tbuckley/cabot-search huggingface dataset:
Lifestyle and the risk of rheumatoid arthritis: cigarette smoking and alcohol consumption.
Authors: J M Hazes, B A Dijkmans, J P Vandenbroucke, R R de Vries, A Cats
Journal: Annals of the Rheumatic Diseases (1990)

In a search for aspects of behaviour related to oral contraceptive use which might explain the favourable effect of oral contraception on the onset of rheumatoid arthritis (RA), cigarette smoking and alcohol consumption were studied as possible risk factors. Information on cigarette smoking and alcohol consumption was obtained by interview at the first visit to the outpatient clinic of 135 young women with confirmed definite or classical RA of recent onset and 378 control patients with soft tissue rheumatism or osteoarthritis. The diagnosis in all patients was confirmed by at least two years of follow up. Of the patients with RA, 44/135 (33%) were current cigarette smokers compared with 181/378 (48%) of the controls. The percentage of smokers among the controls was similar to that of women smokers in the general population. The adjusted risk of RA in women who smoked at least one cigarette a day was 0.61 (95% confidence interval (CI) 0.42 to 0.89). Thirty one (23%) patients with RA and 137 (36%) controls were alcohol drinkers. The risk of RA in women who consumed alcohol at least once a day was 0.52 (95% CI 0.33 to 0.84). The low relative risk estimates for cigarette smoking and alcohol consumption were mutually independent and also independent of oral contraceptive use, the presence of the HLA-DR4 antigen, or a positive family history of RA. The low incidence of alcohol consumption in the patients with RA might be due to the discontinuation of alcohol consumption after disease onset. The low incidence of cigarette smoking in the patients might reflect a protective effect of cigarette smoking on RA onset, possibly induced by changes in the immune system.
Constitutive Expression of AID Leads to Tumorigenesis
Authors: Il-mi Okazaki, Hiroshi Hiai, Naoki Kakazu, Shuichi Yamada, Masamichi Muramatsu, Kazuo Kinoshita, Tasuku Honjo
Journal: The Journal of Experimental Medicine (2003)

Genome stability is regulated by the balance between efficiencies of the repair machinery and genetic alterations such as mutations and chromosomal rearrangements. It has been postulated that deregulation of class switch recombination (CSR) and somatic hypermutation (SHM), which modify the immunoglobulin (Ig) genes in activated B cells, may be responsible for aberrant chromosomal translocations and mutations of non-Ig genes that lead to lymphocyte malignancy. However, the molecular basis for these genetic instabilities is not clearly understood. Activation-induced cytidine deaminase (AID) is shown to be essential and sufficient to induce both CSR and SHM in artificial substrates in fibroblasts as well as B cells. Here we show that constitutive and ubiquitous expression of AID in transgenic mice caused both T cell lymphomas and dysgenetic lesions of epithelium of respiratory bronchioles (micro-adenomas) in all individual mice. Point mutations, but not translocations, were massively introduced in expressed T cell receptor (TCR) and c-myc genes in T lymphoma cells. The results indicate that AID can mutate non-Ig genes including oncogenes, implying that aberrant AID expression could be a cause of human malignancy.
A systematic review of sperm donors: demographic characteristics, attitudes, motives and experiences of the process of sperm donation
Authors: U. Van den Broeck, M. Vandermeeren, D. Vanderschueren, P. Enzlin, K. Demyttenaere, T. D'Hooghe
Journal: Human Reproduction Update (2012)

BACKGROUNDThis systematic review aimed first to integrate the current body of knowledge on the demographic, institutional and psychosocial information on sperm donors, and second to provide insight into the actual experiences of men who donate and the attitudes towards potential donation.
The Stoke CNEP Saga – a view from the General Medical Council
Authors: Graeme Catto
Journal: Journal of the Royal Society of Medicine (2010)

The General Medical Council’s (GMC) purpose is to protect, promote and maintain the health and safety of the public by ensuring proper standards in the practice of medicine. To support that purpose, the GMC has four main regulatory functions: registration (which, in future, will include revalidation); education and training; standards and ethics; and the fitness-to-practise procedures (sometimes misleadingly labelled disciplinary procedures). The fitness-to-practise procedures seem guaranteed to polarize opinions; over the years, there have been criticisms from both sides of the yawning divide that separates those who believe the GMC is too lenient and those who believe it is too harsh. Neither caricature is accurate, as evidenced by the outcomes of appeals and other referrals to the High Court. As with all activities based on human judgements, errors are made but the numbers are very small and they do not reflect systemic bias. The GMC is committed to having processes and procedures that are fair, objective, transparent and free from discrimination. Nevertheless, some criticisms of the fitness-topractise procedures have been justified. The procedures that operated in the 1990s and in the early part of the 2000s were no longer fit for purpose. That is why the GMC launched a programme of fundamental review in 2000 and introduced reformed procedures in November 2004. It is also why, at the Shipman Inquiry in November 2003, the GMC frankly recognized past deficiencies in three areas – operational effectiveness; consistency and quality of decision-making; and the architecture of the procedures. Other criticisms are not justified. Some reflect a historical rather than a current perspective; some are based on misunderstanding; and some are partisan. They include that the GMC bears down
Myocardial energetics during ventricular fibrillation investigated by magnetization transfer nuclear magnetic resonance spectroscopy.
Authors: H Kusuoka, V P Chacko, E Marban
Journal: Circulation Research (1992)

Ventricular fibrillation (VF) is known to produce alterations in myocardial energetics, but the mechanism of these changes remains unclear. To investigate energy metabolism during VF, phosphorus nuclear magnetic resonance spectroscopy and magnetization transfer were applied to isolated perfused ferret hearts. VF was induced either by perfusion with digitalis (strophanthidin, 30 microM) or by high-frequency electrical stimulation. We measured the flux in two critical reactions: from inorganic phosphate (Pi) to ATP (ATP synthesis rate) and from phosphocreatine (PCr) to ATP (energy transfer capacity). During digitalis-induced VF, energy-related phosphates showed changes similar to those during hypoxia: myocardial [Pi] increased and [PCr] decreased. Concomitantly, the ATP synthesis rate increased to levels about threefold higher than control, whereas oxygen consumption increased by only 16%. The ATP synthesis rate exhibited a strong negative correlation with left ventricular pressure during VF (r = -0.95, n = 5, p &lt; 0.02), whereas oxygen consumption did not (r = 0.19, p &gt; 0.05). On the other hand, energy transfer capacity catalyzed by creatine kinase was significantly smaller during VF than in the control condition but still higher than the simultaneous ATP synthesis rate. In contrast to the marked energetic deterioration during VF induced by digitalis, electrically induced VF led to only a small increase in [Pi] and a small decrease in [PCr], and there were no significant changes in the ATP synthesis rate, energy transfer capacity, or O2 consumption. These results indicate that the rundown in energy metabolism during VF induced by digitalis was mainly attributable to a limitation of energy production through oxidative phosphorylation as well as to a marked increase in energy consumption. In contrast, myocardial energy generation remained unimpaired during VF induced by electrical stimulation. Intracellular calcium overload is more severe during VF induced by digitalis than during electrically induced VF (Circ Res 1991;68:1378-1389); severe calcium overload would be expected to compromise the capacity for energy generation by mitochondria. Thus, we propose that known differences in cellular calcium loading underlie the discrepant energetic patterns of the two types of VF.
Antidepressants for irritable bowel syndrome
Authors: R E Clouse
Journal: Gut (2003)

Systematic reports of antidepressant use in irritable bowel syndrome (IBS) first appeared in the medical literature three decades ago. Recent meta-analyses of the cumulative controlled experience confirm the efficacy of antidepressants in IBS and other functional gastrointestinal disorders: only 3–4 patients require treatment to demonstrate a benefit over placebo—numbers indicating a solid treatment effect.1–3 Although many of the earlier reports would be considered scientifically flawed by today’s standards, the effects are consistent across studies. Odds ratios of treatment over placebo for primary study outcome, global (or syndromic) response, and pain exceeded 4.0 for each determination in one analysis, and the effect sizes of antidepressant treatment on continuous outcome measures were large.3 These observations in conjunction with reported open label experience and general clinical success have given antidepressants an important position in the therapeutic armamentarium for IBS.4

Most studies have employed tricyclic antidepressants (TCAs), medications that appear to have benefits not necessarily shared across the antidepressant class. Daily dosages of TCAs (25–125 mg/day) that are below the psychiatric range for antidepressant effect typically are effective in IBS, producing at least a moderate response in more than 85% of patients in open label use.5 With the TCAs, onset of action is rapid, effects appear sustained without tachyphylaxis, and the benefits are unrelated …
Detection of Anti–β1-AR Autoantibodies in Heart Failure by a Cell-Based Competition ELISA
Authors: Hans-Peter Holthoff, Stefan Zeibig, Valerie Jahns-Boivin, Johannes Bauer, Martin J. Lohse, Stefan Kääb, Sebastian Clauss, Roland Jahns, Angela Schlipp, Götz Münch, Martin Ungerer
Journal: Circulation Research (2012)

Autoantibodies directed against the second extracellular loop of the cardiac β1-adrenergic receptor (β1-AR) are thought to contribute to the pathogenesis of dilated cardiomyopathy (DCM) and Chagas heart disease. Various approaches have been used to detect such autoantibodies; however, the reported prevalence varies largely, depending on the detection method used.We analyzed sera from 167 DCM patients (ejection fraction<45%) and from 110 age-matched volunteers who did not report any heart disease themselves, with an often used simple peptide-ELISA approach, and compared it with a novel whole cell-based ELISA, using cells expressing the full transgene for the human β1-AR. Additionally, 35 patients with hypertensive heart disease with preserved ejection fraction were investigated.The novel assay was designed according to the currently most reliable anti-TSH receptor antibody-ELISA used to diagnose Graves disease ("third-generation assay") and also detects the target antibodies by competition with a specific monoclonal anti-β1-AR antibody (β1-AR MAb) directed against the functionally relevant β1-AR epitope. Anti-β1-AR antibodies were detected in ≈60% of DCM patients and in ≈8% of healthy volunteers using the same cutoff values. The prevalence of these antibodies was 17% in patients with hypertensive heart disease. Anti-β1-AR antibody titers (defined as inhibition of β1-AR MAb-binding) were no longer detected after depleting sera from IgG antibodies by protein G adsorption. In contrast, a previously used ELISA conducted with a linear 26-meric peptide derived from the second extracellular β1-AR loop yielded a high number of false-positive results precluding any specific identification of DCM patients.We established a simple and efficient screening assay detecting disease-relevant β1-AR autoantibodies in patient sera yielding a high reproducibility also in high throughput screening. The assay was validated according to "good laboratory practice" and can serve as a companion biodiagnostic assay for the development and evaluation of antibody-directed therapies in antibody-positive heart failure.
Clinical characteristics of chemotherapy-induced alopecia in childhood
Authors: Mira Choi, Min Sun Kim, Song Youn Park, Gyeong Hun Park, Seong Jin Jo, Kwang Hyun Cho, Ji Won Lee, Kyung Duk Park, Hee Young Shin, Hyoung Jin Kang, Ohsang Kwon
Journal: Journal of the American Academy of Dermatology (2013)
Activated alveolar macrophages in subclinical pulmonary inflammation in collagen vascular diseases.
Authors: B Wallaert, F Bart, C Aerts, A Ouaissi, P Y Hatron, A B Tonnel, C Voisin
Journal: Thorax (1988)

A study was initiated to determine whether alveolar macrophages from patients with collagen vascular diseases but free of pulmonary symptoms were spontaneously activated and whether they released various mediators related to the pathogenesis of pulmonary fibrosis. Alveolar macrophages obtained by bronchoalveolar lavage from 32 patients with proved collagen vascular disease but no evidence of lung disease were compared with those from 10 patients with collagen vascular disease with interstitial lung disease (CVD-ILD) and from 10 healthy controls. The total number of alveolar macrophages did not differ between patients with collagen vascular disease and controls but were substantially increased in the CVD-ILD group. Alveolar macrophages from 31 of the 32 patients with collagen vascular disease and from all 10 in the CVD-ILD group had at least one criterion of activation. Neutrophil chemotactic activity was detected in supernatants from alveolar macrophage culture in 23 of the 32 patients with collagen vascular disease and from nine of the 10 in the CVD-ILD group; fibronectin secretion by alveolar macrophages was increased in 12 of the 32 patients with collagen vascular disease and in nine of the 10 in the CVD-ILD group. Furthermore, alveolar macrophages from 20 of the 32 patients with collagen vascular disease and four of the 10 CVD-ILD patients spontaneously released increased amounts of superoxide anion. Thus alveolar macrophages were spontaneously activated in a high proportion of patients with collagen vascular disease.
Depression and Cancer; Depression and Diabetes; and Depression and Heart Diseaseedited by KissaneDavid W., MajMario, and SartoriusNorman. Chichester, United Kingdom, Wiley-Blackwell, 2011, 264 pp., $49.50.edited by KatonWayne, MajMario, and SartoriusNorman. Chichester, United Kingdom, Wiley-Blackwell, 2010, 192 pp., $44.95.edited by GlassmanAlexander, MajMario, and SartoriusNorman. Chichester, United Kingdom, Wiley-Blackwell, 2011, 190 pp., $49.50.
Authors: Thomas P. Beresford
Journal: American Journal of Psychiatry (2012)

1 0 2 a jp.p sych ia tryo n lin e.o rg A m J Psych ia try 1 6 9 :1 , Ja nu a ry 2 0 1 2 her family.The authors emphasize the need to be part of an interdisciplinary team.These two chapters demonstrate the unique understanding that we can bring to our patients and their families as well as to our colleagues.Looking into the future, psychosomatic medicine psychiatrists will develop more of an outpatient practice, including an integrated role in the medical home.In the third edition of this textbook, I look forward to an expanded vision for the future of this subspecialty.I would also like to anticipate that each chapter will incorporate specific attitudes and skills needed in the field, along with the prescribed knowledge base.This would be helpful to trainees who are trying to integrate their medical knowledge and psychotherapeutic skills.An integrated approach to patient care is the distinguishing feature of who we are as psychosomatic medicine psychiatrists.In summary, almost all psychosomatic medicine psychiatrists use this book to prepare for the psychosomatic medicine board examination, in psychosomatic medicine fellowship programs, and as the "must have on your shelf" reference text.This subspecialty has come a long way since 2005, and we have the textbook to prove it.
Epidermal Growth Factor Receptor Mutations and Gene Amplification in Non–Small-Cell Lung Cancer: Molecular Analysis of the IDEAL/INTACT Gefitinib Trials
Authors: Daphne W. Bell, Thomas J. Lynch, Sara M. Haserlat, Patricia L. Harris, Ross A. Okimoto, Brian W. Brannigan, Dennis C. Sgroi, Beth Muir, Markus J. Riemenschneider, Renee Bailey Iacona, Annetta D. Krebs, David H. Johnson, Giuseppe Giaccone, Roy S. Herbst, Christian Manegold, Masahiro Fukuoka, Mark G. Kris, José Baselga, Judith S. Ochs, Daniel A. Haber
Journal: Journal of Clinical Oncology (2005)

Purpose Most cases of non–small-cell lung cancer (NSCLC) with dramatic responses to gefitinib have specific activating mutations in the epidermal growth factor receptor (EGFR), but the predictive value of these mutations has not been defined in large clinical trials. The goal of this study was to determine the contribution of molecular alterations in EGFR to response and survival within the phase II (IDEAL) and phase III (INTACT) trials of gefitinib. Patients and Methods We analyzed the frequency of EGFR mutations in lung cancer specimens from both the IDEAL and INTACT trials and compared it with EGFR gene amplification, another genetic abnormality in NSCLC. Results EGFR mutations correlated with previously identified clinical features of gefitinib response, including adenocarcinoma histology, absence of smoking history, female sex, and Asian ethnicity. No such association was seen in patients whose tumors had EGFR amplification, suggesting that these molecular markers identify different biologic subsets of NSCLC. In the IDEAL trials, responses to gefitinib were seen in six of 13 tumors (46%) with an EGFR mutation, two of seven tumors (29%) with amplification, and five of 56 tumors (9%) with neither mutation nor amplification (P = .001 for either EGFR mutation or amplification v neither abnormality). Analysis of the INTACT trials did not show a statistically significant difference in response to gefitinib plus chemotherapy according to EGFR genotype. Conclusion EGFR mutations and, to a lesser extent, amplification appear to identify distinct subsets of NSCLC with an increased response to gefitinib. The combination of gefitinib with chemotherapy does not improve survival in patients with these molecular markers.
Search for the Evolutionary Origin of a Brain: Planarian Brain Characterized by Microarray
Authors: M. Nakazawa
Journal: Molecular Biology and Evolution (2003)

The origin of the brain remains a challenging problem in evolutionary studies. To understand when and how the structural brain emerged, we analyzed the central nervous system (CNS) of a lower invertebrate, planarian. We conducted a large-scale screening of the head part–specific genes in the planarian by constructing a cDNA microarray. Competitive hybridization of cDNAs between a head portion and the other body portion of planarians revealed 205 genes with head part–specific spikes, including essential genes in the vertebrate nervous system. The expression patterns of the top 30 genes showing the strongest spikes implied that the planarian brain has undergone functional regionalization. We demonstrate the complex cytoarchitecture of the planarian brain, despite its simple superficiality of the morphology.
The Inferior Vena Cava Filter—Reply
Authors: Vinay Prasad, Jason Rho, Adam Cifu
Journal: JAMA Internal Medicine (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 Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Internal Medicine journal
Rifaximin maintained remission from hepatic encephalopathy longer than placebo in patients with cirrhosis
Authors: Brian T. Story
Journal: Annals of Internal Medicine (2010)

ACP Journal Club17 August 2010Rifaximin maintained remission from hepatic encephalopathy longer than placebo in patients with cirrhosisBrian T. Story, MD, Kris V. Kowdley, MD, FACPBrian T. Story, MDVirginia Mason Medical Center, Seattle, Washington, USA (B.T.S., K.V.K.), Kris V. Kowdley, MD, FACPVirginia Mason Medical Center, Seattle, Washington, USA (B.T.S., K.V.K.)Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-153-4-201008170-02008 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Source CitationBass NM, Mullen KD, Sanyal A, et al. Rifaximin treatment in hepatic encephalopathy. N Engl J Med. 2010;362:1071-81. https://pubmed.ncbi.nlm.nih.gov/20335583Clinical Impact RatingsGastroenterology: References1 Bajaj JS. Review article: the modern management of hepatic encephalopathy. Aliment Pharmacol Ther. 2010;31:537-47. [PMID: 20002027] Google Scholar2 Sharma BC, Sharma P, Agrawal A, Sarin SK. Secondary prophylaxis of hepatic encephalopathy: an open-label randomized controlled trial of lactulose versus placebo. Gastroenterology. 2009;137:885-91. [PMID: 19501587] Google Scholar Author, Article, and Disclosure InformationAffiliations: Virginia Mason Medical Center, Seattle, Washington, USA (B.T.S., K.V.K.)This article was published at Annals.org on 3 August 2010. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByProbiotics for patients with hepatic encephalopathy 17 August 2010Volume 153, Issue 4Page: JC2-8KeywordsAdverse eventsAntibioticsBrain diseasesCirrhosisHospitalizationsLiver diseasesLiver transplantationProteinsRespiratory failureStatistical data ePublished: 17 August 2010 Issue Published: 17 August 2010 CopyrightCopyright © 2010 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...