tbuckley/cabot-search huggingface dataset:
Unusual Locations of Involvement by Malignancies
Authors: Geetha N. Varma, Janet S. Winston, Hank C. Hill, John F. Gibbs, Gary M. Proulx, Brian E. McGrath, Milind M. Javle
Journal: Journal of Clinical Oncology (2003)

Article Tools DIAGNOSIS IN ONCOLOGY Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.2003.09.089 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 12947076 Unusual Locations of Involvement by Malignancies CASE 3. GASTRIC SIGNET RING CARCINOMA PRESENTING AS A DIFFUSE THIGH MASS Geetha N. VarmaxGeetha N. VarmaSearch for articles by this author , Janet S. WinstonxJanet S. WinstonSearch for articles by this author , Hank C. HillxHank C. HillSearch for articles by this author , John F. GibbsxJohn F. GibbsSearch for articles by this author , Gary M. ProulxxGary M. ProulxSearch for articles by this author , Brian E. McGrathxBrian E. McGrathSearch for articles by this author , Milind M. JavlexMilind M. JavleSearch for articles by this author Show More Roswell Park Cancer Institute, Buffalo, NY https://doi.org/10.1200/JCO.2003.09.089 First Page Full Text PDF Figures and Tables © 2003 by American Society of Clinical Oncology
Trends in Private and Public Health Insurance for Adolescents
Authors: Paul W. Newacheck
Journal: JAMA (2004)

Previous studies (1984-1995) of adolescent health insurance have shown little change in the proportion with coverage. Federally mandated expansions in Medicaid were offset by declines in private coverage. Further expansions of Medicaid and implementation of the State Children's Health Insurance Program (SCHIP) have opened new avenues for increasing coverage rates.To assess the current health insurance status of adolescents, the demographic and socioeconomic correlates of insurance coverage, and document recent changes in public and private coverage rates.We analyzed data on 12 995 adolescents aged 10 to 18 years, who had been included in the 2002 National Health Interview Survey. We conducted multivariate analyses to assess the independent association of age, sex, race, poverty status, family structure, family size, and region on the likelihood of having insurance coverage. Results are compared with previously published findings on adolescent health insurance coverage spanning 1984 to 1995.Insurance coverage for adolescents.An estimated 12.2% of adolescents were uninsured in 2002, which is a decrease from 14.1% in 1995 (P<.003). The decrease occurred entirely because of an expansion of public coverage and is concentrated among children in poor (<100% of the federal poverty level) and near-poor (100%-199% of the federal poverty level) families. A substantial decrease in the differences between poor and higher-income groups occurred between 1995 and 2002 due to gains in coverage for adolescents in poor and near-poor families and losses in coverage among those in middle- and upper-income families (> or =200% of the federal poverty level). Specifically, the proportion of adolescents in poor families without coverage declined from 27.4% in 1995 to 19.7% in 2002 (P<.001). The proportion of adolescents in near-poor families without coverage declined from 24.8% in 1995 to 19.2% in 2002 (P<.002). In contrast, the proportion of adolescents in middle- and higher-income families without insurance increased from 4.1% in 1995 to 6.3% in 2002 because availability of insurance through the private market declined (P<.001).A modest but significant reduction in the percentage of adolescents without insurance has occurred since 1995, largely as a result of expansions in public coverage. An even larger reduction in the proportion of adolescents without coverage would have occurred, if not for a reduction in private coverage for adolescents in middle- and higher-income families.
Potent Antitumor Immunity Generated by a CD40-Targeted Adenoviral Vaccine
Authors: Basav N. Hangalapura, Dinja Oosterhoff, Jan de Groot, Louis Boon, Thomas Tüting, Alfons J. van den Eertwegh, Winald R. Gerritsen, Victor W. van Beusechem, Alexander Pereboev, David T. Curiel, Rik J. Scheper, Tanja D. de Gruijl
Journal: Cancer Research (2011)

In situ delivery of tumor-associated antigen (TAA) genes into dendritic cells (DC) has great potential as a generally applicable tumor vaccination approach. Although adenoviruses (Ad) are an attractive vaccine vehicle in this regard, Ad-mediated transduction of DCs is hampered by the lack of expression of the Ad receptor CAR on the DC surface. DC activation also requires interaction of CD40 with its ligand CD40L to generate protective T-cell-mediated tumor immunity. Therefore, to create a strategy to target Ads to DCs in vivo, we constructed a bispecific adaptor molecule with the CAR ectodomain linked to the CD40L extracellular domain via a trimerization motif (CFm40L). By targeting Ad to CD40 with the use of CFm40L, we enhanced both transduction and maturation of cultured bone marrow-derived DCs. Moreover, we improved transduction efficiency of DCs in lymph node and splenic cell suspensions in vitro and in skin and vaccination site-draining lymph nodes in vivo. Furthermore, CD40 targeting improved the induction of specific CD8(+) T cells along with therapeutic efficacy in a mouse model of melanoma. Taken together, our findings support the use of CD40-targeted Ad vectors encoding full-length TAA for in vivo targeting of DCs and high-efficacy induction of antitumor immunity.
Metabolic Hypotheses in Schizophrenia
Authors: Ross J. Baldessarini
Journal: New England Journal of Medicine (1975)

The report by Freeman et al. in this issue (page 491) of another case of psychosis and mental retardation in homocystinuria raises a number of interesting points about metabolic research in psychiatry. There has been repeated discussion in recent decades of the possibility that some features of the idiopathic psychoses could be attributed to the abnormal accumulation in the brain of toxic chemical substances, including methylated amines. This methylation hypothesis for schizophrenia1 was initially based on the structural similarity of some endogenous metabolites to methylated hallucinogenic alkaloids such as mescaline and certain N-methylated tryptamines. The idea was given further . . .
Evidence base: rock of certainty or shifting sands?
Authors: Harold A Maio
Journal: BMJ (2004)

National Programme for Information Technology (NPfIT), has highlighted the lack of clinicians' engagement with this £6bn project.The advisory board represents a much needed injection of resources to NHS information technology systems, which could bring many benefits to care for patients and clinicians' working practices.The Wanless reports have emphasised the importance of information technology in the future of healthcare in the United Kingdom. 1 A national programme could avoid the problems around interoperability associated with past failures in NHS information technology systems.However, the secrecy surrounding the procurement phase of the programme has led to an increasing feeling of unease among clinician end users.Anxieties prevail about changes in working practices, usability of systems, training needs, and the possibility that political expediency will overshadow clinical needs.Aidan Halligan, the deputy chief medical officer, has been charged with ensuring clinical engagement with the programme. 2 The good news for the Department of Health comes from its survey, carried out by Medix, which shows that many doctors are enthusiastic about the potential of the national programme, with three quarters of respondents endorsing it as an important NHS priority. 3 Only 4% of respondents thought, however, that they had been adequately consulted.The recently announced new Front Line Support Academy aims to correct omissions at the leadership level.
How Does Measles Virus Cause Subacute Sclerosing Panencephalitis?
Authors: Samuel L. Katz
Journal: New England Journal of Medicine (1969)

IN March, 1967, John H. Connolly and his colleagues1 provided the crucial clue that linked measles-virus infection, in some unique manner, with subacute sclerosing panencephalitis (SSPE). Two and a half years later, one can survey the results of a flurry of clinical and laboratory activities stimulated by their Lancet publication. More than 50 new medical manuscripts dealing with the disorder have appeared in print. There have been repeated corroborations and some refinements of the Connolly data. Electron microscopists have duplicated and sharpened the focus of Bouteille's earlier work,2 which was given clear direction and significance by the implication of measles . . .
Preservation of venous endothelial function in the forearm venous capacitance bed of patients with chronic heart failure despite arterial endothelial dysfunction
Authors: Angus K Nightingale, Daniel J Blackman, Gethin R Ellis, Matthias Schmitt, Jayne A Morris-Thurgood, Elizabeth A Jones, Michael P Frenneaux
Journal: Journal of the American College of Cardiology (2001)
Hepatocyte IKKβ/NF-κB Inhibits Tumor Promotion and Progression by Preventing Oxidative Stress-Driven STAT3 Activation
Authors: Guobin He, Guann-Yi Yu, Vladislav Temkin, Hisanobu Ogata, Christian Kuntzen, Toshiharu Sakurai, Wolfgang Sieghart, Markus Peck-Radosavljevic, Hyam L. Leffert, Michael Karin
Journal: Cancer Cell (2010)
Toward a Model That Encourages the Recruitment of Ethics Consultants With Clinical Experience
Authors: Rogelio Altisent, Maria Teresa Delgado-Marroquín, Nieves Martín-Espildora
Journal: The American Journal of Bioethics (2014)

The maturity shown by the American model of clinical ethics consultation is undisputed. The proposal by White, Jankowski, and Shelton (2014) to assess and accredit future consultants is based on th...
Abstract 2040: Adenomatous polyposis coli mediated signaling, self renewal and differentiation of breast epithelial cells
Authors: Alyssa Lesko, Harikrishna Nakshatri, Manjushree Anjanappa, Poornima Bhat-Nakshatri, Jenifer Prosperi
Journal: Cancer Research (2014)

Abstract Breast cancer is the leading cause of cancer-related death in non-smoking women in the United States. Despite tremendous amounts of information about the etiology of breast cancer, many questions remain unanswered. It has been demonstrated that specific subtypes of breast cancer differ in their sensitivity to chemotherapeutic and targeted therapies. The oncogenic events and signaling pathways driving these tumor subtypes are distinct. This indicates that increased knowledge of the molecular events defining the unique subtypes will provide opportunities for novel therapeutic approaches tailored to fit the specific subtypes and will therefore lead to improvement in patient outcomes. The Adenomatous Polyposis Coli (APC) tumor suppressor is mutated or hypermethylated in 18-70% of sporadic breast cancers depending on subtype. Oncomine database analysis revealed reduced expression of APC in aggressive estrogen receptor (ER) negative breast cancers compared to ER-positive breast cancer or normal breast. Using the ApcMin/+ mouse model, we identified pre-neoplastic lesions in the breast and enhanced breast tumorigenesis in the presence of the Polyoma middle T antigen (PyMT) oncogene. Apc mutation changed the tumor histopathology from solid to squamous adenocarcinomas, resembling the highly aggressive human metaplastic breast cancer. In this model of mouse mammary tumorigenesis, these changes occurred independent of Wnt/b-catenin signaling and required activation of focal adhesion kinase (FAK)/Src signaling, with a subsequent increase in cyclooxygenase-2 (COX-2). The applicability of these signaling pathways to human breast cancer remains unclear. Using the epithelial cell reprogramming assay for growing normal breast epithelial cells, we have begun to characterize expression of cell surface markers to delineate subtypes of epithelial cells. We have also assessed APC expression and correlated APC expression with risk and well-established clinical markers, such as ErbB2. Future studies will modulate APC expression in specific compartments of breast epithelial hierarchy to accomplish our objectives of dissecting the molecular alterations specifically downstream of APC loss and its role in the self-renewal and differentiation of breast epithelial cells. Citation Format: Alyssa Lesko, Harikrishna Nakshatri, Manjushree Anjanappa, Poornima Bhat-Nakshatri, Jenifer Prosperi. Adenomatous polyposis coli mediated signaling, self renewal and differentiation of breast epithelial cells. [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 2040. doi:10.1158/1538-7445.AM2014-2040
Global Crises, Global Solutions
Authors: Henry Greenberg
Journal: BMJ (2005)

What an intriguing idea. Convene serious thinkers to create a list of critical issues facing the global community that are amenable to governmental intervention, prune and prioritise the list to the top 10, enlist leading economists to outline the challenges, add thoughtful commentaries, and then rank the final 10. A group called the Copenhagen Consensus under the leadership of Bj⊘rn Lomborg did just this and teamed up with the Economist to disseminate the results. Global Crises, Global Solutions is the result, and disappointing it is, garnering at best two stars.
CHARACTERISTICS OF THOSE WITH SIGNIFICANT SUBCLINICAL ATHEROSCLEROSIS WITHOUT TRADITIONAL RISK FACTORS: THE DALLAS HEART STUDY
Authors: Jacob P. Kelly, Nitin Gupta, Colby Ayers, Sandeep R. Das, Jarett D. Berry, Darren K. McGuire, James A. de Lemos, Amit Khera
Journal: Journal of the American College of Cardiology (2011)
Inoculation of the Measles
Authors: M. Von Katona
Journal: BMJ (1842)

<h3>Objectives</h3> To identify novel DNA methylation sites significant for rheumatoid arthritis (RA) and comprehensively understand their underlying pathological mechanism. <h3>Methods</h3> We performed (1) genome-wide DNA methylation and mRNA expression profiling in peripheral blood mononuclear cells from RA patients and health controls; (2) correlation analysis and causal inference tests for DNA methylation and mRNA expression data; (3) differential methylation genes regulatory network construction; (4) validation tests of 10 differential methylation positions (DMPs) of interest and corresponding gene expressions; (5) correlation between <i>PARP9</i> methylation and its mRNA expression level in Jurkat cells and T cells from patients with RA; (6) testing the pathological functions of <i>PARP9</i> in Jurkat cells. <h3>Results</h3> A total of 1046 DNA methylation positions were associated with RA. The identified DMPs have regulatory effects on mRNA expressions. Causal inference tests identified six DNA methylation–mRNA–RA regulatory chains (eg, cg00959259-PARP9-RA). The identified DMPs and genes formed an interferon-inducible gene interaction network (eg, <i>MX1</i>, <i>IFI44L</i>, <i>DTX3L</i> and <i>PARP9</i>). Key DMPs and corresponding genes were validated their differences in additional samples. Methylation of PARP9 was correlated with mRNA level in Jurkat cells and T lymphocytes isolated from patients with RA. The <i>PARP9</i> gene exerted significant effects on Jurkat cells (eg, cell cycle, cell proliferation, cell activation and expression of inflammatory factor IL-2). <h3>Conclusions</h3> This multistage study identified an interferon-inducible gene interaction network associated with RA and highlighted the importance of <i>PARP9</i> gene in RA pathogenesis. The results enhanced our understanding of the important role of DNA methylation in pathology of RA.
Abstract 3408: RNAi screening identifies STK10 as a novel therapeutic target for Ewing's sarcoma
Authors: Shilpi Arora, Irma M. Gonzales, Chao Sima, Javed Khan, Spyro Mousses, David O. Azorsa
Journal: Cancer Research (2010)

Abstract Ewing sarcoma family tumors (ESFT) represent ∼ 3% of pediatric cancers and are the second most common bone malignancy in children and adolescents. Rearrangement of the EWS gene on chromosome 22q12 with an ETS gene family member is the underlying molecular genetic abnormality for Ewing's sarcoma. These translocations provide a valuable tool for accurate diagnosis of ESFTs and also represent ideal targets for the development of targeted therapeutics. The most common translocation is t(11;22)(q24;q12), which involves the proteins EWS and Friend Leukemia Integration Site 1 (FLI1). The newly formed EWS-FLI1 fusion protein is a transcription factor that could then lead to aberrant transcription and gives the ES cells a specific tumorigenic context. We employed a functional genomics approach based on high throughput RNA interference (HT-RNAi) analysis to identify “Achilles heel” targets or genes who's silencing affect the proliferation and survival of Ewing's sarcoma cells. We used a human “kinome” library targeting 572 kinases and four ES cell lines, TC-32, TC-71, SK-ES-1 and RD-ES for the HT-RNAi screening. All the screens were done in duplicate and the data was normalized and analyzed using the Z-score method. One gene that was a significant “hit” across all the four cell lines was serine threonine kinase 10 or STK10. Our validation confirmed that reduction in ES cell growth by STK10 siRNA was due to specific STK10 silencing and was not an off target effect. Moreover, silencing of STK10 in ES cells resulted in increased apoptosis. We also showed that normal human fibroblasts did not depend on STK10 for cell growth. Our results have confirmed that STK10, which belongs to the polo like kinase family, is required for the growth of ES cells. After further validation we will use these results for the development of specific drugs targeting STK10 and thereby accelerate the development of improved therapeutics for Ewing's sarcoma. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3408.
Pitavastatin ameliorates albuminuria and renal mesangial expansion by downregulating NOX4 in db/db mice
Authors: M. Fujii, T. Inoguchi, Y. Maeda, S. Sasaki, F. Sawada, R. Saito, K. Kobayashi, H. Sumimoto, R. Takayanagi
Journal: Kidney International (2007)
Mongolism — Implications of the Dental Anomalies
Authors: Theodore H. Ingalls, Richard L. Butler
Journal: New England Journal of Medicine (1953)

ALTHOUGH the dental defects in mongolism have not been systematically analyzed, scattered observations are recorded. Nash1 reported that the teeth of his mongoloid patients, three to thirty-five years of age, were frequently missing, abnormally shaped or smaller than normal.2 In a study of 3 mongoloid skulls, Greig3 observed irregularities of the teeth that were more pronounced in the upper than in the lower jaw. In 1 skull, showing congenital absence of the nasal bones, there was a congenitally absent right upper lateral incisor (Fig. 1A); in the second skull the same tooth was markedly dwarfed, and the left upper . . .
Cancer risk and parental pesticide application in children of Agricultural Health Study participants.
Authors: Kori B Flower, Jane A Hoppin, Charles F Lynch, Aaron Blair, Charles Knott, David L Shore, Dale P Sandler
Journal: Environmental Health Perspectives (2003)

Parental exposure to pesticides may contribute to childhood cancer risk. Through the Agricultural Health Study, a prospective study of pesticide applicators in Iowa and North Carolina, we examined childhood cancer risk and associations with parental pesticide application. Identifying information for 17,357 children of Iowa pesticide applicators was provided by parents via questionnaires (1993-1997) and matched against the Iowa Cancer Registry. Fifty incident childhood cancers were identified (1975-1998). Risk of all childhood cancers combined was increased [standardized incidence ratio (SIR) = 1.36; 95% confidence interval (CI), 1.03-1.79]. Risk of all lymphomas combined was also increased (SIR = 2.18; 95% CI, 1.13-4.19), as was risk of Hodgkin's lymphoma (SIR = 2.56; 95% CI, 1.06-6.14). We used logistic regression to explore associations between self-reported parental pesticide application practices and childhood cancer risk. No association was detected between frequency of parental pesticide application and childhood cancer risk. An increased risk of cancer was detected among children whose fathers did not use chemically resistant gloves [odds ratio (OR) = 1.98; 95% CI, 1.05-3.76] compared with children whose fathers used gloves. Of 16 specific pesticides used by fathers prenatally, ORs were increased for aldrin (OR = 2.66), dichlorvos (OR = 2.06), and ethyl dipropylthiocarbamate (OR = 1.91). However, these results were based on small numbers and not supported by prior biologic evidence. Identification of excess lymphoma risk suggests that farm exposures including pesticides may play a role in the etiology of childhood lymphoma.
The Use of Isotopes in Haematology
Authors: Lawrence C. Parish
Journal: JAMA (1961)

peculiar to the neonatal period -these differences should not be over-emphasized.The separation of 'pmdiatric hxematology' from 'adult hmmatology' seems both unnecessary and undesirable, and as the present book illustrates, is difficult to achieve in practice.The book is however, well produced, authoritative, and up to date.
The Metabolic Syndrome and Chronic Kidney Disease in U.S. Adults
Authors: Jing Chen, Paul Muntner, L. Lee Hamm, Daniel W. Jones, Vecihi Batuman, Vivian Fonseca, Paul K. Whelton, Jiang He
Journal: Annals of Internal Medicine (2004)

Background: The metabolic syndrome is a common risk factor for cardiovascular disease. Objective: To examine the association between the metabolic syndrome and risk for chronic kidney disease and microalbuminuria. Design: Cross-sectional study. Setting: The Third National Health and Nutrition Examination Survey. Patients: Participants 20 years of age or older were studied in the chronic kidney disease (n = 6217) and microalbuminuria (n = 6125) analyses. Measurements: The metabolic syndrome was defined as the presence of 3 or more of the following risk factors: elevated blood pressure, low high-density lipoprotein cholesterol level, high triglyceride level, elevated glucose level, and abdominal obesity. Chronic kidney disease was defined as a glomerular filtration rate less than 60 mL/min per 1.73 m2, and microalbuminuria was defined as a urinary albumin–creatinine ratio of 30 to 300 mg/g. Results: The multivariate-adjusted odds ratios of chronic kidney disease and microalbuminuria in participants with the metabolic syndrome compared with participants without the metabolic syndrome were 2.60 (95% CI, 1.68 to 4.03) and 1.89 (CI, 1.34 to 2.67), respectively. Compared with participants with 0 or 1 component of the metabolic syndrome, participants with 2, 3, 4, and 5 components of chronic kidney disease had multivariate-adjusted odds ratios of 2.21 (CI, 1.16 to 4.24), 3.38 (CI, 1.48 to 7.69), 4.23 (CI, 2.06 to 8.63), and 5.85 (CI, 3.11 to 11.0), respectively. The corresponding multivariate-adjusted odds ratios of microalbuminuria for participants with 3, 4, and 5 components were 1.62 (CI, 1.10 to 2.38), 2.45 (CI, 1.55 to 3.85), and 3.19 (CI, 1.96 to 5.19), respectively. Conclusions: These findings suggest that the metabolic syndrome might be an important factor in the cause of chronic kidney disease.