tbuckley/cabot-search huggingface dataset:
Abstract 4338: The follicle-stimulating hormone receptor: A new tumor vascular endothelial target for imaging and therapy in animal models
Authors: Aurelian Radu, Ahsan Siraj, Francis Vacherot, Regi Thomas, Dennis K. Fujii, Adrian D. Nunn, Nicolae Ghinea
Journal: Cancer Research (2010)

Abstract The follicle stimulating hormone receptor (FSHR) is a cell surface receptor expressed in the adult human organism only in the ovary and testis by granulosa and Sertoli cells, respectively, and to a lower extent by the endothelial cells (ECs) of gonadal blood vessels. Here we report that FSHR is also expressed by the vascular ECs of some types of tumors in mice and it is accessible to ligands delivered intravenously. We analyzed by immunohistochemistry tumors generated in nude mice by injecting human cell lines and also tumors that occur in transgenic mice that express oncogenes. Consistent FSHR expression by the ECs has been found in mouse tumors generated by the human prostate cell line LNCaP, and in tumors that appear in the polyoma virus middle T oncogene mouse model of breast carcinogenesis. The most robust expression of FSHR by ECs was found in the xenograft tumors generated by injecting the cell line A431 derived from a human epidermoid carcinoma. In a few other tumor types the expression of FSHR by the tumor vascular ECs was less frequent or absent. We investigated also by immunohistochemistry in mouse models the relation between expression by ECs of FSHR and VEGFR2/KDR, a well established marker of angiogenesis. The possibility of using FSHR expressed by tumor ECs for targeted imaging and therapy was explored in mice that carried xenograft LNCaP tumors. We coupled anti-FSHR extracellular domain antibodies to gold particles and perfused the mice with the complexes for 20 minutes. The vasculature was subsequently washed by perfusion and the tissues have been fixed and processed for electron microscopy. Numerous FSHR-gold particles bound to the surface of the tumor endothelium were visible, while there were no particles attached to the ECs in the normal tissues (prostate and lung). The reported data are relevant in the context of our recent finding that FSHR is expressed by ECs in a wide range of human tumors (manuscript submitted). The mentioned animal models can be used to evaluate the potential of FSHR for targeted tumor imaging and therapy based on FSHR ligands delivered intravenously. The mouse models could be also useful for investigating the mechanism of induction of FSHR expression in the tumor ECs and its potential role in tumor growth. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4338.
Abeloff’s Clinical Oncology
Authors: James R. Egner
Journal: JAMA (2010)

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 consequences of not having eosinophils
Authors: G. J. Gleich, A. D. Klion, J. J. Lee, P. F. Weller
Journal: Allergy (2013)

Abstract Several lines of evidence suggest that deficiency of eosinophils is not associated with any characteristic abnormality. Patients lacking eosinophils, in the setting of immunodeficiency or as a consequence of I g G ‐mediated eosinophil precursor destruction, do not display any distinguishing abnormalities related to eosinophil reduction. The observation that eosinophil‐deficient mice do not display any distinctive syndrome or failure of their health is evidence that, under ordinary laboratory conditions, the eosinophil does not play a critical role in the well‐being of mammals. Observations that monoclonal antibodies to interleukin‐5 ( IL ‐5) are well tolerated appear unsurprising in light of these findings. For example, patients with the hypereosinophilic syndrome have received mepolizumab, an anti‐ IL ‐5 monoclonal antibody, for as long as 6 years and have not developed any characteristic set of adverse events. Safety data for reslizumab, another anti‐ IL ‐5 monoclonal antibody, and benralizumab, a monoclonal antibody to the IL ‐5 receptor α ‐ chain, are comparatively limited, especially for benralizumab, although reports of administration of these antibodies to humans suggest that they are well tolerated. Thus, data to the present suggest that reduction of eosinophils appears to have no characteristic ill effects on normal health, and monoclonal antibodies that deplete eosinophils have the potential to be widely employed in the treatment of eosinophil‐associated diseases.
Prevention and Management of Tardive Dyskinesia
Authors: GEORGE E. CRANE
Journal: American Journal of Psychiatry (1972)

Because no adequate therapy is available, the prevention of tardive dyskinesia is of great importance. The disorder may be prevented by periodic evaluations of the neurologic status of patients on long-term drug treatment, followed by reducing the drug dosage or discontinuing administration. Withdrawing neuroleptics, particularly in patients with pseudoparkinsonism, may uncover latent dyskinesia. For patients already exhibiting this disorder, the use of small doses of neuroleptics may be safe, provided changes in neurological symptoms are monitored carefully.
OX40-Deficient Mice Are Defective in Th Cell Proliferation but Are Competent in Generating B Cell and CTL Responses after Virus Infection
Authors: Manfred Kopf, Christiane Ruedl, Nicole Schmitz, Awen Gallimore, Karin Lefrang, Barbara Ecabert, Bernhard Odermatt, Martin F Bachmann
Journal: Immunity (1999)
Publication Criteria for Statistical Prediction Models
Authors: Kerry L. Lee
Journal: Annals of Internal Medicine (1993)

Letters1 February 1993Publication Criteria for Statistical Prediction ModelsKerry L. Lee, MD, Nina A. Bickell, MD, and Karen S. Pieper, MDKerry L. Lee, MDSearch for more papers by this author, Nina A. Bickell, MDSearch for more papers by this author, and Karen S. Pieper, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-118-3-199302010-00022 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:Our perspective on the publication of regression coefficients and the disclosure of modeling details to allow others to apply predictive models has evolved over time, and our current position is in complete accord with the philosophy expressed by Drs. Palmas, Denton, and Diamond. Thus, the coefficients for several different diagnostic and prognostic models developed using data from the Duke Cardiovascular Disease Database will appear in a forthcoming article in this journal [1]. The particular prognostic models that were used to calculate the hazard score and the difference between medical and surgical survival probabilities, which in turn were used ...References1. Pryor DB, Shaw LK, McCants CB, Lee KL, Mark DB, Harrell FE, et al. Value of the history and physical examination in identifying patients at increased risk for coronary artery disease. Ann Intern Med. 1993; 118:81-90. Google Scholar2. Pryor DB, Shaw LK, Lee KL, Harrell FE, Mark DB, Califf RM. Validation of models for predicting survival in patients with coronary artery disease. Ann. Intern. Med. 1993 (In press). Google Scholar Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 February 1993Volume 118, Issue 3Page: 231-232KeywordsCardiovascular diseasesDatabasesDisclosureGender discriminationRegression analysisStatistical modelsSurgery ePublished: 15 August 2000 Issue Published: 1 February 1993 Copyright & PermissionsCopyright © 1993 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Comparative genomic hybridization in epithelioid sarcoma
Authors: M-W. Lee, K-J. Jee, S-S. Han, G-Y. Gong, J-H. Choi, K-C. Moon, J-K. Koh
Journal: British Journal of Dermatology (2004)

Epithelioid sarcoma is a rare mesenchymal neoplasm of unknown histogenesis. Data on genome-wide surveys for chromosomal aberrations in epithelioid sarcoma are limited.To investigate genetic aberrations in epithelioid sarcoma.We analysed seven cases of epithelioid sarcoma (classic type, three cases and proximal type, four cases) by comparative genomic hybridization (CGH), and correlated findings with the results of additional immunohistochemical study.CGH analysis showed DNA copy number changes at one to five different genomic sites in six of seven cases (86%). The majority of the changes were gains. The most frequent gain was at 22q (six cases). Other recurrent changes include gains of 12q24-qter (four cases), 17 (four cases), and 5q32-qter (three cases). High-level homology was seen in chromosomal aberration in both types. In addition, expression of interleukin-2 receptorbeta, located in 22q, was revealed by immunohistochemical method in six cases with gain of 22q, suggesting it may play a role in epithelioid sarcoma tumorigenesis.
Hypertrophic stimuli induce transforming growth factor-beta 1 expression in rat ventricular myocytes.
Authors: N Takahashi, A Calderone, N J Izzo, T M Mäki, J D Marsh, W S Colucci
Journal: Journal of Clinical Investigation (1994)

Transforming growth factor-beta 1 (TGF-beta 1) is a peptide growth factor that may play a role in the myocardial response to hypertrophic stimuli. However, the cellular distribution, mechanism of induction, and source of increased TGF-beta 1 in response to hypertrophic stimuli are not known. We tested the hypothesis that the cardiac myocyte responds to hypertrophic stimuli with the increased expression of TGF-beta 1. In adult rat ventricular myocardium freshly dissociated into myocyte and nonmyocyte cellular fractions, the preponderance of TGF-beta 1 mRNA visualized by Northern hybridization was in the nonmyocyte fraction. Abdominal aortic constriction (7 d) and subcutaneous norepinephrine infusion (36 h) each caused ventricular hypertrophy associated with 3.1-fold and 3.8-fold increases, respectively, in TGF-beta 1 mRNA in the myocyte fraction, but had no effect on the level of TGF-beta 1 mRNA in the nonmyocyte fraction. In ventricular myocytes, norepinephrine likewise caused a 4.1-fold increase in TGF-beta 1 mRNA associated with an increase in TGF-beta bioactivity. This induction of TGF-beta 1 mRNA occurred at norepinephrine concentrations as low as 1 nM and was blocked by prazosin, but not propranolol. NE did not increase the TGF-beta 1 mRNA level in nonmyocytes, primarily fibroblasts, cultured from neonatal rat ventricle. Thus, the cardiac myocyte responds to two hypertrophic stimuli, pressure overload and norepinephrine, with the induction of TGF-beta 1. These data support the view that TGF-beta 1, released by myocytes and acting in an autocrine and/or paracrine manner, is involved in myocardial remodeling by hypertrophic stimuli.
Thromboxane A <sub>2</sub> Receptor Agonists Antagonize the Proangiogenic Effects of Fibroblast Growth Factor-2
Authors: Anthony W. Ashton, Yan Cheng, Armin Helisch, J. Anthony Ware
Journal: Circulation Research (2004)

Thromboxane (TX) A2 is released from multiple cell types and is a prime mediator of the pathogenesis of many vascular events, including angiogenesis. Endothelial cells express TXA2 receptors (TP) but the effects of TP stimulation on angiogenesis remain controversial. In this study, we show that stimulation of endothelial cell TP impairs ligand-induced FGF receptor internalization and consequently abrogates FGF-2-induced endothelial cell migration in vitro and angiogenesis in vivo. Prevention of FGF-2-induced angiogenesis was associated with expression of the TPbeta isoform. The deficit in FGFR1 internalization was mediated through activation of TPbeta preventing the FGF-2-mediated decrease in p53 expression, thus enhancing thrombospondin-1 (TSP-1) release from EC and reducing FGFR1 internalization. Once released TSP-1 interacted with the alpha(v)beta3 integrin on the EC surface. On stimulation, FGFR1 and alpha(v)beta3 were found to associate in a complex. We determined that complex formation was important for receptor internalization as conditions that inhibit FGFR1 internalization, such as inappropriate ligation of alpha(v)beta3 by either TSP-1 or a neutralizing antibody, disrupted the complex. These results establish a novel role for isoform specific regulation of angiogenesis by TP, provide the first functional significance for the existence of two TP isoforms in humans, and clarify the mechanism by which TP signaling regulates FGFR1 kinetics and signaling.
Pennyroyal Metabolites in Human Poisoning
Authors: Ilene B. Anderson
Journal: Annals of Internal Medicine (1997)

Letters1 February 1997Pennyroyal Metabolites in Human PoisoningIlene B. Anderson, PharmD, Sidney D. Nelson, PhD, and Paul D. Blanc, MDIlene B. Anderson, PharmDSan Francisco Bay Area Regional Poison Control Center, San Francisco, CA 94110University of Washington, Seattle, WA 98195University of California, San Francisco, San Francisco, CA 94143Search for more papers by this author, Sidney D. Nelson, PhDSan Francisco Bay Area Regional Poison Control Center, San Francisco, CA 94110University of Washington, Seattle, WA 98195University of California, San Francisco, San Francisco, CA 94143Search for more papers by this author, and Paul D. Blanc, MDSan Francisco Bay Area Regional Poison Control Center, San Francisco, CA 94110University of Washington, Seattle, WA 98195University of California, San Francisco, San Francisco, CA 94143Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-126-3-199702010-00017 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:Dr. Carmichael raises pertinent points. There was no evidence that the patient had attempted to induce abortion by any means other than the ingestion of pennyroyal extract and black cohosh root. On physical examination, the patient's uterus was about 4 cm in size and was firm, with a closed os. No blood was present. No abnormalities of the cervix or vagina were noted. On autopsy, the uterine corpus was slightly enlarged and its mucosa was hemorrhagic; the ovaries were slightly enlarged and otherwise unremarkable. The patient had received intravenous Unasyn (ampicillin and sulbactam), gentamicin, and clindamycin on an ...References1. Vallance WB. Pennyroyal poisoning: a fatal case. Lancet. 1955; 850. Google Scholar2. Sullivan JB Jr, Rumack BH, Thomas H Jr, Peterson RG, Bryson P. Pennyroyal oil poisoning and hepatotoxicity. JAMA. 1979; 242:2873-4. Google Scholar Author, Article, and Disclosure InformationAffiliations: San Francisco Bay Area Regional Poison Control Center, San Francisco, CA 94110University of Washington, Seattle, WA 98195University of California, San Francisco, San Francisco, CA 94143 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byAdvances of Molecular Clinical Pharmacology in Gastroenterology and Hepatology 1 February 1997Volume 126, Issue 3Page: 250-251KeywordsAutopsyHemorrhageIngestionMetabolitesPlaguePregnancyProtein structureProteinsShockWestern blot ePublished: 15 August 2000 Issue Published: 1 February 1997 Copyright & PermissionsCopyright © 1997 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
<i>STAT1</i> gene variations, IgE regulation and atopy
Authors: L. A. Pinto, L. Steudemann, M. Depner, N. Klopp, T. Illig, S. K. Weiland, E. Von Mutius, M. Kabesch
Journal: Allergy (2007)

Background: Signal transducer and activator of transcription 1 (STAT1), an intracellular signal transducer and activator of transcription centrally involved in many inflammatory pathways, was recently suggested to play an important role in allergy related immune responses. Aim: Thus, we investigated the effect of polymorphisms in the STAT1 gene on the development of atopic sensitization and allergic diseases. Methods: Haplotype tagging single nucleotide polymorphisms (SNPs) previously described in the STAT1 gene were genotyped by matrix‐assisted laser desorption/ionization time‐of‐flight mass spectrometry technology in a cross‐sectional study population of 3099 German children recruited and phenotyped by the International Study of Asthma and Allergy in Childhood, phase II (ISAAC II). Effects of single SNPs and haplotypes were studied using SAS/Genetics and Haploview. Results: The polymorphism C39134A (rs3771300), located in a potentially cis acting regulatory element in STAT1 intron 24, was inversely related to atopy measured by skin prick test, total and specific serum IgE levels while no effect on atopic disease risk was observed. Conclusion: Our results indicate that STAT1 SNP C39134A may protect from atopic sensitization. Because of its location in a highly conserved noncoding sequence near a putative GATA3 binding site, this polymorphism represents an interesting target for further studies.
Vascular addressins are induced on islet vessels during insulitis in nonobese diabetic mice and are involved in lymphoid cell binding to islet endothelium.
Authors: A Hänninen, C Taylor, P R Streeter, L S Stark, J M Sarte, J A Shizuru, O Simell, S A Michie
Journal: Journal of Clinical Investigation (1993)

In the nonobese diabetic (NOD) mouse, lymphocytic and monocytic infiltration of the pancreatic islets leads to beta cell destruction. To investigate the mechanisms by which lymphocytes enter the NOD pancreas, pancreata were immunostained using monoclonal antibodies to a variety of adhesion molecules known to be involved in lymphocyte binding to vascular endothelium, an initial step in the migration of lymphocytes from blood into organized lymphoid and inflamed tissues. These adhesion molecules include: lymphocyte homing receptors involved in tissue-selective binding of lymphocytes to peripheral lymph node (L-selectin) or mucosal lymphoid tissue (LPAM-1, alpha 4 beta 7-integrin) high-endothelial venules (HEV); and HEV ligands peripheral vascular addressin (PNAd) and mucosal vascular addressin (MAdCAM-1). In NOD pancreata, alpha 4 beta 7 is expressed on most infiltrating cells at all stages of insulitis, whereas L-selectin expression is more pronounced on cells in the islets at later stages. During the development of insulitis, MAdCAM-1 and to a lesser extent PNAd became detectable on vascular endothelium adjacent to and within the inflamed islets. The Stamper-Woodruff in vitro assay was used to examine lymphoid cell binding to such vessels. These functional assays show that both the mucosal (MAdCAM-1/alpha 4 beta 7) and the peripheral (PNAd/L-selectin) recognition systems are involved in this binding. Our findings demonstrate that expression of peripheral and mucosal vascular addressins is induced on endothelium in inflamed islets in NOD pancreas, and that these addressins participate in binding lymphoid cells via their homing receptors. This suggests that these adhesion molecules play a role in the pathogenesis of diabetes in these mice by being involved in the migration of lymphocytes from blood into the inflamed pancreas.
The Urinary Output of Catechol Derivatives Including Adrenaline in Normal Individuals, in Essential Hypertension, and in Myocardial Infarction
Authors: FRANKLIN R. NUZUM, FRITZ BISCHOFF
Journal: Circulation (1953)

Based on Shaw's specific test, the adrenaline content of the urine of some normal individuals was considerably higher than has been reported by those using the von Euler technic (adsorption at an alkaline pH, elution and bioassay). One patient with myocardial infarction showed highly significant amounts on four occasions. The marked elevation in the Kroneberg-Schümann catechol ratio for hypertension patients as compared with normals, reported by these authors, was not confirmed by our findings. In three cases of myocardial infarction the ratio was elevated. Our ratios for normals confirm the original work.
Book Review Diseases of the Nervous System: Clinical neurobiology Second edition. Edited by Arthur K. Asbury, Guy M. McKhann, and W. Ian McDonald. 1619 pp. in two volumes, illustrated. Philadelphia, W.B. Saunders, 1992. $250. ISBN 0–7216–3208–4 .
Authors: David A. Greenberg
Journal: New England Journal of Medicine (1992)
Patients and the new contracts
Authors: P. Davies
Journal: BMJ (2003)

It is said that behind every disagreement there are the bones of an old philosophy rattling around. Surveying the wreckage of the consultants' contract,1 and seeing also that the general practitioners' contract2–4 is floundering in heavy seas—such that even if it is rescued5 it will start life half drowned—has made us wonder what has gone wrong with the process of making contracts for doctors. We want to look deeper, to open out more fundamental debate about what medicine could and should be for, and so what should and should not be in doctors' contracts.

Doctors and managers historically have prided themselves on their pragmatism rather than their philosophy. Getting the task done has been more important than asking whether the task is valid in the first place. To the negotiators from the BMA, the Department of Health, and the NHS Confederation, setting out in 2001 to draw up a contract will therefore have seemed a sensible and achievable task, whereas debating the …
Pleural Effusion and Breast Cancer
Authors: B. A. Stoll
Journal: BMJ (1965)

JOURINALof Tristan da Cunha.'Our findings were based on general clinical examinations of the islanders carried out during the first three months of their period of involuntary exile in England.Some of the findings of a specialized psychiatric and sociological inquiry have now been published by Rawnsley and Loudon.'We should like to draw attention to certain important discrepancies between these find- ings and our own impressions of the mental state of the Tristan people.We reported that they were ". . .noticeably free, with very few exceptions, of anxieties and worries.... Rawnsley and Loudon had the opportunity to make an intensive study over the subsequent months.It was found that there were four current cases (2.1%) of psychotic disorder, and that 240/%, of the adults suffered from headache precipitated by anxiety and worry.This symptom was endemic both on Tristan and in England.There was also shown to be a most interest- ing association between the occurrence of headache at the present day and the occur- rence of an epidemic of hysteria which affected over 10% of the population in 1937When they arrived here their polite friendliness in a new and strange environment, together with mounting nostalgia, led them to present an idealized picture of them- selves and their life on Tristan which more detailed study has corrected.