tbuckley/cabot-search huggingface dataset:
915 CLINICAL PREDICTION OF FAILURE IN ANTI-VIRAL PROPHYLAXIS FOR PATIENTS WITH HEPATITIS B INFECTION UNDERGOING CYTOTOXIC CHEMOTHERAPY FOR MALIGNANT TUMORS
Authors: I.K. Kim, W. Kim, B.S. Kim, Y.J. Jung, J.B. Bong Jeong, B.G. Kim, K.L. Lee, Y.J. Kim, J.-H. Yoon, H.S. Lee
Journal: Journal of Hepatology (2009)
Preparation and drug release behaviors of nimodipine-loaded poly(caprolactone)–poly(ethylene oxide)–polylactide amphiphilic copolymer nanoparticles
Authors: Yong Hu, Xiqun Jiang, Yin Ding, Leyang Zhang, Changzheng Yang, Junfeng Zhang, Jiangning Chen, Yonghua Yang
Journal: Biomaterials (2003)
<i>SMARCB1/INI1</i> Tumor Suppressor Gene Is Frequently Inactivated in Epithelioid Sarcomas
Authors: Piergiorgio Modena, Elena Lualdi, Federica Facchinetti, Lisa Galli, Manuel R. Teixeira, Silvana Pilotti, Gabriella Sozzi
Journal: Cancer Research (2005)

Abstract Epithelioid sarcoma is a rare soft tissue neoplasm of uncertain lineage that usually arises in the distal extremities of adults, presents a high rate of recurrences and metastases and frequently poses diagnostic dilemmas. The recently reported large-cell “proximal-type” variant is characterized by increased aggressiveness, deep location, preferential occurrence in proximal/axial regions of older patients, and rhabdoid features. Previous cytogenetic studies indicated that the most frequent alterations associated with this tumor entity affect chromosome 22. In this study, combined spectral karyotyping, fluorescence in situ hybridization, and array-based comparative genomic hybridization analyses of two proximal-type cases harboring a rearrangement involving 10q26 and 22q11 revealed that the 22q11 breakpoints were located in a 150-kb region containing the SMARCB1/INI1 gene, and that homozygous deletion of the gene was present in the tumor tissue. The SMARCB1/INI1 gene encodes for an invariant subunit of SWI/SNF chromatin remodeling complex and has been previously reported to act as a tumor suppressor gene frequently inactivated in infantile malignant rhabdoid tumors. We analyzed SMARCB1/INI1 gene status in nine additional epithelioid sarcoma cases (four proximal types and five conventional types) and altogether we identified deletions of SMARCB1/INI1 gene in 5 of 11 cases, all proximal types. We confirmed and further extended the number of cases with SMARCB1/INI1 inactivation to 6 of 11 cases, by real-time quantitative PCR analysis of mRNA expression and by SMARCB1/INI1 immunohistochemistry. Overall, these results point to SMARCB1/INI1 gene involvement in the genesis and/or progression of epithelioid sarcomas. Analysis of larger series of epithelioid sarcomas will be necessary to highlight putative clinically relevant features related to SMARCB1/INI1 inactivation.
Interferon gamma and interleukin 4 stimulate prolonged expression of inducible nitric oxide synthase in human airway epithelium through synthesis of soluble mediators.
Authors: F H Guo, K Uetani, S J Haque, B R Williams, R A Dweik, F B Thunnissen, W Calhoun, S C Erzurum
Journal: Journal of Clinical Investigation (1997)

Human respiratory epithelium expresses inducible nitric oxide synthase (iNOS) continuously in vivo, however mechanisms responsible for maintenance of expression are not known. We show that IFNgamma is sufficient for induction of iNOS in primary human airway epithelial cells (HAEC) in vitro, and IL-4 potentiates IFNgamma-induced iNOS expression in HAEC through stabilization of iNOS mRNA. IFNgamma/IL-4- induced iNOS expression in HAEC was delayed in onset and prolonged with expression up to 1 wk. Removal of overlying culture media resulted in loss of expression, while transfer of conditioned media induced iNOS mRNA in other HAEC. IFNgamma and IL-4 stimulation activated STAT1 and STAT6 in HAEC, but conditioned media transfer to HAEC produced even higher levels of STAT1 activation than achieved by direct addition of cytokines. Although cytokine induction of iNOS was dependent on new protein synthesis, conditioned media induction of iNOS in HAEC was not. Further, removal of overlying culture media from cells at different times after cytokine stimulation demonstrated that mediator synthesis and/or secretion important for induction and maintenance of iNOS occurs early after cytokine stimulation. In conclusion, a combination of IFNgamma/ IL-4, which occurs naturally in the lung epithelial lining fluid, leads to maintenance of iNOS expression in human airway epithelium through production of soluble mediators and stabilization of mRNA.
Pathologists' views on consent for autopsy
Authors: A T Williams, D Morris, N K Patel
Journal: Journal of the Royal Society of Medicine (2002)

Consent to autopsy is usually obtained by a doctor other than the one who will perform the procedure. There is an argument that, for proper informed consent, a pathologist should participate. We ascertained the views of consultant pathologists in south-east England. 53 (87%) of 61 consultants responded, of whom 50 currently do autopsies. Only 2 at present participate directly in obtaining consent, and 10 of the remaining 48 expressed willingness to do so. The general view was that consent is best obtained by a senior clinician from the team that has looked after the patient. Pathologists see their primary role as to provide guidance to clinicians. Few see it as their function to obtain consent for autopsy.
Treatment of Localized Myxoedema
Authors: R. H. G. Charles
Journal: BMJ (1965)

Towards the end of August a numtber of young girls weredseen with a different pattern of acne vulgaris.Tohe lesions were either confined to the forehead or most marked on the forehead (Fig. 1).All these girls had in common a popular hair style with a fringe coming down to the eyebrows (Fig. 2).It .,.,
Randomized Trial of High Dose Chemotherapy With Autologous Bone Marrow Support as Adjuvant Therapy for High-Risk, Multi-Node Positive Malignant Melanoma
Authors: B. R. Meisenberg, M. Ross, J. J. Vredenburgh, R. Jones, E.J. Shpall, H. F. Seigler, D. M. Coniglio, K. Wu, W. P. Peters
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Randomized Trial of High Dose Chemotherapy With Autologous Bone Marrow Support as Adjuvant Therapy for High-Risk, Multi-Node Positive Malignant Melanoma Get access Barry R. Meisenberg, Barry R. Meisenberg Duke University Bone Marrow Transplant Program, Duke University Medical CenterDurham, N.C. Correspondence to: William P. Peters, M D., Ph.D., Box 3961, Duke University Medical Center, Durham, NC 27710. Search for other works by this author on: Oxford Academic PubMed Google Scholar Maureen Ross, Maureen Ross Duke University Bone Marrow Transplant Program, Duke University Medical CenterDurham, N.C. Search for other works by this author on: Oxford Academic PubMed Google Scholar James J. Vredenburgh, James J. Vredenburgh Duke University Bone Marrow Transplant Program, Duke University Medical CenterDurham, N.C. Search for other works by this author on: Oxford Academic PubMed Google Scholar Roy Jones, Roy Jones Duke University Bone Marrow Transplant Program, Duke University Medical CenterDurham, N.C. Current address: R. Jones, E. J. Shpall, Bone Marrow Transplant Program, University of Colorado, Denver. Search for other works by this author on: Oxford Academic PubMed Google Scholar E.J. Shpall, E.J. Shpall Duke University Bone Marrow Transplant Program, Duke University Medical CenterDurham, N.C. Search for other works by this author on: Oxford Academic PubMed Google Scholar Hillard F. Seigler, Hillard F. Seigler Duke University Bone Marrow Transplant Program, Duke University Medical CenterDurham, N.C. Search for other works by this author on: Oxford Academic PubMed Google Scholar David M. Coniglio, David M. Coniglio Duke University Bone Marrow Transplant Program, Duke University Medical CenterDurham, N.C. Search for other works by this author on: Oxford Academic PubMed Google Scholar Katherine Wu, Katherine Wu Duke University Bone Marrow Transplant Program, Duke University Medical CenterDurham, N.C. Search for other works by this author on: Oxford Academic PubMed Google Scholar William P. Peters William P. Peters Duke University Bone Marrow Transplant Program, Duke University Medical CenterDurham, N.C. * See “Notes” section following “References.” Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 13, 7 July 1993, Pages 1080–1085, https://doi.org/10.1093/jnci/85.13.1080 Published: 07 July 1993 Article history Received: 31 December 1992 Revision received: 08 April 1993 Accepted: 13 April 1993 Published: 07 July 1993
CRANIECTOMY FOR EPILEPTIFORM SEIZURES AND GRAVE MENTAL DISTURBANCES FOLLOWING HEAD INJURY WITHOUT APPARENT FRACTURE. WITH REPORT OF A CASE.
Authors: H. REINEKING
Journal: JAMA (1900)

The following case is reported, partly because it is somewhat unique in the pronounced character of its symptoms, the absence of demonstrable organic lesion, and the promptness and completeness of relief following operative treatment; partly because it illustrates, better perhaps than any description I could give, a rare but important group of morbid phenomena following injury to the cranium; but chiefly for the purpose and with the desire of calling forth an expression of the views and experience of the Fellows of the Academy in regard to this interesting class of head injuries. C. M., aged 20 years, American, wood carver, single, gave a family history negative as regards any neurotic or other hereditary tendencies. He was well-nourished, not addicted to the use of tobacco or spirituous beverages, had never been sick, never showed any tendency to nervousness, had had no occasion for worry, no overwork, no mental excitement, and
576. Hypoxic Adipocytes Support Early Heterotopic Bone Formation
Authors: Elizabeth A. Olmsted-Davis, Francis H. Gannon, Zbigniew Gugala, John A. Hipp, Christine Foultier-Dilling, Michael H. Heggeness, Alan R. Davis
Journal: Molecular Therapy (2006)

Top of pageAbstract
The factors contributing to heterotopic ossification, the formation of bone in abnormal soft-tissue locations, are beginning to emerge, but very little is known about the microenvironmental conditions that promote this often devastating disease. Using a murine model in which endochondral bone formation is triggered in muscle by bone morphogenetic protein 2 (BMP2), we studied the cellular and biochemical changes near the site of injection of BMP2- expressing cells. As early as 24 hours after BMP2 stimulation, brown adipocytes began to accumulate in the lesional area. These cells stained positively for pimonidazole and therefore generated hypoxic stress (most likely through uncoupled mitochondrial respiration) within the target tissue, a prerequisite for the differentiation of stem cells to chondrocytes and subsequent heterotopic bone formation. They also expressed the angiogenic growth factor VEGF-D, which is required for normal vascularization and remodeling of the cartilaginous matrix formed by chondrocytes. We propose that aberrant expression of BMPs in soft tissue stimulates the production of brown adipocytes, which drive the early steps of heterotopic ossification by lowering the oxygen tension in adjacent tissue and secreting VEGF-D. Further results, obtained in mutant mice that do not produce brown fat, suggest that white adipocytes can convert to fat-oxidizing cells when brown adipocytes are not available, providing a compensatory mechanism for the generation of a hypoxic microenvironment. Manipulation of the transcriptional control of adipocyte fate in local soft-tissue environments may offer a means to prevent or treat the development of bone in extraskeletal sites.
Osteoblastic Response in Patients with Non-small Cell Lung Cancer with Activating EGFR Mutations and Bone Metastases during Treatment with EGFR Kinase Inhibitors
Authors: Sascha Ansén, Christopher Bangard, Silvia Querings, Franziska Gabler, Matthias Scheffler, Daniela Seidel, Beate Saal, Thomas Zander, Lucia Nogová, Karin Töpelt, Eva Markert, Erich Stoelben, Karen Ernestus, Roman K. Thomas, Jürgen Wolf
Journal: Journal of Thoracic Oncology (2010)
The Standard of Care
Authors: JANE KELLEY RODEHEFFER
Journal: Annals of Internal Medicine (1988)

Letters and Corrections1 April 1988The Standard of CareJANE KELLEY RODEHEFFERJANE KELLEY RODEHEFFERSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-108-4-636_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: I sympathize with the authors' (1) use of the Aristotelian concept of phronesis to characterize clinical judgement in the article on the standard of care. Their account of phronesis, or practical wisdom, and of its relation to techne and medical practice is, however, incomplete.The authors do not consider the specific characteristics of medical training that bring about phronesis. In Aristotle's account phronesis is a virtue, and one is habituated into the virtues through participation in which one learns both the goals or ends of a practice, and what means best promote those ends. In medical training,...References1. LA PUMASCHIEDERMAYERTOULMINMILESMCATEE JDSSJ. The standard of care: a case report and ethical analysis. Ann Intern Med. 1988;108:121-4. LinkGoogle Scholar2. KASS L. Toward A More Natural Science. New York: The Free Press; 1985. Google Scholar3. ARISTOTLE . The Nicomachean Ethics, Book VI. Indianapolis: Hackett; 1985. Google Scholar1. LA PUMASCHIEDERMAYERTOULMINMILESMCATEE JDSSJ. The standard of care: a case report and ethical analysis. Ann Intern Med. 1988;108:121-4. LinkGoogle Scholar2. VEVAINABONEKASSOFF JRE, eds. Legal Aspects of Medicine. New York: Springer-Verlag; 1988. Google Scholar3. ORLOWSKIKANOTI JG, eds. Ethical Moments in Critical Care Medicine. Philadelphia: W.B. Saunders; 1986. Google Scholar4. GARDNER F. Death Without Dignity: The Nursing Home Scandal. New York: Pergamon Press; 1962. Google Scholar5. VEVAINA J. The be happy attitudes [Letter]. Chest. 1987;91:150. CrossrefMedlineGoogle Scholar1. LA PUMASCHIEDERMAYERTOULMINMILESMCATEE JDSSJ. The standard of care: a case report and ethical analysis. Ann Intern Med. 1988;108:121-4. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: JANE KELLEY RODEHEFFERAffiliations: Mayo Medical School Rochester, MN 55905 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 April 1988Volume 108, Issue 4Page: 636-637 ePublished: 1 December 2008 Issue Published: 1 April 1988 PDF downloadLoading ...
Ellenberg and Rifkin's Diabetes Mellitus: Theory and Practice
Authors: Barry Z. Izenstein
Journal: JAMA (1991)

Diabetes mellitus has become one of the most common afflictions in Western society. Most internists, practicing endocrinologists, and diabetologists must deal with the intricacies of controlling blood glucose levels and the complications of the disease, both short- and long-term. Certainly such a common disease merits its own textbook. To whom will this edition appeal? The fourth edition of<i>Ellenberg and Rifkin's Diabetes Mellitus: Theory and Practice</i>, edited now by Drs Harold Rifkin and Daniel Forte, Jr, continues, like its predecessors, to be an encyclopedic source of information concerning diabetes. It is now largely rewritten and, as its title boasts, it is both theoretical-academic and practical-clinical. The editors have assembled world-renowned experts in the field, who have written 60 well-organized, up-to-date, and well-referenced chapters. The text has two sections. Chapters 1 through 21 are concerned with the basic physiology of metabolism and the pathophysiology of diabetic complications. Here the actions of
SETBP1 mutations in 658 patients with myelodysplastic syndromes, chronic myelomonocytic leukemia and secondary acute myeloid leukemias
Authors: F Damm, R Itzykson, O Kosmider, N Droin, A Renneville, V Chesnais, V Gelsi-Boyer, S de Botton, N Vey, C Preudhomme, A Clavert, E Delabesse, S Park, D Birnbaum, M Fontenay, O A Bernard, E Solary
Journal: Leukemia (2013)
Brentuximab Vedotin (SGN-35) for Relapsed CD30-Positive Lymphomas
Authors: Anas Younes, Nancy L. Bartlett, John P. Leonard, Dana A. Kennedy, Carmel M. Lynch, Eric L. Sievers, Andres Forero-Torres
Journal: New England Journal of Medicine (2010)

Hodgkin's lymphoma and anaplastic large-cell lymphoma are the two most common tumors expressing CD30. Previous attempts to target the CD30 antigen with monoclonal-based therapies have shown minimal activity. To enhance the antitumor activity of CD30-directed therapy, the antitubulin agent monomethyl auristatin E (MMAE) was attached to a CD30-specific monoclonal antibody by an enzyme-cleavable linker, producing the antibody-drug conjugate brentuximab vedotin (SGN-35).In this phase 1, open-label, multicenter dose-escalation study, we administered brentuximab vedotin (at a dose of 0.1 to 3.6 mg per kilogram of body weight) every 3 weeks to 45 patients with relapsed or refractory CD30-positive hematologic cancers, primarily Hodgkin's lymphoma and anaplastic large-cell lymphoma. Patients had received a median of three previous chemotherapy regimens (range, one to seven), and 73% had undergone autologous stem-cell transplantation.The maximum tolerated dose was 1.8 mg per kilogram, administered every 3 weeks. Objective responses, including 11 complete remissions, were observed in 17 patients. Of 12 patients who received the 1.8-mg-per-kilogram dose, 6 (50%) had an objective response. The median duration of response was at least 9.7 months. Tumor regression was observed in 36 of 42 patients who could be evaluated (86%). The most common adverse events were fatigue, pyrexia, diarrhea, nausea, neutropenia, and peripheral neuropathy.Brentuximab vedotin induced durable objective responses and resulted in tumor regression for most patients with relapsed or refractory CD30-positive lymphomas in this phase 1 study. Treatment was associated primarily with grade 1 or 2 (mild-to-moderate) toxic effects. (Funded by Seattle Genetics; ClinicalTrials.gov number, NCT00430846.).
Testing Times: We Are Still Some Way From Getting the Best Out of Sensitive Troponin Assays
Authors: Edward Watts Carlton, James Hugo Phillimore Gamble, Kim Greaves
Journal: JAMA Internal Medicine (2013)

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 Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Journals 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) 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 Internal Medicine journal
Carcinoid tumour secreting dopa.
Authors: B K Sharma, B J Smits, R Robinson, S Burns, E N Trounson
Journal: BMJ (1984)

A middle aged woman referred for an abdominal mass was found to have large amounts of dopa (3-4-dihydroxyphenylalanine) metabolites in her urine. At operation a tumour affecting almost the entire left lobe of the liver was removed. Histologically the tumour was a metastatic carcinoid. After operation the excretion of dopa metabolites fell substantially, confirming that the tumour was the source. Apparently, owing to an enzyme defect the tumour had been unable to decarboxylate dopa. These findings are further evidence of a neural origin for the endocrine system of the gut.
Effects of vasopressin on portal-systemic collaterals in portal hypertensive rats: Role of nitric oxide and prostaglandin
Authors: Che-Chang Chan, Fa-Yauh Lee, Sun-Sang Wang, Full-Young Chang, Han-Chieh Lin, Chi-Jen Chu, Chun-Ching Tai, I-Nien Lai, Shou-Dong Lee
Journal: Hepatology (1999)

This study investigated the effect of vasopressin on portal-systemic collaterals in portal hypertensive rats and the influence of nitric oxide (NO) and prostaglandin on the responsiveness of collateral vessels to vasopressin. The vascular responsiveness to graded concentrations of vasopressin was tested with or without the incubation of n(omega)-nitro-L-arginine (NNA) (100 micromol/L) and/or indomethacin (10 micromol/L) in perfused collateral vascular beds of rats with portal hypertension induced by partial portal vein ligation. In addition, concentration-response curves to vasopressin with incubation of a vasopressin V(1) receptor antagonist d(CH(2))(5)Tyr(Me) arginine vasopressin and concentration-response curves to a V(2) receptor agonist 1-desamino-8-D-arginine vasopressin were performed. Vasopressin significantly increased the perfusion pressure of collaterals, and this effect was suppressed by the addition of the V(1) receptor antagonist. Perfusion with the V(2) receptor agonist had no effect on the collaterals. Incubation with NNA, indomethacin, or both significantly potentiated the response of collaterals to vasopressin. In addition, the pressor response to vasopressin in the combination group was significantly higher than that in the NNA-alone group. The results show that vasopressin produces a direct vasoconstrictive effect on the portal-systemic collaterals of portal hypertensive rats. This effect is mediated by the vasopressin V(1,) but not V(2), receptors. The attenuation of the response to vasopressin by NO and prostaglandin suggest a function role of both mediators in the regulation of the portal-systemic collateral circulation in portal hypertensive rats.
SOME THERAPEUTIC EXPERIENCES WITH HODGKIN'S DISEASE
Authors: OVID O. MEYER
Journal: JAMA (1941)

The cause of Hodgkin's disease remains obscure, but the theories of the causative factors are well known. The possible significance of the recent reports of Wise and Poston,<sup>1</sup>who have demonstrated the frequent presence of Brucella melitensis in the lymph nodes of patients with lymphogranulomatosis, is yet to be established. These workers have analyzed their results with commendable objectivity and without ascribing a final etiologic relationship to these organisms. Dr. E. A. Birge<sup>2</sup>has cultured specimens from the lymph nodes of 10 patients with Hodgkin's disease seen at the Wisconsin General Hospital but has been unable to demonstrate Brucella organisms. It should be observed, however, that brucellosis is much less common in Wisconsin than in the regions where the patients of Wise and Poston<sup>1</sup>live. This factor has already been weighed by these observers, and further discussion of it is unnecessary. The therapy of Hodgkin's disease is