tbuckley/cabot-search huggingface dataset:
Corrigendum
Authors: B Euston
Journal: BMJ (1940)

Disfigurement of NailsDiGcrr writes: Could any of your readers give assistance with the following case?The patient is a young bank official in his early twenties.About five years ago he noticed that his finger and toe nails were becoming rough and brittle, and now all his nails are furrowed, thick, and constantly breaking off at the distal enid.There is no pain, and his sole complaint is that they are very unsightly.He has-seen a-specialist, who tr-ied var-ious remedies, including x rays, but all without any real benetit.Onie nail was even removed, but the new nail was as bad as ever; otherwise he is quite healthly.
Proceedings of the 239th Meeting of the Netherlands Society for Dermatology and Venereology Amsterdam, 14 February 1987
Authors: W.A. VLOTENT, E. DIJK
Journal: British Journal of Dermatology (1987)

Journal Article Proceedings of the 239th Meeting of the Netherlands Society for Dermatology and Venereology Amsterdam, 14 February 1987 Get access W.A. VAN VLOTENT, W.A. VAN VLOTENT Search for other works by this author on: Oxford Academic Google Scholar E. VAN DIJK E. VAN DIJK Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 117, Issue 6, 1 December 1987, Pages 783–795, https://doi.org/10.1111/j.1365-2133.1987.tb07361.x Published: 01 December 1987
Aneurysm of Cholecystic Artery
Authors: John H. Schaefer
Journal: JAMA (1961)

<h3>To the Editor:—</h3> Several years ago I reported, in the<i>Military Surgeon</i>, a case of fatal hemorrhage from an aneurysm of the cholecystic artery which had ruptured into the cystic duct and from thence had bled into the intestinal tract. The hemorrhage was intermittent over a period of several weeks before ultimate death. I found the source of the hemorrhage at autopsy. Until last week I had heard of no analogous case. I have just received a letter from a pathologist in Italy who is familiar with my report and who recently performed an autopsy on a person in whom an aneurysm of the cholecystic artery caused obstruction of the hepatic duct, with consequent increasing jaundice and death. He would like to know if I have any bibliographic data on such an occurrence. I have not. I will appreciate it very much if anyone who has any knowledge of other cases of aneurysm of the
THE DEVIL'S DILEMMA
Journal: JAMA (1967)

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
Infectious corneal ulcer with overextended wearing of disposable contact lenses
Authors: R. M. Kershner
Journal: JAMA (1989)

<h3>To the Editor.—</h3> The availability of extended-wear soft contact lenses and the recently developed disposable lenses has provided particular advantages to certain contact lens wearers. However, ophthalmologists have been concerned that the use of extended-wear contact lenses will increase the incidence of serious corneal infections. Few data have been available to support this contention because the history of long-term use of disposable contact lenses is not yet available. I herein report a corneal ulcer infected by<i>Pseudomonas</i>sp in a man who was wearing disposable contact lenses for 2 1/2 weeks at a time. <h3>Report of a Case. —</h3> A 19-year-old soft contact lens wearer was switched to disposable contact lenses by his optometrist. He was doing well with them for 10 months and gradually increased his wearing time from 2 to 3 weeks. He developed redness, pain, and loss of vision in his right eye after a 2 1/2week
Abstract 2113: <i>KRAS</i> amplification mediates resistance to osimertinib in acquired afatinib-resistant NSCLC harboring exon 19 deletion/T790M in EGFR
Authors: Toshimitsu Yamaoka, Ohba Motoi, Yasunari Kishino, Sojiro Kusumoto, Junji Tsurutani, Tohru Ohmori
Journal: Cancer Research (2019)

Abstract Background: The second mutation of T790M in epidermal growth factor receptor (EGFR) exon 20 mediates resistance to first- and second-generation EGFR tyrosine kinase inhibitors (TKIs; gefitinib, erlotinib, and afatinib). The critical T790M mutation in EGFR has facilitated the development of third-generation mutation-selective EGFR TKIs (rociletinib and osimertinib). We previously reported heterogeneous afatinib resistance in lung adenocarcinoma PC-9 cells, harboring 15bp deletions in EGFR exon 19. Among the afatinib-resistant PC-9 cells, we noted the emergence of T790M in EGFR exon 20 and responses to third-generation EGFR-TKIs. Here, we used afatinib-resistant lung adenocarcinoma PC-9 cells, called AfaR, harboring the exon 19 deletion/T790M in EGFR. Purpose: To identify novel resistance mechanisms in post-afatinib treatment, two osimertinib-resistant cell lines, OsiR1 and OsiR2, were established using increasing concentrations of osimertinib by stepwise dose escalation up to 1 μmol/L over 10 to 12 months. Results: A linear and reversible KRAS amplification and overexpression with increased osimertinib concentrations in OsiR1 and OsiR2 cells, respectively, was detected. OsiR1 cells maintained osimertinib resistance with KRAS amplification after osimertinib withdrawal for 2 months. After osimertinib withdrawal for 2 months, OsiR2 cells exhibited KRAS attenuation and osimertinib sensitivity was entirely recovered in vitro and in vivo. Phospho-EGFR (Y1068) and growth factor receptor-bound protein 2 (GRB2)/son of sevenless homolog 1 (SOS1) complex was found to mediate osimertinib resistance in OsiR1 cells with sustained KRAS activation. The association of phosphorylated EGFR with the GRB2/SOS1 complex leads to KRAS activation. After 2 months of osimertinib withdrawal, the GRB2/SOS1 complex was dissociated, and the EGFR signal but not the GRB2/SOS1 signal was activated. Concomitant inhibition of mitogen-activated protein kinase kinase and EGFR could overcome osimertinib-resistance in OsiR1 cells. Conclusion: We characterized novel acquired resistance mechanisms for third-generation EGFR-TKI, osimertinib, providing insights into the development of novel treatment strategies. Citation Format: Toshimitsu Yamaoka, Ohba Motoi, Yasunari Kishino, Sojiro Kusumoto, Junji Tsurutani, Tohru Ohmori. KRAS amplification mediates resistance to osimertinib in acquired afatinib-resistant NSCLC harboring exon 19 deletion/T790M in EGFR [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 2113.
Second International Conference on the Adjuvant Therapy of Cancer
Journal: JNCI Journal of the National Cancer Institute (1978)

Journal Article Second International Conference on the Adjuvant Therapy of Cancer Get access JNCI: Journal of the National Cancer Institute, Volume 61, Issue 2, August 1978, Page 619, https://doi.org/10.1093/jnci/61.2.619-c Published: 01 August 1978
SYPHILITIC AORTITIS AND ANEURYSM.
Journal: JAMA (1900)

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
Pediatrics
Authors: Edwin L. Kendig
Journal: JAMA (1969)

In this 14th edition, Dr. Barnett, intending a different approach, has invited outstanding specialists to serve as associate editors and to share in the responsibility for the major chapters. In addition he has included an "extensive and sophisticated discussion" of the mechanisms underlying both human development and disease in infants and children. Actually, the presentation of material in this volume is comparable to that of the leading competition. But there is indeed a vast difference between this and the earlier editions by Holt and McIntosh. These were excellent books at the time, but the present volume is a complete, up-to-date presentation of material for the pediatrician of 1968-1969. In a multiauthored book there will always be unevenness, no matter how well the book is edited, and this is no exception. As the editor himself has suggested, this is a "first" edition, and it will require subsequent editions to achieve the
Bioequivalence of levothyroxine preparations: industry sponsorship and academic freedom
Authors: C. H. Eckert
Journal: JAMA (1997)

<h3>To the Editor.</h3> —Knoll Pharmaceutical Company appreciates the opportunity to comment on the study by Dr Dong and colleagues.<sup>1</sup> In 1987, Knoll's predecessor, Flint Laboratories, entered into an agreement with Dong and colleagues to study 4 levothyroxine preparations, including Flint's Synthroid (levothyroxine sodium tablets) brand. The protocol included a provision that "all data obtained by the investigator... is also considered confidential and is not to be published or otherwise released without written permission from Flint...." In April 1989, while the study was ongoing, the company communicated concerns about the study's execution to Dong and colleagues. Despite repeated requests, we were unable to reach agreement with the investigators on the resolution of these concerns. We did not withdraw funding because the study was nearly complete when the flaws were discovered and dialogue with the investigators on their resolution had just begun. As a partner in research, we have a responsibility
THE EPIDEMIC RECEDING.
Journal: JAMA (1905)

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 THERAPEUTIC VALUE OF SILENCE.
Journal: JAMA (1905)

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
Electroenceph &amp;amp; Clin Neurophysiol, Amsterdam
Journal: JAMA (1964)

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
Changes in xylosyltransferase activity and in proteoglycan deposition in bleomycin-induced lung injury in rat. R. Koslowski, U. Pfeil, H. Fehrenbach, M. Kasper, E. Skutelsky, K-W. Wenzel. Eur Respir J 2001; 18: 347-356.
Journal: European Respiratory Journal (2001)

Unfortunately, the wrong image was shown in figure 3a.The correct figure is reproduced below with the legend.
DUODENAL PERFORATION DUE TO PROPHYLACTIC PANCREATIC STENT
Authors: C Loras, X Andújar
Journal: Endoscopy (2020)

An ERCP was performed in 85 years old woman due to choledocholithiasis. Precut pancreatic sphincterotomy was performed to allow biliary cannulation. A stone was removed with Fogarty balloon and plastic stent of 5cmx5Fr was placed to prevent acute pancreatitis.
<i>HFE</i> Genotype in Patients with Hemochromatosis and Other Liver Diseases
Authors: Adele L. Franks, Wylie Burke
Journal: Annals of Internal Medicine (2000)

Letters1 February 2000HFE Genotype in Patients with Hemochromatosis and Other Liver DiseasesAdele L. Franks, MD and Wylie Burke, MD, PhDAdele L. Franks, MDThe Prudential Center for Health Care Research; Atlanta, GA 30339 (Franks)University of Washington; Seattle, WA 98105 (Burke)Search for more papers by this author and Wylie Burke, MD, PhDThe Prudential Center for Health Care Research; Atlanta, GA 30339 (Franks)University of Washington; Seattle, WA 98105 (Burke)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-132-3-200002010-00020 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:Because Bacon and colleagues (1) explored the utility of genetic testing, it is by definition circular to use the genetic test to discredit previously accepted diagnostic criteria for hemochromatosis in the absence of an independent gold standard. They found that some patients with liver disease who did not meet previously established criteria for hemochromatosis were homozygous for C282Y. The authors assumed that genotype should take precedence over the prior criteria, even though the predictive value of the various HFE genotypes has not yet been established. Indeed, given that C282Y homozygosity has been identified in patients with limited iron ...References1. Bacon BR, Olynyk JK, Brunt EM, Britton RS, Wolff RK. HFE genotype in patients with hemochromatosis and other liver diseases. Ann Intern Med. 1999;130:953-62. LinkGoogle Scholar2. Olynyk JK, Cullen DJ, Aquilia S, Rossi E, Summerville L, Powell LW. A population-based study of the clinical expression of the hemochromatosis gene. N Engl J Med. 1999;341:718-24. CrossrefMedlineGoogle Scholar3. Pietrangelo A, Montosi G, Totaro A, Garuti C, Conte D, Cassanelli S, et al . Hereditary hemochromatosis in adults without pathogenic mutations in the hemochromatosis gene. N Engl J Med. 1999;341:725-32. CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAffiliations: The Prudential Center for Health Care Research; Atlanta, GA 30339 (Franks)University of Washington; Seattle, WA 98105 (Burke) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoHFE Genotype in Patients with Hemochromatosis and Other Liver Diseases Bruce R. Bacon , John K. Olynyk , Elizabeth M. Brunt , Robert S. Britton , and Roger K. Wolff HFE Genotype in Patients with Hemochromatosis and Other Liver Diseases Gordon D. McLaren HFE Genotype in Patients with Hemochromatosis and Other Liver Diseases Lawrie W. Powell Metrics 1 February 2000Volume 132, Issue 3Page: 246KeywordsGenetic diseasesGenetic testingGenotypingHealth screeningHemochromatosisHomozygosityLiver diseasesMutationPatientsPhenotypes Issue Published: 1 February 2000 Copyright & PermissionsCopyright © 2000 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
ANIMAL AND VEGETABLE PATHOLOGY IN RELATION TO HUMAN DISEASES
Journal: JAMA (1923)

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 antiandrogen cyproterone acetate induces synthesis of transforming growth factor beta 1 in the parenchymal cells of the liver accompanied by an enhanced sensitivity to undergo apoptosis and necrosis without inflammation
Authors: F Oberhammer
Journal: Hepatology (1996)

Recently, cases of liver damage and liver tumors have been reported after treatment of prostate cancer patients with the antiandrogen cyproterone acetate (CPA). In rat liver, CPA initiates a wave of DNA synthesis that is accompanied by apoptosis. In apoptotic hepatocytes, a latent form of transforming growth factor beta 1 (TGF-beta 1) is detectable by immunohistochemistry. Injection of a single dose of TGF- beta 1 induces apoptosis in the liver of animals pretreated with CPA but has an insignificant effect in untreated animals. In this study, we show by Northern analysis that there is increased expression of TGF-beta 1 in the liver after CPA treatment. Detection of TGF-beta 1 with in situ hybridization showed that TGF-beta 1 was synthesized in the parenchymal cells. Time course and dose-response experiments performed 48 hours after the last application of CPA showed that apoptotic nuclei with chromatin condensed at the nuclear periphery (AN) were already visible 2 hours after injection (0.13%), and apoptotic bodies (ABs) increased 2 to 9 hours after the injection (from 1.28% to 6.67%) after 25 micrograms TGF-beta 1/kg. At 4.5 hours after injection, an induction of apoptosis could be detected with 0.25 microgram TGF-beta 1/kg and after the maximum dose (250 micrograms TGF-beta 1/kg) ANs (0.24%) and ABs (16.74%) were homogeneously distributed throughout the liver lobe. Irrespective of the dose or time after injection of TGF-beta 1, 82% of the ABs were localized within hepatocytes. Liver enzymes were detected in high amounts in the serum (eightfold elevation of glutamate dehydrogenase, fivefold elevation of alanine transaminase [ALT]) 7 hours after the first visible sign of apoptosis. After an additional 20 hours, the liver contained many necrotic figures. These results suggest that the combination of TGF-beta 1 expression coupled with a strikingly enhanced sensitivity to the induction of apoptosis could be responsible both for the liver damage and the development of liver tumors observed after treatment with CPA. (Hepatology 1996 Feb;23(2):329-37)