tbuckley/cabot-search huggingface dataset:
Nitrofurantoin and Chronic Active Hepatitis
Authors: ALASTAIR R.O. MILLER
Journal: Annals of Internal Medicine (1982)

Letters and Corrections1 September 1982Nitrofurantoin and Chronic Active HepatitisALASTAIR R.O. MILLER, R.N., BRUCE J. ADDIS, R.N., PAUL D. CLARKE, R.N.ALASTAIR R.O. MILLER, R.N.Search for more papers by this author, BRUCE J. ADDIS, R.N.Search for more papers by this author, PAUL D. CLARKE, R.N.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-97-3-452_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Chronic active hepatitis is a recognized complication of treatment with nitrofurantoin. All the cases previously described have occurred in women. We would like to describe the first case in a man.A 65-year-old white man was admitted for investigation of nonresolving jaundice and developing liver failure. The patient's illness had begun 6 months previously as viral hepatitis but had persisted, and his condition had deteriorated, with the appearance of ascites and ankle edema. Alcohol intake was small before the onset of illness and nil after it began. For the 12 months before admission the patient had been...References1. LINDBERG J, LINDHOLM A, LUNDIN P, and IWARSON S. Trigger factors and HLA-A antigens in chronic active hepatitis. Br Med J. 1975;4:77-9. CrossrefMedlineGoogle Scholar2. TOLMAN K. Nitrofurantoin and chronic active hepatitis [Editorial]. Ann Intern Med. 1980;92:119-20. LinkGoogle Scholar3. HOLMBERG L, BOMAN G, and BOTTINGER L. Adverse reaction to nitrofurantoin: analysis of 921 reports. Am J Med. 1980;69:733-9. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: ALASTAIR R.O. MILLER, R.N.; BRUCE J. ADDIS, R.N.; PAUL D. CLARKE, R.N.Affiliations: Royal Naval Hospital Gosport, Hampshire United Kingdom PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byAutoimmune Hepatitis Induced by Nitrofurantoin. The Importance of the Autoantibodies for an Early Diagnosis of Immune DiseaseHepatotoxicity of antibiotics and antifungalsCombined nitrofurantoin toxicity to liver and lung 1 September 1982Volume 97, Issue 3Page: 452-452KeywordsAlcoholsAnklesAscitesChronic hepatitisEdemaHepatitisHepatitis ALiver ePublished: 1 December 2008 Issue Published: 1 September 1982 PDF downloadLoading ...
N-terminal prohormone brain natriuretic peptide: a biomarker for detecting cardiovascular risks in patients with rheumatoid arthritis or osteoarthritis?
Authors: T. Haupl, G. R Burmester, E. Giannitsis, T. Rohrlach, E. Spanuth, H. Parsch, K. Brune
Journal: Annals of the Rheumatic Diseases (2007)

Rheumatoid arthritis (RA) is associated with an increased risk for cardiovascular (CV) events including cardiac insufficiency, acute myocardial infarction and stroke.1 It is assumed that the release of proinflammatory cytokines and acute-phase proteins furthers the progression of atherosclerosis.2,3 This process seems to be further accelerated and aggravated by the administration of cyclooxygenase (Cox) inhibitors (coxibs and non-steroidal anti-inflammatory drugs (NSAIDs)). Therefore, without defining how this could be done, the Food and Drug Administration and European Agency for the Evaluation of Medicinal Products have recommended CV-risk stratification and individualised risk assessment in patients with RA before using coxibs or NSAIDs.

The B type natriuretic peptide (BNP) is a hormone synthesised by cardiomyocytes in response to increased wall tension. The plasma level of its stable, inactive breakdown product, N-terminal prohormone BNP (NT-proBNP), has been identified as a universal predictor of CV risks4 even in patients with clinically inapparent impaired CV function. Patients with RA are known to be burdened with an increased incidence of CV impairment.1 There is preliminary evidence that the serum levels of NT-proBNP in these patients reflect this burden.5

Recently, we observed that the use of NSAIDs and …
A Comparative Study of the Tissue-destroying Effect of the Laser and Electrocoagulation
Authors: W. Matek, H.-D. Reidenbach, A. Wittmann, L. Beierlein, P. Hermanek
Journal: Endoscopy (1989)

The effect of the laser on compact, glandular tissue at the dosage employed for the local palliative treatment of tumors, can largely be mimicked with the aid of high-frequency current (HF-current), applied with the aid of an electro-hydro-thermo-probe: The experiments described in the present study were performed on the livers of 70 male Wistar rats. The laser was applied for 2 seconds at an output of 80 J at a distance to the tissue of 0.5 cm. In the first stage, in the acute experiment, the effect of the HF-current was matched to that of the laser by varying the modulated and unmodulated current components. It was found that the depths of penetration into the tissue at the given laser settings could be achieved with modulated HF-current (so-called coagulation current) at an output of more than 72 watts (equipment setting K 10) coagulation being performed for 10 seconds. The admixture of modulated HF-current (so-called cutting current) reduces the depth of penetration into the tissue. In the first 5 days, the depth of penetration increases after both laser irradiation and HF-coagulation, by a factor of 2 to 3. With respect to the depths of penetration (DP), the scatter ranges, and the histological changes, no difference is to be seen between laser and HF lesions: Laser DP = 5.7 mm (confidence range: 4.4-7.0 mm); HF DP (equipment setting K 10) = 4.8 mm (confidence range: 3.6-5.4 mm).(ABSTRACT TRUNCATED AT 250 WORDS)
A Road Less Traveled
Authors: Helen W.
Journal: Annals of Internal Medicine (2003)

On Being a Patient17 June 2003A Road Less TraveledHelen W.Helen W.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-138-12-200306170-00017 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail I kept buttoning and unbuttoning my black leather coat, responding to the alternating waves of heat and chill typical of narcotic withdrawal. It was a familiar sensation, but instead of being at home with the flu, I was sitting in a circle of fellow substance abusers sharing the misery and confusion of early sobriety.We were a mixed bag of personalities, ages, ethnicities, income levels, and drugs of choice. There was a housewife who smoked pot daily, a young Filipino with a new baby and a methamphetamine habit, a 25-year-old blonde facing prison for her fifth DUI, an alcoholic ex-policeman ... Author, Article, and Disclosure InformationAffiliations: Note: Helen W. is a pseudonym. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byPhysician Impairment and ProfessionalismLife on the Receiving End: A Qualitative Analysis of Health Providers??? Illness Narratives 17 June 2003Volume 138, Issue 12Page: 1004-1005KeywordsAddictsAlcoholicsAlcoholsChildrenCoffeeDrugsEmotionsSigns and symptomsSleepUrine ePublished: 17 June 2003 Issue Published: 17 June 2003 Copyright & PermissionsCopyright © 2003 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Nodal/Activin Signaling Predicts Human Pluripotent Stem Cell Lines Prone to Differentiate Toward the Hematopoietic Lineage
Authors: Veronica Ramos-Mejia, Gustavo J Melen, Laura Sanchez, Ivan Gutierrez-Aranda, Gertrudis Ligero, Jose L Cortes, Pedro J Real, Clara Bueno, Pablo Menendez
Journal: Molecular Therapy (2010)

Lineage-specific differentiation potential varies among different human pluripotent stem cell (hPSC) lines, becoming therefore highly desirable to prospectively know which hPSC lines exhibit the highest differentiation potential for a certain lineage. We have compared the hematopoietic potential of 14 human embryonic stem cell (hESC)/induced pluripotent stem cell (iPSC) lines. The emergence of hemogenic progenitors, primitive and mature blood cells, and colony-forming unit (CFU) potential was analyzed at different time points. Significant differences in the propensity to differentiate toward blood were observed among hPSCs: some hPSCs exhibited good blood differentiation potential, whereas others barely displayed blood-differentiation capacity. Correlation studies revealed that the CFU potential robustly correlates with hemogenic progenitors and primitive but not mature blood cells. Developmental progression of mesoendodermal and hematopoietic transcription factors expression revealed no correlation with either hematopoietic initiation or maturation efficiency. Microarray studies showed distinct gene expression profile between hPSCs with good versus poor hematopoietic potential. Although neuroectoderm-associated genes were downregulated in hPSCs prone to hematopoietic differentiation many members of the Nodal/Activin signaling were upregulated, suggesting that this signaling predicts those hPSC lines with good blood-differentiation potential. The association between Nodal/Activin signaling and the hematopoietic differentiation potential was confirmed using loss- and gain-of-function functional assays. Our data reinforce the value of prospective comparative studies aimed at determining the lineage-specific differentiation potential among different hPSCs and indicate that Nodal/Activin signaling seems to predict those hPSC lines prone to hematopoietic specification.
Age-Dependent Heart Damage
Authors: Tracy Hampton
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
Does Laughter Make Good Medicine?
Authors: Rachel K. Sobel
Journal: New England Journal of Medicine (2006)

The medical teams convened for a ritual snack break at 10:45 on a recent call night. We ate our ice cream in the far corner of the Moffiteria — as we affectionately call the cafeteria at UCSF's Moffit–Long Hospital — fueling up before the onslaught of admissions. The evening's theme: funniest beeper pages in the middle of the night."I once got this page from a nurse," said an intern. "`Doctor, your patient is covered in ants.'" The table erupted in laughter. Apparently, the patient had come in off the streets and brought the ants with him. They crawled out . . .
Influence of thyroid hormone status on mevalonate metabolism in rats.
Authors: K R Feingold, M H Wiley, G MacRae, M D Siperstein
Journal: Journal of Clinical Investigation (1980)

Mevalonate, an essential intermediate in cholesterol synthesis, is metabolized either to cholesterol or, by the shunt pathway, to CO2. Previous investigations have demonstrated that the kidneys are the chief site of circulating mevalonate metabolism and that sex hormones as well as insulin markedly influence circulating mevalonate metabolism. The present study examined in rats the influence of thyroid hormone status on mevalonate metabolism in vivo and in vitro. L-thyroxine administration increased renal conversion of circulating mevalonate to cholesterol, 41% in the females and 22% in the males. Conversely, hypothyroidism induced by 6 N propyl-2-thiouracil reduced renal conversion of circulatng mevalonate to cholesterol by 45% in females and 27% in males; thyroid hormone replacement in these animals returned cholesterogenesis in the kidneys to supranormal levels. Neither L-thyroxine nor hypothyroidism altered circulating mevalonate conversion to cholesterol in the liver or carcass. In vitro studies confirmed the in vivo observations. Changes in thyroid hormone produced only minor changes in the shunt pathway of mevalonate metabolism. This study demonstrates that the major effect of the thyroid hormone on the metabolism of circulating mevalonate is to alter the conversion of mevalonate to cholesterol, an effect localized solely to the kidneys.
Primary biliary cirrhosis: Report of a focus study group
Authors: Nora V. Bergasa, Andrew Mason, Annarosa Floreani, Jenny Heathcote, Mark G. Swain, David E. J. Jones, Keith M. Lindor, Margaret F. Bassendine, Howard J. Worman
Journal: Hepatology (2004)

Liver Disease (AASLD) conceived the Focus Study Group.The first Focus Study Group was organized by Nora V. Bergasa and
Acute Myelofibrosis Evolving into Acute Myeloblastic Leukemia
Authors: JAMES B. PUCKETT
Journal: Annals of Internal Medicine (1981)

Letters and Corrections1 April 1981Acute Myelofibrosis Evolving into Acute Myeloblastic LeukemiaJAMES B. PUCKETT, M.D., M. ROBERT COOPER, M.D.JAMES B. PUCKETT, M.D.Search for more papers by this author, M. ROBERT COOPER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-94-4-545_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: We recently reported to this journal the case of a patient in whom acute myelofibrosis developed 3 years after successful multimodality therapy of a non-Hodgkin's lymphoma (1). This patient subsequently showed a gradual evolution into acute myeloblastic leukemia.A 54-year-old woman developed acute myelofibrosis in April 1980, 3 years after successful multimodality therapy for a diffuse mixed lymphocytic-histiocytic gastric lymphoma. The myelofibrosis was treated with exymetholone and prednisone without improvement. She required weekly erythrocyte and platelet transfusions. Her initial marrow and peripheral smears showed no myeloblastic activity. In July 1980, a repeat bone marrow biopsy showed myelofibrosis...References1. PUCKETTCOOPER JM. Acute myelofibrosis after treatment for non-Hodgkin's lymphoma. Ann Intern Med. 1980;93:510. Letter. LinkGoogle Scholar2. BEARMANPANGALISRAPPAPORT RGH. Acute "malignant" myelosclerosis. Cancer. 1979;43:279-93. CrossrefMedlineGoogle Scholar3. BIRDPROCTOR TS. Malignant myelosclerosis: myeloproliferative disorder or leukemia? Am J Clin Pathol. 1977;67:512-20. CrossrefMedlineGoogle Scholar4. WEISENBURGER D. Acute myelofibrosis terminating as acute myeloblastic leukemia. Am J Clin Pathol. 1980;73:128-32. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Bowman-Gray School of Medicine Winston-Salem, NC 27103 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByAcute panmyelosis with myelofibrosis: an entity distinct from acute megakaryoblastic leukemiaGranulocytic sarcoma of megakaryoblastic differentiation complicating chronic idiopathic myelofibrosisAcute myelofibrosis: Response to recombinant human interferon alpha-2aMyelofibrosis: A review of clinical and pathologic features and treatmentAkute Leukämien und Myelodysplasien 1 April 1981Volume 94, Issue 4_Part_1Page: 545-546KeywordsAcute myeloid leukemiaBiopsyBone marrowLymphomaPlatelets Issue Published: 1 April 1981 PDF DownloadLoading ...
Infectious background of patients with a history of acute anterior uveitis
Authors: M Huhtinen
Journal: Annals of the Rheumatic Diseases (2002)

To study the infectious background of patients with a history of acute anterior uveitis (AAU) and healthy control subjects.Sixty four patients with previous AAU and 64 sex and age matched controls were studied. Serum antibodies to Salmonellae, Yersiniae, Klebsiella pneumoniae, Escherichia coli, Proteus mirabilis, Campylobacter jejuni, and Borrelia burgdorferi were measured using enzyme linked immunosorbent assay (ELISA), and antibodies to Chlamydia trachomatis and Chlamydia pneumoniae by microimmunofluorescence test. Peripheral blood mononuclear cells (PBMCs), separated by density gradient centrifugation, were studied for Salmonella and Yersinia antigens by means of an immunofluorescence test, and for C pneumoniae DNA with a polymerase chain reaction (PCR).Neither prevalence nor levels of single microbial antibodies studied differed between the patients and control subjects, or between subgroups of patients created on the basis of clinical characteristics. In logistic regression analysis, the high number of recurrences (>10) of AAU was independently related to the presence of single or multiple bacterial antibodies (p=0.04). None of the PBMC samples of the patients were positive for Yersinia or Salmonella antigens. C pneumoniae PCR was positive in a patient who was negative for C pneumoniae antibodies.Although neither the prevalence nor the levels of single microbial antibodies studied differed between the patients and the controls, current data suggest that the presence of single or multiple antibodies in patients with many recurrences of AAU compared with patients with none or few recurrences may be a sign of repeated infections, antigen persistence, or raised innate immune responsiveness.
The new public health strategy for England
Authors: L. Davies
Journal: BMJ (2010)

Healthy Lives, Healthy People has great potential but implementing it will be challenging

The government’s new public health strategy for England, Healthy Lives, Healthy People ,1 is a welcome commitment to protecting and improving health and reducing health inequalities. Action is clearly needed. Although people are generally living longer, the overall burden of chronic physical and mental ill health is increasing,2 and the poor are worse off than the rich. If, as some have predicted,3 the recent comprehensive spending review affects the poor more than the rich, this is likely to be exacerbated⇓.4



The strategy, which promises to be radical and new, is evidence based and rooted in an approach that engages and integrates the efforts of national and local government, the NHS, charities, schools, higher education, voluntary groups, businesses, and employers. The strategy accepts a place for government leadership and, albeit when other approaches have failed, for regulation. However, it takes the view that the balance of responsibility and action should shift from central government to local communities, and that people should be “nudged” towards taking on more responsibility for their health by living more healthily. A cabinet subcommittee has been established to engage relevant government departments, and the strategy includes an encouraging list of related initiatives.

In the spirit of national engagement, county and unitary local authorities …
The Ways in Which Hormones Change Cyclic Adenosine 3′,5′-Monophosphate-Dependent Protein Kinase Subunits, and How Such Changes Affect Cell Behavior*
Authors: STEPHEN W. SPAULDING
Journal: Endocrine Reviews (1993)

Hormones and cytokines regulate many cellular functions by activating the ubiquitous cAMP-dependent protein kinase (A kinase) system. Newly synthesized cAMP molecules bind to regulatory (R) subunits in A kinase holoenzymes, causing them to release their catalytic (C) subunits. These free C subunits then phosphorylate proteins until the cAMP level falls, whereupon the R subunits regain their affinity for free C subunits, and thus form inactive holoenzymes again. However if cAMP levels remain persistently elevated, many cells change their A kinase system. Some cells alter the rate of degradation of subunits, and some cells change the level or stability of the messages encoding subunits. Cellular behavior often changes if cAMP levels remain elevated: many cells differentiate, some cells proliferate, and some cells die, depending on the stage of the cell cycle. The two forms of A kinase holoenzyme (type I and type II) contain identical C subunits, but contain either an RI dimer or an RII dimer. In some tissues, type II holoenzyme is compartmentalized to subcellular organelles via specific anchoring proteins, whereas type I holoenzyme is generally cytosolic. Free RI subunits turn over more rapidly than free RII subunits in most cells, but all free subunits are degraded more rapidly than when they are associated together in holoenzymes. Free C subunits can phosphorylate a broad spectrum of proteins in both the cytoplasm and nucleus, depending on the type of cell, its state of differentiation, and the hormonal milieux. If free C subunit is microinjected into the cytoplasm of some intact cells, it migrates to the nucleus, whereas if free R subunit is microinjected, it remains in the cytoplasm. If both subunits are coinjected, R subunit blocks the nuclear migration of the C subunit. A major nuclear target for free C subunits is the CREB family of nuclear proteins, which bind to cAMP response elements (CREs) in the promoter regions of cAMP-responsive genes. Phosphorylation of CREB proteins alters their ability to form dimers and to interact with CREs. Many CREB proteins can be phosphorylated by other kinases as well, indicating this is one means by which cells coordinate cAMP- and non-cAMP-mediated gene responses. However, interactions between CREB and a number of other nuclear proteins with which they can dimerize, especially proteins whose levels are rapidly altered in response to hormones, provide an even higher degree of complexity of gene regulation than is possible from various kinases phosphorylating the different sites in CREB proteins.(ABSTRACT TRUNCATED AT 400 WORDS)
Selection of Anesthetic
Authors: C. R. Swanbeck
Journal: JAMA (1974)

<h3>To the Editor.—</h3> The comments of Edwin J. Goldman, MD (226:1120, 1973) regarding the central nervous system (CNS) excitation produced by enflurane ("Enflurane and Catch 22×3") may be well taken, in that it is sometimes difficult for us in clinical anesthesiology to make a rational decision regarding which of the halogenated agents to use in a given case. In our department, however, the advent of enflurane (ethrane) has dovetailed very nicely with our prior trend from halothane to more so-called balanced anesthesia, and has enabled us to get by with low concentrations of enflurane that are probably insufficient to produce any considerable degree of CNS excitation or other organ damage. We use primarily either a mixture of droperidol and fentanyl citrate (Innovar) or fentanyl citrate (Sublimaze) with the N20:02 for this purpose, and naloxone hydrochloride (Narcan) reverses the narcotic so effectively at the termination of the case that most patients