tbuckley/cabot-search huggingface dataset:
Chlamydia trachomatis and Cervical Squamous Cell Carcinoma
Authors: Jennifer S. Smith, Nubia Muñoz, Silvia Franceschi, José Eluf-Neto, Rolando Herrero, Rosanna W. Peeling
Journal: JAMA (2001)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Regulation of mitosis by P190RhoGAP and ECT2 RhoGEF through Rho-dependent pathways
Authors: Masahito Mikawa, Ling Su, Sarah J. Parsons
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

4904 

P190RhoGAP (P190) is a Rho GTPase activator protein (GAP) that has been shown to regulate actin cytoskeletal dynamics via Rho-dependent signaling pathways. This P190 gene localizes to chromosome 19q13.3, which is often rearranged in glioma, pancreatic, ovarian, and thyroid cancers, suggesting that it plays a role in the genesis of these diseases. In support of this hypothesis, P190 reduces the incidence of PDGF induced-glioma in a mouse model and suppresses v-Ha-Ras induced transformation in NIH3T3 cells. The tumor suppressive effect of P190 is mediated by its GAP activity through negative regulation of Rho. By enhancing the Rho-mediated hydrolysis of RhoGTP to RhoGDP, P190 prevents association of RhoGTP with its downstream effectors. However, which cellular process(es) are affected by P190 has not been fully elucidated. Recently, P190 was shown to localize to the cleavage furrow and contractile ring during cytokinesis. Overexpression of P190 induces multinucleation in breast cancer cells, suggesting that it regulates events in late mitosis. The GAP domain of P190 is required for this abnormal phenotype, indicating that downregulation of Rho activity by P190 leads to multinucleation. In addition, downregulation of Rho and inhibition of its downstream effector, ROCK, are known to induce multinucleated cells. In this study, multinucleation induced by overexpressed P190 could be prevented or rescued by ECT2 RhoGEF (ECT2), a guanine nucleotide exchange factor (GEF) that facilitates conversion of RhoGDP to RhoGTP. Endogenous P190 and ECT2 colocalized at the cleavage furrow during cytokinesis, indicating that each had the ability to associate with and regulate Rho at that site. Cotransfection of wild type ECT2 and P190 resulted in reduced numbers of multinucleated cells as compared to P190-only transfected cells, while cotransfection of constitutively active ECT2 and P190 reduced the number of multinucleated cells to basal levels. Furthermore, a dominant negative ECT2 generated multinucleation. These results indicate that antagonistic regulation of Rho by RhoGEF and RhoGAP during mitosis leads to proper completion of cytokinesis, but deregulation of either can result in improper distribution of genomic DNA to daughter cells and contribute to tumorgenesis.
Langerhans cell histiocytosis first presenting in the skin in adults: frequent association with a second haematological malignancy
Authors: J.R. Edelbroek, M.H. Vermeer, P.M. Jansen, T.J. Stoof, M.M.D. van der Linden, B. Horváth, J. van Baarlen, R. Willemze
Journal: British Journal of Dermatology (2012)

Background Langerhans cell histiocytosis (LCH) in adults first presenting in the skin is rare. Guidelines for staging, treatment and follow-up are lacking. Objectives To better define staging procedures, treatment results and clinical course in adult patients with LCH first presenting in the skin. Methods Eighteen adult patients with LCH first presenting in the skin were collected from five centres collaborating in the Dutch Cutaneous Lymphoma Group. Clinical records and (skin) biopsy specimens were reviewed and follow-up data were obtained. A literature search on adult patients with LCH presenting in the skin was performed. Results Staging procedures showed extracutaneous disease in three of 16 patients who were adequately staged. One patient had a histologically confirmed lytic LCH bone lesion, while two patients had a myelodysplastic syndrome. During follow-up two of 18 patients developed extracutaneous localizations of LCH. Five patients developed a second haematological malignancy, including (myelo)monocytic leukaemia (two cases), histiocytic sarcoma (one case), diffuse large B-cell lymphoma (one case) and peripheral T-cell lymphoma (one case). Review of the literature revealed six other adult patients with a second haematological malignancy preceding or following a diagnosis of LCH. Conclusions The results of the present study suggest an increased risk of a second haematological malignancy in adult patients with LCH presenting in the skin. Extensive staging at presentation and long-term follow-up are therefore warranted in such patients.
Abstract 11292: Impact of Chronic Obstructive Pulmonary Disease on Cardiovascular Function and Prognosis in Heart Failure Patients
Authors: Takeshi Shimizu, Akiomi Yoshihisa, Mai Takiguchi, Minoru Nodera, Shunsuke Miura, Yuichi Nakamura, Hiroyuki Yamauchi, Takashi Owada, Satoshi Abe, Satoshi Suzuki, Masayoshi Oikawa, Atsushi Kobayashi, Takayoshi Yamaki, Koichi Sugimoto, Hiroyuki Kunii, Kazuhiko Nakazato, Hitoshi Suzuki, Shu-ichi Saitoh, Yasuchika Takeishi
Journal: Circulation (2014)

Background: Chronic obstructive pulmonary disease (COPD) often coexists with heart failure (HF), and is thought to have a critical association with mortality and morbidity in HF patients. However, the impact of COPD on cardiovascular function and the detailed all-cause mortality of HF remain unclear. Methods and Results: Consecutive 378 patients admitted for HF who underwent spirometry were divided into 3 groups: HF without COPD (Non-COPD group, n = 272), HF with mild COPD (GOLD I group, n = 82), and HF with moderate COPD (GOLD II group, n = 24). We compared echocardiographic findings, vascular function including flow mediated dilatation (FMD) and cardio-ankle vascular index and circulating levels of troponin T, BNP, CRP, and estimated GFR among the three groups. The GOLD II group, as compared to Non-COPD group, had 1) higher troponin T (0.030 vs. 0.020 ng/ml, P = 0.009), 2) greater cardio-ankle vascular index (8.99 vs. 8.29, P = 0.032), 3) similar levels of FMD, BNP, CRP, and estimated GFR, and 4) similar cardiac systolic and diastolic function of the right and left ventricle. In addition, rates of cardiac (P = 0.049), non-cardiac (P = 0.001), and all-cause mortality (P = 0.002) were higher in GOLD II group than in Non-COPD and GOLD I groups. Importantly, in the Cox proportional hazard analyses, the GOLD stage II was an independent predictor of cardiac (P = 0.038), non-cardiac (P = 0.036), and all-cause mortality (P = 0.015) in HF patients. Conclusions: HF patients with coexistent moderate COPD (GOLD stage II) have greater myocardial damage, greater arterial stiffness, and higher cardiac and non-cardiac mortality. Thus, taking appropriate management to control COPD may improve the prognosis of HF patients with COPD.
Celebrating the ACP Centennial: From the <i>Annals</i> Archive—Smoking Cessation
Authors: Deborah Cotton
Journal: Annals of Internal Medicine (2015)

Editorials7 July 2015Celebrating the ACP Centennial: From the Annals Archive—Smoking CessationDeborah Cotton, MD, MPH, Deputy EditorDeborah Cotton, MD, MPH, Deputy EditorSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/M15-1145 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail During the 2015 centennial year of the American College of Physicians, publisher of Annals of Internal Medicine, Annals editors will link an article in each issue with an earlier paper from our archives addressing the same disease or clinical question. We hope our readers find this interesting and we welcome comments, especially from physicians who were practicing at the time of publication of the original paper who might offer insight into the impact of the earlier paper on their knowledge or practice.In this issue, Bartter (1) and Drummond (2) debate the pros and cons of electronic cigarettes.Nearly 30 ...References1. Bartter T. Electronic cigarettes: aggregate harm. Ann Intern Med. 2015;163:59-60. doi:10.7326/M15-0450 LinkGoogle Scholar2. Drummond MB. Electronic cigarettes: perhaps the devil unknown is better than the devil known. Ann Intern Med. 2015;163:61-2. doi:10.7326/M15-0361 LinkGoogle Scholar3. Health and Public Policy Committee, American College of Physicians. Methods for stopping cigarette smoking. Ann Intern Med. 1986;105:281-91. [PMID: 3729208] doi:10.7326/0003-4819-105-2-281 LinkGoogle Scholar Author, Article, and Disclosure InformationAuthors: Deborah Cotton, MD, MPH, Deputy Editor PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoMethods for Stopping Cigarette SmokingElectronic Cigarettes: Aggregate Harm Thaddeus Bartter Electronic Cigarettes: Perhaps the Devil Unknown Is Better Than the Devil Known M. Bradley Drummond Electronic Cigarettes: Aggregate Harm Thaddeus Bartter Electronic Cigarettes: Perhaps the Devil Unknown Is Better Than the Devil Known M. Bradley Drummond Metrics 7 July 2015Volume 163, Issue 1Page: 63KeywordsArchivesBehaviorDrug therapyElectroconvulsive therapyElectronic cigarettesFood and Drug AdministrationNicotinePrevention, policy, and public healthPublic policySmoking cessation ePublished: 7 July 2015 Issue Published: 7 July 2015 Copyright & PermissionsCopyright © 2015 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Intestinal epithelial cells express galectin-9 in patients with food allergy that plays a critical role in sustaining allergic status in mouse intestine
Authors: X. Chen, C.-H. Song, Z.-Q. Liu, B.-S. Feng, P.-Y. Zheng, P. Li, S. H. In, S.-G. Tang, P.-C. Yang
Journal: Allergy (2011)

To cite this article: Chen X, Song C-H, Liu Z-Q, Feng B-S, Zheng P-Y, Li P, In SH, Tang S-G, Yang P-C. Intestinal epithelial cells express galectin-9 in patients with food allergy that plays a critical role in sustaining allergic status in mouse intestine. Allergy 2011; 66: 1038–1046. Background and aims: Mechanisms in sustaining the allergic hypersensitivity status in the body are unclear. Galectin-9 (Gal-9) has strong immune regulatory capacity. The present study aims to elucidate the role of Gal-9 in sustaining allergic status in the intestine. Methods: Duodenal biopsies were obtained from 20 patients with peptic ulcer and food allergy (FA). The expression of Gal-9 in intestinal tissue was examined at both protein level and mRNA level. Two coculture systems with intestinal epithelial cells (IEC) and mast cells, or dendritic cells (DC) and T cells were established to investigate the source of Gal-9 in the intestine and the mechanism by which Gal-9 modulated DC's phenotyping and sustained the T helper 2 polarization. Results: Normal IEC showed mild expression of Gal-9 that was markedly enhanced in patients with FA. Mast cells had the capability to induce IEC to produce Gal-9 via releasing tryptase that activated the proteinase-activated receptor 2 on IEC. Gal-9 activated DC to produce TIM4 (T-cell immunoglobulin mucin domain) via ligating TIM3 on DC via activating the cyclic guanosine monophosphate (cGMP) pathway. In a mouse FA model, blocking Gal-9 inhibited the allergic hypersensitivity status and the antigen-specific Th2 response in the intestine. Conclusions: IEC-derived Gal-9 contributes to sustaining the allergic status in the intestine.
Portrait of the Artist
Authors: M Therese Southgate
Journal: JAMA (2006)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Abstract 276: Appalachian mountaintop mining particulate matter induces malignant transformation and tumorigenesis of human lung epithelial cells
Authors: Sudjit Luanpitpong, Juhua Luo, Travis Kneuckles, Michael Hendryx, Yon Rojanasakul
Journal: Cancer Research (2014)

Abstract Lung cancer is the leading cause of cancer death, and after smoking, environmental and occupational exposure is the major cause. West Virginia (WV), the biggest coal mining state in Appalachia, ranks the third highest rate of lung cancer incidence in the United States. Our epidemiological studies suggest that living near WV mountaintop coal mining (MTM) activities is a contributing factor of the high lung cancer risk. The purpose of this study was to investigate the effect of MTM particle exposure on cell transformation and tumorigenesis of human lung epithelial cells. Air particulate matter (PM) collected within one mile of active MTM site in Edwight, WV (PMMTM), consisting of silica (Si, 48%) and molybdenum (Mo, 29%) as major constituents, was used for cell exposure studies. As control, PM collected from the neighboring areas that do not have coal mining in Green Bank, WV (PMCON) was used. Chronic exposure (3 months) of non-tumorigenic human lung epithelial BEAS-2B cells to sub-cytotoxic concentration (1 μg/mL) of PMMTM, but not PMCON, was found to induce malignant transformation of the cells, as indicated by loss of contact inhibition and anchorage-independent cell growth. The PMMTM-transformed cells also induced tumor formation in vivo using a xenograft mouse model. Exposure to Mo (1 μg/mL), but not Si, similarly induced malignant transformation and tumorigenesis of the lung epithelial cells, suggesting that Mo may be a key contributing factor of PMMTM pathologic effects. Citation Format: Sudjit Luanpitpong, Juhua Luo, Travis Kneuckles, Michael Hendryx, Yon Rojanasakul. Appalachian mountaintop mining particulate matter induces malignant transformation and tumorigenesis of human lung 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 276. doi:10.1158/1538-7445.AM2014-276
Quantifying the variability of physical activity in daily life caused by seasonality in smokers
Authors: Karina Couto Furlanetto, Jully Anne Felici, Gianna Kelren Waldrish Bisca, Andrea Akemi Morita, Mahara Proença, Juliana Zabatiero, Leandro Cruz Mantoani, Demetria Kovelis, Fabio Pitta
Journal: European Respiratory Journal (2012)

Background:  The level of physical activity in daily life (PADL) depends on many factors, such as social, economical, physiological and demographic aspects. Despite these many causes of variability, the influence of the seasons of the year on PADL is unknown in smokers.  Aims:  To compare changes in the level of PADL in apparently healthy smokers who started in different climatic conditions a protocol aiming at improving PADL; and to quantify the proportion of subjects who achieved 8000 steps/day before and after the intervention.  Methods:  20 smokers with normal lung function were submitted to a 5-month protocol using booklets and pedometers (or step counters) in order to improve PADL by aiming to increase the number of steps/day. They had their baseline PADL assessed for 6 days with a pedometer during Spring/Summer (SS: n=10, 5 men, 51[39-59] years, BMI 26[23-29] Kg/m 2 , 36[14-49] pack-years) or Autumn/Winter (AW: n=10, 5 men, 53[48-57] years, BMI 26[24-28] Kg/m 2 , 38[17-50] pack-years). Reassessment was performed after the protocol, in the opposite climatic condition as compared to baseline.  Results:  Both groups improved their PADL after the protocol (Δ steps/day = SS: 3191[1888-4461] and AW: 2903[517-5377]; p=0.002 for both). There were no between-groups statistical differences concerning baseline PADL, changes after the protocol, and proportion of subjects who reach 8000 steps/day before and after the protocol (SS: from 40% to 80%; AW: from 30% to 70%).  Conclusions:  These preliminary results showed that climatic variation does not incur in significant impact in the level of PADL in apparently healthy smokers, since the same benefits could be achieved regardless of the seasonality.
Detection of Kaposi’s Sarcoma Herpesvirus DNA Sequences in Multiple Myeloma Bone Marrow Stromal Cells
Authors: Dharminder Chauhan, Ajit Bharti, Noopur Raje, Eric Gustafson, Geraldine S. Pinkus, Jack L. Pinkus, Gerrard Teoh, Teru Hideshima, Steve P. Treon, Joyce D. Fingeroth, Kenneth C. Anderson
Journal: Blood (1999)
Comparison of cardiovascular safety in a pooled analysis of COPD trials comparing tiotropium with salmeterol
Authors: Claus Vogelmeier, Leonardo Fabbri, Thomas Glaab, Diego Wyszynski, Inge Leimer, Norbert Metzdorf, Kai-Michael Beeh, Klaus Rabe
Journal: European Respiratory Journal (2013)

Background: Guidelines recommend long-acting bronchodilators as preferred options for maintenance treatment of COPD. Cardiovascular (CV) safety of these treatments is of interest.

Aims and objectives: To compare the CV safety of tiotropium vs the long-acting β2-agonist salmeterol in a large number of patients (pts) with COPD.

Methods: Pooled analysis of 4 double-blind, randomized, parallel-group clinical trials comparing the CV adverse event profile of tiotropium HandiHaler® (HH) vs salmeterol metered dose inhaler (MDI). Incidence rates (IR): number of pts with event divided by pt-years at risk. Rate ratios (RR) and 95%CI: derived from Cochran-Mantel-Haenszel test stratified by study.

Results: In total, 8836 pts were included; 25.3% had a cardiac disorder and 53.7% used CV medication at baseline. IRs (per 100 pt-yrs) for tiotropium vs salmeterol were: all-cause mortality, 1.74 vs 2.08 (RR: 0.84, 95% CI: 0.61, 1.16); fatal major adverse cardiac events (MACE), including death unknown, 0.72 vs 0.92 (RR: 0.78, 95% CI: 0.47, 1.28). IRs of serious adverse CV events during treatment for selected major CV diagnoses are in the table.

View this table:



Conclusion: Tiotropium HH once daily showed a comparable CV safety profile to salmeterol MDI treatment in a pooled analysis of double-blind, randomized, parallel group studies.
Abstract 4844: Serum Organ-Specific Anti-Heart Autoantibodies in Arrhythmogenic Right Ventricular Cardiomyopathy Patients and Relatives: Evidence for Autoimmune Involvement in a Genetically-Determined Myocarditis
Authors: Alida L Caforio, Elisabetta Zachara, Annalisa Vinci, Federica Re, Pasquale Baratta, Francesco Tona, Gaetano Thiene, Sabino Iliceto, Claudio Tondo, William J McKenna
Journal: Circulation (2008)

Objective: Serum anti-heart autoantibodies (AHA) are organ and disease-specific autoimmune markers in myocarditis, dilated cardiomyopathy (DCM), and their relatives. Myocarditis is frequently repor...
Abstract 11543: Resolution of Mitochondrial Oxidant Stress Improves Aged-Cardiac Performance
Authors: Takashi Owada, Hiroyuki Yamauchi, Shu-ichi Saitoh, Hirofumi Machii, Yasuchika Takeishi
Journal: Circulation (2014)

Senescence is a major factor to increase mitochondrial oxidant stress, which contributes to the pathogenesis of heart disease. However, the effect of antioxidant therapy on cardiac mitochondria in aged-cardiac performance remains elusive. We postulated that mitochondrial targeting of superoxide scavenging would have benefit in the aged heart. Increased levels of superoxide and NADPH oxidase activity were appeared in cardiac myocytes isolated from old mice (52W) compared to those from young mice (8W) (Superoxide: 2.6±0.4 vs. 1.2±0.2 nmol/mg protein; NADPH oxidase activity: 2654±282 vs. 1124±156 RLU, P&lt;0.01, n=12, respectively). In old mice treated with the mitochondria-targeted antioxidant MitoTEMPO (180 μg/kg/day, 28 days) coinfusion using subcutaneously implanted minipump, levels of superoxide and NADPH oxidase activity markedly decreased (0.2±0.2 nmol/mg protein and 342±45 RLU, respectively, P&lt;0.01) and eliminated fluorescence intensity of MitoSox Red in cardiomyocytes (from 11.2±2.1 to 0.4±1.1 arbitrary unit, P&lt;0.01). Treatment with MitoTEMPO in old mice improved left ventricle ejection fraction (from 48±5% to 62±5%, P&lt;0.01) and diastolic dysfunction assessed by echocardiography. Endothelium-dependent vasodilation in isolated coronary arterioles was impaired in old mice compared to that in young mice, which was improved by MitoTEMPO treatment (Figure). Mitochondria from the old mouse myocardium exhibited lower rate in complex I (-38±5%) and complex II (-34±6%) -dependent respiration compared with young mice. Supplementation of MitoTEMPO in old mice improved the respiration rates in mitochondria to the level similar to those in young mice. Resolution of mitochondrial oxidant stress by MitoTEMPO in old mice restored cardiac function and coronary vasodilative capacity to the same magnitude observed in young mice. Therefore, antioxidant strategy targeting mitochondria could have therapeutic benefit in heart diseases with senescence.
Abstract 9450: Allogeneic Fetal Membrane-Derived Mesenchymal Stem Cells Sheet Transplantation Therapy for Myocardial Infarction
Authors: Shin Ishikane, Kenichi Yamahara, Jung Kyungsook, Kenichi Mishima, Katsunori Iwasaki, Michihiro Fujiwara, Kenji Kangawa, Tomoaki Ikeda
Journal: Circulation (2010)