tbuckley/cabot-search huggingface dataset:
Is There a Doctor in the Home?
Authors: Roy C. Ziegelstein
Journal: Annals of Internal Medicine (2009)

On Being a Doctor1 September 2009Is There a Doctor in the Home?Roy C. Ziegelstein, MD and Ronald ZaczekRoy C. Ziegelstein, MDFrom Johns Hopkins University School of Medicine, Baltimore, MD 21224, and Baltimore, MD 21201.Search for more papers by this author and Ronald ZaczekFrom Johns Hopkins University School of Medicine, Baltimore, MD 21224, and Baltimore, MD 21201.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-151-5-200909010-00015 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail I am a cardiologist, and one of my patients sent an e-mail to me and his primary care physician today. That's not all that unusual in this day and age. Patients are increasingly using e-mail to communicate with their doctors, and I receive at least a couple e-mails each week. What was unusual here is that the patient wrote from his hospital room. A man who had coronary artery bypass graft surgery just this past summer was writing on his computer from the room of a hospital just 15 minutes away, having been admitted there with chest pain. He was ...Reference1. American College of Emergency Physicians. The patient-centered medical home model. Ann Emerg Med. 2009;53:289-91. [PMID: 19167629] CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAffiliations: From Johns Hopkins University School of Medicine, Baltimore, MD 21224, and Baltimore, MD 21201.Grant Support: Dr. Ziegelstein is supported by the Miller Family Scholar Program of the Johns Hopkins Center for Innovative Medicine.Corresponding Author: Roy C. Ziegelstein, MD, Department of Medicine, Johns Hopkins Bayview Medical Center, 4940 Eastern Avenue, Baltimore, MD 21224.Current Author Addresses: Dr. Ziegelstein: Department of Medicine, Johns Hopkins Bayview Medical Center, 4940 Eastern Avenue, Baltimore, MD 21224.Mr. Zaczek: 912 Tyson Street, Baltimore, MD 21201. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byThe Patient-Centered Medical Home and Health Information Technology 1 September 2009Volume 151, Issue 5Page: 361-362KeywordsBreathingComplex systemsComputersHealth careIschemiaNauseaPatientsPrimary care physiciansSub-specialty careSurgery ePublished: 1 September 2009 Issue Published: 1 September 2009 Copyright & PermissionsCopyright © 2009 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Effects of acute exercise on high density lipoprotein cholesterol and high density lipoprotein subfractions in moderately trained females
Authors: P M Gordon, S Fowler, V Warty, M Danduran, P Visich, S Keteyian
Journal: British Journal of Sports Medicine (1998)

Increases in high density lipoprotein cholesterol (HDL-C) levels have previously been reported after moderate exercise bouts lasting less than two hours in men. Little information exists, however, on HDL-C responses after moderate duration exercise in women. Post-exercise HDL-C modifications may appear differently in women because of higher baseline HDL-C concentrations and differences in lipolytic activity. To determine the influence of exercise on acute HDL-C responses in women, 12 trained premenopausal women (22 (4) years old; mean (SD)) who ran 24-48 km a week exercised on a motor driven treadmill at 75% VO2MAX until 3.34 MJ (800 kcal) were expended (72 (9) min). Subjects were all tested during the early follicular phase of their menstrual cycle. Fasting blood samples were obtained before exercise (baseline), immediately after (IPE), one hour after (1 h PE), 24 hours after (24 h PE), and 48 hours after (48 h PE) exercise. Plasma was analysed for HDL-C, HDL2-C, and HDL3-C. A significant increase in HDL-C was observed 48 h PE (p<0.05). HDL3-C increased IPE (p<0.01) but returned to baseline at 1 h PE. In contrast, HDL2-C was not significantly different from baseline at any time point. The rise in HDL-C, however, was attributed to an increase in both HDL2 and HDL3. Moreover, at 48 h PE, the increase in HDL-C correlated highly with changes in HDL2-C (r = 0.92). Thus it appears that exercise of moderate duration can elicit similar post-exercise increases in HDL-C in women to those previously reported in men. However, the changes in HDL subfractions leading to the rise in HDL-C may be different in women.
CIRCUMSTANCES OF DEATH IN ADULT CONGENITAL HEART DISEASE
Authors: A.C. Zomer, Cuno S.P.M. Uiterwaal, Enno T. v.d. Velde, Lambert F.M. van den Merkhof, L.H.B. Bauer, J.M. Ansink, L. Cozijnsen, Petronella G. Pieper, Folkert J. Meiboom, Diederick E. Grobbee, Barbara J.M. Mulder
Journal: Journal of the American College of Cardiology (2010)
Prolonged Exposure: a Rapid Treatment for Phobias
Authors: J. P. Watson, R. Gaind, I. M. Marks
Journal: BMJ (1971)

Ten adult patients with long-standing specific phobias were treated by prolonged continuous exposure to their phobic objects in fantasy and reality without avoidance. All patients were greatly helped by four to five hours9 treatment in two or three sessions, and all improved more after practice than after imaginal sessions. The treatment method is more economical and efficient than other methods described so far.
Surgeon who operated without insurance is suspended
Authors: C. Dyer
Journal: BMJ (2013)

A surgeon who operated for nearly five years at private hospitals without indemnity insurance has been suspended for four months by a panel of the Medical Practitioners Tribunal Service (MPTS).

Ihimire Paul Okojie, who was employed by the NHS as a consultant surgeon, also practised at Nuneaton Private Hospital and at BMI’s Meriden Hospital in Warwickshire. He operated on approximately 260 patients between August 2007, when his insurance lapsed, and June 2012, when his practising privileges were suspended by the Meriden Hospital.

Okojie had been reminded by the hospital in 2006 that his Medical Defence Union indemnity insurance had lapsed. …
Motor Involvement in Herpes Zoster.
Authors: John J. Massarelli
Journal: Annals of Internal Medicine (1968)

s1 May 1968Motor Involvement in Herpes Zoster.John J. Massarelli, M.D. (Associate)John J. Massarelli, M.D. (Associate)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-68-5-1175_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptRecords of 60 hospitalized patients with herpes zoster were reviewed to study the clinical features of motor involvement. Three cases of upper extremity paralysis and one of the lower extremity were found. In addition, a rare case (eight others have been reported) of diaphragmatic paralysis associated with cervical zoster was presented.Motor involvement is not unusual in herpes zoster. It becomes manifest a few days to a few weeks after the eruption appears. Symptoms and signs depend on the level attacked. Diplopia, facial palsy, hoarseness, dyspnea, weakness of an extremity, abdominal pseudohernia, and urinary urgency or retention have all been... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Worcester, Massachusetts PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1968Volume 68, Issue 5Page: 1175-1175KeywordsDyspneaParalysisSigns and symptoms Issue Published: 1 May 1968 PDF downloadLoading ...
Matrix metalloproteinase inhibition reduces axial tensile strength in the arterial wall
Authors: Marion J. Sierevogel, Evelyn Velema, Carolien J. van Andel, Manon Oude Nijhuis, Freek J. van der Meer, Chris L. de Korte, Chaylendra Strijder, Mirjam B. Smeets, Dominique P. De Kleijn, Cornelius Borst, Gerard Pasterkamp
Journal: Journal of the American College of Cardiology (2002)
Alexander Jenkins Semmes
Authors: Robert S. O'Leary
Journal: New England Journal of Medicine (1954)

VARIED are the ways in which, through the ages, doctors have turned afield from the practice of medicine. As poets, scholars, philosophers, musicians and warriors they have won enduring fame, and their names have become household words to generations often unaware of their earlier dedication to medicine. Dr. Alexander Jenkins Semmes, who holds a modest place indeed among these greats and near greats, won distinction solely by virtue of the vocation for which he forsook his profession:after nearly a generation of industrious, conscientious and successful medical practice, he was ordained in the Roman Catholic priesthood.The first fifty years of . . .
Phosphorylation of Troponin I Controls Cardiac Twitch Dynamics
Authors: YeQing Pi, Kara R. Kemnitz, Dahua Zhang, Evangelia G. Kranias, Jeffery W. Walker
Journal: Circulation Research (2002)

The cardiac myofilament protein troponin I (cTnI) is phosphorylated by protein kinase C (PKC), a family of serine/threonine kinases activated within heart muscle by a variety of agonists. cTnI is also a substrate for cAMP-dependent protein kinase (PKA) activated during β-adrenergic signaling. To investigate the role of cTnI phosphorylation in contractile regulation by these pathways, we generated transgenic mice harboring a mutated cTnI protein lacking phosphorylation sites for PKC (serine 43/45 and threonine 144 mutated to alanine) and for PKA (serine 23/24 mutated to alanine). Transgenic mice were interbred with cTnI-knockout mice to ensure the absence of endogenous phosphorylatable cTnI. Here, we report that regulation of myocyte twitch kinetics by β-stimulation and by endothelin-1 was altered in myocytes containing mutant cTnI. In wild-type myocytes, the β-agonist isoproterenol decreased twitch duration and relaxation time constant (τ) by 37% to 44%. These lusitropic effects of isoproterenol were reduced by about half in nonphosphorylatable cTnI mutant myocytes and were absent in cTnI mutants also lacking phospholamban (generated by crossing cTnI mutants with phospholamban-knockout mice). These observations are consistent with important roles for both cTnI and phospholamban phosphorylation in accelerating relaxation after β-adrenergic stimulation. In contrast, endothelin-1 increased twitch duration by 32% and increased τ by 58%. These endothelin-1 effects were substantially blunted in nonphosphorylatable cTnI myocytes, indicating that PKC phosphorylation of cTnI slows cardiac relaxation and increases twitch duration. We propose that β-agonists and endothelin-1 regulate cardiac twitch dynamics in opposite directions in part through phosphorylation of the myofilament protein cTnI on distinct sites.
Repeat cycles of rituximab on clinical relapse in ANCA-associated vasculitis: identifying B cell biomarkers for relapse to guide retreatment decisions
Authors: Md Yuzaiful Md Yusof, Edward M Vital, Sudipto Das, Shouvik Dass, Gururaj Arumugakani, Sinisa Savic, Andrew C Rawstron, Paul Emery
Journal: Annals of the Rheumatic Diseases (2015)

<h3>Objective</h3> To assess clinical and B cell biomarkers to predict relapse after rituximab in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) using retreatment on clinical relapse strategy. <h3>Methods</h3> 35 patients with AAV received treatment with 2×1000 mg rituximab, repeated on clinical relapse (up to 5 cycles). Disease activity was assessed by Birmingham Vasculitis Activity Score (BVAS) and peripheral B cell subsets using highly sensitive flow cytometry (HSFC) as previously described; both performed at baseline and every 3 months. <h3>Results</h3> Response rates were high: &gt;83%, with median time-to-relapse of 82 weeks for cycle 1 (C1) and &gt;54 weeks for all cycles. Prior to rituximab, AAV was characterised by naïve B-lymphopenia compared to healthy controls. This dysregulation was more marked in patients with raised C-reactive protein (CRP) (p&lt;0.05). In C1, no clinical feature predicted relapse. However, repopulation of naïve B cell at 6 months was associated with a reduced risk of relapse (HR: 0.326, 95% 0.114 to 0.930, p=0.036). Relapse rates at 12 and 18 months were 0% and 14% with naïve repopulation at 6 months, and 31% and 54% without naïve repopulation. <h3>Conclusions</h3> Responses to B cell depletion therapy are long-lasting and relapse post-treatment may be predicted by absence of naïve B cell repopulation at 6 months. Naïve B-lymphopenia may be a biomarker of disease activity in AAV.
REQUIREMENT OF ABSTRACTS OR SUMMARIES OF PUBLISHED ARTICLES
Authors: C. M. Jackson
Journal: JAMA (1924)

To the Editor:  —Some of the fundamental scientific journals require that each article published be accompanied with a brief abstract, which has proved very useful to readers in general, as well as to various abstracting journals. A step in this direction is the requirement of a summary at the close of each article. Recognizing the advantage of some such requirement, the Division of Medical Sciences of the National Research Council authorized a committee (Dr. D. R. Hooker, chairman) to call the matter to the attention of all the medical journals, and to gather information as to the desirability of such a requirement. A questionnaire was therefore sent recently to the editors of all the American journals (about ninety) on the list reviewed in the section on Current Medical Literature ofThe Journal of the American Medical Association. Forty-seven replies were received. Only five of these now publish separate abstracts, and
Effect of Duration of Anaesthesia on Apnoea Neonatorum After Caesarean Section
Authors: J. Ozinsky, G. G. Harrison
Journal: BMJ (1956)

Outside Greater London, where fog was also wide- spread, the corresponding increase in deaths in the Great Towns of England and Wales was from 8,443 to 9,141, an increase of only 8%.Morbidity Although this paper is concerned with the effects of the London fog on mortality, two tables have been added to show certain concomitant morbidity trends in other statistics routinely published in the Registrar-General's Weekly Re- turns.Weekly notifications of pneumonia are shown in Table XII and National Insurance claims for sickness benefit in Table XIII.During weeks ended January 10 and 17TABLE XI.-Deaths Registered in Five Groups (see Table X) of Great Towns in the Outer Ring of Greater London.Weeks
Fruits, Vegetables, and Cancer Prevention Trials
Authors: N. J. Temple
Journal: JNCI Journal of the National Cancer Institute (1999)

Fruits, Vegetables, and Cancer Prevention TrialsThe negative results from intervention trials that sought to prevent cancer by use of ␤-carotene supplements underline the difficulty in choosing the appropriate prophylactic agent (1).Hindsight, which is of course always 20-20, should have cautioned us that the association between ␤-carotene and cancer was just that, an association, and that association does not mean causation.But have the lessons from this saga really been learned?It appears that many researchers are of the opinion that the ␤-carotene trials failed only because the wrong carotenoid was chosen or else was given at the wrong dose.I would argue that the problem is more fundamental.As discussed elsewhere (2), only weak evidence supports a major role for antioxidants in cancer.There are other equally plausible substances in fruits and vegetables that may be responsible, for instance, folate (3) and phytochemicals (4).Prostate cancer may be a special case where the protective substance is lycopene, a carotenoid found in tomatoes (5).Clearly, if the research strategy is to conduct intervention trials, each using one substance at one dose, then it will probably take several decades to discover an effective anticancer substance.This is especially true if there is no "magic bullet" in fruits and vegetables but rather a "team" of substances, each of which is needed for optimal effectiveness.Accordingly, the most appropriate step may be to conduct a randomized intervention trial using a mixture of fruits and vegetables.A suitable mixture might be oranges, tomatoes, broccoli, and carrots.A placebo of similar taste and appearance could easily be formulated.In addition to this rationale, such a trial would achieve the following objectives: 1) It would prove that fruits and vegetables do indeed prevent cancer, 2) it would demonstrate the feasibility of this study design, and 3) there is strong evidence that fruits and vegetables should also prevent coronary heart disease (6) and help correct hypertension (7).
Reduction of liver iron content following tratment of chronic hepatitis C
Authors: E BOUCHER
Journal: Hepatology (1995)

La enfermedad tiroidea subclínica (ETS) es una condición asintomática de alta prevalencia que incluye el hipertiroidismo subclínico (HiperSC) y el hipotiroidismo subclínico (HipoSC). Ambas formas no tienen síntomas ni signos específicos y solamente pueden ser detectados mediante exámenes hormonales. Las causas más frecuentes de HiperSC son la enfermedad de Graves y el bocio multinodular. De HipoSC la causa más frecuente es la tiroiditis crónica autoinmune (enfermedad de Hashimoto). El criterio diagnóstico para HiperSC es TSH sérica de ≤0.4 mU/L y valores normales deT4 total o libre. El criterio diagnóstico para HipoSC es TSH sérica de 4.5-10mU/L junto con valores normales de T4 total o libre. Ambas se consideran más severas cuando los valores de TSH se alejan del valor normal: <0.1 mU/L HiperSC y >10mU/L en HipoSC. En la ETS las alteraciones cardiovasculares son frecuentes, pero de distinta índole, así en el HiperSC hay mayor riesgo de arritmias supraventriculares mientras en el HipoSC hay un riesgo aumentado de dislipidemia y ateroesclerosis. En este artículo se analizan los aspectos diagnósticos de la ETS, sus complicaciones y se propone un plan de manejo desde una perspectiva clínica.Subclinical thyroid disease is a highly prevalent asymptomatic entity that includes subclinical hyperthyroidism and subclinical hypothyroidism. Both forms lack of specific signs and symptoms and only can be detected by hormonal tests. The most frequent etiologies for subclinical hyperthyroidism are Graves’ disease and multinodular goiter, and for subclinical hypothyroidism is Chronic autoimmune thyroiditis. Accepted diagnostic criteria for subclinical hyper and hypothyroidism are a TSH ≤ 0.4 mU/L with normal T3, T4 or FT4 and a TSH ≥ 4.5 mU/L with a normal T4 or FT4 respectively. Both conditions have frequent cardiovascular and metabolic complications such as supraventricular arrhythmia (subclinical hyperthyroidism) and hyperlipidemia with atherogenesis (subclinical hypothyroidism). Diagnostic criteria and abnormalities associated with this conditions are reviewed. In addition, a clinical treatment approach is proposed.
Jagged1-induced Notch signaling drives proliferation of multiple myeloma cells
Authors: Franziska Jundt, Kristina Schulze Pröbsting, Ioannis Anagnostopoulos, Gwendolin Muehlinghaus, Manik Chatterjee, Stephan Mathas, Ralf C. Bargou, Rudolf Manz, Harald Stein, Bernd Dörken
Journal: Blood (2004)
CD203c expression on human basophils is associated with asthma exacerbation
Authors: Emiko Ono, Masami Taniguchi, Noritaka Higashi, Haruhisa Mita, Keiichi Kajiwara, Hiromichi Yamaguchi, Sayaka Tatsuno, Yuma Fukutomi, Hidenori Tanimoto, Kiyoshi Sekiya, Chiyako Oshikata, Takahiro Tsuburai, Naomi Tsurikisawa, Mamoru Otomo, Yuji Maeda, Maki Hasegawa, Eishi Miyazaki, Toshihide Kumamoto, Kazuo Akiyama
Journal: Journal of Allergy and Clinical Immunology (2010)
Genetic Epidemiology and Nonsyndromic Structural Birth Defects
Authors: Charlotte A. Hobbs, Shimul Chowdhury, Mario A. Cleves, Stephen Erickson, Stewart L. MacLeod, Gary M. Shaw, Sanjay Shete, John S. Witte, Benjamin Tycko
Journal: JAMA Pediatrics (2014)

Birth defects are a leading cause of infant morbidity and mortality worldwide. The vast majority of birth defects are nonsyndromic, and although their etiologies remain mostly unknown, evidence supports the hypothesis that they result from the complex interaction of genetic, epigenetic, environmental, and lifestyle factors. Since our last review published in 2002 describing the basic tools of genetic epidemiology used to study nonsyndromic structural birth defects, many new approaches have become available and have been used with varying success. Through rapid advances in genomic technologies, investigators are now able to investigate large portions of the genome at a fraction of previous costs. With next-generation sequencing, research has progressed from assessing a small percentage of single-nucleotide polymorphisms to assessing the entire human protein-coding repertoire (exome)-an approach that is starting to uncover rare but informative mutations associated with nonsyndromic birth defects. Herein, we report on the current state of the genetic epidemiology of birth defects and comment on future challenges and opportunities. We consider issues of study design, and we discuss common variant approaches, including candidate gene studies and genome-wide association studies. We also discuss the complexities embedded in exploring interactions between genes and the environment. We complete our review by describing new and promising next-generation sequencing technologies and examining how the study of epigenetic mechanisms could become the key to unraveling the complex etiologies of nonsyndromic structural birth defects.
Of Designer Drugs, Magic Bullets, and Gold Standards
Authors: Basil M. Rifkind
Journal: JAMA (1998)

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
Role of the cardiac Na+/H+ exchanger during ischemia and reperfusion
Authors: D Allen
Journal: Cardiovascular Research (2003)

The coupled exchanger theory describes one of the central mechanisms of damage in the ischemic heart. The theory proposes that anaerobic glycolysis produces lactate and protons and that the protons can leave the cardiac cell on the cardiac Na+/H+ exchanger (NHE1). The subsequent rise in [Na+]i stimulates the cardiac Na+/Ca2+ exchanger (NCX) and results in an increase in [Ca2+]i which promotes myocardial cell damage. Although the general features of this theory are widely accepted, there is dispute about some aspects, specifically whether the NHE1 remains active during ischemia or not. We review the evidence on this issue and conclude that NHE1 is substantially inhibited during ischemia. This issue is central to the design of a clinical trial of NHE1 inhibitors in the treatment of human cardiac ischemia and the existing clinical trials are considered in this light.