signaling for cell proliferation, survival, and motility. During tumor metastasis, integrin-mediated cell adhesion to and migration on the ECM proteins are required for cancer cell survival and adaptation to the new microenvironment. Using stable isotope labeling by amino acids in cell culture–mass spectrometry, we profiled the phosphoproteomic changes induced by the interactions of cell integrins with type I collagen, the most common ECM substratum. Integrin-ECM interactions modulate phosphorylation of 517 serine, threonine, or tyrosine residues in 513 peptides, corresponding to 357 proteins. Among these proteins, 33 key signaling mediators with kinase or phosphatase activity were subjected to small interfering RNA–based functional screening. Three integrin-regulated kinases, DBF4, PAK2, and GRK6, were identified for their critical role in cell adhesion and migration possibly through their regulation of actin cytoskeleton arrangement. Altogether, we not only depict an integrin-modulated phosphorylation network during cell-ECM protein interactions but also reveal novel regulators for cell adhesion and migration. [Cancer Res 2009;69(8):3713–20]
Non–Small Cell Lung Cancer Exhibits Transcript Overexpression of Genes Associated with Homologous Recombination and DNA Replication Pathways
Authors: Saviozzi Silvia , Ceppi Paolo , Novello Silvia , Ghio Paolo , Lo Iacono Marco , Borasio Piero , Cambieri Alberto , Volante Marco , Papotti Mauro , Calogero Raffaele A. , Scagliotti Giorgio V. 
Published: April 2009

Abstract
Genes involved in DNA repair and replication have been recently investigated as predictive markers of response to chemotherapy in non–small cell lung cancer (NSCLC). However, few data on the expression of these genes in tumor compared with corresponding normal lung are available. The aim of this study was to evaluate differential mRNA levels of 22 DNA repair genes of five different DNA repair pathways: direct, base excision, nucleotide excision (NER), double-strand break (DSBR), and postreplicative repair. In addition, six genes involved in DNA replication (REP) and three telomere maintenance genes were investigated. Total RNAs extracted from fresh-frozen tumors and corresponding normal tissues of 50 consecutive chemo-naïve resected NSCLC patients were analyzed. Transcript levels were quantified by real-time PCR. A significant overexpression was detected in 20 of 30 (67%) genes, mostly belonging to DSBR pathways, whereas others (XPA, XPC, and UBE2N; 10%) were significantly underexpressed. For 7 of 30 (23%) genes, mostly belonging to NER pathway, no significant difference between paired tumor and normal samples was observed. Transcript overexpression of DSBR and REP genes was significantly higher in poorly differentiated carcinomas and DSBR levels were higher in men compared with women. The transcriptional overexpression of four genes (XRCC5, TOP3B, TYMS, and UNG) showed significant correlation with a shorter patients' outcome at the univariate, whereas only stage of disease appeared as an independent factor affecting prognosis, as assessed by multivariate analysis. In conclusion, genes belonging to DNA repair/replication pathways are overexpressed in NSCLC and are associated with a more aggressive phenotype. [Cancer Res 2009;69(8):3390–6]
Suppression of Human Solid Tumor Growth in Mice by Intratumor and Systemic Inoculation of Histidine-Rich and pH-Dependent Host Defense–like Lytic Peptides
Authors: Makovitzki Arik , Fink Avner , Shai Yechiel 
Published: April 2009

Abstract
Previously, we reported that intratumor or systemic inoculation of a cationic 15-mer, innate immunity-like lytic peptide composed of d- and l-amino acids ([D]-K6L9) caused growth arrest of 22RV1 prostate carcinoma xenografts in a mouse model. However, despite its therapeutic potential, this peptide has significant systemic toxicity at concentrations slightly higher than the therapeutic one. Here, we used the acidic environment created by solid tumors as a trigger to activate anticancer lytic peptides by making them cationic only at low pH levels. We achieved this selectivity by substituting lysines (pKa, ∼10.5) for histidines (pKa, ∼6.1) in the parental peptide [D]-K6L9. Histidine is protonated below pH 7. For that purpose, we replaced either three or all six lysines in the parental peptide with histidines to obtain the peptides [D]-K3H3L9 and [D]-H6L9. Interestingly, in vitro experiments showed pH-dependent activity only with [D]-H6L9 mainly toward cancer cell lines. However, both peptides showed reduced systemic toxicity compared with the parental peptide. Intratumor and systemic inoculation of these peptides resulted in a significant decrease in the 22RV1 prostate cancer tumor volume and systemic secretion of prostate-specific antigen in a xenograft mice model. Moreover, histologic modifications revealed a significant reduction in new blood vessels selectively in tumor tissues after treatment with the peptides compared with the untreated tumors. The lytic mode of action of these new peptides, which makes it difficult for the cancer cells to develop resistance, and their selective and pH-dependent activity make them potential candidates for treatment of solid cancer tumors. [Cancer Res 2009;69(8):3458–63]
Akt Phosphorylation of Merlin Enhances Its Binding to Phosphatidylinositols and Inhibits the Tumor-Suppressive Activities of Merlin
Authors: Okada Masashi , Wang Yanru , Jang Sung-Wuk , Tang Xiaoling , Neri Luca M. , Ye Keqiang 
Published: April 2009

Abstract
The NF2 tumor suppressor gene encodes an intracellular membrane-associated protein, called merlin, which belongs to the band 4.1 family of cytoskeleton-associated proteins that link cell surface glycoproteins to the actin cytoskeleton. Merlin suppresses phosphatidylinositol 3-kinase (PI3K)/Akt signaling by directly binding and inhibiting the stimulatory activity of PIKE-L on PI3K. Akt feeds back and phosphorylates merlin and provokes its polyubiquitination and degradation. Here, we show that Akt phosphorylation and PI(3,4,5)P3 binding mediate the tumor-suppressive activity of merlin. The extreme NH2 terminus of merlin directly interacts with phosphatidylinositols, for which the unfolded conformation is required. Moreover, Akt phosphorylation enhances merlin binding affinity to phosphatidylinositols and inhibits its proapoptotic actions. Furthermore, Akt phosphorylation and phosphatidylinositols increase merlin binding to CD44. Epidermal growth factor treatment and Akt phosphorylation provoke merlin to aggregate in the ruffled plasma membrane and promote cell migration. Thus, these results suggest that PI3K signaling regulates the tumor-suppressive activity of merlin via both Akt phosphorylation and phosphatidylinositol lipids binding to merlin. [Cancer Res 2009;69(9):4043–51]
PTEN Loss Contributes to Erlotinib Resistance in EGFR-Mutant Lung Cancer by Activation of Akt and EGFR
Authors: Sos Martin L. , Koker Mirjam , Weir Barbara A. , Heynck Stefanie , Rabinovsky Rosalia , Zander Thomas , Seeger Jens M. , Weiss Jonathan , Fischer Florian , Frommolt Peter , Michel Kathrin , Peifer Martin , Mermel Craig , Girard Luc , Peyton Michael , Gazdar Adi F. , Minna John D. , Garraway Levi A. , Kashkar Hamid , Pao William , Meyerson Matthew , Thomas Roman K. 
Published: April 2009

Abstract
Clinical resistance to epidermal growth factor receptor (EGFR) inhibition in lung cancer has been linked to the emergence of the EGFR T790M resistance mutation or amplification of MET. Additional mechanisms contributing to EGFR inhibitor resistance remain elusive. By applying combined analyses of gene expression, copy number, and biochemical analyses of EGFR inhibitor responsiveness, we identified homozygous loss of PTEN to segregate EGFR-dependent and EGFR-independent cells. We show that in EGFR-dependent cells, PTEN loss partially uncouples mutant EGFR from downstream signaling and activates EGFR, thereby contributing to erlotinib resistance. The clinical relevance of our findings is supported by the observation of PTEN loss in 1 out of 24 primary EGFR-mutant non–small cell lung cancer (NSCLC) tumors. These results suggest a novel resistance mechanism in EGFR-mutant NSCLC involving PTEN loss. [Cancer Res 2009;69(8):3256–61]
The Role of microRNA-221 and microRNA-222 in Androgen-Independent Prostate Cancer Cell Lines
Authors: Sun Tong , Wang Qianben , Balk Steven , Brown Myles , Lee Gwo-Shu Mary , Kantoff Philip 
Published: April 2009

Abstract
Androgen-dependent prostate cancer typically progresses to castration-resistant prostate cancer (CRPC) after the androgen deprivation therapy. MicroRNAs (miR) are noncoding small RNAs (19-25nt) that play an important role in the regulation of gene expression. Recent studies have shown that miR expression patterns are significantly different in normal and neoplastic prostate epithelial cells. However, the importance of miRs in the development of CRPC has not yet been explored. By performing genome-wide expression profiling of miRs, we found that expression levels of several miRs, in particular miR-221 and miR-222, were significantly increased in CRPC cells (the LNCaP-derived cell line LNCaP-Abl), compared with those in the androgen-dependent prostate cancer cell line (LNCaP). Overexpression of miR-221 or miR-222 in LNCaP or another androgen-dependent cell line, LAPC-4, significantly reduced the level of the dihydrotestosterone (DHT) induced up-regulation of prostate-specific antigen (PSA) expression and increased androgen-independent growth of LNCaP cells. Knocking down the expression level of miR-221 and miR-222 with antagonist miRs in the LNCaP-Abl cell line restored the response to the DHT induction of PSA transcription and also increased the growth response of the LNCaP-Abl cells to the androgen treatment. Changing the expression level of p27/kip1, a known target of miR-221 and miR-222, alone in LNCaP cells affected the DHT-independent cell growth but did not significantly influence the response of PSA transcription to the DHT treatment. In conclusion, our data suggest the involvement of miR-221 and miR-222 in the development or maintenance of the CRPC phenotype. [Cancer Res 2009;69(8):3356–63]
Characterization of the HDAC1 Complex That Regulates the Sensitivity of Cancer Cells to Oxidative Stress
Authors: Kato Takuya , Shimono Yohei , Hasegawa Masaki , Jijiwa Mayumi , Enomoto Atsushi , Asai Naoya , Murakumo Yoshiki , Takahashi Masahide 
Published: April 2009

Abstract
Histone deacetylases (HDAC) are involved in carcinogenesis through their regulation of cell proliferation, differentiation, and survival. The inhibitors of HDAC exhibit profound synergistic effects in cancer treatment when combined with other anticancer drugs. However, the molecular mechanisms underlying this synergy are not fully understood. Here, we show that HDAC1 increases the resistance of cancer cells to oxidative stress by negatively regulating the expression of thioredoxin binding protein 2 (TBP-2). We found that the recruitment of HDAC1 to the TBP-2 promoter is mediated by a protein complex consisting of RET finger protein (RFP; also called TRIM27) and the trimeric transcription factor NF-Y. Accordingly, RNA interference–mediated depletion of RFP led to the disruption of the protein complex and a marked increase in the sensitivity of cancer cells to cisplatin, a potent inducer of oxidative stress. Furthermore, high levels of RFP expression correlated with down-regulation of TBP-2 in human colon cancers and were associated with poor clinical outcome. These findings reveal the diverse cancer-promoting activities of HDAC1 and identify RFP as a key regulator that provides cancer cells with resistance to anticancer drugs. [Cancer Res 2009;69(8):3597–604]
Folate Intake, Methylenetetrahydrofolate Reductase Polymorphisms, and Breast Cancer Risk in Women from the Malmö Diet and Cancer Cohort
Authors: Ericson Ulrika , Sonestedt Emily , Ivarsson Malin I.L. , Gullberg Bo , Carlson Joyce , Olsson Håkan , Wirfält Elisabet 
Published: April 2009

AbstractBackground: Single nucleotide polymorphisms (SNP) of the folate-metabolizing enzyme methylenetetrahydrofolate reductase (MTHFR) may modify associations between folate intake and breast cancer. We examined if the association between tertiles of dietary folate equivalents (DFE) and breast cancer was different in subgroups according to genotypes of the MTHFR 677 C&gt;T (rs1801133) and 1298A&gt;C (rs1801131) SNPs and if the polymorphisms per se were associated with breast cancer.Methods: This nested case-control study included 544 incident cases with invasive breast cancer and 1,088 controls matched on age and blood sampling date from the population-based Malmö Diet and Cancer cohort. Genotyping of the MTHFR SNPs was done with PCR-based matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Odds ratios (OR) were obtained by unconditional logistic regression.Results: DFE was positively associated with breast cancer in MTHFR 677CT/TT−1298AA women (P for trend = 0.01) but inversely associated in compound heterozygous women (P for trend = 0.01). Interaction was observed between DFE and the 1298C allele (P = 0.03). The 677T allele was associated with increased breast cancer risk in women above 55 years [multivariate adjusted OR, 1.34; 95% confidence interval (95% CI), 1.01-1.76] and an interaction was observed between the T allele and age (P = 0.03). Homozygosis for the 1298C allele was associated with increased risk in women between 45 and 55 years (multivariate adjusted OR, 1.89; 95% CI, 1.09-3.29).Conclusion: In conclusion, a positive association between DFE and breast cancer was observed in MTHFR 677CT/TT−1298AA women but an inverse association was observed in 677CT−1298AC women. The 677T allele was associated with higher breast cancer risk in women above 55 years of age. (Cancer Epidemiol Biomarkers Prev 2009;18(4):1101–10)