tbuckley/cabot-search huggingface dataset:
FEATURES OF LIFE INSURANCE EXAMINING WHICH DEMAND CORRECTION.
Journal: JAMA (1906)

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
Editorial Board
Authors: Zuhair Ballas, Iowa City, Iowa Deputy, David Huston, Rachel Miller, New York, N Associate, Andrea Apter, Leonard Philadelphia, St Bacharier, Claus Louis, Joshua Bachert, Boston Boyce, Robert Bush, Javier Chinen, Raif Geha, Corinne Keet, Carole Ober, David Peden, Harald Renz, Marburg Germany, Marc Rothenberg, Cincinnati Ohio, Hirohisa Saito
Journal: Journal of Allergy and Clinical Immunology (2020)
Rings and Nodules on Trabecular Fibers
Journal: JAMA (1963)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Correction:<i>S140 Interim results from a prospective study of tablet and web- based audiometry to detect ototoxicity in adults with cystic fibrosis</i>
Authors: A Vijayasingam, E Frost, J Wilkins, L Picinali, P Premachandra, L Gillen, D Morris- Rosendahl, M Ni, C Elston, N Simmonds, A Shah
Journal: Thorax (2019)
Vascular endothelial growth factor receptor 2–mediated angiogenesis is essential for gonadotropin-dependent follicle development
Authors: Ralf C. Zimmermann, Tipton Hartman, Suzanne Kavic, Samuel A. Pauli, Peter Bohlen, Mark V. Sauer, Jan Kitajewski
Journal: Journal of Clinical Investigation (2003)

Gonadotropins induce ovarian follicle growth that is coincident with increased follicular vasculature, suggesting a role of angiogenesis in follicle development. Functional studies performed in nonhuman primates show that administration of substances that inactivate VEGF block the development and function of preovulatory follicles as demonstrated by histological analysis or hormone measurements. Blockage of function of VEGF receptor 2 (VEGFR-2) alters follicular hormone secretion, suggesting that the intraovarian effect of VEGF might be mediated by this receptor. The specific mechanism by which follicular development was blocked in these previous studies remains unclear, however. Here we characterize the intraovarian role of VEGFR-2 activity on follicular development by choosing a model in which active feedback is absent, the prepuberally hypophysectomized mouse. Hypophysectomy prevents advanced follicle growth and maturation; however, follicle development to the preovulatory stage can be stimulated by administration of gonadotropins. We report that exogenously administered gonadotropins are unable to drive follicle development to the preovulatory stage in the presence of antiangiogenic agent, VEGFR-2–neutralizing Ab's. This inhibition of follicular development is caused by arrests to both angiogenesis and antrum formation. We conclude that the intraovarian VEGF/VEGFR-2 pathway is critical for gonadotropin-dependent angiogenesis and follicular development.
CORRIGENDUM
Journal: Allergy (2017)

In the article "Effect of omalizumab on angioedema in H1-antihistamine-resistant chronic spontaneous urticaria patients: results from X-ACT, a randomized controlled trial," Figure 2 has to be corrected.The asterisks denoting P < 0.05 are missing in Figure 2. The revised figure is shown below: Figure 2 legend: Change in CU-Q2oL total scores from baseline.CU-Q2oL, Chronic Urticaria Quality of Life Questionnaire.Arrows indicate omalizumab/placebo administration.The valus represented are for the full analysis set, using analysis of covariance.Last observation carried forward (LOCF) was used for missing values.ANCOVA model: variable = baseline, centre, treatment.* indicates P < 0.05 (95% CI at week 28 = À30.9,À12.1).[Colour figure can be viewed at wileyonlinelibrary.com]We apologize for any inconvenience caused.
Possible tobramycin delirium
Authors: C. F. McCartney
Journal: JAMA (1982)

TOBRAMYCIN sulfate and a related aminoglycoside, gentamicin sulfate, are valued for their efficacy in treating serious Gram-negative infections despite their narrow therapeutic ratio.<sup>1</sup>Their widespread use is reflected in 1978 projections from demographic and clinical data that estimated that 3.9 million patients received one course of treatment with an aminoglycoside that year.<sup>2</sup>Reports of serious adverse reactions to these drugs have usually described nephrotoxicity or ototoxicity. Though we can find no published description of tobramycin's corticoneuronal toxicity, there are several case reports of acute toxic psychosis with gentamicin.<sup>3,4</sup>These led us to suspect tobramycin as the cause of delirium in the patient described here. <h3>Report of a Case</h3> The patient was a 66-year-old woman with urinary incontinence. Following radical hysterectomy and radiation therapy for cervical cancer, she had required three surgical procedures for stress urinary incontinence. Intermittent self-catheterization was then offered to relieve the resultant increased residual
TRTH-03. CYTO-MITO™ - A NOVEL CLASS OF DUAL-ACTING HSP90 INHIBITORS FOR THE TREATMENT OF GLIOBLASTOMA
Authors: Srinivasa Reddy Natala, Shyama Siddique, David Carney, Ann Mladek, Jeffrey Stebbins, Li Yang, Pooi San Lee, Daniel Brimberry, Robert Ardecky, Peter Teriete, Allan Rubenstein, Jann Sarkaria, Nicholas Cosford, Sridhar Prasad
Journal: Neuro-Oncology (2017)

Glioblastoma (GBM) is a highly invasive and aggressive primary brain tumor and is considered one of the deadliest forms of cancer. Despite aggressive therapies, half of GBM patients die within 15 months after diagnosis and only 2% survive more than 5 years. Therefore, effective treatments for GBM represent an urgent unmet medical need. Genetic profiling of glioma has shown multiple oncogenes critical for cell-signaling are not only mutated and/or amplified but can also circumvent the otherwise clinically promising targeted therapeutics. Therefore, a therapy that can simultaneously suppress multiple cell-signaling oncogenes using a single agent may be a more effective therapeutic strategy for GBM. Cytosolic Hsp90 facilitates GBM tumor cell growth and survival by assisting in the proper folding and active conformation maintenance of many oncoproteins. The mitochondrial Hsp90 homolog, TNF Receptor Associated Protein-1 (TRAP1) is also elevated in GBM tumors and participates in pleiotropic signaling circuitries of organelle integrity and cellular homeostasis. Thus, dual-acting Hsp90/TRAP1 inhibitors benefit from the advantage of simultaneously disrupting a multitude of cancer-promoting pathways and have successfully demonstrated anti-tumor effectiveness against a number of glioma cell lines and in vivo preclinical models. Taken together, these data support concomitant inhibition of cytosolic Hsp90 and the mitochondrial TRAP1 using a single agent represents a novel “double-pronged” approach for effective GBM treatment. Plex has discovered dual-acting (Hsp90/TRAP1) inhibitors demonstrating low sub-micromolar efficacy in multiple clinically relevant Mayo Clinic GBM patient-derived cell lines. Consistent with sub-micromolar efficacy, our compounds caused ≥50% suppression in EGFR and Akt1 levels in these cell lines. In addition, the compounds induced mitochondrial dysfunction, both in cells and in isolated mitochondria. Preliminary studies also show, a compound in our Hsp90/TRAP1 inhibitor series achieved effective concentrations in normal rat brains, indicating effective blood brain barrier crossing. This work was supported by National Institutes of Health grant (1R43GM090383).
Protective action of hepatocyte growth factor for acute liver injury caused by ?-galactosamine in transgenic mice.
Authors: J Okano
Journal: Hepatology (1997)

Hepatocyte growth factor (HGF) has been reported to be a potent mitogen for hepatocytes in vivo and in vitro. Recent reports have shown that HGF has cytoprotective actions in acute liver injury models, but its mechanisms remain to be resolved. In the present study, we investigated whether HGF could work as an anti-hepatitis agent for acute liver injury caused by D-galactosamine (D-GalN) using transgenic (TG) mice expressing HGF in hepatocytes, compared with wild-type (WT) mice of their siblings. After administration of 3 g/kg body weight of D-GalN, elevated serum transaminase levels and severe liver damage that were observed in WT mice were significantly improved in TG mice. In TG mice, the percentage of proliferating cell nuclear antigen (PCNA)-positive hepatocytes was high at 0 hours after D-GalN treatment, and increased at 24 hours. The percentage of PCNA-positive cells in WT mice was very low at 0 hours and 24 hours after treatment, but increased at 48 hours. To clarify the mechanisms via which HGF acts, we measured hepatic HGF and prostaglandin E2 (PGE2) contents after D-GalN administration by an enzyme immunoassay. Total hepatic HGF contents, which were composed of murine (endogeneous) and human (derived from transgene) HGF, in TG mice were higher than those in WT mice at 0, 12, and 24 hours after administration of 3 g/kg body weight of D-GalN. Hepatic PGE2 contents in TG mice were also significantly higher than those in WT mice. Hepatic PGE2 contents had a positive correlation with total HGF contents at both 12 hours and 24 hours after the treatment. Moreover, an administration of 0.5 microg of anti-HGF antibody into the portal vein suppressed hepatic PGE2 contents of mice, compared with saline-injected mice in acute liver injury. Anti-PGE2 antibody administration caused more severe liver damage than saline solution. A survival rate of TG mice that were given 6 g/kg body weight of D-GalN-a lethal dose of D-GalN-was improved compared with WT mice. These results provided direct evidences that HGF worked as an anti-hepatitis agent against acute liver injury caused by D-GalN, and that this action might be exerted through accelerated hepatic PGE2 production.
Abstract LB-26: The N-terminal projection domain of the microtubule associated protein Tau inhibits TNFα signaling
Authors: Shawon Debnath, Peter Hannon, Kristina Toropova, Nelson Nunez-Rodriguez, Alejandra Alonso, Jimmie E. Fata
Journal: Cancer Research (2012)

Abstract Tumor Necrosis Factor-alpha (TNFα) is a multifunctional pro-inflammatory cytokine implicated in inducing both tumor promotion and tumor inhibition. This paradoxical effect can be partly explained by the fact that TNFα acts as a regulator of both proliferation and apoptosis; however the mechanisms and factors associated with how or whether a tumor cell responds to a microenvironment rich in TNFα have not been fully resolved. Here we provide evidence that the microtubule associate protein Tau inhibits TNFα signaling through its N-terminal domain and implicate it as a novel regulator of the cellular response to this key cytokine. Our findings indicate that over-expression of Tau in the human breast cancer cell lines MCF7, SkBr3 and in the pheochromocytoma cell line PC12 suppresses TNFα-induced apoptosis evident in the control cells. TNFα-induced cell apoptosis in control cells is triggered as early as 6 hrs post-treatment with hallmark features of cell shrinkage, membrane blebbing, disruption of tubulin architecture and caspase-3 activation. While over-expression of wild type full length Tau isoform in these cell lines, completely abrogates all TNFα-associated apoptotic phenotypes. Aside from inhibiting TNFα-induced apoptosis, Tau over-expression also interferes with TNFα-induced NFKB activation. This is evident by a significant decrease in NFKB nuclear translocation in Tau over-expressed cells compared to controls. Suppression of TNFα-signaling by Tau is not associated with its tubulin interaction since a truncated N-terminal projection domain lacking all microtubule binding domains still provides resistance to TNFα-induced apoptosis and NFKB activation. These findings lead us to conclude that the functional domain of Tau that regulates TNFα response lies within its N-terminal region and current studies investigating regions within this domain are ongoing. Our data provide direct evidence that the N-terminal domain of the microtubule associated protein Tau can inhibit TNFα signaling in tumor cells. These findings indicate a novel function for Tau and add to our knowledge of how a tumor cell responds to TNFα-signaling. 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 LB-26. doi:1538-7445.AM2012-LB-26
Detection of antigens related to hepatitis C virus RNA encoding the NS5 region in the livers of patients with chronic type C hepatitis
Authors: M Tsutsumi
Journal: Hepatology (1994)

Hepatitis C virus is a positive single-strand RNA virus distantly related to flaviviruses. Therefore RNA replicase, an RNA-dependent RNA polymerase, may be essential for the replication of hepatitis C virus, as well as other RNA viruses. In this study we synthesized the recombinant polypeptide (HCV-NS5 antigen) with a 576 bp cDNA encoding a part of the NS5 region of the HCV genome that has the Gly-Asp-Asp motif. The antibody against this polypeptide was obtained from rabbit serum. In Western-blot analysis with NS5 IgG HCV antibody, an 84-kD protein was clearly detected as a single band in the microsomal fraction but not in the nuclear and mitochondrial fractions or in the cytosol fraction. Immunohistochemically, HCV-NS5 antigen was clearly stained in the cytoplasm of hepatocytes but not in the nucleus or cell membrane. Moreover, as determined on immunoelectron microscopy, HCV-NS5 antigen was demonstrated with fine granular distribution along the endoplasmic reticulum but not in other organelles, including the nucleus and mitochondria. Immunoreaction in other cell types was negative. These results indicate that replication of HCV may occur only in hepatocytes and that HCV-NS5 may be produced in the endoplasmic reticulum of these cells. HCV-NS5 antigen was stained only in the livers of hepatitis C virus–positive patients but not in sections from patients with chronic type B hepatitis or alcoholic fibrosis. In chronic type C liver disease, the overall detection rate of HCV-NS5 antigen was 56 (33 in chronic persistent hepatitis, 52 in chronic active hepatitis and 86 in cirrhosis). These results indicate that the replication of HCV may occur more frequently in the advanced than in the early stages of type C hepatitis. Recently, interferon has been used for treatment of chronic type C hepatitis. However, it is very difficult to determine when HCV is eliminated from the liver, even if hepatitis C virus RNA is not detected in serum. Immunostaining of HCV-NS5 antigen in liver biopsy sections may be helpful in evaluating the cessation of HCV replication. (Hepatology 1994;19:265–272).
King's College Hospital Reports.—Being the annual report of King's College Hospital and the Medical Department of King's College.
Journal: JAMA (1897)

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
Future of postgraduate medical centres.
Authors: J Williams, Elizabeth Maughan, Lister Hospital, J Austin, B Astedt, Rosemary Gardner, Joyce Mcguckin, British Medical, L Van Der Kuip, J Gardner, British Yournal
Journal: BMJ (1972)

lung metastases of adenocarcinoma of the colon in another.A temporary improvement in neurological signs occurred in another patient with spinal deposits of adenocarcinoma of the colon.In a patient with lung and liver metastases of rectal adenocarcinoma there was a reduction in the size of the liver, but this may have been due to treatment of congestive cardiac failure with digoxin and diuretics.There was no improvement in two patients with metastases of anaplastic carcinoma of the breast and ovary although the latter showed exceptionally high F.D.P. levels (1,500 ,ug/ml) during treatment.Fibrin degradation products have been observed in women with malignant ovarian metastases,2 3and may be derived from breakdown of plasma fibrin following release of thromboplastic substances into the circu- lation.We suggest that some of the F.D.P. occurring during ancrod therapy may be de- rived not only from the expected breakdown of microclots in the circulation but also from degradation of fibrin filaments in the tumour.It may well be that the malignant cells are exposed free from their surrounding sheath of fibrin filament and may perhaps be more susceptible to cytotoxic therapy.-We are, etc.,
Alterations in Morphology, Arginase, and β-Glucuronidase Within a Clone of Mouse Tumor Cells &lt;italic&gt;In Vitro&lt;/italic&gt;
Journal: JNCI Journal of the National Cancer Institute (1961)

Journal Article Alterations in Morphology, Arginase, and β-Glucuronidase Within a Clone of Mouse Tumor Cells In Vitro Get access Katherine K. Sanford, Katherine K. Sanford Laboratory of Biology, National Cancer Institute,4Bethesda, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar Benton B. Westfall, Benton B. Westfall Laboratory of Biology, National Cancer Institute,4Bethesda, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar Ernest H. Y. Chu, Ernest H. Y. Chu Laboratory of Biology, National Cancer Institute,4Bethesda, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar Edward L. Kuff, Edward L. Kuff Laboratory of Biology, National Cancer Institute,4Bethesda, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar Anne B. Covalesky, Anne B. Covalesky Laboratory of Biology, National Cancer Institute,4Bethesda, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar Lartius T. Dupree, Lartius T. Dupree Laboratory of Biology, National Cancer Institute,4Bethesda, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar Gwendolyn L. Hobbs, Gwendolyn L. Hobbs Laboratory of Biology, National Cancer Institute,4Bethesda, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar Wilton R. Earle Wilton R. Earle Laboratory of Biology, National Cancer Institute,4Bethesda, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 26, Issue 5, May 1961, Pages 1193–1219, https://doi.org/10.1093/jnci/26.5.1193 Published: 01 May 1961 Article history Received: 29 November 1960 Published: 01 May 1961