tbuckley/cabot-search huggingface dataset:
Correction.
Journal: JAMA (1884)

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Proceedings of the Fifty-Eighth Annual Meeting of the American Society for Clinical Investigation, Inc., Held in Atlantic City, N.J., May 2, 1966: Abstracts
Authors: Roger Lester, Peter Klein, Franz Ingelfinger, B Le- Vine, A Redmond
Journal: Journal of Clinical Investigation (1966)

To determine if correlations exist between structure and glucuronide formation, we studied the excretion of bilirubin and several other bile pigments in rats.Bili- +2H +4H +4Kverdin -> bilirubin mesobilirubin -> mesobilirubinogen -2H> i-urobilin, a series of tetrapyrrols differing only in the number of their double bonds, form a convenient spectrum with which to assess the effect of structure on conjugation.11 Radiochemically pure, specifically labeled, tritiated forms of the latter four tetrapyrrols were prepared and administered intravenously to rats with external biliary drainage.In normal Sprague- Dawley rats, 74 to 87% of each administered tetrapyrrol appeared in bile within 90 minutes of injection.Bilirubin and mesobilirubin were excreted as glucuronide conju- gates, but conjugate formation did not appear to be requisite for the excretion of mesobilirubinogen and i-urobilin.Confirmation of this distinction was obtained in rats lacking the conjugating enzyme glucuronyl trans- ferase (Gunn rats).In these animals, less than 10% of the injected bilirubin-8H and mesobilirubin-8H ap- peared in bile during the 90 minutes after injection.In a comparable period, however, 83 to 92% of injected mesobilirubinogen-?H and i-urobilin-'H was excreted by the liver.Thus, unlike biliverdin (previously shown to be excreted as the glucuronide in rabbits), bilirubin, and mesobilirubin, the excretion of mesobilirubinogen and i-urobilin occurs without glucuronide formation.IT When Dreiding molecular models of the tetrapyrrols were constructed, it was apparent that biliverdin, bilirubin, and mesobilirubin possessed a marked degree of steric rigidity resulting from the methyne (-CH=) bridges between the outer and inner pyrrol rings.These bridges are saturated (-CH2-) in mesobilirubinogen and i-urobilin, and, as a result, models of these molecules exhibit a high degree of flexibility.IT These studies suggest that glu- curonide conjugation is not an essential step in the excretion of all bile pigments, but is specifically associated with the excretion of those tetrapyrrols having un- saturated bridges linking their outer ring structures.
Medical Education Staff.
Journal: JAMA (1963)

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COLLIER'S WEEKLY AND PATENT MEDICINES.
Journal: JAMA (1905)

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<i>Erratum:</i> Vol. 70, No. 18
Journal: MMWR Morbidity and Mortality Weekly Report (2021)

In the report "Emergency Department Visits and Hospitalizations for Selected Nonfatal Injuries Among Adults Aged ≥65 Years -United States, 2018," on page 663, in the first paragraph, the third complete sentence should have read, "Rates of ED visits for unintentional fall injuries per 100,000 persons increased with age, from 2,678 among adults aged 65-74 years to 4,900 among adults aged 75-84 years and 9,867 among adults aged ≥85 years."
Is the Mayo model for predicting survival useful after the introduction of ursodeoxycholic acid treatment for primary biliary cirrhosis
Authors: M Kilmurry
Journal: Hepatology (1996)

Treatment of patients with primary biliary cirrhosis (PBC) using ursodeoxycholic acid (UDCA) leads to a reduction in serum bilirubin. The first objective of this study was to assess the performance of certain prognostic indicators for PBC after the introduction of treatment with UDCA. Serum bilirubin is an important prognostic indicator for PBC and an important component of the Mayo model for grading patients into risk categories. In an analysis of patients enrolled in the Canadian multicenter trial, the Mayo score was calculated before and after treatment with UDCA. After treatment, the Mayo score continued to divide patients with PBC into groups with varying risk. In addition, the serum bilirubin alone was shown to do the same even after the introduction of treatment with UDCA. A second objective was to establish whether UDCA had an effect on long-term (2- to 6-year) survival in patients with PBC. (Hepatology 1996 May;23(5):1148-53)
Lack of Synergy by Mixtures of Weakly Estrogenic Hydroxylated Polychlorinated Biphenyls and Pesticides
Authors: Kathleen F. Arcaro, Dilip D. Vakharia, Yi Yang, John F. Gierthy
Journal: Environmental Health Perspectives (1998)

We examined the estrogenicity of binary mixtures of the hydroxylated polychlorinated biphenyls (OHPCBs) 2,4,6-trichloro-4'-biphenylol (2,4,6-TCB-4'-OH) and 2,3,4,5,-tetrachloro-4'-biphenylol and the pesticides endosulfan and dieldrin.The OHPCBs and pesticides were tested in both the MCF-7 focus assay and a competitive estrogen-receptor binding assay.Although the individual OHPCBs were estrogenic in both assays, there was no synergy when they were combined at various concentrations as equimolar mixtures.Of the pesticides, only endosulfan was estrogenic.Its weak estrogenicity was seen only in the MCF-7 focus assay at the highest concentration tested-10 pM.There was no synergy of the equimolar mixture of pesticides.To determine whether OHPCBs might respond synergistically when combined with the natural estrogen 17-estradiol (E2), we tested various concentrations of 2,4,6-TCB-4'-OH in the MCF-7 focus assay in combination with physiologically relevant concentrations of E2.There was no synergy between 2,4,6-TCB-4'-OH and E2.Pretreatment for 3 or 7 days with 2,4,6-TCB-4'-OH had no effect on subsequent foci induced by a combination of 2,4,6-TCB-4'-OH and E2.Although our results showing no synergy between the pesticides or the OHPCBs are in contrast to a recent report that binary mixtures of these same compounds produce synergistic responses in estrogen-sensitive assays, they are in agreement with the results from other assays showing a lack of synergy.Considering all results, it appears that synergy of these weakly estrogenic compounds acting through the estrogen receptor is unlikely.
ENDEMIC MYCOBACTERIAL ULCERATION
Journal: JAMA (1966)

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Omission
Journal: JAMA (1985)

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How to be good
Authors: Richard Smith, Gaby Shockley, Rajendra Kale, Jane Smith, Annabel Ferriman, Lynn Eaton, Kamran Abbasi General, Trish Groves, Sandra Goldbeck-Wood, Tessa Richards, Sharon Davies, Trevor Jackson, Rhona Macdonald, Andrew Woodward, John Gary, Bryan Standing, Susan Minns, Marita Batten Picture, Jan Croot, Abi Berger, Margaret Cooter, Jackie Annis, Greg Cotton, Liz Payne, Miriam Pinchuk, Barbara Squire, Julia Thompson, Tony Delamothe, Christopher Martyn, Marcus Müllner, Roger Robinson, Tony North, Ron Davis, Jennifer Leaning, John Roberts, James Barrett, Nick Booth, Peter Cantillon, Tim Coleman, Teifion Davies, Brendan Delaney, Nick Dunn, Jon Emery, Ben Essex, John Essex, David Fitzmaurice, Robin Ferner, Ian Forgacs, Marcia Hall, Julia Hippisley-Cox, Linda Hutchinson, Kevin Jones, Tim Lancaster, Ben Lloyd, Diana Lockwood, Azeem Majeed, Pippa Oakeshott, Michael O'brien, Ed Peile, John Rees, Stephen Rose, Adam Sandell, Aziz Sheik, Nicholas Steel, Frank Sullivan, Sheila Teasdale, Tom Treasure, John Williams, Diana Wood, Jeremy Wyatt, Doug Altman, Mike Campbell, Tim Cole, Jon Deeks, Stephen Evans, Hazel Inskip, Julie Morris, Gordon Murray, Jackie Connor, Andy Josephides, Bernadette Kearney Display, Catherine Harding-Wiltshire, Simon Walker, Alan Walker, Nick Gray, Nadia Gurney-Randall, David Evans, Jeremy Anderson, Mary Australia, Lisa Baker, Donald Bero, Nicholas Berwick, Luis-Gabriel Christakis, Michael Cuervo, Paul Dixon, Roger Australia, Peter Goss, Tony Denmark, Yuan Grabham, China Gu, Canada Haynes, Georgia Kirtava, Cindy Austria, Hong Lam, Leonard Kong, Israel Lebovici, Michel Liberati, France Lievre, Daniel Mulrow, Gretchen Purcell, Lois Quam, Paula Rochon, Canada Sepulveda, Rosalind Smyth, Fiona Stanley, Paul Stewart, Tessa Torres-Edejer, Susumu Wakai, Hugh Japan
Journal: BMJ (2001)
SELECTIONS.
Journal: JAMA (1894)

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Update: Acquired Immunodeficiency Syndrome— United States, 1981-1988
Journal: JAMA (1989)

During 1992, state and territorial health departments reported 47,095 cases of acquired immunodeficiency syndrome (AIDS) to CDC, an increase of 3.5% over the 45,499 cases reported in 1991. As in previous years, most (50.8%) cases were attributable to transmission of human immunodeficiency virus (HIV) among homosexual/bisexual men (Table 1). This report summarizes the characteristics of persons reported with AIDS in 1992, compares them with data from 1991 (Table 1), and describes selected trends since 1988.
Privacy matters
Journal: Nature Genetics (1998)

Privacy mattersFamily trees (or pedigrees) can reveal sensitive information that can be used to stigmatize or discriminate against family members.Until recently, information published in scientific journals stayed within a small circle of scholars; the public at large was neither interested nor, for the most part, educated enough to read research papers.This has changed.Patients and their relatives are often well-educated about their condition and organized in support groups that function as information relay stations.Public interest has increased dramatically, and many journals (including this one), universities and funding agencies spend considerable effort in communicating with the general media, recognizing that an educated populace is necessary if society is to benefit from scientific knowledge.However, increased public access to primary research articles, often over the internet, has raised concerns about the privacy of research participants.Recognizing the special status of genetic information presented in pedigrees, the National Institutes of Health (NIH) are currently funding a project on privacy and confidentiality issues associated with their publication.As part of the project, Jeffrey Botkin and colleagues surveyed the existing practices of investigators and scientific journals with respect to pedigree publication.The results have just been published 1 , and it is apparent that all is not well.Two sets of guidelines exist on the publication of pedigrees, one from the NIH's Office for Protection from Research Risks (OPPR) and one from the International Committee of Medical Journal Editors (ICMJE).The OPPR guidebook 2 suggests that the Institutional Review Boards (IRBs) should examine potentially problematic manuscripts, and consider whether a pedigree is essential to publication, whether identifying information could be omitted and whether the subjects have given consent to publication.The ICMJE statement 3 is more explicit.It requests that written informed consent for publication is obtained after the patient is shown the manuscript.It also states that complete anonymity is hard to achieve, that consent should be obtained if there is any doubt, that the requirement for informed consent be included in a journal's instructions to authors, and that individual articles mention that informed consent has been obtained.In surveying the practices of 20 journals, Botkin et al. found that few have strict guidelines, and none of them enforces them rigorously.(Nature Genetics has no explicit policy on privacy protection of research participants, but does expect that informed consent is obtained from participants of studies submitted and encourages reviewers to point out potential problems.)Specific guidelines on the publication of volume 19 no. 3
INDIANA PATHOLOGIC EXHIBIT.
Journal: JAMA (1899)

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
Mutagenicity and Metabolism of Vinyl Chloride and Related Compounds
Authors: H. Bartsch, C. Malaveille, A. Barbin, H. Bresil, L. Tomatis, R. Montesano
Journal: Environmental Health Perspectives (1976)

The various adverse biological effects of vinyl chloride appear to be dependent upon the metabolic conversion of this compound into chemically reactive metabolites. The metabolism of vinyl chloride in mammals and in man, including the formation of monochloroacetic acid and some identified sulfur conjugates is reviewed. Hepatic microsomal mixed function oxidases from rats, mice, and humans were equally effective in transforming vinyl chloride into alkylating agents in vitro. Two of the enzyme reaction products, i.e., chloroethylene oxide and 2-chloroacetaldehyde, showed potent genetic activity in microorganisms and Chinese hamster V79 cells. The role of liver microsomal enzymes in the generation of electrophilic mutagenic vinyl chloride metabolites is discussed.
Serratia marcescens Endocarditis
Journal: JAMA (1970)

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