tbuckley/cabot-search huggingface dataset:
More on Medical Malpractice
Authors: Randall R. Bovbjerg
Journal: Annals of Internal Medicine (1993)

Letters1 June 1993More on Medical MalpracticeRandall R. Bovbjerg, JDRandall R. Bovbjerg, JDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-118-11-199306010-00031 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:Taken together, these letters make four points. First, legal performance is unsatisfactory. My editorial agreed, although with different emphasis. Second, the correspondents all find claims much too frequent (myriad suits, alarming frequency). Claims are certainly high relative to the placid 1950s, when lifetime chance of suit was only 1/7 [1]. For 1991, 1/7 was the national average annual rate (13.9%, down from all-time high of 17.7% in 1985 [data from the St. Paul Fire & Marine Insurance Co. Personal Communication]). The typical doctor's risk of claim is lower, however, because claims are concentrated disproportionately in high-claims areas and ...References1. American Medical Association. Opinion survey on medical malpractice. JAMA. 1957; 164:1583-94. Google Scholar2. Localio AR, Lawthers AG, Brennan TA, et al. Relation between malpractice claims and adverse events due to negligence. N Engl J Med. 1991; 325:245-51. Google Scholar3. Curran WJ. How lawyers handle medical malpractice cases: an analysis of an important medicolegal study. Rockville, Maryland: National Center for Health Services Research; 1977. DHEW pub. no. (HRA) 77-3152. Google Scholar4. What price justice? The Economist. 1993; 326:16-7. Google Scholar5. Bovbjerg RR, Sloan FA, Blumstein FA. Valuing life and limb in tort: scheduling pain and suffering Nw Univ L Rev. 1989; 83:908-76. Google Scholar Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 June 1993Volume 118, Issue 11Page: 909-910KeywordsArmed forcesMotivationShockTaxes ePublished: 15 August 2000 Issue Published: 1 June 1993 Copyright & PermissionsCopyright © 1993 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Anorexia Nervosa: A Factitial Disease
Authors: IVAN FRAS
Journal: Annals of Internal Medicine (1973)

Comments and Corrections1 September 1973Anorexia Nervosa: A Factitial DiseaseIVAN FRAS, M.D., F.A.C.PIVAN FRAS, M.D., F.A.C.PSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-79-3-458 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The study on prognosis in anorexia nervosa by Drs. Halmi, Brodland, and Loney (Ann Intern Med 78:907-909, 1973) leads me to draw parallels between anorexia nervosa and factitial disease in general.Whether we can consider anorexia nervosa as a special form of factitial or self-induced disease is open to more discussion than can be undertaken in this letter. But there are similarities in the prognosis for the two conditions: the authors of the above-mentioned study suggest that vomiting and laxative abuse are among the criteria presaging a poor outcome. Both are conscious acts. So are the acts...References1. OBERMAYER M: Dynamics and management of self-induced eruptions. Calif Med 94:61-65, February 1961 MedlineGoogle Scholar2. PETERSON W: Self-induced eruptions. Minn Med 52:103-104, 1969 MedlineGoogle Scholar3. ZAIDENS S: Self-inflicted dermatoses and their psychodynamics. J Nerv Ment Dis 113:395-404, 1951 MedlineGoogle Scholar4. FRAS I: Factitial Disease. Proceedings of the First International College of Psychosomatic Medicine, Guadalajara, Mexico, 1971. In press Google Scholar5. BLISSBRANCH EC: Anorexia Nervosa. New York, Harper & Row Publishers, Hoeber Medical Division, 1960 Google Scholar6. AGLERATNOFFSPRING DOG: The anticoagulant malingerer. Psychiatric studies of three patients. Ann Intern Med 73:67-72, 1970 LinkGoogle Scholar7. DAILYCOLESCREGER WJW: Factitious anemia. Ann Intern Med 58:533-538, 1963 LinkGoogle Scholar8. MILLER A: Factitial disease. Tex Med 65:65-69, 1969 MedlineGoogle Scholar9. WHITEPEARSONCODDINGTON JHR: Purpura factitia. Attracting attention by self-inflicted lesions. Clin Pediatr (Phila) 5:157-160, 1966 CrossrefMedlineGoogle Scholar10. HOFFMANBAER HP: Gingival mutilation in children. Phychiatry 31:380-386, 1968 Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByDenial of illness and the use of self-reporting measures in anorexia nervosa patients 1 September 1973Volume 79, Issue 3Page: 458-459KeywordsAnorexia nervosaVomiting Issue Published: 1 September 1973 PDF DownloadLoading ...
Abstract 2173: Heterozygosity for Mtap accelerates lymphomagenesis in Emu-Myc and Pten +/− mice
Authors: Warren D. Kruger, Yuwaraj Kadariya, Baiqing Tang, Tahseen Al-Saleem, Kyoko Haykawa
Journal: Cancer Research (2012)

Abstract The gene encoding the methionine salvage pathway methylthioadenosine phosphorylase (MTAP) is a tumor suppressor gene that is frequently inactivated in a wide variety of human cancers. Loss of MTAP is associated with elevated expression of ornithine decarboxylase (ODC), a key enzyme in the synthesis of polyamines and a known oncogene. Here, we have examined if heterozygosity for a null mutation in Mtap could accelerate tumor development in two different mouse cancer models, Eα-myc transgenic and Pten+/−. We found that the median age of tumor formation in both models was significantly accelerated in Mtap+/− compared to Mtap+/+ mice. In Eα-myc mice, Mtap mutations accelerated the formation of lymphomas from cells in the early pre-B stage and these tumors tended to be of higher grade and have higher expression levels of ODC protein compared to those observed in control Emu-myc Mtap+/+ mice. Supprisingly, examination of Mtap mRNA and protein in highly lymphoma infiltrated tissue in heterozygous animals indicates that &amp;gt;80% of the tumors maintain expression of the Mtap allele. Our findings show that germline inactivation of a single Mtap allele enhances lymphomagenesis in both Emu-myc and Pten+/− mice and is associated with elevated levels of ODC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2173. doi:1538-7445.AM2012-2173
piggyBac Transposon-mediated Long-term Gene Expression in Mice
Authors: Hideyuki Nakanishi, Yuriko Higuchi, Shigeru Kawakami, Fumiyoshi Yamashita, Mitsuru Hashida
Journal: Molecular Therapy (2010)

Transposons are promising systems for somatic gene integration because they can not only integrate exogenous genes efficiently, but also be delivered to a variety of organs using a range of transfection methods. piggyBac (PB) transposon has a high transposability in mammalian cells in vitro, and has been used for genetic and preclinical studies. However, the transposability of PB in mammalian somatic cells in vivo has not been demonstrated yet. Here, we demonstrated PB-mediated sustained gene expression in adult mice. We constructed PB-based plasmid DNA (pDNA) containing reporter [firefly and Gaussia luciferase (Gluc)] genes. Mice were transfected by injection of these pDNAs using a hydrodynamics-based procedure, and the conditions for high-level sustained gene expression were examined. Consequently, gene expressions were sustained over 2 months. Our results suggest that PB is useful for organ-selective somatic integration and sustained gene expression in mammals, and will contribute to basic genetic studies and gene therapies.
Filling the Void
Authors: Peter Vash
Journal: JAMA (2012)

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
Gene Therapy Continues to Mature and to Face Challenges
Authors: David A Williams
Journal: Molecular Therapy (2009)

Two recent reports of note for readers of Molecular Therapy—one in the scientific literature and one in the "regulatory cyperspace"—point to continued success and ongoing challenges of the gene therapy field. Pule et al. recently reported that they had successfully engineered virus-specific T cells that demonstrated apparent antitumor efficacy against neuroblastoma, a rare but deadly tumor seen in children.1 At the same time, many of us received a "Notification of Serious Adverse Event" from the National Institutes of Health Office of Biotechnology Activities that was based on a press release by the French Health Products Safety Agency (Agence Française de Sécurité Sanitaire des Produits de Santé; AFSSAPS) reporting "a biological observation in one treated patient" in a trial in France using a lentivirus (HIV-1) vector containing the gene for human β-globin to transduce CD34+ hematopoietic stem cells in patients with severe forms of thalassemia or sickle cell disease.
Science, medicine, and the future: Nutritional genomics
Authors: R. Elliott
Journal: BMJ (2002)

alpha M beta 2, a beta 2 integrin expressed on cells of myelomonocytic differentiation, functions as a receptor for factor X (X) and fibrinogen (Fg) and participates in leukocyte adhesion to vascular endothelium. Acquisition of high affinity ligand binding has been suggested to result from a conformational change of alpha M beta 2 in response to agonist-induced leukocyte stimulation. We now describe mAb 7A10, which preferentially binds to alpha M beta 2 on activated cells and reports the functional activation of this integrin. Agonist-stimulated monocytes and monocytic cells, but not resting cells, maximally expressed the 7A10 neoepitope, whereas expression of other selected alpha M beta 2 epitopes remained unchanged. The neoepitope was elicited equally by exposure of cells to either ADP or FMLP and did not require divalent cations for expression. Saturation of the 7A10 neoepitope by this Ab on stimulated THP-1 cells inhibited both X and Fg binding and abolished the alpha M beta 2-driven cellular coagulant response. Stimulated monocytic cells, which bound X and/or Fg, exhibited a sustained adhesion to unstimulated endothelial cell monolayers and Ab 7A10 inhibited this sustained adhesion. We conclude that activated conformers of alpha M beta 2 mediate X and Fg binding, that assembly of either X or Fg or both on alpha M beta 2 mediates leukocyte adhesion to unstimulated endothelium through sparse ICAM-1, and that mAb 7A10 can report and functionally inhibit this pathway of leukocyte adhesion.
Phthalate ester residues--their metabolism and analysis in fish.
Authors: D L Stalling, J W Hogan, J L Johnson
Journal: Environmental Health Perspectives (1973)

During the course of our analysis of fish and other aquatic materials for pesticide residues, unknown components were often detected.Concern about the identity of late eluting gas-liquid chromatographic (GLC) peaks in fish and water extracts led to the identification of phthalic acid esters (PAEs) as environmental contaminants (1).Further study of these contaminants with a GLC-mass spectrometer (GLC-MS) led to their identification as di-2-ethylhexyl phtha- late (DEHP) and di-n-butyl phthalate (DBP).Preliminary data from acute toxicity tests indicate that these compounds are relatively low in toxicity.Chronic studies, however, indicate that they may have more subtle effects on reproduction of some aquatic species (2).Residue data obtained from a variety of areas, dietary materials, and samples related to fish rearing operations have established some information on the incidence of PAEs in relation to pesticides and polychlorinated biphenyl contaminants (Table 1).PAE residues in water appeared to be correlated with rivers draining industrialized or heavily popu- lated areas (John Hesse, Michigan Depart- ment of Natural Resources, East Lansing, Michigan 1972 personal communication).However, the distribution of PAEs in the aquatic environment remains to be defined.PAEs are commonly used as plasticizers, especially in poly(vinyl chloride) plastics.In
Clinical reactions to systemic provocation with gold sodium thiomalate in patients with contact allergy to gold
Authors: H. MÖLLER, B. BJÖRKNER, M. BRUZE
Journal: British Journal of Dermatology (1996)

In a double blind experimental study, 20 patients with a contact allergy to gold sodium thiosulphate were challenged intramuscularly with the chemically similar gold sodium thiomalate and with placebo. The most spectacular clinical reaction in the 10 patients given the active agent, was an epidermal and dermal flare up of healed patch-test reactions to the gold salts, as well as a high, but transient, rise in body temperature. Previous intradermal tests were similarly reactivated. In addition, toxicoderma-like rashes were observed in several cases, but a flare up of a previous contact dermatitis site was seen in one patient only. The specificity of the positive provocations was demonstrated.
Low income scheme index: a new deprivation scale based on prescribing in general practice
Authors: D. C E F Lloyd, C. M Harris, D. W Clucas
Journal: BMJ (1995)

<h3>Abstract</h3> <b>Objectives</b>: To describe and validate a new deprivation index, based on the percentage of prescribed items exempt from the prescription charge under the low income scheme, at both family health services authority and practice level. <b>Design</b>: Comparison of the index with three other deprivation indices and correlation of index values with the use of drugs given for conditions with known social class gradients. <b>Setting</b>: All 90 family health services authorities and 7619/9289 practices in England. <b>Results</b>: The ranking of family health services authorities on the new index correlated highly with rankings on the other indices. Values in relation to the use of drugs given for conditions with known social class gradients were in the predicted direction at both family health services authority level and practice level; correlation was highly significant at the authority level, but less significant at practice level. <b>Conclusions</b>: The new index provides a good measure of deprivation at family health services authority level, and at practice level the results are sufficiently encouraging to warrant further research. It provides the best available instrument for relating deprivation to the use of drugs in any population that can be defined by prescribing data, but an attempt to use it in determining allocation of resources would at this stage be premature. <h3>Key messages</h3> Key messages The scheme can be updated annually or even quarterly At family health services authority level the index is valid and easy to use At practice level a deprivation score is calcul-able but it is affected by the individual habits of prescribers It would be premature at the moment to use the index to allocate resources at practice level
Differential modulation of rat hepatic stellate phenotype by natural and synthetic retinoids
Authors: Karine Hellemans, Peggy Verbuyst, Erik Quartier, Frans Schuit, Krista Rombouts, Ross A.S. Chandraratna, Detlef Schuppan, Albert Geerts
Journal: Hepatology (2004)

Activation of hepatic stellate cells (HSC) is a central event in the pathogenesis of liver fibrosis during chronic liver injury. We examined the expression of retinoic acid (RAR) and retinoid X receptors (RXR) during HSC activation and evaluated the influence of natural and synthetic retinoic acids (RA) on the phenotype of culture-activated HSC. The expression of the major RAR/RXR subtypes and isoforms was analyzed by Northern hybridization. Presence of functional receptor proteins was established by gel shift analysis. Retinoic acids, RAR, and RXR selective agonists and an RAR antagonist were used to evaluate the effects of retinoid signalling on matrix synthesis by Northern blotting and immunoprecipitation, and on cell proliferation by BrdU incorporation. The 9- cis RA and synthetic RXR agonists reduced HSC proliferation and synthesis of collagen I and fibronectin. All- trans RA and RAR agonists both reduced the synthesis of collagen I, collagen III, and fibronectin, but showed a different effect on cell proliferation. Synthetic RAR agonists did not affect HSC proliferation, indicating that ATRA inhibits cell growth independent of its interaction with RARs. In contrast, RAR specific antagonists enhance HSC proliferation and demonstrate that RARs control proliferation in a negative way. In conclusion, natural RAs and synthetic RAR or RXR specific ligands exert differential effects on activated HSC. Our observations may explain prior divergent results obtained following retinoid administration to cultured stellate cells or to animals subjected to fibrogenic stimuli. (Hepatology 2004;39:97-108.)
Epinephrine potentiation of arachidonate‐induced aggregation of cyclooxygenase‐deficient platelets
Authors: Gundu H. R. Rao, James G. White
Journal: American Journal of Hematology (1981)

Evaluation of platelet physiology, biochemistry, ultrastructure, and function in a young woman without history of hemorrhagic problems revealed that her platelets were deficient in cyclooxygenase activity. Her citrate platelet-rich plasma (C-PRP) responded monophasically when stirred with aggregating agents in the same manner as aspirin-treated normal C-PRP, but could be irreversible aggregated by high concentrations of thrombin, collagen, and ADP. Her platelets did not aggregate when stirred with AA at concentrations as high as 2 mM. Ultrastructure and levels of serotonin and adenine nucleotides wer normal. Amounts of 14C-AA released after stirring with thrombin were similar to normal cells. However, evaluation of prostaglandin synthesis after stirring with 14C-AA revealed no evidence of endoperoxide or thromboxane production, although products of the lipoxygenase pathway were produced in normal amounts. Aggregation in response to AA was completely corrected after mixing with 10% normal C-PRP. However, equal volumes of her C-PRP and normal aspirin-treated C-PRP did not respond to AA, whereas 10% normal platelets combined with aspirin-treated cells corrected aggregation to AA. Since epinephrine pretreatment corrects the response of dog platelets that are not aggregated by AA, we evaluated the influence of epinephrine on her platelets. Preexposure to 5 micro M epinephrine, a concentration that gave only primary waves of aggregation, resulted in normalization of her response to AA, even though correction was not associated with the generation of endoperoxides or thromboxanes. The results may explain why patients with platelet cyclooxygenase deficiency have mild or absent bleeding symptoms.
Binding and metabolism of platelet-activating factor by human neutrophils.
Authors: J T O'Flaherty, J R Surles, J Redman, D Jacobson, C Piantadosi, R L Wykle
Journal: Journal of Clinical Investigation (1986)

Human polymorphonuclear neutrophils rapidly incorporated radiolabeled platelet-activating factor, 1-O-[hexadecyl-9, 10-3H2]-2-acetyl-sn-glycero-3-phosphocholine ([3H]PAF), and then metabolized it into its sn-2-fatty acyl derivative. Fractionation of radiolabel-pretreated cells over Percoll gradients revealed that virtually all of the intact [3H]PAF was located in nongranule membranes that were enriched with alkaline phosphatase and cell surface glycoproteins. While still membrane associated, the ligand was rapidly converted to its acyl derivative and then more slowly transferred to specific granules and, to a lesser extent, azurophilic granules. In contrast, neutrophils did not metabolize [3H]PAF at 4 degrees C but rather gradually accumulated it in their alkaline phosphatase-enriched membrane subfractions. These same subfractions contained receptors for the ligand, as determined by their capacity to bind [3H]PAF specifically. Binding was readily saturated, partially reversible, and fit a two receptor model; dissociation constant (Kd) values for high and low affinity sites were 0.2 and 500 nM, respectively. Receptors with similar affinities were detected in whole cells. Furthermore, the potencies of several structural analogues in inhibiting binding of [3H]PAF to membranes correlated closely with their respective potencies in stimulating degranulation responses. Finally, quantitative studies suggested all or most of the cell's receptors were membrane associated. We conclude that PAF rapidly enters cellular membranes to bind with specific receptors that trigger function. The intramembranous ligand is also deacetylated, acylated, and then transferred to granules. This metabolism may be sufficiently rapid to limit ligand-receptor binding and distort quantitative analyses of receptors.
Mechanical Circulatory Assistance: Current Status
Authors: Charles A. Sanders, Mortimer J. Buckley, W. Gerald Austen
Journal: New England Journal of Medicine (1971)

Mechanical circulatory assistance (MCA) has been applied to support the circulation of patients in cardiogenic shock for over a decade. Initially, the standard cardiopulmonary bypass machine was employed, a device proved to be safe and effective for limited periods during open-heart surgery. The results were meager and discouraging.1 There was the legitimate question, however, whether delay in applying MCA had allowed the shock state to progress so far as to preclude survival with any therapy. Moreover, the short duration over which the circulation could be sustained by extracorporeal means did not test fully the hypothesis that the severely injured heart . . .