tbuckley/cabot-search huggingface dataset:
FURTHER OBSERVATIONS ON SMOKER'S RESPIRATORY SYNDROME
Authors: G L WALDBOTT
Journal: Annals of Internal Medicine (1953)

Article1 November 1953FURTHER OBSERVATIONS ON SMOKER'S RESPIRATORY SYNDROMEGEORGE L. WALDBOTT, M.D., F.A.C.P.GEORGE L. WALDBOTT, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-39-5-1026 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe literature concerning the effect of tobacco on the human organism is mainly concerned with the cardiovascular system. In a review on the subject, Scott1 notes that during smoking the blood pressure shows a transient rise, averaging 15 mm., the pulse rate increases about eight beats a minute, and skin temperature falls due to capillary constriction. Bryant and Wood2 observed the occurrence of anginal pains from smoking. Smoking is believed by some to be responsible for the occurrence of thromboangiitis obliterans.Relative to the respiratory tract, there is some evidence—and much speculation—that smoking contributes to the development of lung cancer....Bibliography1. Scott RB: Some medical aspects of tobacco smoking, Brit. M. J. 1: 671-675 (Mar. 29) 1952. CrossrefMedlineGoogle Scholar2. BryantWood JMJE: Tobacco angina; electrocardiographic study, Am. Heart J. 34: 20-34 (July) 1947. CrossrefMedlineGoogle Scholar3. WynderGraham ELEA: Tobacco smoking as a possible etiologic factor in bronchogenic carcinoma, J. A. M. A. 143: 329-336 (May 27) 1950. CrossrefMedlineGoogle Scholar4. WhitfieldArnottWaterhouse AGWMJA: Effect of ephedrine in asthma and emphysema, Quart. J. Med. 19: 319-326 (Oct.) 1950. MedlineGoogle Scholar5. Myerson MC: Smoker's larynx, Ann. Otol., Rhin. and Laryng. 59: 541-546, 1950. CrossrefGoogle Scholar6. Waldbott GL: Smoker's syndrome, J. A. M. A. 151: 1398-1400 (April) 1953. MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Presented at the Thirty-Fourth Annual Session of the American College of Physicians, Atlantic City, New Jersey, April 17, 1953. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byManagement of the Asthma-COPD Overlap Syndrome (ACOS): a Review of the EvidenceHUMAN BIOCHEMICAL GENETICS"SMOKER'S COUGH " 1 November 1953Volume 39, Issue 5Page: 1026-1031KeywordsBlood pressureCapillariesFallsHeart rateLung and intrathoracic tumorsRespiratory systemTemperature ePublished: 1 December 2008 Issue Published: 1 November 1953 PDF downloadLoading ...
Abstract 18216: Epigenetic Up-regulation of α-smooth Muscle Actin Expression and Cell Aggregation in Human Aortic Valve Interstitial Cells Promotes Calcific Nodule Formation
Authors: Rui Song, David A. Fullerton, Lihua Ao, Kesen Zhao, Xianzhong Meng
Journal: Circulation (2014)

Older people are at risk of calcific aortic valve disease. Aortic valve interstitial cells (AVICs) play an important role in nodular calcification in aortic valve leaflets. AVICs in human aortic valves consist of fibroblasts and myofibroblasts that express α-smooth muscle actin (α-SMA). We have observed that AVICs of diseased aortic valves have greater osteogenic activities. However, molecular mechanism underlying AVIC formation of calcification nodules is not well understood. We hypothesized that an epigenetic mechanism promotes AVIC calcification nodule formation through induction of α-SMA expression and cell aggregation. Methods and Results: MiRNA profiles in AVICs from normal and diseased human aortic valves were analyzed by miRNA array and real-time qPCR. Diseased AVICs displayed higher levels of miR-486. Immunoblotting and immunofluorescence staining revealed that diseased AVICs had higher levels of α-SMA and α-SMA fibers. Inhibition of miR-486 by lentiviral-delivered miR-486 antagomir in diseased AVICs suppressed α-SMA expression and cell aggregation, resulting in reduced calcification nodule formation. Conversely, lentiviral-delivered miR-486 mimic in normal AVICs induced α-SMA expression and cell aggregation, leading to exacerbated calcification nodule formation. Stimulation of normal AVICs with pro-osteogenic mediators TGF-β1 and BMP-2 up-regulated miR-486 levels. MiR-486 antagomir reduced α-SMA expression, cell aggregation and calcification nodule formation in cells exposed to TGF-β1 or BMP-2. Further, miR-486 mimic induced AKT phosphorylation. Inhibition of AKT decreased α-SMA expression and cell aggregation induced by miR-486 mimic in normal AVICs. Knockdown of α-SMA suppressed cell aggregation and calcification nodule formation. Conclusions: The pro-osteogenic phenotype of AVICs of diseased aortic valves is associated with up-regulated levels of miR-486 and α-SMA. MiR-486 modulates the AKT pathway to up-regulate α-SMA expression and cell aggregation that are required for calcification nodule formation. These novel findings indicate that miR-486 contributes to the mechanism underlying aortic valve calcification and appears to be a therapeutic target for suppression of valvular osteogenic activity.
Increased proteasome degradation of cyclin-dependent kinase inhibitor p27 is associated with a decreased overall survival in mantle cell lymphoma
Authors: Roberto Chiarle, Leo M. Budel, Jeffrey Skolnik, Glauco Frizzera, Marco Chilosi, Alessandra Corato, Gianni Pizzolo, Jory Magidson, Alessia Montagnoli, Michele Pagano, Brigitte Maes, Christine De Wolf-Peeters, Giorgio Inghirami
Journal: Blood (2000)
Update on Firearm Use in G- and PG-Rated Movies
Authors: Leigh T Ramsey, Andrew R Pelletier
Journal: JAMA (2004)

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
Dual treatment with lopinavir–ritonavir plus lamivudine versus triple treatment with lopinavir–ritonavir plus lamivudine or emtricitabine and a second nucleos(t)ide reverse transcriptase inhibitor for maintenance of HIV-1 viral suppression (OLE): a randomised, open-label, non-inferiority trial
Authors: José R Arribas, Pierre-Marie Girard, Roland Landman, Judit Pich, Josep Mallolas, María Martínez-Rebollar, Francisco X Zamora, Vicente Estrada, Manuel Crespo, Daniel Podzamczer, Joaquín Portilla, Fernando Dronda, José A Iribarren, Pere Domingo, Federico Pulido, Marta Montero, Hernando Knobel, André Cabié, Laurence Weiss, José M Gatell
Journal: The Lancet Infectious Diseases (2015)
Mutant U2AF1 Expression Alters Hematopoiesis and Pre-mRNA Splicing In Vivo
Authors: Cara Lunn Shirai, James N. Ley, Brian S. White, Sanghyun Kim, Justin Tibbitts, Jin Shao, Matthew Ndonwi, Brian Wadugu, Eric J. Duncavage, Theresa Okeyo-Owuor, Tuoen Liu, Malachi Griffith, Sean McGrath, Vincent Magrini, Robert S. Fulton, Catrina Fronick, Michelle O’Laughlin, Timothy A. Graubert, Matthew J. Walter
Journal: Cancer Cell (2015)
Respiratory morbidity 10 years after the Union Carbide gas leak at Bhopal: a cross sectional survey
Authors: P Cullinan, S Acquilla, V R. Dhara
Journal: BMJ (1997)

<h3>Abstract</h3> <b>Objective:</b> To examine the role of exposure to the 1984 Bhopal gas leak in the development of persistent obstructive airways disease. <b>Design:</b> Cross sectional survey. <b>Setting:</b> Bhopal, India. <b>Subjects:</b> Random sample of 454 adults stratified by distance of residence from the Union Carbide plant. <b>Main outcome measures:</b> Self reported respiratory symptoms; indices of lung function measured by simple spirometry and adjusted for age, sex, and height according to Indian derived regression equations. <b>Results:</b> Respiratory symptoms were significantly more common and lung function (percentage predicted forced expiratory volume in one second (FEV<sub>1</sub>), forced vital capacity (FVC), forced expiratory flow between 25% and 75% of vital capacity (FEF<sub>25-75</sub>), and FEV<sub>1</sub>/FVC ratio) was reduced among those reporting exposure to the gas leak. The frequency of symptoms fell as exposure decreased (as estimated by distance lived from the plant), and lung function measurements displayed similar trends. These findings were not wholly accounted for by confounding by smoking or literacy, a measure of socioeconomic status. Lung function measurements were consistently lower in those reporting symptoms. <b>Conclusion:</b> Our results suggest that persistent small airways obstruction among survivors of the 1984 disaster may be attributed to gas exposure. <h3>Key messages</h3> Many people died as a result of exposure to gas after the 1984 Union Carbide disaster in Bhopal but long term effects remain unclear In this study respiratory disease attributable to gas exposure was detected in adult survivors The frequency of symptoms decreased with decreasing exposure (as estimated by distance of home from the plant) Lung function showed similar trends, although the number of subjects was much smaller Much of the disease is probably due to irreversible obstruction in small airways
Examination of Autoantibody Status and Clinical Features Associated With Cancer Risk and Cancer‐Associated Scleroderma
Authors: Ami A. Shah, Laura K. Hummers, Livia Casciola‐Rosen, Kala Visvanathan, Antony Rosen, Fredrick M. Wigley
Journal: Arthritis & Rheumatology (2015)

Objective We previously reported a contemporaneous onset of cancer and scleroderma in patients with anti–RNA polymerase III antibodies, and we identified a biologic link between cancer and scleroderma. This investigation was designed to further evaluate whether autoantibody status and other characteristics are associated with cancer and a clustering of cancer with scleroderma onset. Methods Logistic regression analysis was performed to assess the relationship of 2 outcomes, cancer (model 1) and a short (±2 years) cancer–scleroderma interval (model 2), with autoantibody status and scleroderma covariates. Results Of 1,044 scleroderma patients, 168 (16.1%) had cancer. In the adjusted model 1, only older age at scleroderma onset (odds ratio 1.04 [95% confidence interval 1.02–1.05]) and white race (odds ratio 2.71 [95% confidence interval 1.22–6.04]) were significantly associated with an increased overall risk of cancer. In the adjusted model 2, only anti–RNA polymerase III positivity (odds ratio 5.08 [95% confidence interval 1.60–16.1]) and older age at scleroderma onset (odds ratio 1.04 [95% confidence interval 1.00–1.08]) were significantly associated with a short cancer–scleroderma interval. While anti–RNA polymerase III positivity was associated with a short cancer–scleroderma interval independent of age at scleroderma onset, the cancer–scleroderma interval shortened with older age at scleroderma onset in other antibody groups (Spearman's correlation P &lt; 0.05), particularly among patients with anti–topoisomerase I antibodies and patients who were negative for anticentromere, anti–topoisomerase I, and anti–RNA polymerase III antibodies. Conclusion Increased age at scleroderma onset is strongly associated with cancer risk overall. While anti–RNA polymerase III status is an independent marker of coincident cancer and scleroderma at any age, a clustering of cancer with scleroderma is also seen in patients with anti–topoisomerase I and other autoantibody specificities who develop scleroderma at older ages.
Abstract 13031: Real-Time Three-Dimensional Transesophageal Echocardiography for Diagnosis of Pannus Formation in Mechanical Aortic Valves: Comparison with Multi-detector Computed Tomography and Surgical Findings
Authors: Sahmin Lee, Seung-Pyo Lee, Eun-Ah Park, Mi-Kyung Hong, Ji-Hyun Kim, Han Mo Yang, Hyung-Kwan Kim, Whal Lee, Yong-Jin Kim, Dae-Won Sohn
Journal: Circulation (2014)

Introduction: Pannus formation is a rare but important complication that can be missed in patients with prosthetic valves. However, currently available methodologies are not sufficient to diagnose subvalvular pannus formation especially in mechanical aortic valves. Hypothesis: In this study, we explored a series of experiences with three-dimensional transesophageal echocardiography (3D-TEE) for the visualization and accurate assessment of subvalvular pannus in patients with mechanical aortic valve. Methods: We enrolled 11 patients (mean age 64±8.6 years, 10 patients with either double or triple valve replacement) who had previously implanted mechanical aortic valve, with transaortic mean pressure gradient &gt;40mmHg or transaortic maximal velocity &gt;4m/sec despite normal occluder motion. All patients underwent 3D-TEE examination to rule out pannus formation and these findings were compared with multi-detector computed tomography (MDCT) images and/or surgical findings. Results: In 10 patients, 3D-TEE allowed good visualization of subaortic pannus formation whereas there was no significant pannus ingrowth in one patient. Through cropping full-volume 3D-TEE images, subaortic pannus formation could be visualized well in en face view, which was confirmed by MDCT images. The 3D-TEE images of the pannus were also matched with intraoperative findings in 7 patients undergoing reoperation of the mechanical aortic valve (Figure). Quantitative measurement of geometric subvalvular area using 3D planimetry was feasible and correlated well with the area measured by MDCT and with transaortic mean pressure gradient on transthoracic echocardiography (Spearman’s ρ=0.761 and -0.726, all p-value&lt;0.05). Conclusions: Real-time 3D-TEE is a useful diagnostic tool for the anatomical assessment of subvalvular pannus formation in mechanical aortic valves.
Induction of G1 arrest and apoptosis by new benzylidene derivatives of andrographolide in breast and colon cancer cells
Authors: Srinivasa Jada, Charles Matthews, Mohamad Saad, Ahmad Hamzah, Nordin Lajis, Malcolm Stevens, Johnson Stanslas
Journal: Clinical Cancer Research (2007)

C29   Andrographolide, a major diterpenoid lactone from the herb  Andrographis paniculata  Nees was previously shown by us to have promising antitumour activities in breast cancer models. Owing to this, a series of new andrographolide analogues were then synthesised and evaluated for  in vitro  antitumour activities against a 2-cancer cell line panel consisting of MCF-7 (breast) and HCT-116 (colon) cells. Majority of the analogues exhibited submicromolar concentrations of growth inhibition and cytotoxicity. Out of the fourteen compounds tested against the 60 NCI human cancer cell lines, 3,19-(2-bromobenzylidene)andrographolide (SRJ09) and 3,19-(3-chloro-4-fluorobenzylidene)andrographolide (SRJ23) showed selectivity towards leukaemia, melanoma and colon, non-small cell lung and prostate cancers. SRJ09 and its related compound, SRJ10 induced a consistent G 1  phase arrest in MCF-7 cells. In HCT-116 cells, SRJ23 provoked a G 1  arrest and induced apoptosis (subG1 population). Western blot analysis revealed that SRJ09 down-regulated CDK4 level in MCF-7 cells upon treatment with 1 and 7 μM for 72 h but did not alter CDK1 level. Induction of cell death by apoptosis in SRJ09 and SRJ23 treated HCT-116 cells was confirmed by annexin V-FITC/PI flow cytometry analysis. In conclusion, these data suggest SRJ09 being the lead compound in this study, possessed antitumour activity by down-regulating CDK4 and inducing apoptosis.
Abstract 895: Use of Contraindicated Anti-Thrombotics in Dialysis Patients Undergoing Percutaneous Coronary Interventions: Insights From the NCDR Cath-PCI Registry
Authors: Thomas T Tsai, Thomas M Maddox, Matthew T Roe, David Dai, Karen P Alexander, P Michael Ho, John C Messenger, Brahmajee K Nallamothu, Eric D Peterson, John S Rumsfeld
Journal: Circulation (2009)

Background: Because of their renal clearance, two commonly used anti-thrombotics in percutaneous coronary interventions (PCI), eptifibatide and enoxaparin, are relatively contra-indicated in dialys...
An Atlas of Radiology of Rheumatic Disorders.
Authors: Jan Dequeker
Journal: Annals of Internal Medicine (1982)

An atlas of radiology of rheumatic disorders , An atlas of radiology of rheumatic disorders , کتابخانه دیجیتالی دانشگاه علوم پزشکی و خدمات درمانی شهید بهشتی
microRNA profiling in pulmonary fibroblasts in COPD
Authors: Corry-Anke Brandsma, Stephanie Christenson, Joshua Campbell, Marnix Jonker, Marc Lenburg, Avi Spira, James Hogg, Dirkje Postma, Wim Timens
Journal: European Respiratory Journal (2011)

COPD is characterized by emphysema with loss of extracellular matrix (ECM), and (small) airways disease with increased ECM deposition and airway wall thickening. How both processes can occur in close proximity in one lung is unknown and needs more attention. Fibroblasts are the principal cells involved in ECM production in the lung. MicroRNAs are small RNAs that can cause downregulation of target protein expression. We hypothesize that microRNA-mediated differences between COPD and healthy fibroblasts, and additionally airway and parenchymal fibroblasts, contribute to the airway and parenchymal changes in COPD.

We profiled microRNA expression in pulmonary fibroblasts from severe COPD patients and controls to investigate effects of COPD, smoking (ex-smokers vs current smokers) and fibroblast type (airway vs parenchymal fibroblasts).

Using linear models we found 42 microRNAs differentially expressed in COPD patients, 25 between ex-smokers and current smokers and 45 between airway and parenchymal fibroblasts in COPD (p<0.01). Interestingly some of the microRNAs differentially expressed in COPD fibroblasts, i.e. mir-181d and mir-296-5p, are also differentially expressed in lung tissue in relation to emphysema severity (Christenson, S.A. et al. Am J Resp Crit Care Med 2010;181:A2024) . COPD and smoking had similar effects on several microRNAs, including mir-181d, mir-296-5p, mir-29b1*, mir-23* and mir-202, suggesting a possible mechanism for the link between smoking and COPD development. Furthermore, mir-155 expression was decreased in COPD and within COPD in airway fibroblasts. Given the role of mir-155 in airway remodeling (Rodriguez, A. et al. Science 2007; 316:608-11) this microRNA could be important in the airway changes in COPD.
<i>Clostridium difficile</i>infection
Authors: V. K. Viswanathan, Michael Mallozzi, Gayatri Vedantam
Journal: Gut Microbes (2010)

Clostridium difficile infection (CDI) is the primary cause of antibiotic-associated diarrhea, and is a significant nosocomial disease. In the past ten years, variant toxin-producing strains of C. difficile have emerged, that have been associated with severe disease as well as outbreaks worldwide. This review summarizes current information on C. difficile pathogenesis and disease, and highlights interventions used to combat single and recurrent episodes of CDI.
Lesson of the week: Wound botulism associated with subcutaneous drug use
Authors: A F A Merrison
Journal: BMJ (2002)

Wound botulism in drug users is a rare but important cause of weakness and neuropathy 

Botulism has long been considered a foodborne infection, the causative agent, Clostridium botulinum usually being transmitted in preserved foods. Yet C botulinum is widely distributed in soil and may be transmitted through wounds. An important distinction is that infections from food are limited to the amount of toxin ingested whereas in infections from wounds the toxin can be produced in situ until infection is eliminated from the wound.1

A new mode of presentation is occurring in drug users, the organism entering at sites of subcutaneous injection. The first reported case due to subcutaneous injection was in New York in 1982.2 As drug use has increased so has the number of people exposed to C botulinum . Over 90% of cases of wound botulism have been reported in the United States (75% in California), with only a small number of cases in the United Kingdom and elsewhere in Europe. 1 3–6

Botulism manifests as an acute descending paralysis, with involvement of autonomic and cranial nerves. C botulinum produces a potent exotoxin that binds irreversibly to the presynaptic membrane causing failure of transmission at the neuromuscular junction, autonomic ganglia, and parasympathetic nerve terminals. Diagnosis is based on clinical and neurophysiological findings, serology, and by identifying the organism or toxin. An antitoxin is available, but treatment remains largely supportive. We report a case of wound botulism in a subcutaneous heroin user who posed diagnostic difficulties.

A 50 …
75. The Optimization of a Single-LTR HIV-1 Vectors for Functional Genomic Applications
Authors: Hong Ma, Tal Kafri
Journal: Molecular Therapy (2004)

The development of high throughput methods for converting simple expression cassettes into lentiviral vectors, and retrieving vector genomes carrying candidate genes from a host, will significantly facilitate the use of lentiviral vectors as an efficient means of screening novel gene function.
Abstract MP11: Association of Sick Sinus Syndrome with Incident Cardiovascular Disease and Mortality: the Atherosclerosis Risk in Communities Study and Cardiovascular Health Study
Authors: Alvaro Alonso, Paul N Jensen, Faye L Lopez, Lin Y Chen, Bruce M Psaty, Aaron R Folsom, Susan R Heckbert
Journal: Circulation (2014)

Background: Sick sinus syndrome (SSS) is a disorder characterized by symptomatic dysfunction of the sinoatrial node. Despite being relatively frequent and a major indication for pacemaker implantation (PMI), the impact of SSS on the risk of other cardiovascular diseases (CVD) and mortality is unclear. Thus, we assessed whether SSS incidence was associated with mortality and CVD in two community-based studies. Methods: We included 19,893 men and women age 45 and older enrolled in the Atherosclerosis Risk in Communities (ARIC) study and the Cardiovascular Health Study (CHS), without pacemaker and free of atrial fibrillation (AF) at baseline. Incident cases of SSS were adjudicated after review of medical charts from hospitalizations with a 427.81 ICD-9 code. Ascertainment of incident CVD (heart failure, myocardial infarction, stroke, AF, PMI) and mortality was done according to standard validated protocols. The association between SSS and the selected outcomes was assessed using age, sex, and race-standardized rates and multivariable Cox models adjusted for potential confounders. Results: During a mean follow-up of 17 years, 213 incident SSS events were identified and validated (incidence = 6 events per 10,000 person-years). Age, sex, and race-standardized rates for each of the outcomes in those with and without SSS are presented in the Table. Overall, individuals with SSS had higher rates of mortality and CVD. These differences were still present, though weakened, after adjustment for baseline cardiovascular risk factors (Table, Model 2). After additional adjustment for incident CVD (Model 3), SSS was no longer associated with higher mortality, myocardial infarction or stroke, but an association with heart failure, AF and PMI remained. Conclusion: Individuals who develop SSS are at increased risk of death and incident CVD. Their management should incorporate comprehensive cardiovascular prevention in addition to symptom relief. The mechanisms underlying these associations warrant further investigation.