tbuckley/cabot-search huggingface dataset:
Resistance of cytolytic lymphocytes to perforin-mediated killing. Induction of resistance correlates with increase in cytotoxicity.
Authors: C C Liu, S Jiang, P M Persechini, A Zychlinsky, Y Kaufmann, J D Young
Journal: The Journal of Experimental Medicine (1989)

CTL and NK cells cultured in vitro are known to produce a cytolytic pore-forming protein (PFP, perforin) localized in their cytoplasmic granules. Using purified perforin, we showed here that both cloned CTL and primary killer cell populations, including allospecific CTL, NK/lymphokine-activated killer cells, and MHC-non-restricted CTL, were more resistant to perforin-mediated killing than other lymphocyte populations and cell types. Similar results were obtained with both murine and human cytolytic lymphocyte populations. Resistance of killer cells to perforin correlated in general with their cytolytic capability. Thus, cells that have acquired competence to kill after stimulation with Con A, IL-2, or leukocyte-conditioned medium, were also the more resistant cells. IL-2-independent CTL lines and hybridomas derived in our laboratories could be triggered to become cytotoxic and perforin resistant by short-term stimulation with various cytokines, indicating that the acquisition of resistance to perforin-mediated lysis was independent of cell proliferation. Activation of one IL-2-independent CTL line with IL-2 also resulted in enhanced production of perforin and in enhanced serine esterase activity. The acquisition of cell resistance to perforin by these IL-2-independent cell lines after activation with stimulatory reagents was independent of protein and RNA neosynthesis: emetine, cycloheximide, and actinomycin D, while effectively blocking the incorporation of [35S]methionine into cell proteins, did not affect the induced increase in perforin resistance.
Inhibitors in hemophilia patients: Current status and management
Authors: Louis Aledort
Journal: American Journal of Hematology (1994)

The development of inhibitor antibodies is a long-standing, well-documented complication of coagulation factor replacement therapy and is difficult to treat. Previous estimates of 5-15% of patients developing inhibitors may be low, since newer data suggest a wider range of occurrence. Factors that appear to affect inhibitor development include the severity of hemophilia, age, genetics, and, possibly, the type of replacement therapy administered. Recent studies raise the concern that recombinant factor therapies may be associated with more rapid development and higher levels of inhibitors in previously untreated patients. However, results of different studies are often difficult to compare owing to differences in methodology and populations studied. Further studies standardized in design and methods are clearly needed. Management of patients with inhibitors involves control of acute bleeding episodes and, over the long term, induction of immune tolerance for the coagulation replacement therapy. Many with low or moderate levels of inhibitors may be treated simply by administering higher doses of clotting factor. Other therapies appropriate for those with high levels of inhibitors include porcine F VIII and factor VIII "bypassing" agents, such as recombinant factor VIIa. Long-term immune tolerance has been achieved through the high-dose "Bonn" regimen and immunosuppressive regimens such as the "Malmö" method. Although management of inhibitor patients has improved, it still represents a major challenge. Further research is needed to identify which patients will develop inhibitors and tolerance, as well as to develop better methods to manage, reduce, or eliminate inhibitors from these patients.
Abstract 2291: Inhibition of c-Src restores estrogen stimulated growth in estrogen-deprivation resistant MCF-7 breast cancer cells
Authors: Ping Fan, Helen Kim, Russell McDaniel, V. Craig Jordan
Journal: Cancer Research (2011)

Abstract Resistance to aromatase inhibitors used for the treatment of estrogen receptor (ER) positive breast cancer is an increasing clinical problem. Previously we showed that physiological concentrations estradiol (E2) could trigger apoptosis of long-term E2 deprived breast cancer cells (MCF-7:5C) (Lewis et al. JNCI 2005; 97:1746-59). This new targeted strategy provides novel therapeutic approaches to endocrine resistant breast cancer. A recent phase II clinical trial reported that E2 provided a clinical benefit for aromatase inhibitor-resistant advanced breast cancer patients. However, only 30% of patients receive clinical benefit (Ellis MJ et al. JAMA 2009;302:774-80). This prompted us to investigate strategies to increase the therapeutic responsiveness in aromatase inhibitor resistant breast cancer. c-Src is currently of interest, as it mediates survival pathways of breast cancer cells. Here, we investigate the therapeutic potential of combination c-Src inhibitor PP2 and E2 on the MCF-7:5C cells. In the short-term treatment, c-Src inhibitor could block both Akt and MAPK pathways and decreased growth rates of MCF-7:5C cells. c-Src inhibitor could continuously block phosphor-Akt, but phosphor-MAPK pathway was increased after long-term treatment. Long-term treatment with E2 alone initially caused massive apoptosis, but a small population of surviving cells subsequently re-grew. In contrast, a combination of PP2 and E2 actually blocked apoptosis and the resulting cell line (MCF-7:PF) was unique, as they grew vigorously in culture with physiological levels of E2, which could be blocked by the pure antiestrogen ICI182,780. The mechanistic change underlying the action of combination treatment was that the c-Src inhibitor blocked E2 initiated apoptosis and collaborate with E2 to up-regulate endogenous ERα target genes and insulin-like growth factor-1 receptor (IGF-1Rβ) in MCF-7:PF cells. Furthermore, the inhibitor of IGF-1Rβ, AG1024, completely blocked E2 stimulated growth. This provides the evidence that IGF-1Rβ plays an important role in E2 stimulated growth in MCF-7:PF cells. These data illustrate that caution must be exercised when considering the evaluation of c-Src inhibitors in clinical trial following the development of acquired resistance to aromatase inhibitors, especially in combination with physiological levels of E2. Key words: c-Src, long-term estrogen deprivation, apoptosis, breast cancer Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2291. doi:10.1158/1538-7445.AM2011-2291
Concurrent acute myeloid leukemia with inv(16)(p13.1q22) and chronic lymphocytic leukemia: Molecular evidence of two separate diseases
Authors: Chuanyi M. Lu, Joyce L. Murata‐Collins, Endi Wang, Imran Siddiqi, H. Jeffrey Lawrence
Journal: American Journal of Hematology (2006)

Abstract Acute myeloid leukemia (AML) occurring concurrently with or after untreated chronic lymphocytic leukemia (CLL) is rare. We report a case of a 59‐year‐old man who was evaluated for anemia, thrombocytopenia, and leukocytosis with circulating blasts. On the basis of the morphology and immunophenotyping results, a preliminary diagnosis of chronic myelomonocytic leukemia with concurrent CLL was considered. Subsequently, cytogenetic analysis of the leukemic blood specimen revealed inv(16)(p13.1q22) with secondary trisomy 22 in a sideline clone. Fluorescence in situ hybridization confirmed the CBFβ rearrangement associated with inv(16) in myeloblasts and myelomonocytic cells, but not in CLL cells. Therefore, a final diagnosis of AML with inv(16) with concurrent CLL was made. After standard chemotherapy for AML, the patient achieved complete remission for both his AML and CLL. The unique aspects of this case include concomitant AML and CLL, which do not share clonality, complex cytogenetic abnormalities with trisomy 22 as a secondary abnormality associated with inv(16), and achievement of remission for both AML and CLL by AML chemotherapy regimen. This case also represents one of the rare instances where a diagnosis of AML can be established even when the blast percentage in the marrow and blood is less than 20%. Am. J. Hematol., 2006. © 2006 Wiley‐Liss, Inc.
Die impotenten Don Juans
Authors: Gustav Hans Graber
Journal: Psychotherapy and Psychosomatics (1956)

Research Articles| February 10 2010 Die impotenten Don Juans Subject Area: Psychiatry and Psychology Gustav Hans Graber Gustav Hans Graber Bern Search for other works by this author on: This Site PubMed Google Scholar Acta Psychotherapeutica et Psychosomatica (1956) 4 (2): 137–143. https://doi.org/10.1159/000285232 Article history Published Online: February 10 2010 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Gustav Hans Graber; Die impotenten Don Juans. Acta Psychotherapeutica et Psychosomatica 1 February 1956; 4 (2): 137–143. https://doi.org/10.1159/000285232 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsActa Psychotherapeutica et Psychosomatica Search Advanced Search Article PDF first page preview Close Modal This content is only available via PDF. 1956Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.
Safety of Dyclonine
Authors: David O. Merifield
Journal: JAMA (1964)

<h3>To the Editor:—</h3> I read with interest the recent communication, "Clinical Effectiveness of Drugs Used for Topical Anesthesia" (<i>JAMA</i><b>188:</b>711 [May 25] 1964). In the discussion of dyclonine hydrochloride it is stated that the drug does "... not cause systemic reactions..." and that it "... has been used during the past seven years... without any disquieting episodes." The authors also state that "As many as 30 cc may be sprayed or applied to the mucous membranes of the pharynx or trachea at one sitting without systemic or residual local manifestations." I would like to draw attention to a report of three untoward reactions (<i>Arch Otolaryng</i><b>74:</b>437 [Oct] 1961). One was of a severe nature, associated with convulsions and coma; the patient had received only 9 cc of the 0.5% solution. While the newer topical anesthetics appear to have a fairly great margin of safety, no topical anesthetic should be considered
Role of the GRO family of chemokines in monocyte adhesion to MM-LDL-stimulated endothelium.
Authors: D Schwartz, A Andalibi, L Chaverri-Almada, J A Berliner, T Kirchgessner, Z T Fang, P Tekamp-Olson, A J Lusis, C Gallegos, A M Fogelman
Journal: Journal of Clinical Investigation (1994)

We have previously shown that treatment of endothelial cells with minimally modified LDL (MM-LDL) induces the binding of monocytes to unknown endothelial receptor molecules. We now report that a member of the GRO family of chemokines plays a role in MM-LDL-induced monocyte binding. A cDNA library made from rabbit aortic endothelial cells (RAEC) treated with MM-LDL was expression screened for molecules inducing binding of a human monocyte cell line (THP-1). A cDNA was isolated with 75% homology to GRO. GRO mRNA levels were significantly elevated after exposure of RAEC or human aortic endothelial cells (HAEC) to MM-LDL. HAEC treated with MM-LDL displayed an increase in a surface-associated protein that bound to antibody against GRO despite low levels of GRO in the medium. Antibody to GRO significantly inhibited the binding of monocytes to MM-LDL-treated RAEC and HAEC. The increase in GRO expression and monocyte binding were reduced by incubating MM-LDL-treated endothelial cells with heparin (in a method that releases heparan sulfate bound molecules from the cell surface). These results suggest that GRO related chemokines are bound to the surface of MM-LDL-treated endothelial cells and may contribute to the monocyte adhesion induced by MM-LDL.
P318FGF10 regulates regional proliferation in the fetal heart through a FOXO3/p27kip1 pathway and promotes cell cycle reentry of adult cardiomyocytes
Authors: F Rochais, R Sturny, CM Chao, K Mesbah, M Bennett, TJ Mohun, S Bellusci, RG Kelly
Journal: Cardiovascular Research (2014)

Cardiomyocyte proliferation gradually declines during embryogenesis resulting in severely limited regenerative capacities in the adult heart. Understanding the developmental processes controlling cardiomyocyte proliferation may thus identify new therapeutic targets to modulate the cell cycle activity of cardiomyocytes in the adult heart. In the present study, we investigate the mechanism by which FGF10 controls fetal cardiomyocyte proliferation and test the hypothesis that FGF10 promotes the proliferative capacity of adult cardiomyocytes. Analysis of Fgf10-/- hearts and primary cardiomyocyte cultures reveals that altered ventricular morphology is associated with impaired proliferation of right ventricular myocytes. Decreased FOXO3 phosphorylation associated with upregulated p27kip1 levels were observed specifically in the right ventricle of Fgf10-/- hearts. In addition, cell type specific expression analysis revealed that Fgf10 and its receptor, Fgfr2b, are predominantly expressed in cardiomyocytes rather than cardiac fibroblasts, consistent with a cell-type autonomous role of FGF10 in regulating regional specific myocyte proliferation in the fetal heart. Furthermore, we demonstrate that in vivo overexpression of Fgf10 in adult mice results in an upregulation of cardiomyocyte but not cardiac fibroblast proliferation. In conclusion, this study identifies FGF10 as a regulator of regional cardiomyocyte-autonomous proliferation in the fetal heart through a FOXO3/p27kip1 pathway. In addition, FGF10 triggers cell cycle reentry of adult cardiomyocytes and is thus a potential target for cardiac repair.
F-18 FDG PET Identification of Right Atrium Metastasis From a Vesical Carcinoma
Authors: I Biancheri, R Zsigmond, O Angoué, O Blagosklonov, S Klingelschmitt, P Legalery, B Kastler, H Boulahdour
Journal: Clinical Nuclear Medicine (2007)

Fluorodeoxyglucose (FDG) positron emission tomography (PET) has been shown to be useful in the diagnosis and staging of various malignancies. The main advantage of PET is its high sensitivity in identifying malignancies at an early stage. The authors present a patient in whom transthoracic echography and MRI revealed a right atrial mass. The diagnosis was difficult between tumor and thrombus, but PET imaging correctly suggested a malignant tumor.
Mitral valve replacement with mounted aortic valve homografts
Authors: M. A. Rogers, R. J. Chambers, M. S. Gotsman, W. S. Winship
Journal: Thorax (1972)

The clinical results of isolated mitral valve replacement with mounted aortic valve homografts undertaken in 29 patients is presented. In 15 of these patients haemodynamic evaluations were made before and after operation. The results attest to the haemodynamic suitability of the homograft aortic valve in the mitral position and it would appear from this initial study that there will be little difference in the durability of orthotopic and heterotopic aortic homograft valves.
Hematocrit and Prognosis in Patients With Acute Myocardial Infarction
Authors: Philip I. Hershberg
Journal: JAMA (1972)

It has previously been demonstrated that the mean hematocrit value in patients with acute myocardial infarction is higher than that in control subjects. Although never studied on a statistical basis, it has long been suspected that those patients with coronary heart disease who have higher hematocrit values tend to have poorer prognoses. However, when hematocrit values of 190 patients on admission to a coronary care unit were correlated with their ultimate hospital course, patients having higher hematocrit values tended to have slightly, but not significantly, better prognoses than those with lower hematocrit values. It has also been noted that, at least on a statistical basis, all of the fall in mean hematocrit values which occurred during the first three hospital days could be attributed to diagnostic phlebotomy rather than to previously suspected plasma volume alterations.
Factors in the Death of President Kennedy
Authors: John K. Lattimer
Journal: JAMA (1966)

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
Abstract 1698: Resveratrol potentiates the cytotoxic profile of docetaxel and doxorubicin via inhibiting the activity and expression of p-glycoprotein molecules
Authors: Ahmed M. Al-Abd, Ali M. Mahmoud, Salwa M. Nofal, Gamal A. El-sherbiny, Mohammed A. El-Moselhy, Hekma A. Ahmed Abdel-Tawab, Wafaa I. El-Eraky, Hany A. El-Shemy
Journal: Cancer Research (2011)

Abstract P-glycoprotein is membrane protein highly abundant in tumor cells which facilitate the effluxes of several chemotherapeutic agents to the extracellular compartment. Several P-glycoprotein blockers of synthetic origin were suggested as adjuvant therapy for cancer; however, manifested several toxic side effects. Resveratrol was found to block p-glycoprotein with potential use as adjuvant therapy for several p-glycoprotein substrates such as docetaxel and doxorubicin. Herein, we have assessed the interactive characteristics of resveratrol with docetaxel and doxorubicin and further investigated the molecular bases of this interaction in three different solid tumor cell lines (MCF-7, HeLa and HepG2). Resveratrol per se was found to possess anti-cancer properties; however with relatively low potency in all tested cell lines (IC50 ranges from 8.0 to 19.1µg/ml). Doxorubicin and docetaxel showed IC50‘s ranged from 0.28 to 0.42 µg/ml and from 22.3 to 67.1 ng/ml, respectively. Resveratrol combination with doxorubicin and docetaxel significantly increased the potencies of both chemotherapeutic agents showing IC50‘s ranging from 0.07 to 0.2 µg/ml and from 6.2 to 45.7 ng/ml, respectively. The combination index showed synergistic interaction between resveratrol and doxorubicin or docetaxel in MCF-7 cell line, while additive interaction in HeLa and Hep-G2 cell lines. Real time PCR revealed that the expression of BAX and BcL2 were simultaneously elevated due to combination of resveratrol with doxorubicin or docetaxel in all tested cell lines while p-53 showed marginal elevation in MCF-7 and HepG2 cell lines. The p-glycoprotein efflux activity was significantly inhibited with subsequent accumulation of p-glycoprotein substrate within the intracellular compartment of all tested cell lines. Also the expression level of mdr1 gene was down regulated after resveratrol combination with doxorubicin or docetaxel in all tested cell lines. In conclusion, resveratrol potentiates the anti-cancer effects of doxorubicin and docetaxel via increasing their intracellular level due to p-glycoprotein activity inhibition and down regulation of mdr1 gene. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1698. doi:10.1158/1538-7445.AM2011-1698
Arterial Hypertension Associated with Acute Anterior Poliomyelitis
Authors: Fletcher H. McDowell, Fred Plum
Journal: New England Journal of Medicine (1951)

AN ABNORMALLY elevated arterial blood A pressure has been a striking finding in over half the patients with acute paralytic poliomyelitis seen at the New York Hospital in the past two years. The hypertension appeared in the acute stage of the disease and sometimes lasted well into convalescence; its degree has in general been proportionate to the severity of the patient's illness.Although high blood pressure has not been widely commented on as being a concomitant or a sequela of poliomyelitis, the phenomenon has been previously recorded. Grulee and Panos,1 for example, found transient hypertension in 51 out of 70 . . .
949 IMPACT OF NON-ALCOHOLIC FATTY LIVER DISEASE (NAFLD) ON CHRONIC HEPATITIS B (CHB) AND C (CHC)
Authors: A.A. Markova, S.S. Dragneva, K. Antonov, D. Jelev, O. Kosseva, R. Ivanova, A. Gegova, L. Mateva
Journal: Journal of Hepatology (2008)