tbuckley/cabot-search huggingface dataset:
The global burden of periodontal disease: towards integration with chronic disease prevention and control
Authors: Poul E. Petersen, Hiroshi Ogawa
Journal: Periodontology 2000 (2012)

Abstract Chronic diseases are accelerating globally, advancing across all regions and pervading all socioeconomic classes. Unhealthy diet and poor nutrition, physical inactivity, tobacco use, excessive use of alcohol and psychosocial stress are the most important risk factors. Periodontal disease is a component of the global burden of chronic disease, and chronic disease and periodontal disease have the same essential risk factors. In addition, severe periodontal disease is related to poor oral hygiene and to poor general health (e.g. the presence of diabetes mellitus and other systemic diseases). The present report highlights the global burden of periodontal disease: the ultimate burden of periodontal disease (tooth loss), as well as signs of periodontal disease, are described from World Health Organization (WHO) epidemiological data. High prevalence rates of complete tooth loss are found in upper middle‐income countries, whereas the tooth‐loss rates, at the time of writing, are modest for low‐income countries. In high‐income countries somewhat lower rates for edentulism are found when compared with upper middle‐income countries. Around the world, social inequality in tooth loss is profound within countries. The Community Periodontal Index was introduced by the WHO in 1987 for countries to produce periodontal health profiles and to assist countries in the planning and evaluation of intervention programs. Globally, gingival bleeding is the most prevalent sign of disease, whereas the presence of deep periodontal pockets (≥6 mm) varies from 10% to 15% in adult populations. Intercountry and intracountry variations are found in the prevalence of periodontal disease, and these variations relate to socio‐environmental conditions, behavioral risk factors, general health status of people (e.g. diabetes and HIV status) and oral health systems. National public health initiatives for the control and prevention of periodontal disease should include oral health promotion and integrated disease‐prevention strategies based on common risk‐factor approaches. Capacity building of oral health systems must consider the establishment of a financially fair service in periodontal care. Health systems research is needed for the evaluation of population‐oriented oral health programs.
Combined Effects of 3-Methylcholanthrene, Mammary Tumor Virus, Nodule-Inducing Virus, and Prolonged Hormonal Stimulation on the Tumor-Producing Capabilities of the Nodule Outgrowth Line D1&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: Daniel Medina, L. J. Faulkin, K. B. DeOme
Journal: JNCI Journal of the National Cancer Institute (1970)

The scheme for mouse mammary tumorigenesis has been extended to include 3-mefhylcholanthrene (MCA) as an effective tumorigenic agent. Methylcholanthrene is a very poor noduligenic agent in intact virgin BALB/c mice, and the hyperplastic alveolar nodules induced have low tumor-producing capabilities. However, D1 mammary-nodule outgrowths responded to MCA with a relatively high rate of tumor production (50%). Prolonged hormone stimulation by pituitary isografts increased the tumor incidence in MCA-treated D1 nodule outgrowths in a similar fashion, as was shown previously for mammary tumor virus (MTV)-positive and nodule-inducing virus (NIV)-positive D1 nodule outgrowths exposed to prolonged hormone stimulation. When MCA was given to MTV-positive mice bearing D1 nodule outgrowths, the effect appeared to be additive, rather than synergistic. There was no evidence that MCA acted hormonally in the neoplastic transformation. Rather, the results suggested that MCA acted on the D1 nodule cell population to increase the production of tumors from this population, whereas hormone stimulation acted synergistically with MTV and NIV to increase tumor formation from D1 nodule outgrowths.
T cells in peripheral blood during viral acute exacerbation of COPD
Authors: María Inés Vargas-Rojas, Alejandra Ramírez-Venegas, Leonardo Limón-Camacho, Oliver Pérez-Bautista, Helena Solleiro-Villavicencio, Raúl H. Sansores
Journal: European Respiratory Journal (2012)

Introduction: Exacerbations in COPD patients increase premature mortality.The main cause of AECOPD are viral infections however, the type of predominant cellular immune response is unknown.  Objective: To quantify the T cell subpopulations in peripheral blood of patients with viral AECOPD and compare them with patients in a stable disease (COPD) and healthy controls (HC).  Methods: We included 82 patients from the Cohort of COPD Clinic, between May 2009 and December 2011, 49 of them were exacerbated and we included 19 HC. Viral diagnosis was performed by using real-time PCR and we used flow cytometry to determine T-cell subpopulations. Differences between groups were evaluated by Kruskal-Wallis and we performed a post-hoc U-Mann-Whitney test.  Results: 26 patients (53%) had a viral exacerbation (Influenza A 54%, Coronavirus 14%, Influenza B 7%, RSV 7%, H1N1 7%, MPV 4%). In these patients predominated the Th1 response 8.6(6.2-11) versus COPD 2.5(1.3-4.29) and HC 1.1(0.8-1.4) p  Conclusions: Our data show a polarization Th1, Tc1, Tc2 and Tc17 in AECOPD patients suggesting the involvement of these populations in the cellular immune response during viral infections. We did not find a higher prevalence of H1N1 infections in patients in the cohort.
Infectivity of Cell Cultures by a Virus Isolated From a Mammary Carcinoma of a Rhesus Monkey&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: Harish C. Chopra, Inna Zelljadt, Erling M. Jensen, Marcus M. Mason, Norman J. Woodside
Journal: JNCI Journal of the National Cancer Institute (1971)

Infectivity studies of various cell lines of primate origin, inoculated with virus isolated from the monkey mammary carcinoma, were conducted by electron microscopy. The cell cultures did not show any cytopathic effect and the infectivity was demonstrated by the presence of virus particles in the infected cells. The cell cultures of rhesus monkey embryo, rhesus monkey lung, and chimpanzee lung were found to be infected. Most significantly, human embryonic cell cultures and an established human leukocyte (NC-37) culture were infected with cell-free virus. The latter is chronically infected and continues to produce new virus particles. The development of virus in these cultures was similar to that observed in the original monkey mammary tumor cells. Electron microscopy of infected cells revealed the presence of intracytoplasmic A-type and budding extracellular forms, resembling oncogenic RNA viruses.
HLA-DPB1 and chronic sarcoidosis
Authors: Annika Wennerström, Anne Pietinalho, Jagoda Lasota, Krista Salli, Marja-Liisa Lokki, Olof Selroos
Journal: European Respiratory Journal (2012)

Background: Beryllium disease and sarcoidosis have clinical similarities. Beryllium exposure together with the HLA-DPB1 alleles containing a glutamic acid at amino acid position 69 (Glu69) is associated with beryllium sensitization and chronic beryllium disease (CBD).

Aim: To determinate whether the same genetic variations of HLA-DPB1 that are found in CBD are associated with chronic sarcoidosis.

Methods: HLA-DPB1 was determined in 98 Finnish patients with chronic sarcoidosis not resolved within 2 years and in 150 control subjects. The DPB1 alleles were genotyped with sequence specific primers (Olerup SSP™) and haplotypes were formed with MHC class II and class III markers.

Results: 17 different DPB1 alleles were observed. The DPB1*04:02 allele was less frequent among the patients (10.2% vs.20.3%; p=0.003, OR=0.45) than controls. A haplotype with DPB1*04:01, one C4A gene and one C4B gene was increased among sarcoidosis patients (30.9% vs. 22.5%; p=0.036, OR=1.5). By studying polymorphic amino acid residues of DPB1, we did not detect an association of Glu69, but a DPB1*04:02 specific amino acid variant was detected at the position 178 (Met) suggesting a protective role for chronic sarcoidosis (p=0.004, OR=0.42). Furthermore, preliminary SNP analyses of HLA class II and III region showed that the SNP associations are independent from DPB1.

Conclusion: We confirm and further describe the contributory role of DPB1 with the risk associated for chronic sarcoidosis. Preliminary results suggest that both DRB1 and certain independent markers in the HLA class II and III region increase the risk for chronic sarcoidosis. However, HLA association analyses are complicated by the extensive linkage disequilibrium (LD) across the HLA region.
Risk of Menopause During the First Year After Breast Cancer Diagnosis
Authors: Pamela J. Goodwin, Marguerite Ennis, Kathleen I. Pritchard, Maureen Trudeau, Nicky Hood
Journal: Journal of Clinical Oncology (1999)

Premenopausal women with breast cancer often enter a premature menopause during initial treatment of their malignancy, with resulting loss of childbearing capacity, onset of menopausal symptoms, and subsequent prolonged exposure to long-term risks of menopause. Adjuvant therapy is believed to contribute to this early menopause.One hundred eighty-three premenopausal women with locoregional breast cancer (tumor-node-metastasis staging system classification, T1-3 N0-1 M0) who had undergone surgical treatment and provided information on menopausal status at diagnosis and 1 year later were enrolled. Systemic adjuvant therapy was recorded. Univariate and multivariate predictors of menopause were examined.Age, weight gain, tumor stage, nodal stage, and systemic adjuvant therapy (chemotherapy, tamoxifen) were all significant univariate correlates of menopause. In multivariate analysis, age, chemotherapy, and hormone therapy (tamoxifen) made significant independent contributions to the onset of menopause.Age and systemic chemotherapy are the strongest predictors of menopause in women with locoregional breast cancer. They independently contribute to menopause. A graphic representation of our multivariate model allows an estimation of risk of menopause according to patient age and planned adjuvant treatment, and it may facilitate clinical decision-making.
Spontaneous Alterations in the Pancreas of the Aging Syrian Golden Hamster2
Authors: Michichito Takahashi, Parviz Pour
Journal: JNCI Journal of the National Cancer Institute (1978)

The systematic histologic examination of the pancreas of aging Syrian golden hamsters revealed distinct alterations that affected the exocrine, endocrine, and supporting tissues. Some of these lesions showed a significant relationship to age and/or sex of the animal. Specific alterations that affected the ductules and islets represented a characteristic, probably genetically linked, process of the hamster pancreas and may have been the decisive factors for the unique carcinogenic response of this species to specific carcinogens.
A sterol mesylate activator of CEBPα signaling induces monocytic differentiation in human leukemia cells in vitro and in vivo
Authors: Erik D. Harris, Constance J. Glover, Joseph W. Adelsberger, Melinda G. Hollingshead, Ronald L. Felsted, Robert H. Shoemaker, Anne Monks
Journal: Cancer Research (2006)

4619  A novel sterol mesylate (NSC 67657) was previously identified as a potent activator of CEBPα signaling in an HTS assay, and it was also demonstrated that this compound could induce myeloid differentiation in U937 and HL60 human leukemia cell lines. The present study compared transcription profiles (generated from 20,000K oligonucleotide arrays) of HL60 cells, treated with NSC 67657 (20μM) and all-trans retinoic acid (ATRA, 5μM), which suggested these two agents produced differentiated cells along different lineages. While ATRA induced gene expression changes related to granulocytic differentiation, NSC 67657 triggered monocytic differentiation as evidenced by prominent induction of CD14 and other related genes. Additional data supporting NSC 67657 induction of monocyte/macrophage differentiation was generated using flow cytometry and the NBT test in HL60 and NB4 (acute promyelocytic leukemia) cells. Both cells lines were induced to differentiate (>99% of the cells) following 2μM ATRA treatment for 5-7 days measured by reduction of nitroblue tetrazolium to its insoluble formazan (NBT assay), and >90% of the cells expressed CD18 and CD35, but not CD14. In contrast only HL60 cells were induced to differentiate (NBT assay) following NSC67675 treatment and 95% of the cells were positive for expression of CD14. However, NB4 cells (which only terminally differentiate into monocytes/macrophages in the presence of phorbol esters), showed no indication of differentiating either by the NBT assay or markers of differentiation following treatment with NSC 67657. When HL60 cells were implanted intraperitoneally into athymic mice, and treated orally beginning on day 3, with 200mg/kg NSC 67657 bid qd x 5, and ascites cells extracted on day 7, these cells were found to express elevated levels of the CD14 mRNA (>20fold), or antigen as measured by flow cytometry. Thus the sterol mesylate agent, NSC 67657, which activates CEBPα signaling, has been shown to primarily initiate monocytes/macrophage differentiation as opposed to granulocytic differentiation in HL60 cells, both in vitro and in vivo. These results indicate that NSC 67657 is a novel differentiating agent that warrants further preclinical evaluation as a potential anti-leukemic drug. Supported by NCI contract # NO1-CO-12400.
Pepsinogen C is a new prognostic marker in primary breast cancer.
Authors: F Vizoso, L M Sánchez, I Díez-Itza, A M Merino, C López-Otín
Journal: Journal of Clinical Oncology (1995)

PURPOSE Here we evaluate in breast cancer patients the prognostic value of pepsinogen C, a proteolytic enzyme involved in the digestion of proteins in the stomach that is also synthesized by a significant percentage of breast carcinomas. PATIENTS AND METHODS Pepsinogen C expression was examined by immunoperoxidase staining in a series of 243 breast cancer tissue sections, and results obtained were quantified using the HSCORE system, which considers both the intensity and the percentage of cells staining at each intensity. Evaluation of the prognostic value of pepsinogen C was performed retrospectively in corresponding patients by multivariate analysis that took into account conventional prognostic factors. The mean follow-up period was 48.5 months. RESULTS A total of 113 carcinomas (46.5%) stained positively for this proteinase, but there were clear differences among them with regard to the intensity and percentage of stained cells. Pepsinogen C values were significantly higher in well differentiated (grade I, 89.1) and moderately differentiated (grade II, 88.5) tumors than in poorly differentiated (grade III, 27.7) tumors (P &lt; .001). Similarly, significant differences in pepsinogen C content were found between estrogen receptor (ER)-positive tumors and ER-negative tumors (85.9 v 41.2, respectively; P &lt; .05). Moreover, results indicated that low pepsinogen C content predicted shorter relapse-free survival duration and overall survival duration (P &lt; .0001). Separate Cox multivariate analysis for relapse-free survival and overall survival in subgroups of patients as defined by node status showed that pepsinogen C expression was the strongest factor to predict both relapse-free survival and overall survival in node-positive patients (P &lt; .0001 for both) and node-negative patients (P &lt; .005 and P &lt; .01, respectively). CONCLUSION Pepsinogen C is a new prognostic factor for early recurrence and death in both node-positive and node-negative breast cancer. In addition, and in contrast to most studies that concern the prognostic significance of proteolytic enzymes in cancer, pepsinogen C production by breast cancer cells is associated with lesions of favorable evolution.
Escherichia coli bacteraemia in pregnant women is life-threatening for foetuses
Authors: Laure Surgers, A Bleibtreu, C Burdet, O. Clermont, C Laouénan, A. Lefort, F Mentré, B Carbonne, E Bingen, J-L. Meynard, E. Denamur, Laurent Mereghetti, Roland Quentin, . Colibafi Group
Journal: Clinical Microbiology and Infection (2014)
Long non-coding RNA ROR decoys gene-specific histone methylation to promote tumorigenesis
Authors: Jiayan Fan, Yue Xing, Xuyang Wen, Renbin Jia, Hongyan Ni, Jie He, Xia Ding, Hui Pan, Guanxiang Qian, Shengfang Ge, Andrew R. Hoffman, He Zhang, Xianqun Fan
Journal: Genome biology (2015)

Abstract Background Long non-coding RNAs (lncRNAs) are not translated into proteins and were initially considered to be part of the ‘dark matter’ of the genome. Recently, it has been shown that lncRNAs play a role in the recruitment of chromatin modifying complexes and can influence gene expression. However, it is unknown if lncRNAs function in a similar way in cancer. Results Here, we show that the lncRNA ROR occupies and activates the TESC promoter by repelling the histone G9A methyltransferase and promoting the release of histone H3K9 methylation. Suppression of ROR in tumors results in silencing of TESC expression, and G9A-mediated histone H3K9 methylation in the TESC promoter is restored, which significantly reduces tumor growth and metastasis. Without ROR silencing, TESC knockdown presents consistent and significant reductions in tumor progression. Conclusions Our results reveal a novel mechanism by which ROR may serve as a decoy oncoRNA that blocks binding surfaces, preventing the recruitment of histone modifying enzymes, thereby specifying a new pattern of histone modifications that promote tumorigenesis.
Gastric Cancer: A Primer on the Epidemiology and Biology of the Disease and an Overview of the Medical Management of Advanced Disease
Authors: Manish A. Shah, David P. Kelsen
Journal: Journal of the National Comprehensive Cancer Network (2010)

Gastric cancer is a cause of significant morbidity and cancer-related mortality worldwide. Despite recent advances in targeted therapy and understanding of the biology and development of the malignancy, progress in the treatment of gastric cancer has been limited. Most newly diagnosed patients will present with incurable disease, and have a median survival of less than 1 year. Although the disease has widespread ethnic and epidemiologic differences, medical management of gastric cancer does not distinguish among the various disease subtypes. The recent report of the ToGA phase III study has validated Her2 as a molecular target in this disease, supporting the concept that a greater understanding of the biology of gastric cancer subsets may improve treatment selection and overall outcome of individual patients. This article summarizes the epidemiology and ethnic variation of this disease to crystalize subtypes of gastric cancer in the context of current and future medical management of advanced disease.
Preoperative Chemotherapy in Non–Small-Cell Lung Cancer: Nothing New in N2 Disease
Authors: Tommaso De Pas, Ugo Pastorino, Lorenzo Spaggiari, Giuseppe Curigliano, Filippo de Braud, Chris Robertson
Journal: Journal of Clinical Oncology (2002)

Article Tools SPECIAL DEPARTMENTS Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.2002.20.10.2603 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 12011140 Preoperative Chemotherapy in Non–Small-Cell Lung Cancer: Nothing New in N2 Disease Tommaso De PasxTommaso De PasSearch for articles by this author , Ugo PastorinoxUgo PastorinoSearch for articles by this author , Lorenzo SpaggiarixLorenzo SpaggiariSearch for articles by this author , Giuseppe CuriglianoxGiuseppe CuriglianoSearch for articles by this author , Filippo de BraudxFilippo de BraudSearch for articles by this author , Chris RobertsonxChris RobertsonSearch for articles by this author Show More European Institute of Oncology, Milan, ItalyUniversity of Strathclyde and Scottish Centre for Infection and Environmental Health, Glasgow, Scotland https://doi.org/10.1200/JCO.2002.20.10.2603 First Page Full Text PDF Figures and Tables © 2002 by American Society of Clinical Oncology
Pandemic influenza in a southern hemisphere setting: the experience in Peru from May to September, 2009
Authors: J Gómez, C V Munayco, J C Arrasco, L Suarez, V A Laguna-Torres, P V Aguilar, G Chowell, T J Kochel
Journal: Eurosurveillance (2009)

This paper presents a description of Peru’s experience with pandemic H1N1 influenza 2009. It is based on data from four main surveillance systems: a) ongoing sentinel surveillance of influenza-like illness cases with virological surveillance of influenza and other respiratory viruses; b) sentinel surveillance of severe acute respiratory infections and associated deaths; c) surveillance of acute respiratory infections in children under the age of five years and pneumonia in all age groups; and d) case and cluster surveillance. On 9 May 2009, the first confirmed case of pandemic H1N1 influenza in Peru was diagnosed in a Peruvian citizen returning from New York with a respiratory illness. By July, community transmission of influenza had been identified and until 27 September 2009, a total of 8,381 cases were confirmed. The incidence rate per 10,000 persons was 4.4 (in the 0–9 year-olds) and 4.1 (in the 10–19 year-olds). During epidemiological weeks (EW) 26 to 37, a total of 143 fatal cases were notified (a case fatality of 1.71%, based on confirmed cases). The maximum peak in the number of cases was reached in EW 30 with 37 deaths. Currently, the impact of the pandemic in the Peruvian population has not been too severe, and fortunately, healthcare centres have not been overwhelmed. However, the future of this pandemic is uncertain and despite the fact that our country has not been seriously affected, we should be prepared for upcoming pandemic waves.
Recombinant interferon alfa given before and in combination with standard chemotherapy in children with acute lymphoblastic leukemia in first marrow relapse: a Pediatric Oncology Group pilot study.
Authors: J Ochs, M L Brecher, D Mahoney, R Vega, B H Pollock, G R Buchanan, V M Whitehead, Y Ravindranath, A I Freeman
Journal: Journal of Clinical Oncology (1991)

Recombinant interferon alfa (rIFN-alpha) was given to 31 children with acute lymphoblastic leukemia (ALL) in first on-therapy marrow relapse as the sole treatment (30 megaunits/m2/d intravenously x 10 days) before standard four-drug reinduction and during multiagent continuation therapy (30 megaunits/m2 subcutaneously x 3 consecutive days every 3 weeks). After 10 days of rIFN-alpha, there were two partial remissions (PRs); seven additional patients had either greater than or equal to 25% reduction in the percentage of marrow blast cells or hypoplastic marrow. Two patients had progressive disease with an increase in leukocyte counts. All patients experienced influenza-like symptoms, and there were isolated instances of severe abdominal pain and personality change. Dose-limiting toxicity comprised grade III/IV transaminase elevation (two patients) and syncope with personality change (one patient). Twenty-three of 31 children (74%) subsequently achieved marrow remission using standard agents. One patient was taken off study during teniposide (VM-26) and cytarabine (ara-C) consolidation due to toxicity. Continuation therapy including rIFN-alpha pulse was well tolerated in the remaining children; only one patient required rIFN-alpha dosage reduction (for CNS toxicity). rIFN-alpha toxicity did not necessitate reductions in doses of standard chemotherapy agents or significant delays in therapy. Five patients remain in remission at 26+ to 36+ months; 13 patients relapsed in marrow, one in the meninges (7 months), and one in meninges, mediastinum, and lymph nodes (2 months). Two children were removed from study for marrow transplant. In summary, high-dose rIFN-alpha alone had a modest antileukemic effect. In contrast to the clinical experience with combined rIFN-alpha and chemotherapy in adults, rIFN-alpha given in a pulse-like manner throughout continuation therapy did not compromise the intensity of the standard chemotherapy regimen.