tbuckley/cabot-search huggingface dataset:
Watchful Waiting with Periodic Liver Biopsy versus Immediate Empirical Therapy for Histologically Mild Chronic Hepatitis C: A Cost-Effectiveness Analysis
Authors: John B. Wong
Journal: Annals of Internal Medicine (2000)

Background: Not all patients with histologically mild chronic hepatitis C progress to cirrhosis. Objective: To compare no antiviral treatment, periodic liver biopsy with subsequent antiviral treatment for moderate hepatitis or cirrhosis, and immediate antiviral therapy. Design: Cost-effectiveness analysis. Data Sources: Clinical trial data and published studies. Target Population: Hepatitis C virus–infected patients with histologically mild hepatitis. Time Horizon: Lifetime. Perspective: Societal. Intervention: Immediate combination antiviral treatment or biopsy every 3 years plus combination antiviral therapy for moderate hepatitis or cirrhosis. Outcome Measures: Life expectancy, quality-adjusted life expectancy, and costs. Results of Base-Case Analysis: Over 20 years, biopsy every 3 years with treatment of moderate hepatitis would avoid treatment in 50% of the cohort and would result in an 18% likelihood of cirrhosis compared with 16% for immediate treatment and 27% for no antiviral therapy. Immediate antiviral treatment should increase life expectancy by 1.0 quality-adjusted life-year compared with biopsy management. Over an average lifetime, biopsy management would lead to six liver biopsies costing $6200; immediate antiviral treatment would cost $5100 less than biopsy management because of savings related to biopsy and prevention of future hepatitis C–related morbidity. Immediate therapy was cost-effective compared with biopsy management and had a cost-effectiveness ratio of $7000 compared with no antiviral therapy. Results of Sensitivity Analysis: When age, sex, genotype, and estimates of histologic progression or compliance with follow-up are varied, immediate therapy should result in an increase of at least 0.8 quality-adjusted life-year compared with biopsy management. Conclusion: For histologically mild chronic hepatitis C, initial combination treatment compared with periodic liver biopsy should reduce the future risk for cirrhosis, prolong life, and be cost-effective.
MOVEMENTS OF THE MANDIBULAR CONDYLES AND DENTAL ARTICULATION.
Authors: W. E. WALKER
Journal: JAMA (1897)

This paper is a continuation of the line of thought and investigation indicated in my paper entitled "The Glenoid Fossa; the Movements of the Mandible; the Cusps of the Teeth," read before the Southern Dental Association in November, 1895.<sup>1</sup> Up to that time I had not been able to find mention of the facts that, in the movements of mastication, the mandibular condyle moves "not only forward but also downward, causing the ramus to drop, in the anterior and lateral movements of the mandible" and that the condyle on the side toward which the jaw is advancing, in the lateral movements, does not merely "rotate on its axis," otherwise "remaining stationary" as we are taught, but that it also moves both upward and backward, very slightly in many subjects, and not at all in some, but considerably in others. I enlisted the services of men who have access to
The Canadian Experience with Intensive Fluorouracil, Epirubicin and Cyclophosphamide in Patients with Early Stage Breast Cancer
Authors: M.N. Levine, V. Bramwell, K. Pritchard, D. Perrault, B. Findlay, H. Abu-Zahra, D. Warr, A. Arnold, J. Skillings
Journal: Drugs (1993)
IMPORTANCE OF LOCAL FACTORS IN THE ONSET OF PULMONARY TUBERCULOSIS
Authors: W. Pagel
Journal: BMJ (1934)

jsA -~~~~~~~~~~~~~~~~~~~~~~~~~MEIA ORAThe usual symptoms came on, aind some burning of the face, lips, and -tongue with oedema were observed on arrival at hospital shortly after.This appeared to be a mild case, and after two days the parents removed the child against medical advice.The subsequent history illustrates the necessity for
Bariatric Surgery and Long-term Control of Morbid Obesity
Authors: Robert E. Brolin
Journal: JAMA (2002)

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 nursing profession's coming of age: Sign of the times
Authors: Vinay P Rao
Journal: BMJ (2006)

The nursing profession's coming of age The end of medicine as a professionEditor-Young describes the coming of age of the nursing profession. 1 All professions and occupations are human creations and therefore are subject to change.With the widening of roles of many professions, it becomes harder to define what a doctor can do that can't be done by an appropriately trained member of another profession.Perhaps major surgery and certifying cause of death are all that remains.With the increasing difficulty of getting junior doctors to do anything that may be regarded as work (rather than education) we doctors may be engineering the abolition of our profession, and we may move from distinct professions to practitioners from varied backgrounds being trained for a particular function.
Suppression of ovulation by transdermal oestradiol patches.
Authors: N. R. Watson, J. W. Studd, A. F. Riddle, M. Savvas
Journal: BMJ (1988)

Gynaecological history and details of development of osteoarthritis and rheumatoid arthritis in middle aged women Median Median age Median time from Median age at at onset of Median age No (%/O) who Median age at hysterectomy No in age No (% menopause symptoms at referral had had hysterectomy to referral group (years) nulliparous (years) (years) (years) hysterectomy (years) (years) Osteoarthritis group 292 58 52 (18) 49-5 49 53 82 (28)* 42 6 years Rheumatoid arthritis group 270 59 71(27) 49 5 48 50 39(14)* 45 4 years Electoral register population 243 50 33 (14) 50 37 (15) 43 Local general practice population 346 54 71 (29) 50 38 (11) 41*Sixty three (77%) and 25 (64%) hysterectomies were carried out at least one year before referral to hospital in the osteoarthritis and rheumatoid arthritis groups respectively.implied that the indications for surgery might be more important than surgery itself.There are several poten- tial biases.Early symptoms in women with osteo- arthritis may have been misinterpreted and resulted in hysterectomy.This is unlikely given the long median delay (six years) between operation and diagnosis and that those with spinal osteoarthritis did not have the greatest rate of hysterectomy.The difference in rate of hysterectomy between the women with osteoarthritis and those with rheumatoid arthritis may have been due to fewer gynaecological abnormalities occurring in those with rheumatoid arthritis.Previous studies found no difference between women with rheumatoid arthritis and controls,2 and the rates of hysterectomy in women with rheumatoid arthritis were similar to those in our population controls.By contrast, a link between hysterectomy and predisposition to osteoarthritis is biologically plausible.Dysfunctional uterine bleeding and fibroids, the main reasons for hysterectomy in our study, have both been attributed to an excess of oestrogens.Oestrogens have also been found to affect adversely several different animal models of
Letter: Screening for breast cancer.
Authors: I Burn
Journal: BMJ (1975)

scribing.Too mnany clinicians go into print on insufficient evidence when they have a single case.These are taken up and per- petuated by those who write articles on MAOIs as fact.A confused situation is being compounded by inaccurate and nmisleading evidence where factual and clear authoritative reporting is required for the guidance of both the doctor and the paticnt.-I am, etc.,
The course and correlates of high hospital utilization in sickle cell disease: Evidence from a large, urban Medicaid managed care organization
Authors: C. Patrick Carroll, Carlton Haywood, Peter Fagan, Sophie Lanzkron
Journal: American Journal of Hematology (2009)

Although most patients with sickle cell disease (SCD) are hospitalized infrequently and manage painful crises at home, a small subpopulation is frequently admitted to emergency departments and inpatient units. This small group accounts for the majority of health care expenses for patients with SCD. Using inpatient claims data from a large, urban Medicaid MCO for 5 consecutive years, this study sought to describe the course of high inpatient utilization (averaging four or more admissions enrolled per year for at least 1 year) in members with a diagnosis of SCD and a history of hospitalizations for vaso-occlusive crisis. High utilizers were compared with the other members with SCD on demographics, medical and psychiatric comorbidity, and use of other health care resources. Members who were high utilizers had more diagnostic mentions of sickle cell complications than low utilizers. However, the pattern of high inpatient utilization was likely to moderate over successive years, and return to the pattern after moderation was uncommon. Despite this, a small subpopulation engaged in exceptional levels of inpatient utilization over multiple years.
A High Throughput In Vivo Model for Testing Delivery and Antiviral Effects of siRNAs in Vertebrates
Authors: Brian Dall Schyth, Niels Lorenzen, Finn Skou Pedersen
Journal: Molecular Therapy (2007)

Despite the promise of small interfering RNAs (siRNAs) in antiviral therapy, few in vivostudies of them as inhibitors of viral replication and disease have been published, a lack that is most probably due to problems with obtaining successful delivery. Here we introduce a novel in vivomodel composed of small juvenile rainbow trout and a fish pathogenic virus to analyze the delivery and antiviral effects of formulated siRNAs. Intraperitoneally (IP) injected siRNAs formulated in polycationic liposomes, and to a lesser degree naked siRNAs, primarily entered free IP cells, including macrophage-like cells. Uptake in these cells correlated with antiviral activity, seen as reduced mortality of virus-challenged fish. However, protection at the disease level was not dependent upon which of three tested siRNAs was used, and protection correlated with up-regulation of an interferon (IFN)-related gene in the liver, indicating a systemic IFN response. The results emphasize the compromise in using transfection reagents for improved uptake of siRNAs, where these reagents also increase the risk of the siRNAs ending up in a cellular compartment in which stimulation of non-specific anti-viral defence mechanisms will be initiated.
The TSH receptor reveals itself
Authors: Terry Davies, Russell Marians, Rauf Latif
Journal: Journal of Clinical Investigation (2002)

The thyrotropin receptor (TSHR), one of the primary antigens in autoimmune thyroid disease, is a target of both antigen-specific T cells and antibodies in patients with this condition (1). Autoantibodies to the TSHR (TSHR-Ab) act as thyroid stimulating factor (TSH) agonists in autoimmune hyperthyroidism (Robert Graves disease) but as TSH antagonists in autoimmune hypothyroidism (Hashimoto thyroiditis). The TSHR antigen is primarily expressed in the epithelial cells of the thyroid follicles, but TSHR mRNA and protein have been reported in a variety of cell types, some of which show evidence of receptor activity (Table ​(Table11).



Table 1

Tissue distribution of the TSHR



The TSHR gene, cloned in 1989 (2–5), maps to human chromosome 14q and encodes a predicted seven-transmembrane, G protein–coupled glycoprotein. Although it is similar to the luteinizing hormone receptor and the follicle-stimulating hormone receptor, the TSHR is the largest of the glycoprotein hormone receptors, due primarily to 8– and 50–amino acid insertions in its ectodomain (residues 38–45 and 317–367) (6). As predicted from its cDNA, the TSHR has an unglycosylated molecular weight of 84 kDa but the glycosylated holoreceptor runs on SDS-PAGE with an apparent molecular weight of 95–100 kDa. There are six potential N-linked glycosylation sites on the TSHR, and it was recently shown that the TSHR is also palmitoylated (7). The minimal 5′ promoter region required to confer thyroid-specific expression and cAMP autoregulation extends from 220 to 39 bp upstream of the transcription start site, but there are multiple transcription start sites between –89 and –68 bp (8).
Dynamics of interaction between complement-fixing antibody/dsDNA immune complexes and erythrocytes. In vitro studies and potential general applications to clinical immune complex testing.
Authors: R P Taylor, C Horgan, M Hooper, J Burge
Journal: Journal of Clinical Investigation (1985)

Soluble antibody/3H-double-stranded PM2 DNA (dsDNA) immune complexes were briefly opsonized with complement and then allowed to bind to human erythrocytes (via complement receptors). The cells were washed and subsequently a volume of autologous blood in a variety of media was added, and the release of the bound immune complexes from the erythrocytes was studied as a function of temperature and time. After 1-2 h, the majority of the bound immune complexes were not released into the serum during blood clotting at either 37 degrees C or room temperature, but there was a considerably greater release of the immune complexes into the plasma of blood that was anticoagulated with EDTA. Similar results were obtained using various conditions of opsonization and also using complexes that contained lower molecular weight dsDNA. Thus, the kinetics of release of these antibody/dsDNA immune complexes differed substantially from the kinetics of release of antibody/bovine serum albumin complexes that was reported by others. Studies using the solution phase C1q immune complex binding assay confirmed that in approximately half of the SLE samples that were positive for immune complexes, there was a significantly higher level of detectable immune complexes in plasma vs. serum. Freshly drawn erythrocytes from some SLE patients exhibiting this plasma/serum discrepancy had IgG antigen on their surface that was released by incubation in EDTA plasma. Thus, the higher levels of immune complexes observed in EDTA plasma vs. serum using the C1q assay may often reflect the existence of immune complexes circulating in vivo bound to erythrocytes.
Subcorneal pustular dermatosis and monoclonal IgA
Authors: D. WALLACH, F. COTTENOT, G. PELBOIS, B. CAVELIER, LILIANE DIDIERJEAN, JEAN-H. SAURAT
Journal: British Journal of Dermatology (1982)

A patient with subcorneal pustular dermatosis was found to have a circulating monoclonal IgA kappa immunoglobulin. Direct irnmunofluorcscence studies revealed IgA kappa deposits in the subcorneal zone of the epidermis. Circulating IgA kappa reacting with the subcorneal zone of normal human epidermis was demonstrated by indirect immunofluoresence. It is speculated that IgA deposition might be implicated in the pathogenesis of subcorneal pustular dermatosis.
A nonsense mutation 1669Glu--&gt;Ter within the regulatory domain of human erythroid ankyrin leads to a selective deficiency of the major ankyrin isoform (band 2.1) and a phenotype of autosomal dominant hereditary spherocytosis.
Authors: P Jarolim, H L Rubin, V Brabec, J Palek
Journal: Journal of Clinical Investigation (1995)

We describe a nonsense mutation in the regulatory domain of erythroid ankyrin associated with autosomal dominant hereditary spherocytosis with a selective deficiency of the ankyrin isoform 2.1 (55% of normal), a deficiency of spectrin (58% of normal) proportional to the decrease in an- kyrin 2.1, and a normal content of the other main ankyrin isoform, protein 2.2.PCR amplification of cDNA encoding the regulatory domain of ankyrin revealed a marked de- crease in the ratio of ankyrin 2.1 mRNA to the ankyrin 2.2 mRNA.Sequencing of ankyrin gene in the region where the 2.1 and 2.2 mRNA differ detected a nonsense mutation 1669Glu-Ter (GAA-TAA) in one ankyrin allele.Only nor- mal ankyrin 2.1 mRNA was detected in the reticulocyte RNA.Since the alternative splicing within the regulatory domain of ankyrin retains codon 1669 in ankyrin 2.1 mRNA and removes it from ankyrin 2.2 mRNA, we propose that the 1669Glu-Ter mutation decreases the stability of the abnormal ankyrin 2.1 mRNA allele leading to a decreased synthesis of ankyrin 2.1 and a secondary deficiency of spectrin.(J.Clin.Invest.1995.95
CXC chemokine receptor CXCR4 expression enhances tumorigenesis and angiogenesis of basal cell carcinoma
Authors: G-S. Chen, H-S. Yu, C-C.E. Lan, K-C. Chow, T-Y. Lin, L-F. Kok, M-P. Lu, C-H. Liu, M-T. Wu
Journal: British Journal of Dermatology (2006)

Background Chemokines and their receptors, well known for their ability to attract leucocytes, also play important roles for tumour progression. Objectives To investigate the possible involvement of chemokine receptors in the pathogenesis of cutaneous basal cell carcinoma (BCC). Methods We performed an expression analysis of chemokine receptors using a well‐characterized human BCC cell line. Upon the finding of CXCR4 expression by BCC, retroviral transduction of BCC cells with the CXCR4 gene was employed to address its functional significance for BCC in vitro and in vivo. Results We found expression of the CXC chemokine receptor CXCR4 by a human cell line and a subset of tissue samples from BCC, especially in noduloulcerative and sclerosing types. Following treatment with CXCL12, the ligand for CXCR4, CXCR4‐transduced BCC cells (CXCR4‐BCC) showed increased proliferation under low serum concentration and resistance to apoptosis induced by ultraviolet B irradiation in vitro. Conditioned media from CXCR4‐BCC preincubated with CXCL12 enhanced tubule formation of human endothelial cells in vitro. These responses of CXCR4‐BCC were negated by cotreatment with either neutralizing antibodies or specific blocking peptides for CXCR4 in vitro. Moreover, xenograft tumour transplants produced by injection of CXCR4‐BCC yielded significant tumour progression in nude mice, whereas additional serial injections of CXCR4‐blocking peptides resulted in tumour regression. Conclusions CXCR4 expression may play a critical role in tumour progression and angiogenesis of certain subtypes of BCC with more aggressive nature, and functional blockade of CXCR4 could be a potential therapeutic strategy for these tumours.
Post-infarction remodeling is independent of mitogen-activated protein kinase kinase 3 (MKK3)
Authors: J CLARK, R FLAVELL, M FAIRCLOTH, R DAVIS, R HEADS, M MARBER
Journal: Cardiovascular Research (2007)

Objectives:: Our aim was to examine the role of mitogen-activated protein kinase kinase 3 (MKK3) in the development of left ventricular (LV) remodeling following myocardial infarction (MI).
The Impact of Hospitals 300-2000
Authors: Anne Hardy
Journal: JAMA (2008)

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
Frederick Wynn Wright
Authors: A. Salter
Journal: BMJ (2014)

Frederick Wynn Wright (“Fred” or “FWW”) was born in Blackburn, Lancashire, and moved south to Birmingham. He studied medicine at Lincoln College, Oxford, in 1948, having been in the army (intelligence corps) after leaving King Edward’s School, Birmingham, in 1945. At school he had studied classics, but “mugged up” the necessary sciences for Oxford prelims during military service. He did preclinical studies and courses in Oxford and the honours school in physiology and biochemistry. It was at Southfield House that he shared a sitting room with Donald Johnson, who became best man in August 1952, when Fred married Lilian. Donald was a theology student— later vicar of Funtington and canon of Chichester cathedral. Fred had known Lilian since he was a child, as his middle name Wynn came from her father, his godfather.

After qualifying he became HP to Patrick Mallam in February 1955, after which he did a short rotating HS job, followed by accident service, before joining radiology in 1956. There progressively senior house officer, registrar, senior registrar, and consultant in 1962.

Fred went to …
Buruli ulcer in a visitor to London
Authors: M.R.W. Evans, J. Mawdsley, R. Bull, D.N.J. Lockwood, H. Thangaraj, D. Shanahan, K. Rajakulasingam
Journal: British Journal of Dermatology (2003)

Journal Article Buruli ulcer in a visitor to London Get access M.R.W. Evans, M.R.W. Evans Hospital for Tropical Diseases, London, U.K., Departments of Respiratory Medicine M.R.W. Evans, Communicable Diseases Branch, Department of Health, London, UK E‐mail: mrw.evans@lineone.net Search for other works by this author on: Oxford Academic Google Scholar J. Mawdsley, J. Mawdsley Hospital for Tropical Diseases, London, U.K., Departments of Respiratory Medicine Search for other works by this author on: Oxford Academic Google Scholar R. Bull, R. Bull Dermatology Search for other works by this author on: Oxford Academic Google Scholar D.N.J. Lockwood, D.N.J. Lockwood Hospital for Tropical Diseases, London, U.K., Departments of Respiratory Medicine Search for other works by this author on: Oxford Academic Google Scholar H. Thangaraj, H. Thangaraj Department of Infectious Diseases, St George's Hospital, London, U.K Search for other works by this author on: Oxford Academic Google Scholar D. Shanahan, D. Shanahan Surgery, Homerton Hospital, London, U.K Search for other works by this author on: Oxford Academic Google Scholar K. Rajakulasingam K. Rajakulasingam Hospital for Tropical Diseases, London, U.K., Departments of Respiratory Medicine Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 149, Issue 4, 1 October 2003, Pages 907–909, https://doi.org/10.1046/j.1365-2133.2003.05562.x Published: 01 October 2003
Controlled Demolition: Smurf1 Regulates Neuronal Polarity by Substrate Switching
Authors: Michael Stiess, Frank Bradke
Journal: Neuron (2011)

During axon specification, growth promoting proteins localize selectively to the growing axon. In this issue of <i>Neuron</i>, Cheng et al. report how selective protein degradation, controlled by a substrate switch of the ubiquitin ligase Smurf1, specifies Par6 and RhoA localization and thereby regulates neuronal polarity.