tbuckley/cabot-search huggingface dataset:
Hepatitis A Virus
Authors: Sarah Ringold
Journal: JAMA (2005)

Hepatitis A VirusH epatitis A virus (HAV) is one of several viruses that specifically target the liver.Infection with HAV generally leads to a self-limited illness that causes temporary liver inflammation (damage to cells) but does not require specific treatment.However, in rare cases, the infection may result in a more serious illness, leading to liver failure (loss of liver functions) or death.As many as 30% of individuals in the United States have evidence of past infection with the virus.The virus is found in the feces of infected persons and is most commonly transmitted through person-to-person contact and through the ingestion of water or food that has been contaminated with feces from infected individuals.Infection with HAV is more common in developing countries where poor hygiene may be more common.The July 13, 2005, issue of JAMA includes an article about trends in HAV infection in the United States over the past decade.
Eltrombopag: Is this “24 karat gold platelet” treatment for thrombocytopenia in cirrhosis associated with hepatitis C?
Authors: Amany Zekry, John Freiman, Kris Kowdley, Geoffrey McCaughan, Christian Trautwein
Journal: Hepatology (2008)

Eltrombopag is a new, orally active thrombopoietin-receptor agonist that stimulates thrombopoiesis. We evaluated its ability to increase platelet counts and facilitate treatment for hepatitis C virus (HCV) infection in patients with thrombocytopenia associated with HCV-related cirrhosis. Methods: Seventy-four patients with HCV-related cirrhosis and platelet counts of 20,000 to less than 70,000 per cubic millimeter were randomly assigned to receive eltrombopag (30, 50, or 75 mg daily) or placebo daily for 4 weeks. The primary end point was a platelet count of 100,000 per cubic millimeter or more at week 4. Peginterferon and ribavirin could then be initiated, with continuation of eltrombopag or placebo for 12 additional weeks. Results: At week 4, platelet counts were increased to 100,000 per cubic millimeter or more in a dose-dependent manner among patients for whom these data were available: in 0 of the 17 patients receiving placebo, in 9 of 12 (75%) receiving 30 mg of eltrombopag, in 15 of 19 (79%) receiving 50 mg of eltrombopag, and in 20 of 21 (95%) receiving 75 mg of eltrombopag (P < 0.001). Antiviral therapy was initiated in 49 patients (in 4 of 18 patients receiving placebo, 10 of 14 receiving 30 mg of eltrombopag, 14 of 19 receiving 50 mg of eltrombopag, and 21 of 23 receiving 75 mg of eltrombopag) while the administration of eltrombopag or placebo was continued. Twelve weeks of antiviral therapy, with concurrent receipt of eltrombopag or placebo, were completed by 36%, 53%, and 65% of patients receiving 30 mg, 50 mg, and 75 mg of eltrombopag, respectively, and by 6% of patients in the placebo group. The most common adverse event during the initial 4 weeks was headache; thereafter, the adverse events were those expected with interferon-based therapy. events were those expected with interferon-based therapy. Conclusions: Eltrombopag therapy increases platelet counts in patients with thrombocytopenia due to HCV-related cirrhosis, thereby permitting the initiation of antiviral therapy.
Correction re Myeloproliferative Disorders
Authors: FRANK A. LIZZI
Journal: Annals of Internal Medicine (1970)

Letters and Comments1 January 1970Correction re Myeloproliferative DisordersFRANK A. LIZZI, M.D.FRANK A. LIZZI, M.D.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-72-1-148_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: I would like to point out an error in the otherwise quite thorough report by Glasser and Walker, entitled "Transitions Among the Myelopro-liferative Disorders" (Ann Intern Med 71: 285-307, 1969).In referring to a patient reported by Kemp, Stafford, and Tanner (1), the authors state that "no karyotypes were presented for analysis" to substantiate the presence of the Philadelphia chromosome. In point of fact, however, in the report by Kemp and associates two karyotypes are illustrated showing the Ph1chromosome in their patient....Reference1. KEMPSTAFFORDTANNER NJR: Chromosome studies during early and terminal chronic myeloid leukaemia. Brit Med J 1: 1010, 1964. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Subdepartment of Hematology Albany Medical Center Hospital Albany, N.Y. 12208 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 January 1970Volume 72, Issue 1Page: 148-148KeywordsChromosomesKaryotypesMyeloproliferative disorders Issue Published: 1 January 1970 PDF downloadLoading ...
Inhibition and Genetic Ablation of the B7/CD28 T-Cell Costimulation Axis Prevents Experimental Hypertension
Authors: Antony Vinh, Wei Chen, Yelena Blinder, Daiana Weiss, W. Robert Taylor, Jörg J. Goronzy, Cornelia M. Weyand, David G. Harrison, Tomasz J. Guzik
Journal: Circulation (2010)

Background— The pathogenesis of hypertension remains poorly understood, and treatment is often unsuccessful. Recent evidence suggests that the adaptive immune response plays an important role in this disease. Various hypertensive stimuli cause T-cell activation and infiltration into target organs such as the vessel and the kidney, which promotes vascular dysfunction and blood pressure elevation. Classically, T-cell activation requires T-cell receptor ligation and costimulation. The latter often involves interaction between B7 ligands (CD80 and CD86) on antigen-presenting cells with the T-cell coreceptor CD28. This study was therefore performed to examine the role of this pathway in hypertension. Methods and Results— Angiotensin II–induced hypertension increased the presence of activated (CD86 + ) dendritic cells in secondary lymphatic tissues. Blockade of B7-dependent costimulation with CTLA4-Ig reduced both angiotensin II– and deoxycorticosterone acetate (DOCA)–salt–induced hypertension. Activation of circulating T cells, T-cell cytokine production, and vascular T-cell accumulation caused by these hypertensive stimuli were abrogated by CTLA4-Ig. Furthermore, in mice lacking B7 ligands, angiotensin II caused minimal blood pressure elevation and vascular inflammation, and these effects were restored by transplantation with wild-type bone marrow. Conclusions— T-cell costimulation via B7 ligands is essential for development of experimental hypertension, and inhibition of this process could have therapeutic benefit in the treatment of this disease.
Multiple recurrent intrapulmonary and endobronchial mesenchymomas (hamartomas).
Authors: C M Laroche, S Stewart, F Wells, J Shneerson
Journal: Thorax (1993)

A patient is described with multiple, benign, chondromatous intrapulmonary and endobronchial mesenchymomas of the lung, which recurred after resection on two occasions over a period of 30 years. In such a patient presenting at a young age or with a history of previous recurrence, a wedge excision may be necessary to prevent further recurrence.
Inhibition and Rapid Recovery of Ca <sup>2+</sup> Current During Ca <sup>2+</sup> Release From Sarcoplasmic Reticulum in Guinea Pig Ventricular Myocytes
Authors: Karin R. Sipido, Geert Callewaert, Edward Carmeliet
Journal: Circulation Research (1995)

Abstract We have investigated the modulation of the L-type Ca 2+ channel by Ca 2+ released from the sarcoplasmic reticulum (SR) in single guinea pig ventricular myocytes under whole-cell voltage clamp. [Ca 2+ ] i was monitored by fura 2. By use of impermeant monovalent cations in intracellular and extracellular solutions, the current through Na + channels, K + channels, nonspecific cation channels, and the Na + -Ca 2+ exchanger was effectively blocked. By altering the amount of Ca 2+ loading of the SR, the time course of the Ca 2+ current (I Ca ) could be studied during various amplitudes of Ca 2+ release. In the presence of a large Ca 2+ release, fast inhibition of I Ca occurred, whereas on relaxation of [Ca 2+ ] i , fast recovery was observed. The time course of this transient inhibition of I Ca reflected the time course of [Ca 2+ ] i . However, the inhibition seen in the first 50 ms, ie, the time of net Ca 2+ release from the SR, exceeded the inhibition observed later during the pulse, suggesting the existence of a higher [Ca 2+ ] near the channel during this time. Transient inhibition of I Ca during Ca 2+ release was observed to a similar degree at all potentials. It could still be observed in the presence of intracellular ATP-γ-S and of cAMP. Therefore, we conclude that the modulation of I Ca by Ca 2+ release from the SR is not related to dephosphorylation. It could be related to a reduction in the driving force and to a direct inhibition of the channel by [Ca 2+ ] i . The observation that the degree of inhibition does not depend on membrane potential suggests that the Ca 2+ binding site for this modulation is located outside the pore. The transient nature of the modulation of I Ca by Ca 2+ release will contribute to the recovery of I Ca during prolonged action potentials.
Regression of multiple viral warts in a human immunodeficiency virus-infected patient treated by triple antiretroviral therapy
Authors: J.R. Turnbull, R. Husak, R. Treudler, C.C. Zouboulis, C.E. Orfanos
Journal: British Journal of Dermatology (2002)

Human papillomavirus‐induced viral warts may cause therapeutic problems, especially in human immunodeficiency virus (HIV)‐infected patients. We report a 34‐year‐old homosexual man who, after testing HIV‐positive in January 1998, suffered from multiple, extensive viral warts, particularly on his hands (Fig. 1) and upper lip. He received oral antiretroviral therapy for 2 years, initially with didanosine, stavudine and efavirenz. The efavirenz was changed to abacavir in June 1999. The medication was taken irregularly until November 2000. Following 4 months of closely supervised subsequent therapy, a nearly total regression of the viral warts was seen (Fig. 2), accompanied by a significant improvement in immune status.
Disturbances of heart rhythm produced by 50 Hz leakage currents in dogs
Authors: E. B. RAFTERY, H. L. GREEN, I. C. GREGORY
Journal: Cardiovascular Research (1975)

In healthy dogs and in dogs with experimental myocardial infarct, the smallest current applied through a pacing wire which would produce a disturbance in rhythm was 60 μA. This figure is higher than most recommended standards for earth-free monitoring equipment. Much bigger currents were required to produce a disturbance from a wire in the right atrium, which appears to be a safe location for catheters and pacing wires.
Red cell life span after splenectomy in hereditary spherocytosis
Authors: Robert G. Chapman
Journal: Journal of Clinical Investigation (1968)

Despite the persistence of spherocytosis after splenectomy in hereditary spherocytosis, it has usually been assumed that red cell life span returns completely to normal after this treatment. Diisopropyl fluorophosphate. DF(32)P, a noneluting red cell label, was given intravenously to 11 patients in five unrelated families 2-27 yr after splenectomy for typical hereditary spherocytosis. Hemoglobin ranged from 14.0 to 19.8 g/100 ml in this group and reticulocytes from 1.1 to 2.9%, showing the excellent clinical response to splenectomy. Loss of red cell radioactivity corrected for radiophosphorus decay was linear with time during the 60-70 days of the study. Red cell survival as indicated by this rate of loss was 96 +/- 13 days (range 76-118 days), significantly less than the 123 +/- 14 days observed with the same method in 12 persons with normal red cells (P < 0.0005). I conclude that splenectomy does not eliminate the decreased red cell survival in hereditary spherocytosis. The residual 22% decrease in red cell survival is clinically unimportant, but it must be considered in evaluation of biochemical differences observed in hereditary spherocytic red cells.
Prevalence of Clinical and Isolated Subclinical Cardiovascular Disease in Older Adults With Glucose Disorders
Authors: Joshua I. Barzilay, Charles F. Spiekerman, Lewis H. Kuller, Gregory L. Burke, Vera Bittner, John S. Gottdiener, Fred L. Brancati, Trevor J. Orchard, Daniel H. O’Leary, Peter J. Savage
Journal: Diabetes Care (2001)

OBJECTIVE—Clinical cardiovascular disease (CVD) is highly prevalent among people with diabetes. However, there is little information regarding the prevalence of subclinical CVD and its relation to clinical CVD in diabetes and in the glucose disorders that precede diabetes. RESEARCH DESIGN AND METHODS—Participants in the Cardiovascular Health Study, aged ≥65 years (n = 5,888), underwent vascular and metabolic testing. Individuals with known disease in the coronary, cerebral, or peripheral circulations were considered to have clinical disease. Those without any clinical disease in whom CVD was detected by ultrasonography, electrocardiography, or ankle arm index in any of the three vascular beds were considered to have isolated subclinical disease. RESULTS—Approximately 30% of the cohort had clinical disease, and ∼60% of the remainder had isolated subclinical disease. In those with normal glucose status, isolated subclinical disease made up most of the total CVD. With increasing glucose severity, the proportion of total CVD that was clinical disease increased; 75% of men and 66% of women with normal fasting glucose status had either clinical or subclinical CVD. Among those with known diabetes, the prevalence was ∼88% (odds ratio [OR] 2.46 for men and 4.22 for women, P &amp;lt; 0.0001). There were intermediate prevalences and ORs for those with impaired fasting glucose status and newly diagnosed diabetes. CONCLUSIONS—Isolated subclinical CVD is common among older adults. Glucose disorders are associated with an increased prevalence of total CVD and an increased proportion of clinical disease relative to subclinical disease.
The impact of subendocardial scarring on prediction of improvement of regional wall motion after revascularization by dobutamine echocardiography
Authors: J.J. Bax, J.H. Cornel, A. Elhendy, D. Poldormans, P.M. Fioretti, J.R.T.C. Roelandi
Journal: Journal of the American College of Cardiology (1998)
Shiga Bacillus Infection
Authors: Claude T. H. Friedman
Journal: JAMA (1973)

In August 1970, an 18-month-old girl, who had never been outside of Los Angeles County, was found to have shiga bacillus dysentery. Consequently, we established a surveillance of all cases of this disease in the county. Twenty cases occurred between 1966 and 1971; 19 of them in the last three years. Two patients died. Three had never traveled out of the county. Of 47 family contacts, 5 had evidence of asymptomatic infection. The sudden rise in incidence of this disease and the documented spread within the county are a warning for the future.
There Is No Use Chasing an Illusion
Authors: John Lister
Journal: New England Journal of Medicine (1975)

WHEN I left England in May for another brief visit to the United States, there was still intense concern about the National Health Service (NHS) and about the state of the medical profession itself.As anticipated, the review body that advises the government on doctors' pay had reported to the Prime Minister and recommended substantial pay rises for all doctors working in the NHS. For some groups the increase was about 30 per cent, but took account of the fact that the previous year's award had been restricted by the country's economic circumstances. The government agreed to implement the recommendations . . .
Comparative In Vitro Activity of PD 131628, the Microbiologically Active Constituent of the Prodrug CI-990 (PD 131112)
Authors: D. Felmingham, M.J. Robbins, G. Ghosh, M. Mehta, A. Leakey, S. Clark, G. Mumtaz, G.L. Ridgway, R.N. Gruneberg
Journal: Drugs (1993)
Antibody producing capacity to the bacteriophage phi X174 in rheumatoid arthritis.
Authors: R Bucknall, P Bacon, C Elson, J V Jones
Journal: Annals of the Rheumatic Diseases (1987)

Antibody production in response to the primary immunogen bacteriophage phi X174 was investigated in 14 patients with previous yersinia arthritis (YA) and in 15 controls. HLA-B27 occurred in 10 patients with YA and in three controls. After primary and secondary immunisation the antibody responses were essentially similar both in patients with YA and controls. Consequently our results suggest that antibody response to a foreign antigen does not differ between patients with YA and a normal control population. In addition, there was no difference in peak antibody responses between individuals with HLA-B27 and those without HLA-B27.
GLUT4, AMP kinase, but not the insulin receptor, are required for hepatoportal glucose sensor–stimulated muscle glucose utilization
Authors: Rémy Burcelin, Valerie Crivelli, Christophe Perrin, Anabela Da Costa, James Mu, Barbara B. Kahn, Morris J. Birnbaum, C. Ronald Kahn, Peter Vollenweider, Bernard Thorens
Journal: Journal of Clinical Investigation (2003)

Recent evidence suggests the existence of a hepatoportal vein glucose sensor, whose activation leads to enhanced glucose use in skeletal muscle, heart, and brown adipose tissue. The mechanism leading to this increase in whole body glucose clearance is not known, but previous data suggest that it is insulin independent. Here, we sought to further determine the portal sensor signaling pathway by selectively evaluating its dependence on muscle GLUT4, insulin receptor, and the evolutionarily conserved sensor of metabolic stress, AMP-activated protein kinase (AMPK). We demonstrate that the increase in muscle glucose use was suppressed in mice lacking the expression of GLUT4 in the organ muscle. In contrast, glucose use was stimulated normally in mice with muscle-specific inactivation of the insulin receptor gene, confirming independence from insulin-signaling pathways. Most importantly, the muscle glucose use in response to activation of the hepatoportal vein glucose sensor was completely dependent on the activity of AMPK, because enhanced hexose disposal was prevented by expression of a dominant negative AMPK in muscle. These data demonstrate that the portal sensor induces glucose use and development of hypoglycemia independently of insulin action, but by a mechanism that requires activation of the AMPK and the presence of GLUT4.
Detection of remote myocardial infarction in patients with positron emission transaxial tomography and intravenous 11C-palmitate.
Authors: B E Sobel, E S Weiss, M J Welch, B A Siegel, M M Ter-Pogossian
Journal: Circulation (1977)

Ischemic myocardial injury has been detected recently in isolated perfused hearts and intact experimental animals with positron-emitting 11C-palmitate and reconstructive tomography providing cross-sectional images of the heart free from superimposed activity in overlying structures. To evaluate the applicability of positron emission transaxial tomography in detecting infarction in man, 10 normal human subjects and 12 patients who sustained documented acute myocardial infarction three to 12 months previously were studied. Tomograms were obtained after intravenous injection of 5 to 10 mCi of 11C-labeled palmitate, a physiological substrate of myocardium. Tomograms from all normal subjects exhibited homogeneous distribution of 11C-palmitate throughout each 1.5 cm thick cross section of the ventricle. Tomograms from all patients with remote anterior or inferior and posterior myocardial infarction exhibited diminished accumulation of 11C-palmitate delineating regions corresponding to the electrocardiographic locus of infarction. The distribution of 11C-palmitate detectable by positron emission transaxial tomography in a series of cross sections from apex to base in the same normal subject or patient with remote myocardial infarction was analogous to that observed in normal dogs and animals with experimentally induced myocardial infarction.
Thyroid Hormone Replacement — One Hormone or Two?
Authors: Anthony D. Toft
Journal: New England Journal of Medicine (1999)

Extracts of animal thyroid tissue, first used in 1892, contained both thyroxine and triiodothyronine and were the only available treatment for hypothyroidism for some 50 years. Because of concern about their variable potency,1 these extracts have been considered obsolete for some time by all but a few practitioners, who are often thought by their colleagues to be practicing on the fringes of medicine. Treatment with thyroid extract (or synthetic triiodothyronine) also led to high serum concentrations of triiodothyronine, because of its rapid absorption, and some patients had palpitations one to two hours after taking it. Synthetic thyroxine did not have . . .
Safer healthcare depends on in-depth investigation, not quick fixes, says expert
Authors: J. Feinmann
Journal: BMJ (2011)

Safe healthcare measures should be proactive, building on extensive investigation of the causes of high risk behaviour in medicine, rather than quick fix reactions to harmful incidents, a conference has heard.

Matthew Cooke, professor of emergency medicine at Warwick Medical School and leader of the Health Foundation’s safer clinical systems programme, warned, “We don’t treat patients before we know what’s wrong with them, and in the same way we shouldn’t assume there are transferable quick fixes for human factor issues in healthcare.” He was speaking at a seminar in London last week organised by the Clinical Human Factors Group, an increasingly influential independent coalition of healthcare professionals and managers and users of services. 

Professor Cooke was explaining the need for a second, two year phase of the safer …