bluuebunny/crossref_metadata_2025_split huggingface dataset:
Oral cancer screening: Practices, knowledge, and opinions of dentists working in Ohio nursing homes
Authors: Mahalaha Suparna A. , Cheruvu Vinay K. , Smyth Kathleen A. 
Published: October 2009

ABSTRACTThe state of oral health of nursing homes residents is less than satisfactory. The oral health care in nursing homes is also deficient, therefore it is likely that oral cancer (OC) screening of residents will be inadequate. The purpose of this cross‐sectional study was to determine OC screening practices, knowledge, and opinions of dentists working in nursing homes throughout Ohio. A 28‐item pretested questionnaire was mailed to 75 dentists who were serving 606 nursing homes.The response rate was 49%. The main outcome measures of interest included: OC screening practices of the Ohio dentists, their knowledge of OC detection, and their opinions regarding OC screening competency. Age was found to be a significant factor, with younger dentists being more likely to have higher knowledge scores after adjusting for all other covariates.
Two Kinds of Knowledge in Scientific Discovery
Authors: Bridewell Will , Langley Pat 
Published: October 2009

AbstractResearch on computational models of scientific discovery investigates both the induction of descriptive laws and the construction of explanatory models. Although the work in law discovery centers on knowledge‐lean approaches to searching a problem space, research on deeper modeling tasks emphasizes the pivotal role of domain knowledge. As an example, our own research on inductive process modeling uses information about candidate processes to explain why variables change over time. However, our experience with IPM, an artificial intelligence system that implements this approach, suggests that process knowledge is insufficient to avoid consideration of implausible models. To this end, the discovery system needs additional knowledge that constrains the model structures. We report on an extended system, SC‐IPM, that uses such information to reduce its search through the space of candidates and to produce models that human scientists find more plausible. We also argue that although people carry out less extensive search than SC‐IPM, they rely on the same forms of knowledge—processes and constraints—when constructing explanatory models.
Temporal Variation of Bacterial Respiration and Growth Efficiency in Tropical Coastal Waters
Authors: Lee Choon Weng , Bong Chui Wei , Hii Yii Siang 
Published: October 2009

ABSTRACT

We investigated the temporal variation of bacterial production, respiration, and growth efficiency in the tropical coastal waters of Peninsular Malaysia. We selected five stations including two estuaries and three coastal water stations. The temperature was relatively stable (averaging around 29.5°C), whereas salinity was more variable in the estuaries. We also measured dissolved organic carbon and nitrogen (DOC and DON, respectively) concentrations. DOC generally ranged from 100 to 900 μM, whereas DON ranged from 0 to 32 μM. Bacterial respiration ranged from 0.5 to 3.2 μM O
2
h
−1
, whereas bacterial production ranged from 0.05 to 0.51 μM C h
−1
. Bacterial growth efficiency was calculated as bacterial production/(bacterial production + respiration), and ranged from 0.02 to 0.40. Multiple correlation analyses revealed that bacterial production was dependent upon primary production (

r
2

= 0.169, df = 31, and
P
< 0.02) whereas bacterial respiration was dependent upon both substrate quality (i.e., DOC/DON ratio) (

r
2

= 0.137, df = 32, and
P
= 0.03) and temperature (

r
2

= 0.113, df = 36, and
P
= 0.04). Substrate quality was the most important factor (

r
2

= 0.119, df = 33, and
P
= 0.04) for the regulation of bacterial growth efficiency. Using bacterial growth efficiency values, the average bacterial carbon demand calculated was from 5.30 to 11.28 μM C h
−1
. When the bacterial carbon demand was compared with primary productivity, we found that net heterotrophy was established at only two stations. The ratio of bacterial carbon demand to net primary production correlated significantly with bacterial growth efficiency (

r
2

= 0.341, df = 35, and
P
< 0.001). From nonlinear regression analysis, we found that net heterotrophy was established when bacterial growth efficiency was <0.08. Our study showed the extent of net heterotrophy in these waters and illustrated the importance of heterotrophic microbial processes in coastal aquatic food webs.
Protistan Predation Affects Trichloroethene Biodegradation in a Bedrock Aquifer
Authors: Cunningham Joseph J. , Kinner Nancy E. , Lewis Maureen 
Published: October 2009

ABSTRACT

Despite extensive research on the bottom-up force of resource availability (e.g., electron donors and acceptors), slow biodegradation rates and stalling at
cis
-dichloroethene (cDCE) and vinyl chloride continue to be observed in aquifers contaminated with trichloroethene (TCE). The objective of this research was to gauge the impact of the top-down force of protistan predation on TCE biodegradation in laboratory microcosms. When indigenous bacteria from an electron donor-limited TCE-contaminated bedrock aquifer were present, the indigenous protists inhibited reductive dechlorination altogether. The presence of protists during organic carbon-amended conditions caused the bacteria to elongate (length:width, ≥10:1), but reductive dechlorination was still inhibited. When a commercially available dechlorinating bacterial culture and an organic carbon amendment were added in he presence of protists, the elongated bacteria predominated and reductive dechlorination stalled at cDCE. When protists were removed under organic carbon-amended conditions, reductive dechlorination stalled at cDCE, whereas in the presence organic carbon and bacterial amendments, the total chlorinated ethene concentration decreased, indicating TCE was converted to ethene and/or CO
2
. The data suggested that indigenous protists grazed dechlorinators to extremely low levels, inhibiting dechlorination altogether. Hence, in situ bioremediation/bioaugmentation may not be successful in mineralizing TCE unless the top-down force of protistan predation is inhibited.
Occupational determinants of serum cholinesterase inhibition among organophosphate-exposed agricultural pesticide handlers in Washington State
Authors: Hofmann Jonathan N , Keifer Matthew C , De Roos Anneclaire J , Fenske Richard A , Furlong Clement E , van Belle Gerald , Checkoway Harvey 
Published: October 2009

ObjectiveTo identify potential risk factors for serum cholinesterase (BuChE) inhibition among agricultural pesticide handlers exposed to organophosphate (OP) and N-methyl-carbamate (CB) insecticides.MethodsWe conducted a longitudinal study among 154 agricultural pesticide handlers who participated in the Washington State cholinesterase monitoring program in 2006 and 2007. BuChE inhibition was analysed in relation to reported exposures before and after adjustment for potential confounders using linear regression. ORs estimating the risk of BuChE depression (>20% from baseline) were also calculated for selected exposures based on unconditional logistic regression analyses.ResultsAn overall decrease in mean BuChE activity was observed among study participants at the time of follow-up testing during the OP/CB spray season relative to pre-season baseline levels (mean decrease of 5.6%, p<0.001). Score for estimated cumulative exposure to OP/CB insecticides in the past 30 days was a significant predictor of BuChE inhibition (β=−1.74, p<0.001). Several specific work practices and workplace conditions were associated with greater BuChE inhibition, including mixing/loading pesticides and cleaning spray equipment. Factors that were protective against BuChE inhibition included full-face respirator use, wearing chemical-resistant boots and storing personal protective equipment in a locker at work.ConclusionsDespite existing regulations, agricultural pesticide handlers continue to be exposed to OP/CB insecticides at levels resulting in BuChE inhibition. These findings suggest that modifying certain work practices could potentially reduce BuChE inhibition. Replication from other studies will be valuable.
The detachment era (1977–1982) and its role in revolutionizing continental tectonics
Authors: Wernicke B. 
Published: October 2009

Abstract

After the discovery of thrust-and-nappe structure near the turn of the twentieth century, mountain belts were viewed as a direct expression of horizontal shortening of the continental crust, and continental rifting was viewed as a phenomenon distinct from it. By mid-century, broad consensus had emerged, mainly on the basis of physical reasoning, that thrust-and-nappe structure instead reflected gravity sliding secondary to vertical motions of the crust, as embodied in the influential
stockwerk
folding hypothesis. In a noteworthy period from 1977 to 1982, informally referred to here as the ‘detachment era’, not only did the last vestiges of support for the
stockwerk
hypothesis evaporate, but large-magnitude extension was discovered throughout the Cordillera, manifest primarily by extensional detachments and metamorphic core complexes. Soon afterward extensional detachments were recognized as a global phenomenon, forcing first-order reinterpretation of field relations in most orogens. Although plate tectonics is indisputably the most profound discovery in Earth sciences in the twentieth century, the detachment era arguably had commensurate impact on field-based interpretations of continental tectonics. Three decades later, controversy persists over the origin of metamorphic tectonites in core complexes, and over the existence and mechanics of slip on shallowly dipping extensional detachments.
Candidate Gene Association Study of Esophageal Squamous Cell Carcinoma in a High-Risk Region in Iran
Authors: Akbari Mohammad R. , Malekzadeh Reza , Shakeri Ramin , Nasrollahzadeh Dariush , Foumani Maryam , Sun Yulong , Pourshams Akram , Sadjadi Alireza , Jafari Elham , Sotoudeh Masoud , Kamangar Farin , Boffetta Paolo , Dawsey Sanford M. , Ghadirian Parviz , Narod Steven A. 
Published: October 2009

Abstract
There is a region with a high risk for esophageal squamous cell carcinoma (ESCC) in the northeast of Iran. Previous studies suggest that hereditary factors play a role in the high incidence of cancer in the region. We selected 22 functional variants (and 130 related tagSNPs) from 15 genes that have been associated previously with the risk of ESCC. We genotyped a primary set of samples from 451 Turkmens (197 cases and 254 controls). Seven of 152 variants were associated with ESCC at the P = 0.05 level; these single nucleotide polymorphisms were then studied in a validation set of 549 cases and 1,119 controls, which included both Turkmens and non-Turkmens. The association observed for a functional variant in ADH1B was confirmed in the validation set, and that of a tagSNP in MGMT, the association was borderline significant in the validation set, after correcting for multiple testing. The other 5 variants that were associated in the primary set were not significantly associated in the validation set. The histidine allele at codon 48 of ADH1B gene was associated with a significantly decreased risk of ESCC in the joint data set (primary and validation set) under a recessive model (odds ratio, 0.41; 95% confidence interval, 0.29-0.76; P = 4 × 10−4). The A allele of the rs7087131 variant of MGMT gene was associated with a decreased risk of ESCC under a dominant model (odds ratio, 0.79; 95% confidence interval, 0.64-0.96; P = 0.02). These results support the hypothesis that genetic predisposition plays a role in the high incidence of ESSC in Iran. [Cancer Res 2009;69(20):7994–8000]
Role for Krüppel-Like Factor 4 in Determining the Outcome of p53 Response to DNA Damage
Authors: Zhou Qibing , Hong Yuan , Zhan Qimin , Shen Yan , Liu Zhihua 
Published: October 2009

Abstract
Cells are incessantly exposed to many sources of genotoxic stress. A critical unresolved issue is how the resulting activation of the p53 tumor suppressor can lead to either cell cycle arrest or apoptosis depending on the extent of DNA damage. The present study shows that the level of Krüppel-like factor 4 (KLF4) expression is inversely correlated with the extent of DNA damage. KLF4 is activated by p53 following cytostatic, mild DNA damage, whereas it is strongly repressed via enhanced turnover of mRNA on severe DNA damage that irreversibly drives cells to apoptosis. Blocking the repression of KLF4 on severe DNA damage suppresses p53-mediated apoptosis, whereas ablation of the KLF4 induction on mild DNA damage shifts the p53 response from cell cycle arrest to cell death. Our results suggest that coordinate regulation of KLF4 expression depending on the extent of DNA damage may be an important mechanism that dictates the life and death decisions of p53. [Cancer Res 2009;69(21):8284–92]
Inhibition of Azoxymethane-Induced Colorectal Cancer by CP-31398, a TP53 Modulator, Alone or in Combination with Low Doses of Celecoxib in Male F344 Rats
Authors: Rao Chinthalapally V. , Steele Vernon E. , Swamy Malisetty V. , Patlolla Jagan M.R. , Guruswamy Suresh , Kopelovich Levy 
Published: October 2009

Abstract
Tumor suppressor p53 plays a major role in colorectal cancer development. The present study explores the effects of p53-modulating agent CP-31398 alone and combined with celecoxib on azoxymethane-induced aberrant crypt foci (ACF) and colon adenocarcinomas in F344 rats. Maximum tolerated doses were 400 and 3,000 ppm for CP-31398 and celecoxib, respectively. ACF and tumor efficacy endpoints were carried out on azoxymethane-treated 7-week-old rats (48 per group) fed the control AIN-76A diet. Two weeks after carcinogen treatment, rats were fed the diets containing 0, 150, or 300 ppm CP-31398, 300 ppm celecoxib, or 150 ppm CP-31398 plus 300 ppm celecoxib. ACF and colon adenocarcinomas were determined at 8 and 48 weeks after azoxymethane treatment, respectively. Dietary CP-31398 was shown to suppress mean colonic total ACF by 43% and multicrypt ACF by 63%; dietary CP-31398 at 150 and 300 ppm suppressed adenocarcinoma incidence by 30.4% (P &lt; 0.02) and 44% (P &lt; 0.005), respectively, and adenocarcinoma multiplicity by 51% (P &lt; 0.005) and 65% (P &lt; 0.0001), respectively. Dietary celecoxib suppressed colon adenocarcinoma incidence (60%; P &lt; 0.0003) and multiplicity (70%; P &lt; 0.0001). Importantly, combination of low-dose CP-31398 and celecoxib suppressed colon adenocarcinoma incidence by 78% and multiplicity by 90%. Rats that were fed the high-dose CP-31398 or a combination of low-dose CP-31398 and celecoxib showed considerable enhancement of p53 and p21WAF1/CIP expression, apoptosis, and reduced tumor cell proliferation in colonic tumors. These observations show, for the first time, that CP-31398 possesses significant dose-dependent chemopreventive activity in a well-established colon cancer model and that a combination of low-dose CP-31398 and celecoxib significantly enhanced colon cancer chemopreventive efficacy. [Cancer Res 2009;69(20):8175–82]
Inhibition of the Androgen Receptor as a Novel Mechanism of Taxol Chemotherapy in Prostate Cancer
Authors: Gan Lu , Chen Shuai , Wang Yuwei , Watahiki Akira , Bohrer Laura , Sun Zhen , Wang Yuzhuo , Huang Haojie 
Published: October 2009

Abstract
Taxol chemotherapy is one of the few therapeutic options for men with castration-resistant prostate cancer (CRPC). However, the working mechanisms for Taxol are not fully understood. Here, we showed that treatment of 22Rv1, a PTEN-positive CRPC cell line, with paclitaxel and its semisynthetic analogue docetaxel decreases expression of the androgen receptor (AR)–activated genes prostate-specific antigen (PSA) and Nkx3.1 but increases expression of the AR repression gene maspin, suggesting that Taxol treatment inhibits AR activity. This was further supported by the observation that the activity of AR luciferase reporter genes was inhibited by paclitaxel. In contrast, paclitaxel treatment failed to inhibit AR activity in the PTEN-null CRPC cell line C4-2. However, pretreatment of C4-2 cells with the phosphoinositide 3-kinase inhibitor LY294002 restored paclitaxel inhibition of the AR. Treatment of 22Rv1 xenografts in mice with docetaxel induced mitotic arrest and a decrease in PSA expression in tumor cells adjacent to vascular vessels. We further showed that paclitaxel induces nuclear accumulation of FOXO1, a known AR suppressive nuclear factor, and increases the association of FOXO1 with AR proteins in the nucleus. FOXO1 knockdown with small interfering RNA attenuated the inhibitory effect of paclitaxel on AR transcriptional activity, expression of PSA and Nkx3.1, and cell survival. These data reveal a previously uncharacterized, FOXO1-mediated, AR-inhibitory effect of Taxol in CRPC cells that may play an important role in Taxol-mediated inhibition of CRPC growth. [Cancer Res 2009;69(21):8386–94]
Widespread Estrogen-Dependent Repression of microRNAs Involved in Breast Tumor Cell Growth
Authors: Maillot Gérard , Lacroix-Triki Magali , Pierredon Sandra , Gratadou Lise , Schmidt Sabine , Bénès Vladimir , Roché Henri , Dalenc Florence , Auboeuf Didier , Millevoi Stefania , Vagner Stéphan 
Published: October 2009

Abstract
Altered expression of microRNAs (miRNA), an abundant class of small nonprotein-coding RNAs that mostly function as negative regulators of protein-coding gene expression, is common in cancer. Here, we analyze the regulation of miRNA expression in response to estrogen, a steroid hormone that is involved in the development and progression of breast carcinomas and that is acting via the estrogen receptors (ER) transcription factors. We set out to thoroughly describe miRNA expression, by using miRNA microarrays and real-time reverse transcription-PCR (RT-PCR) experiments, in various breast tumor cell lines in which estrogen signaling has been induced by 17β-estradiol (E2). We show that the expression of a broad set of miRNAs decreases following E2 treatment in an ER-dependent manner. We further show that enforced expression of several of the repressed miRNAs reduces E2-dependent cell growth, thus linking expression of specific miRNAs with estrogen-dependent cellular response. In addition, a transcriptome analysis revealed that the E2-repressed miR-26a and miR-181a regulate many genes associated with cell growth and proliferation, including the progesterone receptor gene, a key actor in estrogen signaling. Strikingly, miRNA expression is also regulated in breast cancers of women who had received antiestrogen neoadjuvant therapy. Overall, our data indicate that the extensive alterations in miRNA regulation upon estrogen signaling pathway play a key role in estrogen-dependent functions and highlight the utility of considering miRNA expression in the understanding of antiestrogen resistance of breast cancer. [Cancer Res 2009;69(21):8332–40]
Cross-Talk between Estrogen Receptor and Epidermal Growth Factor Receptor in Head and Neck Squamous Cell Carcinoma
Authors: Egloff Ann Marie , Rothstein Mary E. , Seethala Raja , Siegfried Jill M. , Grandis Jennifer Rubin , Stabile Laura P. 
Published: October 2009

Abstract
Purpose: This study aimed to characterize estrogen receptor expression and signaling in head and neck squamous cell carcinoma (HNSCC) cell lines and patient tissues, and to evaluate estrogen receptor and epidermal growth factor (EGF) receptor (EGFR) cross-activation in HNSCC.
Experimental Design: Estrogen receptor expression and signaling in HNSCC cell lines were assessed by immunoblotting. In vitro proliferation and invasion were evaluated in HNSCC cell lines in response to estrogen receptor and EGFR ligands or inhibitors. Estrogen receptor and EGFR protein expression in patient tissues was assessed by immunohistochemical staining.
Results: Phospho–mitogen-activated protein kinase (P-MAPK) levels were significantly increased following combined estrogen and EGF treatment. Treatment of HNSCC cells with estrogen and EGF significantly increased cell invasion compared with either treatment alone, whereas inhibiting these two pathways resulted in reduced invasion compared with inhibiting either pathway alone. EGFR (P = 0.008) and nuclear estrogen receptor α (ERαnuc; P &lt; 0.001) levels were significantly increased in HNSCC tumors (n = 56) compared with adjacent mucosa (n = 30), whereas nuclear estrogen receptor β (ERβnuc) levels did not differ (P = 0.67). Patients with high ERαnuc and EGFR tumor levels had significantly reduced progression-free survival compared with patients with low tumor ERαnuc and EGFR levels (hazards ratio, 4.09; P = 0.01; Cox proportional hazards). In contrast, high ERβnuc tumor levels were not associated with reduced progression-free survival alone or when combined with EGFR.
Conclusions: ERα and ERβ were expressed in HNSCC, and stimulation with estrogen receptor ligands resulted in both cytoplasmic signal transduction and transcriptional activation. Estrogen receptor and EGFR cross-talk was observed. Collectively, these studies indicate that estrogen receptor and EGFR together may contribute to HNSCC development and disease progression. (Clin Cancer Res 2009;15(21):6529–40)
Trastuzumab: A Picky Partner?
Authors: McArthur Heather L. , Hudis Clifford A. 
Published: October 2009

Abstract
Preclinical and clinical models of HER2-positive breast cancer show that human epidermal growth factor receptor 2 (HER2)-targeted therapy with trastuzumab adds significant benefits and modest risks to conventional cytotoxic therapies. Building on this advance will likely depend on elucidation of relevant signaling pathways and mechanisms of action for effective HER2-targeted therapies. (Clin Cancer Res 2009;15(20):6311–3)
Estrogen Receptor–Negative Breast Cancer: New Insights into Subclassification and Targeting
Authors: Zhao Jean J. , Silver Daniel P. 
Published: October 2009

Abstract
Classification schemes for disease states can help identify distinctions with useful implications for therapy and prognosis. Speers and colleagues provide a new subclassification scheme for estrogen receptor-negative breast cancer based upon kinome-wide gene expression profiling with interesting findings that are potentially relevant for both treatment and clinical outcome. (Clin Cancer Res 2009;15(20):6309–10)