tbuckley/cabot-search huggingface dataset:
Effect of Screening for Partner Violence on Use of Health Services at 3-Year Follow-up of a Randomized Clinical Trial
Authors: Joanne Klevens, Laura S. Sadowski, Romina Kee, Diana Garcia, Colby Lokey
Journal: JAMA (2015)

The US Preventive Services Task Force recommends women of reproductive age be screened for partner violence.1 However, others, such as the World Health Organization2 and the Cochrane Collaborative,3 conclude there is insufficient evidence for this recommendation.

Our randomized clinical trial allocated women seeking care in outpatient clinics to 1 of 3 study groups: computerized partner violence screening and provision of a local resource list, universal provision of a partner violence resource list without screening, or a no screen/no resource list control group. No differences were found in women’s quality of life, days lost from work or housework, use of health care and partner violence services, or the recurrence of partner violence after 1 year.4

We report women’s use of health services over 3 years, which we hypothesized would be lower in the intervention groups, as delayed effects of acting on the referral information could result from deteriorating health.
Abstract 1626: Exercise Training Has Protective Effects in Acute Cardiac Overload by Preventing Apoptosis and Nf-kB Activation
Authors: Daniel Moreira-Goncalves, Tiago Henriques-Coelho, Helder Fonseca, Jose Alberto Duarte, Adelino Leite-Moreira
Journal: Circulation (2009)

Introduction: Cardiac overload is an important stimulus for triggering HF. We hypothesized that exercise training (ExT) could positively influence the early cardiac adaptation to overload by preser...
Abstract 1768: A novel PDE10 inhibitor suppresses tumor growth in an orthotopic mouse model of lung cancer
Authors: Veronica Ramirez-Alcantara, Michele A. Schuler, Bing Zhu, Nan Li, Evrim Gurpinar, Joshua Canzoneri, Adam Keeton, Bernard Gary, Suzanne Russo, Lori Coward, Gregory S. Gorman, William Grizzle, Xi Chen, Gary A. Piazza
Journal: Cancer Research (2014)

Abstract Background: Conventional chemotherapy and radiation cannot distinguish between cancer and normal cells resulting in dose-limiting toxicity. Molecular targeted drugs hold greater promise, but few targets are unique to cancer cells and drugable. Our laboratory discovered that the cyclic nucleotide phosphodiesterase, PDE10, is elevated in human lung tumor cells and essential for their growth. A novel PDE10 inhibitor, MCI-020 was designed to achieve high lung concentrations and found to selectively inhibit the growth of human lung tumor cells in vitro. Objective: Evaluate pharmacokinetics, tissue distribution and antitumor efficacy of MCI-020 in mice. Material and Methods: MCI-020 (100 mg/kg) was formulated as a suspension and administrated orally to C57BL/6 female mice. Free levels of MCI-020 were quantified in plasma and tissues by reverse-phase chromatography with tandem mass spectrometry detection. For efficacy evaluation, athymic nude-Foxn1nu female mice were treated with MCI-020 (150 mg/kg bid) for 5 days before inoculation with 1x106 A549 cells/mouse into the left lung. After inoculation, MCI-020 treatment continued for 4 weeks. Anti-tumor efficacy of MCI-020 was evaluated by gross and histological grading of the lungs. Results: MCI-020 displayed attractive oral bioavailability and reached appreciably higher concentrations in lungs compared with plasma. MCI-020 treatment showed strong anti-tumor efficacy in the orthotopic mouse model of lung cancer and was well tolerated. Compared with the vehicle group in which 85% of the mice formed lung tumors, only 25% of the mice in the treatment group developed tumors. Histological grading of the extent of tumor formation revealed a score of 0.83 ± 0.3 (low involvement) for the treatment group, compared with 2.6 ± 0.4 (high involvement) for the vehicle group. Conclusions: These observations support a critical role of PDE10 in lung tumor growth and suggest that PDE10 inhibitors will be useful for the prevention or treatment of lung cancer. This project is supported by NIH grant 1R01CA148817. Citation Format: Veronica Ramirez-Alcantara, Michele A. Schuler, Bing Zhu, Nan Li, Evrim Gurpinar, Joshua Canzoneri, Adam Keeton, Bernard Gary, Suzanne Russo, Lori Coward, Gregory S. Gorman, William Grizzle, Xi Chen, Gary A. Piazza. A novel PDE10 inhibitor suppresses tumor growth in an orthotopic mouse model of lung cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1768. doi:10.1158/1538-7445.AM2014-1768
Comprehensive gene expression profile of LPS-stimulated human monocytes by SAGE
Authors: Takuji Suzuki, Shin-ichi Hashimoto, Nobuaki Toyoda, Shigenori Nagai, Nobuyuki Yamazaki, Hong-Yan Dong, Jun Sakai, Taro Yamashita, Toshihiro Nukiwa, Kouji Matsushima
Journal: Blood (2000)
Noninvasive Identification of Ventricular Tachycardia-Related Conducting Channels Using Contrast-Enhanced Magnetic Resonance Imaging in Patients With Chronic Myocardial Infarction
Authors: Esther Perez-David, Ángel Arenal, José L. Rubio-Guivernau, Roberto del Castillo, Leonardo Atea, Elena Arbelo, Eduardo Caballero, Verónica Celorrio, Tomas Datino, Esteban Gonzalez-Torrecilla, Felipe Atienza, Maria J. Ledesma-Carbayo, Javier Bermejo, Alfonso Medina, Francisco Fernández-Avilés
Journal: Journal of the American College of Cardiology (2011)
Liver: Helical Computed Tomography and Magnetic Resonance Imaging
Authors: Yuji Baba, Yasuyuki Yamashita, Kazuo Awai, Koichi Kawanaka
Journal: Liver Cancer (2009)

Both computed tomography (CT) and magnetic resonance (MR) imaging have made major contributions to the evaluation of liver morphology, blood flow and detection and characterization of liver neoplasms.Studies in numerous institutions have established that both CT and MR imaging are highly accurate in the diagnosis of hepatic pathology.
In‐hospital worsening heart failure
Authors: Javed Butler, Mihai Gheorghiade, Anita Kelkar, Gregg C. Fonarow, Stefan Anker, Stephen J. Greene, Lampros Papadimitriou, Sean Collins, Frank Ruschitzka, Clyde W. Yancy, John R. Teerlink, Kirkwood Adams, Gadi Cotter, Piotr Ponikowski, G. Michael Felker, Marco Metra, Gerasimos Filippatos
Journal: European Journal of Heart Failure (2015)
Generation of Plasma Cells From Peripheral Blood Memory B Cells: Synergistic Effect of Interleukin-10 and CD27/CD70 Interaction
Authors: Kazunaga Agematsu, Haruo Nagumo, Yumiko Oguchi, Takayuki Nakazawa, Keitaro Fukushima, Kozo Yasui, Susumu Ito, Tetsuji Kobata, Chikao Morimoto, Atsushi Komiyama
Journal: Blood (1998)
Activity of coumarin and cimetidine in metastatic renal cell carcinoma.
Authors: A P Venook, Y Davenport, A Tseng
Journal: Journal of Clinical Oncology (1989)

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1989.7.3.402 Journal of Clinical Oncology - published online before print September 22, 2016 PMID: 2918335 Activity of coumarin and cimetidine in metastatic renal cell carcinoma. A P VenookxA P VenookSearch for articles by this author , Y DavenportxY DavenportSearch for articles by this author , A Tseng JrxA Tseng JrSearch for articles by this author https://doi.org/10.1200/JCO.1989.7.3.402 PDF "Activity of coumarin and cimetidine in metastatic renal cell carcinoma.." Journal of Clinical Oncology, 7(3), pp. 402–403© 1989 by American Society of Clinical Oncology
Aggressive Public Health Response Prevented Meningitis Cases, Deaths
Authors: Anita Slomski
Journal: JAMA (2015)

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Sydney E. Salmon
Authors: Raymond Alexanian, Kenneth Anderson, Bart Barlogie, James Berenson, William S. Dalton, Robert A. Kyle
Journal: Clinical Cancer Research (2000)

Cancer research lost an eminent scientist, clinician, and educator when Sydney E. Salmon, M.D., died on October 6, 1999 at the age of 63 years after a long battle with pancreatic cancer.

Born in Staten Island, New York, Dr. Salmon attended the University of Arizona in Tucson, Arizona, earning a B.A
Trauma related shin splints
Authors: R. Ashford, M A Macleod
Journal: BMJ (1999)

<h3>Abstract</h3> The increased availability of both open ecological data, and software to interact with it, allows the fast collection and integration of information at all spatial and taxonomic scales. This offers the opportunity to address macroecological questions in a cost-effective way. In this contribution, we illustrate this approach by forecasting the structure of a stream food web at the global scale. In so doing, we highlight the most salient issues needing to be addressed before this approach can be used with a high degree of confidence.
The ABCD (Autologous Bone Marrow Cells in Dilated Cardiomyopathy) Trial
Authors: Sandeep Seth, Balram Bhargava, Rajiv Narang, Ruma Ray, Sujata Mohanty, Gurpreet Gulati, Lalit Kumar, Balram Airan, Panangipalli Venugopal
Journal: Journal of the American College of Cardiology (2010)
Contribution of Inert Mass to Experimental Cancer Cachexia in Rats
Authors: S D Morrison, J F Moley, J A Norton
Journal: JNCI Journal of the National Cancer Institute (1984)

An inert artificial tumor (AFT) was inflated in male F344 rats to simulate, experimentally, the growth in mass of large transplantable tumors that produce cachexia. The AFT depressed host weight gain and skeletal muscle mass up to 30% and food intake up to 20% of the depression induced by tumors of comparable size. When the growth rate of the AFT was low, there was no depression of food intake. Work-induced hypertrophy of skeletal muscles, as assessed by a gastrocnemius tenotomy model, was approximately equal to that of normal, tumor-bearing, and AFT-bearing animals. The AFT elevated host total energy expenditure by 12.5% and compartment-of-energy expenditure attributable to motor activity by 10.5%. The elevation of energy expenditure accounted for most of the depression of weight gain of AFT-bearing animals below that of intact animals. The large mass of most transplantable tumors leads to an overestimate of the malignant tissue-depletive effects of tumor and an under-estimate of the asthenic effects.
Low-level laser therapy effect on the bronchial hyperresponsiveness and the chronic allergy airway inflammation is driven to RhoA signaling and STAT-6
Authors: Priscila Marcondes, Regiane Albertini, Ana Paula Ligeiro de Oliveira, Rodolfo Vieira, Flavio Aimbire
Journal: European Respiratory Journal (2013)

Low-level laser therapy (LLLT) controls the bronchial hyperresponsiveness (BHR) associated with increased RhoA mRNA expression as well as the generation of pro-inflammatory mediators associated with NF-kB signaling in acute lung inflammation. Thus, in the current study, we aimed to explore if LLLT reduce both the BHR and the generation of inflammatory mediators in chronic allergic asthma. Wistar rats were divided in experimental groups for studies of bronchial reactivity and lung inflammation after antigen challenge. The BHR was measured through of isolated organ system and construction of dose-response curves to methacholine. The lung inflammation was measured by the following markers: inflammatory cells, adhesion molecule, mucus production, collagen synthesis and cytokines. To confirm the participation of RhoA in BHR, the animals were pretreated with a RhoA inhibitor, Y-27632, 1 h before the antigenic challenge. LLLT was carried out by a 660 nm diode laser with a dose of 5.4 J during 3 minutes and two irradiation protocols were used. The reduction of BHR post LLLT coincides with decreasing of RhoA expression in bronchial muscle as well as the reduction of eosinophils. Laser effect was also evidenced in E-selectin expression and Th2 cytokines and eotaxin levels. The signal transducer and activator of transduction-6 (STAT6) concentration in lung from challenged rats was also reduced diminished after laser treatment; otherwise, LLLT does not work on IgE in serum. Therefore, our results demonstrated that LLLT reduces the BHR via RhoA and the chronic allergic airway inflammation via STAT6.
Alcohol intake and cancer of the upper digestive tract
Authors: C. L. Vecchia, S. Franceschi, A. Favero, R. Talamini, E. Negri, K K Cheng, C Cummins, R Maric, V. Reed, R. Fitzgerald, C. Caygill, M. Gronbak, T. I A Sorensen
Journal: BMJ (1999)

Editor—A Danish study of 156 subjects with upper digestive tract cancers showed that wine drinkers may be at a lower risk than drinkers with a similar intake of beer or spirits.1 Wine is the most common alcoholic beverage in Italy, accounting for over 80% of alcohol intake.2 We investigated the separate and combined effect of wine drinking in a large dataset.3

Data were collected between 1984 and 1993 in Greater Milan and the province of Pordenone, Northern Italy, on 547 histologically confirmed incident cases of cancer of the oral cavity and pharynx (466 men, 81 women; age 22-74 (median 57)) and 412 cases of cancer of the oesophagus (345 men, 67 women; age 26-74 (median 60)). Controls were 2375 subjects (1797 men, 578 women; age 25-74 (median 56)) admitted to the same network of hospitals with acute non-neoplastic conditions unrelated to alcohol or tobacco consumption. Of these, 570 were admitted for trauma, 593 for non-traumatic orthopaedic conditions, 475 for acute surgical diseases, 428 for eye diseases, and 309 for miscellaneous other illnesses. Trained interviewers questioned cases and controls, using a structured questionnaire; questions on the days per week that each type of alcoholic beverage (wine, beer, and spirits) was consumed and the average number of drinks per day were included. 

The table gives the distribution of cases of oral and pharyngeal and oesophageal cancer and of the comparison group according to consumption of various alcoholic beverages. When non-drinkers and moderate drinkers (<3 drinks a day) were used as the comparison group, the odds ratios of oral and pharyngeal cancer were 4.95 for very heavy (⩾10 drinks per day) wine drinkers and 4.13 for very heavy wine, beer, and spirit drinkers. Corresponding findings for oesophageal cancer were 7.53 and 5.52. The odds ratios for beer or spirit drinkers only were 0.9 (95% confidence interval 0.3 to 2.4) for cancers of the oral cavity (7 cases, 47 controls) and 1.5 (0.6 to 3.9) for oesophageal cancer (7 cases, 47 controls). These results were consistent across separate diagnostic conditions in controls.

This pattern of risk according to type of alcoholic beverage is different from that reported in the Danish study.1 Taken together, these data lead us to conclude that ethanol is the main component of alcoholic beverages that determines the risk of cancer and that the most frequently consumed beverage in each area tends to be the one with the highest risk.4,5 Wine consumption is clearly strongly related to cancers of the upper digestive tract in individuals and populations with heavy consumption.
Patients' descriptions of living with COPD
Authors: Eva Österlund Efraimsson, Carina Holding Eriksson, Anna Håkansson, Katarina Andersson, Hillevi Bengtsson, Sara Lindström, Marie Jensen, Linda Falk, Cecilia Fehrm
Journal: European Respiratory Journal (2013)

Aim:  To explore which problems patients with COPD in all four stages express and describe during visits at nurse-led COPD clinics in primary health care .  Method: A  prospective qualitative observational study comprising two videotaped consultations, first and third re-visit, with each of 20 patients (13 women), all smokers (n=11) or former smokers diagnosed with COPD. The consultations were conducted by six COPD-nurses in primary health care and analysed by qualitative content analysis.  Results:  Smokers wished to quit or reduce their smoking but expressed motivational difficulties in fighting cravings. Concerns about the visits were mainly about the spirometry-examination which they found exhausting and difficult to perform. Also, they were worried about the results. Other concerns included the prospect of increasing symptoms and fears about future health. Symptoms described in all stages were cough, phlegm and dyspnoea connected even with light physical exertion. In stage III and IV, dyspnoea was the most severe symptom affecting daily activities. Patients expressed concern about symptoms that could be dangerous or fatal. Previously independent activities necessitated planning and help from others. They wished to learn about self -management and used various strategies to handle their disease even when offered support and assistance. Patients told that information about COPD, how to handle symptoms and treatment in daily life increased their security and control.  Conclusion:  Patients were concerned about their smoking habits and subsequent symptoms being dangerous or fatal. Dyspnoea was troublesome and limited everyday life already in early stages of COPD, thus not always correlated to the severity stage of the disease.
The effects of mono (2-ethylhexyl) phthalate, mono-n-butyl phthalate and ethanol on PPARs in MCF-7 human breast cancer cells
Authors: N. Gopisetty Venkata, J. A. Robinson, P. J. Cabot, G. R. Monteith, S. J. Roberts-Thomson
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

374 

Di(2-ethylhexyl)phthalate (DEHP) and di- n -butyl phthalate (DBP) belong to a group of chemicals that are used as plasticizers in a wide range of products and are environmental contaminants at levels significant for humans. Both compounds are known reproductive toxins in rodents and DEHP also induces rodent hepatocarcinogenesis in a process believed to be mediated via the peroxisome proliferator-activated receptor α (PPARα). DEHP and DBP are metabolized to their respective active metabolite monoesters, mono-(2-ethylhexyl) phthalate (MEHP) and mono- n -butyl phthalate (MBP). There have been no studies of the effects of these agents on PPARs in breast cancer cell lines. Ethanol is another modulator of PPARs, since changes in PPARβ occur in B12 oligodendrocyte cells upon ethanol exposure. Epidemiological studies show a positive correlation between alcohol intake and breast cancer risk. However, there have been no studies of the effects of ethanol on PPARs in breast cancer cell lines. We hypothesized that MEHP and/or MBP would affect the transactivation of human PPAR isoforms in MCF-7 cells and that ethanol would change the expression of PPARs in MCF-7 cells.. Using a gene reporter assay we looked at the activation of human PPARα, PPARβ and PPARγ by MEHP and MBP. MEHP activated both PPARα and PPARγ but had no activity towards PPARβ. MBP while unable to act as an agonist towards any PPAR isoform showed antagonistic activity against human PPARγ and PPARβ. Using real time RT-PCR we looked at the transcription of PPAR isoforms in the presence of increasing concentrations of ethanol and saw isoform specific effects. Given that the effects of PPARα, PPARβ and PPARγ activation in human breast cells appears to be opposing (PPARα and PPARβ activators in breast cells cause an increase in proliferation, while PPARγ activation in breast cells is associated with differentiation and an inhibition of cell proliferation), the consequences of MEHP and ethanol in the breast are likely to be complex.
In vivo use of recombinant TAT-CRE protein for sporadic lung cancer induction in a orthotopic mouse tumor model.
Authors: Lukas Heukamp, Michael Peitz, Linda Diehl, Ursual Rommerscheidt-Fuss, Luisa Klotz, Jens Hahne, Frank Edenhofer, Reinhard Buettner
Journal: Cancer Research (2007)

3856  Mouse tumor models with spontaneously developing sporadic tumors are important to cancer research to generate new hypotheses in tumor biology and to test new treatment strategies. Ideally tumor induction should mimic natural tumor development and lead to a small number of molecularly well defined tumors. Most Cre recombinase inducible tumor models show a marked field cancerization as most if not all target cells express the oncogen after induction. We have used the transgenic mouse strain RasF (Meuwissen et. al., Oncogene 2001) expressing a Cre recombinase inducible Ras oncogene. In these mice the number of tumors that develop can be influenced by the dose of recombinant Adneo virally encoded CRE that is given. However, a large number of Lung adenocarcinomas develop in both lungs and a strong anti-viral immune response is induced.  To generate a mouse tumor model that more closely resembles the human pathogenesis without the use of Adenoviral vectors, we have used recombinant Cre recombinase fused to the basic membrane translocation peptide TAT (TAT-Cre). Injection of TAT-Cre recombinant protein into one lung of immunocompetent RasF mice yields a small number of pulmonary adenocarcinomas after a short latency in the injected lung without the need for immunsuppression. Since only a limited number of tumors developed in these mice, respiratory distress due to a large tumor burden was greatly reduced and the animals survived for a longer period of time compared to an Adenoviral Cre delivery system. The TAT-Cre protein was not immunstimulatory as pulmonary dendritic cells did not upregulate CD40 or CD86 after TAT-Cre application.  In summary, we present a novel approach to reliably deliver Cre recombinase in vivo to induce a limited number of sporadic orthotopic tumors in mice. The protocol has no need for immune suppression and mimicks human cancer formation with a prolonged observatory window to test new therapeutic approaches.