tbuckley/cabot-search huggingface dataset:
Long term effects of smoking on physical fitness and lung function: a longitudinal study of 1393 middle aged Norwegian men for seven years
Authors: L. Sandvik, G. Erikssen, E. Thaulow
Journal: BMJ (1995)

<h3>Abstract</h3> Objective:to study association between smoking habits and long term decline in physical fitness and lung function in middle aged men who remained healthy. Design: Baseline and follow up measurements performed during 1972-5 and 1980-2 respectively. Setting:National University Hospital of Oslo, Norway. Subjects:1393 men aged 40-59 at baseline who were all healthy at baseline and at follow up. Main outcome measures:Forced expiratory volume in one second and physical fitness (defined as total work done during a symptom limited bicycle ergometer test divided by body weight. Results: Initial fitness was substantially lower among 347 persistent smokers than among 791 persistent non-smokers (1349 J/kg v 1618 J/kg), as was initial forced expiratory volume (3341 ml v 3638 ml). Mean (95% confidence interval) decline in fitness over 7.2 years was 217 (185 to 249) J/kg among smokers compared with 86 (59 to 113) J/kg among non-smokers (P&lt;0.001). Corresponding declines in forced expiratory volume were 271 (226 to 316) ml in smokers and 116 (85 to 147) ml in non-smokers (P&lt;0.001). Differences between smokers and non-smokers remained practically unchanged after adjustment for age and level of physical activity. Changes in fitness and forced expiratory volume among 199 men who had stopped smoking mimicked the findings for persistent non-smokers, and 56 men who started smoking presented findings close to those of persistent smokers Conclusion:Decline in physical fitness and lung function among healthy middle aged men was considerably greater among smokers than among nonsmokers and could not be explained by differences in age and physical activity.
Importance of Failing Vision in Early Diagnosis of Suprasellar Meningiomas
Authors: J. A. Jane, W. McKissock
Journal: BMJ (1962)

Os Acromiale is an anatomic variant that can cause symptoms rarely. Os Acromiale is caused by the failure of the anterior acromial apophysis to fuse to the acromion process. SPECT/CT can play an important role in diagnosing this clinical entity.
The severe combined immunodeficiency (scid) mouse. A laboratory model for the analysis of Lyme arthritis and carditis.
Authors: U E Schaible, M D Kramer, C Museteanu, G Zimmer, H Mossmann, M M Simon
Journal: The Journal of Experimental Medicine (1989)

We report that the spirochete B. burgdorferi induces progressive polyarthritis and carditis in mice with severe combined immunodeficiency syndrome (scid) but not in normal C.B-17 mice. The onset and severity of the disease were dependent on (a) the viability; (b) the infectivity; and (c) the dose of inoculated B. burgdorferi organisms. Infective spirochetes were isolated from both blood and joints of inoculated scid mice. These findings suggest that B. burgdorferi-induced chronic arthritis and carditis in mice develops independently of lymphocyte function and makes the scid mouse an attractive laboratory model to study the role of the immune system in experimental Lyme Borreliosis.
Rearrangement of the MLL Gene in Acute Lymphoblastic and Acute Myeloid Leukemias with 11q23 Chromosomal Translocations
Authors: Michael J. Thirman, Heidi J. Gill, Robert C. Burnett, David Mbangkollo, Norah R. McCabe, Hirofumi Kobayashi, Sheryl Ziemin-van der Poel, Yasuhiko Kaneko, Rodman Morgan, Avery A. Sandberg, R.S.K. Chaganti, Richard A. Larson, Michelle M. Le Beau, Manuel O. Diaz, Janet D. Rowley
Journal: New England Journal of Medicine (1993)

Translocations involving chromosome band 11q23 are very frequent in both acute lymphoblastic and acute myeloid leukemias and are the most common genetic alteration in infants with leukemia. In all age groups and all phenotypes of leukemia, an 11q23 translocation carries a poor prognosis. A major question has been whether one or several genes on band 11q23 are implicated in these leukemias. Previously, we identified the chromosomal breakpoint region in leukemias with the common 11q23 translocations and subsequently cloned a gene named MLL that spans the 11q23 breakpoint.
Casein Kinase-2α1 Induces Hypertrophic Response by Phosphorylation of Histone Deacetylase 2 S394 and its Activation in the Heart
Authors: Gwang Hyeon Eom, Young Kuk Cho, Jeong-Hyeon Ko, Sera Shin, Nakwon Choe, Yoojung Kim, Hosouk Joung, Hyung-Seok Kim, Kwang-Il Nam, Hae Jin Kee, Hyun Kook
Journal: Circulation (2011)

Background— Cardiac hypertrophy is characterized by transcriptional reprogramming of fetal gene expression, and histone deacetylases (HDACs) are tightly linked to the regulation of those genes. We previously demonstrated that activation of HDAC2, 1 of the class I HDACs, mediates hypertrophy. Here, we show that casein kinase-2α1 (CK2α1)–dependent phosphorylation of HDAC2 S394 is required for the development of cardiac hypertrophy. Methods and Results— Hypertrophic stimuli phosphorylated HDAC2 S394, which was necessary for its enzymatic activation, and therefore the development of hypertrophic phenotypes in rat neonatal cardiomyocytes or in isoproterenol-administered mice hearts. Transgenic mice overexpressing HDAC2 wild type exhibited cardiac hypertrophy, whereas those expressing phosphorylation-resistant HDAC2 S394A did not. Compared with that in age-matched normal human hearts, phosphorylation of HDAC2 S394 was dramatically increased in patients with hypertrophic cardiomyopathy. Hypertrophy-induced phosphorylation of HDAC2 S394 and its enzymatic activity were completely blocked either by CK2 blockers or by CK2 α 1 short interfering RNA . Hypertrophic stimuli led CK2α1 to be activated, and its chemical inhibitors blocked hypertrophy in both phenylephrine-treated cardiomyocytes and isoproterenol-administered mice. CK2α1-transgenic mice developed hypertrophy, which was attenuated by administration of trichostatin A, an HDAC inhibitor. Overexpression of CK2α1 caused hypertrophy in cardiomyocytes, whereas chemical inhibitors of both CK2 and HDAC as well as HDAC2 S394A blunted it. Hypertrophy in CK2α1-transgenic mice was exaggerated by crossing these mice with wild-type-HDAC2-overexpressing mice. By contrast, however, it was blocked when CK2α1-transgenic mice were crossed with HDAC2 S394A-transgenic mice. Conclusions— We have demonstrated a novel mechanism in the development of cardiac hypertrophy by which CK2 activates HDAC2 via phosphorylating HDAC2 S394.
Point Estimates of Number Needed to Treat/Screen Are Insufficient Without Characterization of Their Uncertainty
Authors: Paul F. Pinsky
Journal: Journal of Clinical Oncology (2011)

Both Wallang and Rath 2 and Chantada et al 1 suggest that the four study patients who died of disease may have had extraocular disease at presentation.First, the imaging and clinical staging was exactly the same for all children in our study, but the only children who died had delayed enucleation of group E eyes longer than 3 months due to chemotherapy (statistically significant, P Ͻ .001). 3 Second, the suggested high resolution magnetic resonance imaging may have documented extraocular disease at diagnosis, but was unavailable to these and most children in the world.Our statistical analysis indicates that it is more likely that the disease became extraocular while the children were being treated with chemotherapy.Third, the safe option for group E eyes is immediate enucleation to allow microscopic examination and pathologic staging.The advanced pTNM stage in three children longer than 3 months after diagnosis, is not representative of the unknown stage at diagnosis.Wallang and Rath 2 misunderstood our conventional reference to follow-up, which is the time from diagnosis to last visit.The group treated with primary chemotherapy had shorter median follow-up and 91% were diagnosed in 2007; 40% of those treated with primary enucleation were diagnosed in 2007, 60% in 2006.This reflects an increasing clinical practice trend to administer pre-enucleation chemotherapy, 3 not different surveillance protocols.We are alarmed by the idea of Chantada et al 1 that preenucleation chemotherapy may help parents to accept later enucleation.This may have been the rationale for use of chemotherapy for some of our patients, but our results clearly show that this is extremely dangerous.Clinicians have the duty to present the truth to families, not soften the dangers.Despite how harsh it may seem to parents that an eye must be removed, the harsher outcome is death, and when properly explained, no parent would opt for the latter event.
Ste20-Related Kinase SLK Phosphorylates Ser188 of RhoA to Induce Vasodilation in Response to Angiotensin II Type 2 Receptor Activation
Authors: Christophe Guilluy, Malvyne Rolli-Derkinderen, Laurent Loufrani, Anne Bourgé, Daniel Henrion, Luc Sabourin, Gervaise Loirand, Pierre Pacaud
Journal: Circulation Research (2008)

The small G protein Rho signaling pathways are recognized as major regulators of cardiovascular functions, and activation of Rho proteins appears to be a common component for the pathogenesis of hypertension and vascular proliferative disorders. Recent evidence suggests that modulation of Rho protein signaling by phosphorylation of Rho proteins provides an additional simple mechanism for coordinating Rho protein functions. Phosphorylation of RhoA by cAMP- or cGMP-activated kinase on Ser188 induces cytosolic sequestration of RhoA through increased interaction with guanine dissociation inhibitor, thereby resulting in inhibition of RhoA-dependent functions. Here we show that stimulation of angiotensin II (Ang II) type 2 receptor (AT(2)R) in vascular smooth muscle cells induces Ser188 phosphorylation of RhoA independently of cAMP- or cGMP-activated kinase. We identify the Ser/Thr kinase Ste20-related kinase SLK as a new kinase phosphorylating RhoA on Ser188. Activation of the signaling cascade involving Src homology 2 domain-containing protein-tyrosine phosphatase 1, casein kinase II and SLK is responsible for RhoA phosphorylation and inhibition of RhoA-mediated arterial contraction induced by AT(2)R activation. These results thus identify the molecular mechanism linking AT(2)R to RhoA inhibition and vasodilation.
Spirometric reference values for Malagasy adults aged 18–73 years
Authors: Julia Ratomaharo, Olinto Linares Perdomo, Dave S. Collingridge, Rabezanahary Andriamihaja, Matthew Hegewald, Robert L. Jensen, John Hankinson, Alan H. Morris
Journal: European Respiratory Journal (2014)

The American Thoracic Society (ATS) and European Respiratory Society (ERS) recommend that spirometry prediction equations be derived from samples of similar race/ethnicity. Malagasy prediction equations do not exist. The objectives of this study were to establish prediction equations for healthy Malagasy adults, and then compare Malagasy measurements with published prediction equations. We enrolled 2491 healthy Malagasy subjects aged 18–73 years (1428 males) from June 2006 to April 2008. The subjects attempted to meet the ATS/ERS 2005 guidelines when performing forced expiratory spirograms. We compared Malagasy measurements of forced expiratory volume in 1 s (FEV 1 ), forced vital capacity (FVC) and FEV 1 /FVC with predictions from the European Community for Steel and Coal (ECSC), the third National Health and Nutrition Examination Survey (NHANES III) and the ERS Global Lung Function Initiative (GLI) 2012 study. A linear model for the entire population, using age and height as independent variables, best predicted all spirometry parameters for sea level and highland subjects. FEV 1 , FVC and FEV 1 /FVC were most accurately predicted by NHANES III African-American male and female, and by GLI 2012 black male and black and South East Asian female equations. ECSC-predicted FEV 1 , FVC and FEV 1 /FVC were poorly matched to Malagasy measurements. We provide the first spirometry reference equations for a healthy adult Malagasy population, and the first comparison of Malagasy population measurements with ECSC, NHANES III and GLI 2012 prediction equations.
Electrical and mechanical activity in the human lower esophageal sphincter during diaphragmatic contraction.
Authors: R K Mittal, D F Rochester, R W McCallum
Journal: Journal of Clinical Investigation (1988)

To determine the effect of contraction of the diaphragm on the lower esophageal sphincter (LES) pressure, we studied eight healthy volunteers during spontaneous breathing, maximal inspiration, and graded inspiratory efforts against a closed airway (Muller's maneuver). Electrical activity of the crural diaphragm (DEMG) was recorded from bipolar esophageal electrodes, transdiaphragmatic pressure (Pdi) was calculated as the difference between gastric and esophageal pressures, and LES pressure was recorded using a sleeve device. During spontaneous breathing, phasic inspiratory DEMG was accompanied by phasic increases in Pdi and LES pressure. With maximal inspiration, DEMG increased 15-20-fold compared with spontaneous inspiration, and LES pressure rose from an end-expiratory pressure of 21 to 90 mmHg. Similar values were obtained during maximal Muller's maneuvers. LES pressure fell promptly when the diaphragm relaxed. Graded Muller's maneuver resulted in proportional increases in the Pdi, LES pressure, and DEMG. The LES pressure was always greater than Pdi and correlated with it in a linear fashion (P less than 0.001). We conclude that the contraction of the diaphragm exerts a sphincteric action at the LES, and that this effect is an important component of the antireflux barrier.
Drug Postmarketing Studies
Authors: Mwango Kashoki, Cathryn Lee, John Jenkins
Journal: JAMA (2013)

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
The Quest for an Image of Brain: Computerized Tomography in the Perspective of Past and Future Imaging Methods
Authors: Manuel L. Brown
Journal: JAMA (1981)

ABSTRACT This book begins with the interesting concept and enticing title of The Quest for an Image of Brain. The stated objective is to provide an overview of some of the historical and technical landmarks in brain imaging. Dr Oldendorf covers in separate chapters skull radiography, pneumoencephalography, angiography, ultrasound, isotope scanning, and computed tomography, as well as some information on future imaging methods such as positron emission tomography and nuclear magnetic resonance.The historical aspects as presented by the author are fascinating and well-written vignettes. The scientific aspects of the book vary greatly from picturesque description and oversimplification to an in-depth discussion of minute areas, such as contrast agents. Unfortunately, there is often a confusing mixture of history and science and this occasionally detracts from the text. The author seems to have had great difficulty deciding whether he was going to be historical, scientific, or anecdotal. Any one of these approaches
OPERATION FOR EPITHELIOMA OF THE LOWER LIP
Authors: H. A. L. RYFKOGEL
Journal: JAMA (1913)

The ideal operation for lip cancer would be one that permitted the removal of the disease in block with the cervical glands and intervening tissue, as in the radical breast amputation. The method of Stewart<sup>1</sup>accomplishes this, but the resulting infection and sloughing is frequently extensive and severe, so that death has not infrequently occurred. Such a block dissection is unnecessary, however, because these epitheliomas seem to form their glandular metastases by embolism rather than by continuous growth along the lymphatics as in cancer of the breast. Moreover, the lymphatics draining the lips do not run over the point of the chin, which can be left to form a valuable support for the new lip. Lip cancer, on account of the loose tissue of the lip and the constant motion of the muscles, is prone to infiltrate far beyond the visible ulceration, and one should therefore feel free to
Abstract P2-01-04: High-density lipoprotein cholesterol is associated with mammographic density in premenopausal women
Authors: VG Flote, H Frydenberg, G Ursin, T Wilsgaard, A Iversen, PT Ellison, EA Wist, T Egeland, I Thune, A-S Furberg
Journal: Cancer Research (2013)

Abstract Background: High-Density Lipoprotein Cholesterol (HDL-C), and ovarian steroid hormones and mammographic density have independently been associated with breast cancer development. However, little is known regarding the association between HDL-C, ovarian hormones and mammographic density in premenopausal women. Material and Methods: We assessed fasting HDL-C among 202 healthy women, aged 25-35 years, participating in the Energy Balance and Breast cancer Aspects (EBBA) study-I. Progesterone and estrogen were assessed both in serum (three times) and daily saliva across an entire menstrual cycle. Computer-assisted mammographic density (Madena) was obtained from digitized mammograms taken at days 7-12 of the menstrual cycle during a narrow time frame, thereby avoiding potential bias due to variations in mammographic density during the menstrual cycle. The association between HDL-C, in combination with progesterone or estrogen and absolute mammographic density were studied in multivariable linear and logistic regression models, and potential confounding factors and effect modifiers were tested. Results: The participating women had a mean age of 30.7, mean HDL-C of 1.54 mmol/l, and absolute breast density of 34.7 cm2 (median 32.4 cm2). Among women in the lowest tertile of HDL-C (≤1.38mmol/l), we observed a positive association between midmenstrual salivary 17β-estradiol and absolute breast density (p = 0.014), and between luteal salivary progesterone and absolute breast density (p = 0.029). Among these women in the lowest tertile of HDL-C, we also observed that high 17β-estradiol throughout the menstrual cycle was associated with higher absolute mammographic density (above median absolute density, &amp;gt;32.4 cm2). Odds Ratio (OR) per standard deviation (SD) increase in salivary midmenstrual 17β-estradiol was 2.49 (95% confidence interval [CI] 1.12-5.53) for having a higher absolute mammographic density (&amp;gt;32.4 cm2). These associations between HDL-C, ovarian steroids and absolute mammographic density were not observed in the middle or highest tertiles of HDL-C. Conclusion: Our findings suggest that low HDL-C, a marker of dyslipidemia, in combination with high levels of either progesterone or estradiol may be associated with higher absolute mammographic density in premenopausal women. Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P2-01-04.
Effect of Cardiotonic Lactones on Calcium Metabolism of Dog Cardiac Microsomes
Authors: MARK L. ENTMAN, JOSEPH W. COOK, RUBIN BRESSLER
Journal: Circulation Research (1969)

The effects of several lactones were studied in a microsomal fraction of dog myocardium thought to be sarcoplasmic reticulum. The lactones increased the steady-state accumulation and turnover of calcium only in the presence of ATP, and augmented the calcium-stimulated ATPase activity. When the effective concentrations of the lactones were exceeded, there were no further alterations in calcium accumulation or turnover. A correlation between the capacity of these lactones to increase calcium accumulation and turnover and their relative cardiotonic activity, as reported in the literature, was noted. The potency of the lactones in relation to calcium metabolism in the microsomes is influenced by ring saturation, position of the double bond, and presence of a steroid ring system to the lactone moiety.
Effects of bolus injections and continuous infusions of somatostatin and placebo in patients with cirrhosis: A double-blind hemodynamic investigation
Authors: Isabel Cirera, Faust Feu, Angelo Luca, Joan C. García-Pagan, Mercedes Fernández, Angels Escorsell, Jaime Bosch, Joan Rodés
Journal: Hepatology (1995)

The present double-blind study was aimed at investigating the hemodynamic and humoral effects of somatostatin or placebo in patients with cirrhosis. Patients were randomly assigned to receive either an injection of 250 micrograms of somatostatin followed by a constant infusion of somatostatin at 250 micrograms/h (n = 13), an injection of 250 micrograms of somatostatin followed by a 500 micrograms/h continuous infusion (n = 10), or an injection of placebo followed by a placebo infusion (n = 9). Placebo had no effect. Somatostatin bolus markedly decreased the hepatic venous pressure gradient: by 52% at 1 minute; P < .001; 19% at 3 minutes, P < .01; and by 13% at 5 minutes, P < .04. Azygos blood flow decreased similarly by 45% at 1 minute, P < .001; 16% at 3 minutes, P < .02; and 9.5% at 5 minutes, P = .05. Mean arterial pressure increased by 25% (P < .001). Continuous somatostatin infusions (250 or 500 micrograms/h) had no systemic effects, but significantly reduced hepatic venous pressure gradient (250 micrograms/h: -6.1%, P < .05 and 500 micrograms/h: -15%, P < .01) and hepatic blood flow (250 micrograms/h: -10%, 500 micrograms/h: -18%, P < .05). Azygos blood flow was not changed after 250 micrograms/h infusion but was reduced after 500 micrograms/h (-23%, P < .02). Somatostatin but not placebo, suppressed glucagon to normal levels. This study shows that a bolus injection of somatostatin caused an immediate and marked decrease of hepatic venous pressure gradient and azygos blood flow. Continuous infusion of somatostatin had a mild but sustained effect on splanchnic hemodynamics; this effect was more pronounced with the higher dose.