tbuckley/cabot-search huggingface dataset:
Alpha-Interferon-induced Nodular Rheumatoid Arthritis in Renal Cell Carcinoma
Authors: Yukio Ueno, Takaomi Sohma
Journal: Annals of Internal Medicine (1992)

Letters1 August 1992Alpha-Interferon-induced Nodular Rheumatoid Arthritis in Renal Cell CarcinomaYukio Ueno, MD, Takaomi Sohma, MDYukio Ueno, MDSearch for more papers by this author, Takaomi Sohma, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-117-3-266_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editors:Rönnblom and colleagues (1) and Chazerain and colleagues (2) reported the development of rheumatoid arthritis-like disease after alpha-interferon therapy. We describe a similar case of seropositive, nodular rheumatoid arthritis, which occurred during interferon therapy. A 64-year-old man developed gross hematuria on 28 December 1990. A large mass in the upper abdomen detected on physical examination was confirmed by abdominal ultrasonography and computed tomography as a 10 x 1O x 10 cm tumor of the right kidney extending to the pararenal space. The leukocyte count was 6800/mm3, and the hemoglobin level was 17.5 g/dL. Rheumatoid factor and C-reactive...References1. RönnblomAlmOberg LGK. Autoimmunity after alpha-interferon therapy for malignant carcinoid tumors. Ann Intern Med. 1991; 115:178-83. LinkGoogle Scholar2. ChazerainMeyerKahn POM. Rheumatoid arthritis-like disease after alpha-interferon therapy. Ann Intern Med. 1992;116:427. LinkGoogle Scholar3. GarnickBrenner MB. Tumors of the urinary tract. In: Wilson JD, Braunwald E, Isselbacker KJ; eds. Harrison's Principles of Internal Medicine. 12th edition. New York: McGraw-Hill; 1991:1207-12. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Yukio Ueno, MD; Takaomi Sohma, MDAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byArthritis Induced by Interferon-alpha Therapy in a Patient with Essential ThrombocythemiaArthritis during interferon beta-1b treatment in multiple sclerosisManifestations rhumatologiques des anticancéreuxParaneoplastic rheumatic syndromesAutoimmunity induced by interferon-α therapy for chronic viral hepatitisInterferon-?1A-induced polyarthritis in a patient with the HLA-DRB1*0404 alleleAlpha-interferon-induced arthritis: clinical presentation, treatment, and preventionInterferontherapie und AutoimmunitätPsoriatic Arthritis with Spinal Involvement in a Patient Receiving Alpha-interferon for Chronic Hepatitis CDevelopment of Sjögren's syndrome during treatment with recombinant human interferon-alpha-2b for chronic hepatitis CImmunological Adverse Effects of Interferon TreatmentHypothyroidism and arthritis during interferon therapy 1 August 1992Volume 117, Issue 3Page: 266-267KeywordsComputed axial tomographyHemoglobinInterferonsKidneysRenal cell carcinomaRenal diseasesRheumatoid arthritisUltrasound imaging ePublished: 1 December 2008 Issue Published: 1 August 1992 PDF downloadLoading ...
Activated Charcoal in Phenobarbital Overdose
Authors: Mark J. Goldberg
Journal: JAMA (1985)

<h3>To the Editor.—</h3> Previous studies have shown that the administration of multiple oral doses of activated charcoal will decrease the elimination half-life of phenobarbital.<sup>1,2</sup>An uncontrolled trial in patients with phenobarbital overdose treated with this regimen suggested that coma time and duration of mechanical ventilation were decreased consistent with the decrease in phenobarbital halflife.<sup>3</sup>However, the obvious thesis that decreasing the half-life of phenobarbital by administering multiple doses of activated charcoal would result in a decrease in coma time and duration of mechanical ventilation in patients with phenobarbital overdose requires final proof. Pond et al<sup>4</sup>have tested this thesis. In a small randomized controlled trial, they have confirmed that repeated doses of activated charcoal, compared with single doses, decrease the serum half-life of phenobarbital in patients with phenobarbital overdose. But, it is surprising that the duration of mechanical ventilation was not different in the two groups. However,
A Retrospective Review of the Impact of Influenza A(H1N1)v Swine ‘flu Variant on a District General Hospital
Authors: Victoria H. Jeffrey, Philip J.R. Sajik, Cecilia M. Jukka, Rashmi Gupta, Judith A. Bowley, Bridget C. Lees, Andrew Q. Chalmers, Martin A. Kiernan
Journal: Journal of Infection (2011)
Unintended Changes in Cognition, Mood, and Behavior Arising from Cell-Based Interventions for Neurological Conditions: Ethical Challenges
Authors: P. S. Duggan, A. W. Siegel, D. M. Blass, H. Bok, J. T. Coyle, R. Faden, J. Finkel, J. D. Gearhart, H. T. Greely, A. Hillis, A. Hoke, R. Johnson, M. Johnston, J. Kahn, D. Kerr, P. King, J. Kurtzberg, S. M. Liao, J. W. McDonald, G. McKhann, K. B. Nelson, M. Rao, A. Regenberg, K. Smith, D. Solter, H. Song, J. Sugarman, R. J. Traystman, A. Vescovi, J. Yanofski, W. Young, D. J. H. Mathews
Journal: The American Journal of Bioethics (2009)

The prospect of using cell-based interventions (CBIs) to treat neurological conditions raises several important ethical and policy questions. In this target article, we focus on issues related to the unique constellation of traits that characterize CBIs targeted at the central nervous system. In particular, there is at least a theoretical prospect that these cells will alter the recipients' cognition, mood, and behavior-brain functions that are central to our concept of the self. The potential for such changes, although perhaps remote, is cause for concern and careful ethical analysis. Both to enable better informed consent in the future and as an end in itself, we argue that early human trials of CBIs for neurological conditions must monitor subjects for changes in cognition, mood, and behavior; further, we recommend concrete steps for that monitoring. Such steps will help better characterize the potential risks and benefits of CBIs as they are tested and potentially used for treatment.
BCR and BCR-ABL regulation during myeloid differentiation in healthy donors and in chronic phase/blast crisis CML patients
Authors: M Marega, R G Piazza, A Pirola, S Redaelli, A Mogavero, I Iacobucci, I Meneghetti, M Parma, E M Pogliani, C Gambacorti-Passerini
Journal: Leukemia (2010)
High frequency of the 425AG splice-site mutation and novel mutations of the COL7A1 gene in central Europe: significance for future mutation detection strategies in dystrophic epidermolysis bullosa
Authors: M. Csikos, H.I. Szocs, A. Laszik, S. Mecklenbeck, A. Horvath, S. Karpati, L. Bruckner-Tuderman
Journal: British Journal of Dermatology (2005)

Mutations in the type VII collagen gene (COL7A1) are responsible for dominant and recessive forms of dystrophic epidermolysis bullosa (DEB). These mutations are usually specific for individual families; only a few cases of recurring mutations have been identified.Forty-three unrelated Hungarian and German patients with different DEB phenotypes were screened for novel and recurrent COL7A1 mutations.All patients were classified based on clinical and genetic findings, skin immunofluorescent antigen mapping, and electron microscopic studies. Mutation analysis was performed by amplification of genomic DNA with polymerase chain reaction using COL7A1-specific primers, heteroduplex analysis, and direct nucleotide sequencing. Restriction endonuclease digestion was used for family screening and mutation verification. Results In this group of patients, the splice-site mutation 425A-->G was observed frequently, in 11 of 86 alleles (12.8%), once in homozygous form and in nine cases in heterozygous form. One of 100 control alleles from clinically unaffected individuals also carried the mutation. We also identified three novel mutations: the 976-3C-->A splice-site mutation, and the 4929delT and 8441-15del20 deletions.High recurrence of the splice-site mutation 425A-->G in central European patients with DEB should be taken into account when designing COL7A1 mutation detection strategies. Reporting of three novel COL7A1 mutations in this study further emphasizes the molecular heterogeneity of DEB and provides more information for studies on genotype-phenotype correlations in different DEB subtypes.
Prevention of acute gastric erosions in the rat by novel semi-synthetic amphipathic analogues of pepstatin.
Authors: S P Huddy, G Patel, G C Heywood, B M Austen, J Hermon-Taylor
Journal: Gut (1988)

Pepstatin is a potent aspartyl proteinase inhibitor which is virtually insoluble in physiological media. Five semi-synthetic amphipathic analogues of pepstatin, prepared by N terminal substitution of native pepstatin with hydrophilic oligopeptides, have been assessed for their ability to protect the mucosa in two animal models of acute gastric erosions. Concentrations of approximately 90 pmol/mg were achieved in the rat gastric mucosa after oral administration of a 20 mmol solution. These levels are theoretically adequate to inhibit all pepsin like proteinase activity (including zymogens). Each pepstatin analogue was tested by intragastric administration in a controlled hypotension/luminal acid animal model of acute gastric erosions in a group of six animals. All the inhibitors tested produced marked mucosal protection, as measured by a mucosal damage index, compared with control animals (control mean 241, range 100-420; Pepstatinyl-Gly-Orn-Orn-Cys (10 mmol) mean 3, range 0-8, p less than 0.01; Pepstatinyl-Gly-Cysteic acid-Cysteic acid (10 mmol) mean 5, range 0-21, p less than 0.01; Pepstatinyl-Gly-Lys-Lys (10 mmol) mean 18, range 0-60, p less than 0.01; Pepstatinyl-Gly-Cysteic acid-Cysteic acid (1 mmol) mean 24, range 0-86, p less than 0.01; Pepstatinyl-Gly-Orn-Orn-Cys (1 mmol) mean 57, range 0-116, p less than 0.01; Pepstatinyl-Gly-Asp-Asp (1 mg/ml suspension) mean 68, range 19-126, p less than 0.01; Pepstatinyl-Arg-OMe (1 mmol) mean 93, range 4-142, p less than 0.05, Pepstatinyl-Gly-Lys-Lys (1 mmol) mean 157, range 70-286, NS). In a platelet activating factor/20% luminal ethanol model of erosions the pepstatin analogues again provided mucosal protection although this only reached statistical significance for one of three compounds tested.
H1N1 Influenza A Disease — Information for Health Professionals
Authors: Lindsey R. Baden, Jeffrey M. Drazen, Patricia A. Kritek, Gregory D. Curfman, Stephen Morrissey, Edward W. Campion
Journal: New England Journal of Medicine (2009)

In the first 2 weeks in April, cases of infection with an untypable influenza A virus began to be identified in Mexico and southern California.1 Although the exact sequence of events is uncertain, by the third week of April it was established that the illness resulted from a triple recombination of human, avian, and swine influenza viruses; the virus has been found to be H1N1. This virologic analysis allowed for the development of a polymerase-chain-reaction (PCR) test to determine whether, in any given person, illness with the protean manifestations of cough, fever, sore throat, diarrhea, and nausea could be confirmed . . .
Method for detection of bacteriuria suitable for use in general practice.
Authors: J M Bradley, N Crowley, J H Darrell
Journal: BMJ (1967)

A completely satisfactory screening method for bacteriuria requiring the minimum of apparatus and bench expertise and suitable for use in general practice has still to be described. Even where laboratory facilities are readily available to general practitioners transport of the specimen without the delay which would upset the quantitative aspects of the investigation is often impossible. In addition, hospital laboratories would be unable to cope with the demands that ought to be made on them if all diagnosed urinary tract infections were adequately followed. The investigation of patients whose symptoms are less con clusive but who nevertheless may have urinary tract infections (Mond et al., 1965) would add considerably to the volume of work.
Comment on Ågren et al. Increased Incorporation of Antiplasmin Into the Fibrin Network in Patients With Type 1 Diabetes. Diabetes Care 2014;37:2007–2014
Authors: Dingeman C. Rijken, Shirley Uitte de Willige
Journal: Diabetes Care (2014)

Antiplasmin (α2-antiplasmin or plasmin inhibitor) is the main physiological inhibitor of plasmin and efficiently attenuates fibrin clot lysis after being cross-linked to fibrin by the action of activated factor XIII (FXIIIa). Agren et al. (1) recently demonstrated that the fibrin network of plasma clots from patients with type 1 diabetes contains more antiplasmin than the fibrin network of plasma clots from control subjects. This is an interesting finding, as increased clot resistance to fibrinolysis might contribute to cardiovascular disease frequently associated with diabetes.

The authors used a new, still unpublished method for the determination of the incorporation of antiplasmin …
Lifestyle Interventions Are Cost-Effective in People With Different Levels of Diabetes Risk
Authors: Monique A.M. Jacobs-van der Bruggen, Griët Bos, Wanda J. Bemelmans, Rudolf T. Hoogenveen, Sylvia M. Vijgen, Caroline A. Baan
Journal: Diabetes Care (2006)

OBJECTIVE—In the current study we explore the long-term health benefits and cost-effectiveness of both a community-based lifestyle program for the general population (community intervention) and an intensive lifestyle intervention for obese adults, implemented in a health care setting (health care intervention). RESEARCH DESIGN AND METHODS—Short-term intervention effects on BMI and physical activity were estimated from the international literature. The National Institute for Public Health and the Environment Chronic Diseases Model was used to project lifetime health effects and effects on health care costs for minimum and maximum estimates of short-term intervention effects. Cost-effectiveness was evaluated from a health care perspective and included intervention costs and related and unrelated medical costs. Effects and costs were discounted at 1.5 and 4.0% annually. RESULTS—One new case of diabetes per 20 years was prevented for every 7–30 participants in the health care intervention and for every 300–1,500 adults in the community intervention. Intervention costs needed to prevent one new case of diabetes (per 20 years) were lower for the community intervention (€2,000–9,000) than for the health care intervention (€5,000–21,000). The cost-effectiveness ratios were €3,100–3,900 per quality-adjusted life-year (QALY) for the community intervention and €3,900–5,500 per QALY for the health care intervention. CONCLUSIONS—Health care interventions for high-risk groups and community-based lifestyle interventions targeted to the general population (low risk) are both cost-effective ways of curbing the growing burden of diabetes.
Thrombocytopenia and Illicit Drug Use
Authors: Theodore E. Warkentin
Journal: Annals of Internal Medicine (1994)

Letters15 April 1994Thrombocytopenia and Illicit Drug UseTheodore E. Warkentin, MDTheodore E. Warkentin, MDHamilton Civic Hospitals; Hamilton, Ontario, L8L 2X2; CanadaSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-120-8-199404150-00018 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:To Cherubin and Sapira's comprehensive list of medical complications related to illicit drug abuse [1], we add several important thrombocytopenic syndromes. Severe, acute immune thrombocytopenia (platelet counts <20 × 109/L) can occur in some patients after repeated injections of heroin [2] or cocaine [3]. Quinine-dependent, platelet-reactive IgG, treggered by the use of quinine “filler” within the illicit drug preparation, has been implicated [4]. In addition, chronic immune thrombocytopenia is an important complication of intravenous drug abuse [5], often as a manifestation of chronic human immunodeficiency virus (HIV) infection. Illicit drug use should be considered in patients with ...References1. Cherubin CE, Sapira JD. The medical complications of drug addiction and the medical assessment of the intravenous drug user: 25 years later. Ann Intern Med. 1993; 119:1017-28. Google Scholar2. Adams WH, Rufo RA, Talarico L, Silverman SL, Brauer MJ. Thrombocytopenia and intravenous heroin use. Ann Intern Med. 1978; 89:207-11. Google Scholar3. Leissinger CA. Severe thrombocytopenia associated with cocaine use. Ann Intern Med. 1990; 112:708-10. Google Scholar4. Christie DJ, Walker RH, Kolins MD, Wilner FM, Aster RH. Quinine- induced thrombocytopenia following intravenous use of heroin. Arch Intern Med. 1983; 143:1174-5. Google Scholar5. Savona S, Nardi MA, Lennette ET, Karpatkin S. Thrombocytopenia purpura in narcotics addicts. Ann Intern Med. 1985; 102:737-41. Google Scholar Author, Article, and Disclosure InformationAffiliations: Hamilton Civic Hospitals; Hamilton, Ontario, L8L 2X2; Canada PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byPhysician Recognition of Active Injection Drug Use In HIV-Infected Patients Is Lower Than Validity of Patient's Self-Reported Drug UsePistol‐packin' pilfererFactitious quinine‐induced thrombocytopenia 15 April 1994Volume 120, Issue 8Page: 693KeywordsCocaineDrug abuseDrugsHIVHIV infectionsHeroinIdiopathic thrombocytopenic purpuraPlateletsQuinine Issue Published: 15 April 1994 Copyright & PermissionsCopyright © 1994 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
The effect of liver denervation on hepatic hemodynamics during hypovolemic shock in swine
Authors: Michael J. Henderson, Gregory J. Mackay, Alan B. Lumsden, Hussein M. Atta, Richard Brouillard, Michael H. Kutner
Journal: Hepatology (1992)

This study tested the hypothesis that the denervated liver is more susceptible to hypovolemic shock than the normal liver. Fourteen swine, seven nondenervated and seven after liver denervation, were studied during hypovolemic shock to 50% of baseline blood pressure. Hepatic artery and portal vein flows were measured using transonic flow probes, and cardiac output and central venous pressure were measured using Swan-Ganz catheters. Hepatic artery flow fell equivalently in the two groups, from 132 ± 71 to 94 ± 17 ml/min in the nondenervated group compared with 149 ± 56 to 91 ± 55 ml/min in the denervated group. In contrast, portal flow in the denervated group (276 ± 71 to 119 ± 53 ml/min) fell significantly (p &lt; 0.001) more than in the nondenervated group (289 ± 135 to 194 ± 70 ml/min). The 58% reduction from baseline in portal flow in the denervated group compared with the 30% reduction in the nondenervated group suggests that the normal compensatory mechanism to maintain portal flow during hypovolemic shock is neurally mediated. It can be hypothesized that sensory afferent fibers might initiate a feedback to splanchnic vasodilatation in response to reduced portal flow. This study supports the hypothesis that the denervated liver is more susceptible to hypovolemic shock. (Hepatology 1992;15:130-133).
RESULTS OF EXPLORATION IN PATIENTS WITH CLINICAL DIAGNOSIS OF SUBDURAL HEMATOMA
Authors: Philip S. Bergman
Journal: JAMA (1952)

Medical literature contains many descriptions of the clinical features and operative findings in cases of subdural hematoma.<sup>1</sup>The criteria for diagnosis, however, are usually discussed only in terms of proved subdural hematoma. Little attention has been directed to cases in which a subdural hematoma was suspected clinically but was not found at operation. It is our chief purpose in this report to compare two such groups in order to evaluate better the diagnostic and prognostic features of this important clinical entity. Another aspect of this disorder that has received relatively little consideration is the clinical course following surgical treatment. It is often the impression of those not intimately connected with neurological or neurosurgical services that recovery is to be expected after removal of a subdural clot. We shall show that this conception, while sometimes true in the individual case, cannot be applied to subdural hematomas in general. <h3>CLINICAL MATERIAL</h3>
Diagnosis of Acute Cholecystitis
Authors: Josep H. Llaurado
Journal: JAMA (1981)

<h3>To the Editor.—</h3> In the article by Freitas and Gulati (1980;244:1585), "Rapid Evaluation of Acute Abdominal Pain by Hepatobiliary Scanning," it is concluded that hepatobiliary radionuclide scintigraphy "should be the procedure of choice" for evaluation of suspected acute cholecystitis, since "it is simple, rapid, and safe to perform,<i>enabling a diagnosis to be established within one hour</i>" (our italics). We think that the last phrase may be misleading to the clinician. If the radionuclide material is visualized in the gallbladder and intestine in less than one hour (a normal or unremarkable study), the diagnosis of acute cholecystitis is virtually excluded.<sup>1,2</sup>The reader of the article by Freitas and Gulati may conversely construe that if the gallbladder is not visualized in one hour, the diagnosis of acute cholecystitis is established. This would be an unwarranted conclusion that might lead the patient to unnecessary surgery. Early in our scintigraphic studies we
Plasma fenfluramine levels, weight loss, and side effects.
Authors: J A Innes, M L Watson, M J Ford, J F Munro, M E Stoddart, D B Campbell
Journal: BMJ (1977)

Fifty women with refractory obesity received fenfluramine for 20 weeks. Every two weeks details of weight change, drug dose, degree of anorexia, and any side effects were recorded and plasma was obtained for fenfluramine and norfenfluramine measurements. Of the 41 patients available for final analysis 26 achieved a maximum plateau dose of 160 mg/day. Plasma fenfluramine concentrations did not correlate with the degree of anorexia or with the incidence of side effects other than the severity of dream disturbance. There was a highly significant relation between weight loss and plasma fenfluramine and norfenfluramine concentrations and also between weight loss and the presence of sustained anorexia. Women who achieved mean plateau concentrations over 200 ng/ml lost a mean 8.8 kg while those with concentrations less than 100 ng/ml lost a mean of only 2.1 kg. When fenfluramine is prescribed in refractory obesity the dose should be increased stepwise until either satisfactory weight loss is achieved or troublesome side effects appear.