bluuebunny/crossref_metadata_2025_split huggingface dataset:
Oral Health, Related Behaviors and Oral Health Impacts Among Homeless Adults
Authors: Conte Michael , Broder Hillary L. , Jenkins George , Reed Rebecca , Janal Malvin N. 
Published: January 2009

AbstractObjectives:To assess the oral health needs, related behavior and oral health impact among homeless persons in Newark, New Jersey. Methods:Participants represented a convenience sample of adults (n=46) participating in Homeless Services Day, an annual event sponsored by the Homeless Services Division of the Newark, NJ Department of Health and Human Services. Their mean age was 40.4 yr (SD=10.0), and 51.1% were female. The majority (76%) reported African‐American ethnicity; remaining participants self‐identified as Hispanic, White or Asian. Participants reported being homeless for a median of 11 months, with a range of 1 to 108 months. Results:The 46 participants had 745 teeth (averaged 16.2 per person) that were either missing, had fillings or had untreated decay. Diseased teeth averaged 3.8 per person; missing teeth averaged 8.6 per person; and filled teeth averaged 3.7 per person. Only 28.3% had a dental visit in the past year. Approximately 87% reported negative oral health impacts impact: over half (55.6%) had current oral facial pain and two‐thirds of our participants reported having dental‐related face pain during the past year. Additional oral health impacts included: eating (42%), smiling (33%), concentrating (18%) and talking (16%). Conclusions:Consistent with other studies, this homeless sample presented with considerable oral health needs. Newark's homeless, like other homeless cohorts, face access to care and negative oral health impacts. This study informs the need for future research that can provide substantive evidence for care providers and policy makers.
Specific Caries Index: A New System for Describing Untreated Dental Caries Experience in Developing Countries
Authors: Acharya Shashidhar 
Published: January 2009

AbstractObjectives:To develop a reproducible surface‐specific caries index that provided qualitative and quantitative information about untreated dental caries, that could be used in conjunction with the DMFS index and would provide information on not only the caries prevalence but also the location and type of caries lesion in an individual based on clinical examination. Methods:Untreated carious lesions were divided into six types based on the location of the lesions.339 rural school children in the age group of 12–15 years were examined for dental caries using both the DMFS index and the Specific Caries Index. Results:Type 1 and 2 were found to be the most common type of caries lesions. The reproducibility of the Specific Caries Index was also found to be good. Conclusions:Encouraging indications about the validity and reproducibility of this new caries index was found, suggesting the need for further studies to test its applicability in larger and different populations.
Childhood Overweight and Orthodontists: Results of a Survey
Authors: Huang Jeannie S. , Becerra Karen , Walker Edward , Hovell Melbourne F. 
Published: January 2009

AbstractObjectives:A survey among orthodontists to assess clinical procedures of overweight screening and nutrition intervention among youth was conducted. Methods:Orthodontists identified through professional society membership were invited to participate via email. The web‐based survey collected information regarding overweight screening, nutrition counseling, and referral habits. Results:91% of 111 respondents reported counseling children and families on nutrition recommendations. Referral of overweight youth to a dietitian or pediatrician was sporadic. Orthodontists who felt that overweight had a severe negative impact on dental health were more likely to screen patients for overweight and perform dietary counseling for all patients than orthodontists who felt the impact of overweight on dental health was less severe. Conclusions:Orthodontists report regularly engaging in dietary discussions with their pediatric patients and may serve as important clinical advocates for healthy dietary choices among youth. Overweight screening and referral practices among orthodontists to appropriate health professionals should be further evaluated as interventions for pediatric obesity.
Prevalence of preoperative anemia and hematinic deficiencies in patients scheduled for elective major orthopedic surgery
Authors: BISBE ELVIRA , CASTILLO JORGE , SÁEZ MONTSERRAT , SANTIVERI XAVIER , RUÍZ AINA , MUÑOZ MANUEL 
Published: January 2009

SUMMARYPreoperative anemia is an independent risk factor for allogeneic blood transfusion in patients undergoing major orthopedic surgery (MOS) whereas hematinic deficiency can delay the recovery from postoperative anemia. Both conditions can, however, be corrected before elective procedures are undertaken. We therefore evaluated the prevalence of anemia and hematinic deficiencies in MOS patients. Demographic and laboratory data were gathered from all MOS patients from a single institution between January 2001 and December 2002. A total of 715 patients (483 women/232 men) entered the study. According to WHO criteria, the prevalence of anemia was 10.5% and increased with age, without gender‐related differences. Preoperative hemoglobin was < 13 g/dL in 19.4% of patients, and the prevalence of hematinic deficiencies was 33% for iron, 12.3% for vitamin B12 and 3% for folate. In anemic patients, there were 30.8% with hematinic deficiency anemia (20% with iron‐deficiency anemia), 30.8% with anemia of chronic disease and 38.4% with anemia of mixed or indeterminate cause. The prevalence of anemia, as well as of hematinic deficiencies, is high in MOS patients. Therefore, whenever possible, patients undergoing MOS should be assessed early enough to allow for proper investigation and treatment prior to the scheduled procedure.
Anemia, chronic renal disease and chronic heart failure: the cardiorenal anemia syndrome
Authors: SILVERBERG DONALD S. , WEXLER DOV , IAINA ADRIAN , SCHWARTZ DORON 
Published: January 2009

SUMMARYThe mortality and morbidity of congestive heart failure (CHF) have improved slightly over the years but are still very high. Many patients with CHF are anemic, which raises the question, ‘Could uncontrolled anemia be a cause?’ The anemia is associated with more severe CHF and higher mortality, hospitalization and morbidity rates. The only way to prove that anemia is causing this worsening of CHF is to correct it. We review here some of the published papers about correction of anemia. Many, but not all, show a positive effect of erythropoietin or its derivatives when coadministered with oral or intravenous (IV) iron, with improvements in left and right ventricular systolic and diastolic function, dilation, hypertrophy, renal function, New York Heart Association class, exercise capacity, oxygen utilization, caloric intake, quality of life, and the activity of endothelial progenitor cells. A reduction in hospitalizations, diuretic dose, pulmonary artery pressure, plasma volume, heart rate, serum brain natriuretic peptide levels, the inflammatory marker interleukin 6, and soluble Fas ligand (a mediator of apoptosis) were also observed. Iron deficiency may also play an important role in this anemia because improvement in CHF has been seen with IV iron treatment alone. We call the interaction between chronic renal failure, CHF and anemia the cardiorenal anemia syndrome. Each of these three elements causes or exacerbates the others, and their correction can prevent the progression of both renal and heart failure. However, until ongoing large placebo‐controlled studies on darbepoetin alpha or IV iron are completed, we will not know whether these treatments really influence the outcome of renal failure and CHF.
CLUSTERING QUALITY MEASURES BASED ON COMPARING THE PROXIMITY MATRICES FOR THE MEMBERSHIP VECTORS AND THE OBJECTS
Authors: BROUWER ROELOF K. 
Published: January 2009

There are several commonly accepted clustering quality measures (clustering quality as opposed to cluster quality) such as the rand index, the adjusted rand index and the jacquard index. Each of these however is based on comparing the partition produced by the clustering process to a correct partition. They can therefore only be used to determine the quality of a clustering process when the correct partition is known. This paper therefore proposes another clustering quality measure that does not require the comparison to a correct partition. The proposed metric is based on the assumption that the proximities between the membership vectors should correlate positively with the proximities between the objects which may be the proximities between their feature vectors. The values of the components of the membership vector, corresponding to a pattern, are the membership degrees of the pattern in the various clusters. The membership vector is just another object data vector or type of feature vector with the feature values for an object being the membership values of the object in the various clusters. Based on this premise, this paper describes some new cluster quality metrics derived from standard correlation measures and other proposed correlation metrics. Simulations on data with a wide range of clusterability or separability show that the approach of comparing the proximity matrix based on the membership matrix to the object proximity matrix is quite effective.
Protein Kinase D1–Mediated Phosphorylation and Subcellular Localization of β-Catenin
Authors: Du Cheng , Jaggi Meena , Zhang Chuanyou , Balaji K.C. 
Published: January 2009

Abstract
β-Catenin is essential for E-cadherin–mediated cell adhesion in epithelial cells and also acts as a key cofactor for transcription activity. We previously showed that protein kinase D1 (PKD1), founding member of the PKD family of signal transduction proteins, is down-regulated in advanced prostate cancer and interacts with E-cadherin. This study provides evidence that PKD1 interacts with and phosphorylates β-catenin at Thr112 and Thr120 residues in vitro and in vivo; mutation of Thr112 and Thr120 results in increased nuclear localization of β-catenin and is associated with altered β-catenin–mediated transcription activity. It is known that mutation of Thr120 residue abolishes binding of β-catenin to α-catenin, which links to cytoskeleton, suggesting that PKD1 phosphorylation of Thr120 could be critical for cell-cell adhesion. Overexpression of PKD1 represses β-catenin–mediated transcriptional activity and cell proliferation. Epistatic studies suggest that PKD1 and E-cadherin are within the same signaling pathway. Understanding the molecular basis of PKD1–β-catenin interaction provides a novel strategy to target β-catenin function in cells including prostate cancer. [Cancer Res 2009;69(3):1117–24]
Steroid Sulfatase and Estrogen Sulfotransferase in Colon Carcinoma: Regulators of Intratumoral Estrogen Concentrations and Potent Prognostic Factors
Authors: Sato Ryuichiro , Suzuki Takashi , Katayose Yu , Miura Koh , Shiiba Kenichi , Tateno Hiroo , Miki Yasuhiro , Akahira Junichi , Kamogawa Yukiko , Nagasaki Shuji , Yamamoto Kuniharu , Ii Takayuki , Egawa Shinichi , Evans Dean B. , Unno Michiaki , Sasano Hironobu 
Published: January 2009

Abstract
Previous epidemiologic and in vitro studies have indicated a potential involvement of estrogens in the pathogenesis of human colon carcinoma, but the precise roles of estrogens have remained largely unknown. Therefore, in this study, we first measured intratumoral concentrations of estrogens in 53 colon carcinomas using liquid chromatography-electrospray ionization tandem mass spectrometry (LC-ESI-MS). Tissue concentrations of total estrogen [estrone (E1) + estradiol] and E1 were significantly (2.0- and 2.4-fold, respectively) higher in colon carcinoma tissues than in nonneoplastic colonic mucosa (n = 31), and higher intratumoral concentrations of total estrogen and E1 were significantly associated with adverse clinical outcome. Intratumoral concentration of total estrogen was significantly associated with the combined status of steroid sulfatase (STS) and estrogen sulfotransferase (EST), but not with that of aromatase. Thus, we subsequently examined the STS/EST status in 328 colon carcinomas using immunohistochemistry. Immunoreactivities for STS and EST were detected in 61% and 44% of the cases, respectively. The −/+ group of the STS/EST status was inversely associated with Dukes' stage, depth of invasion, lymph node metastasis, and distant metastasis and positively correlated with Ki-67 labeling index of the carcinomas. In addition, this −/+ group had significantly longer survival, and a multivariate analysis revealed the STS/EST status as an independent prognostic factor. Results from our present study showed that the STS/EST status of carcinoma tissue determined intratumoral estrogen levels and could be a significant prognostic factor in colon carcinoma, suggesting that estrogens are locally produced mainly through the sulfatase pathway and play important roles in the progression of the disease. [Cancer Res 2009;69(3):914–22]
Rapid DNA Double-Strand Breaks Resulting from Processing of Cr-DNA Cross-Links by Both MutS Dimers
Authors: Reynolds Mindy F. , Peterson-Roth Elizabeth C. , Bespalov Ivan A. , Johnston Tatiana , Gurel Volkan M. , Menard Haley L. , Zhitkovich Anatoly 
Published: January 2009

Abstract
Mismatch repair (MMR) strongly enhances cyto- and genotoxicity of several chemotherapeutic agents and environmental carcinogens. DNA double-strand breaks (DSB) formed after two replication cycles play a major role in MMR-dependent cell death by DNA alkylating drugs. Here, we examined DNA damage detection and the mechanisms of the unusually rapid induction of DSB by MMR proteins in response to carcinogenic chromium(VI). We found that MSH2-MSH6 (MutSα) dimer effectively bound DNA probes containing ascorbate-Cr-DNA and cysteine-Cr-DNA cross-links. Binary Cr-DNA adducts, the most abundant form of Cr-DNA damage, were poor substrates for MSH2-MSH6, and their toxicity in cells was weak and MMR independent. Although not involved in the initial recognition of Cr-DNA damage, MSH2-MSH3 (MutSβ) complex was essential for the induction of DSB, micronuclei, and apoptosis in human cells by chromate. In situ fractionation of Cr-treated cells revealed MSH6 and MSH3 chromatin foci that originated in late S phase and did not require replication of damaged DNA. Formation of MSH3 foci was MSH6 and MLH1 dependent, whereas MSH6 foci were unaffected by MSH3 status. DSB production was associated with progression of cells from S into G2 phase and was completely blocked by the DNA synthesis inhibitor aphidicolin. Interestingly, chromosome 3 transfer into MSH3-null HCT116 cells activated an alternative, MSH3-like activity that restored dinucleotide repeat stability and sensitivity to chromate. Thus, sequential recruitment and unprecedented cooperation of MutSα and MutSβ branches of MMR in processing of Cr-DNA cross-links is the main cause of DSB and chromosomal breakage at low and moderate Cr(VI) doses. [Cancer Res 2009;69(3):1071–9]
Both TEAD-Binding and WW Domains Are Required for the Growth Stimulation and Oncogenic Transformation Activity of Yes-Associated Protein
Authors: Zhao Bin , Kim Joungmok , Ye Xin , Lai Zhi-Chun , Guan Kun-Liang 
Published: January 2009

Abstract
The Yes-associated protein (YAP) transcription coactivator is a candidate human oncogene and a key regulator of organ size. It is phosphorylated and inhibited by the Hippo tumor suppressor pathway. TEAD family transcription factors were recently shown to play a key role in mediating the biological functions of YAP. Here, we show that the WW domain of YAP has a critical role in inducing a subset of YAP target genes independent of or in cooperation with TEAD. Mutation of the WW domains diminishes the ability of YAP to stimulate cell proliferation and oncogenic transformation. Inhibition of YAP oncogenic-transforming activity depends on intact serine residues 127 and 381, two sites that could be phosphorylated by the Hippo pathway. Furthermore, genetic experiments in Drosophila support that WW domains of YAP and Yki, the fly YAP homologue, have an important role in stimulating tissue growth. Our data suggest a model in which YAP induces gene expression and exerts its biological functions by interacting with transcription factors through both the TEAD-binding and WW domains. [Cancer Res 2009;69(3):1089–98]
Sorafenib induces growth suppression in mouse models of gastrointestinal stromal tumor
Authors: Huynh Hung , Lee Jonathan W.J. , Chow Pierce K.H. , Ngo Van Chanh , Lew Guo Bin , Lam Irene W.L. , Ong Hock Soo , Chung Alexander , Soo Khee Chee 
Published: January 2009

Abstract
Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor of the gastrointestinal tract. Current therapeutic options include surgery and targeted molecular approaches such as imatinib and sunitinib. Our aim was to establish patient-derived GIST xenografts for the use of screening new drugs and improving current treatment regimens used in GIST. In this present study, we investigate the antitumor activity of sorafenib against patient-derived GIST xenografts. Murine xenograft models were given two oral doses of sorafenib daily for 30 days and growth of established tumor xenografts was monitored at least twice weekly by vernier caliper measurements. Western blotting was then used to determine changes in proteins in these xenografts before and after sorafenib therapy. Apoptotic and cell proliferation were analyzed by immunohistochemisty. Our data found that oral administration of sorafenib to mice, bearing patient-derived GIST xenografts, resulted in dose-dependent inhibition of tumor growth. Sorafenib-induced growth inhibition was associated with decreased cell proliferation, increased apoptosis, and reduction in tumor angiogenesis. Western blot analysis revealed that sorafenib inhibited C-Raf, phospho-extracellular signal-regulated kinase 1/2, and phospho-MEK1 (Thr286) slightly as well as phospho-c-Kit (Tyr568/Tyr570), phospho- platelet-derived growth factor receptor β (Tyr1021), and phospho-Flk1 (Tyr951), suggesting that sorafenib inhibited GIST growth by blocking the Raf/MEK/extracellular signal-regulated kinase pathway and angiogenesis. Sorafenib also induced cell cycle arrest, evident through increased levels of p15 and p27 and decreased levels of p21, cyclin A, cyclin B1, and cdc-2. Our study provides a strong rationale for the clinical investigation of sorafenib in patients with GIST as well as an established platform for further drug evaluation studies using GIST xenograft models. [Mol Cancer Ther 2009;8(1):152–9]
Telomerase-specific virotherapy in an animal model of human head and neck cancer
Authors: Nakajima Oumi , Matsunaga Atsuko , Ichimaru Daiju , Urata Yasuo , Fujiwara Toshiyoshi , Kawakami Koji 
Published: January 2009

Abstract
Telomerase-specific replication-competent adenovirus, Telomelysin (OBP-301), has a human telomerase reverse transcriptase promoter that regulates viral replication and efficiently kills human cancer cells. The objectives of this study are to examine the effects of OBP-301 in squamous cell carcinoma of the head and neck cells in vitro and in xenografted animals in vivo. OBP-301 was found to be cytotoxic to the YCUT892, KCCT873, KCCT891, KCCL871, YCUM862, HN12, and KCCOR891 cell lines in vitro. However, the level of cytotoxicity is not correlated with the expression levels of adenoviral receptors, which may be required for adenoviral infection in squamous cell carcinoma of the head and neck cells. OBP-301 shows remarkable antitumor activity against established s.c. KCCT873 tumors in immunodeficient animals in a dose-dependent manner. In addition, no significant toxicity was observed in animals receiving treatment. These results suggest that OBP-301 is a novel therapeutic agent with promise for the treatment of human head and neck cancers. [Mol Cancer Ther 2009;8(1):171–7]
NS-398, ibuprofen, and cyclooxygenase-2 RNA interference produce significantly different gene expression profiles in prostate cancer cells
Authors: John-Aryankalayil Molykutty , Palayoor Sanjeewani T. , Cerna David , Falduto Michael T. , Magnuson Scott R. , Coleman C. Norman 
Published: January 2009

Abstract
Cyclooxygenase-2 (COX-2) plays a significant role in tumor development and progression. Nonsteroidal anti-inflammatory drugs (NSAID) exhibit potent anticancer effects in vitro and in vivo by COX-2-dependent and COX-2-independent mechanisms. In this study, we used microarray analysis to identify the change of expression profile regulated by a COX-2-specific NSAID NS-398 (0.01 and 0.1 mmol/L), a nonspecific NSAID ibuprofen (0.1 and 1.5 mmol/L) and RNA interference (RNAi)-mediated COX-2 inhibition in PC3 prostate cancer cells. A total of 3,362 differentially expressed genes with 2-fold change and P &lt; 0.05 were identified. Low concentrations of NSAIDs and COX-2 RNAi altered very few genes (1-3%) compared with the higher concentration of NS-398 (17%) and ibuprofen (80%). Ingenuity Pathway Analysis was used for distributing the differentially expressed genes into biological networks and for evaluation of functional significance. The top 3 networks for both NSAIDs included functional categories of DNA replication, recombination and repair, and gastrointestinal disease. Immunoresponse function was specific to NS-398, and cell cycle and cellular movement were among the top functions for ibuprofen. Ingenuity Pathway Analysis also identified renal and urologic disease as a function specific for ibuprofen. This comprehensive study identified several COX-2-independent targets of NSAIDs, which may help explain the antitumor and radiosensitizing effects of NSAIDs. However, none of these categories were reflected in the identified networks in PC3 cells treated with clinically relevant low concentrations of NS-398 and ibuprofen or with COX-2 RNAi, suggesting the benefit to fingerprinting preclinical drug concentrations to improve their relevance to the clinical setting. [Mol Cancer Ther 2009;8(1):261–73]
Endocrine-Immune-Paracrine Interactions in Prostate Cells as Targeted by Phytomedicines
Authors: Gray Nora E. , Liu Xunxian , Choi Renee , Blackman Marc R. , Arnold Julia T. 
Published: January 2009

Abstract
Dehydroepiandrosterone (DHEA) is used as a dietary supplement and can be metabolized to androgens and/or estrogens in the prostate. We investigated the hypothesis that DHEA metabolism may be increased in a reactive prostate stroma environment in the presence of proinflammatory cytokines such as transforming growth factor β1 (TGFβ1), and further, whether red clover extract, which contains a variety of compounds including isoflavones, can reverse this effect. LAPC-4 prostate cancer cells were grown in coculture with prostate stromal cells (6S) and treated with DHEA +/− TGFβ1 or interleukin-6. Prostate-specific antigen (PSA) expression and testosterone secretion in LAPC-4/6S cocultures were compared with those in monocultured epithelial and stromal cells by real-time PCR and/or ELISA. Combined administration of TGFβ1 + DHEA to cocultures increased PSA protein secretion two to four times, and PSA gene expression up to 50-fold. DHEA + TGFβ1 also increased coculture production of testosterone over DHEA treatment alone. Red clover isoflavone treatment led to a dose-dependent decrease in PSA protein and gene expression and testosterone metabolism induced by TGFβ1 + DHEA in prostate LAPC-4/6S cocultures. In this coculture model of endocrine-immune-paracrine interactions in the prostate, TGFβ1 greatly increased stromal-mediated DHEA effects on testosterone production and epithelial cell PSA production, whereas red clover isoflavones reversed these effects.