Guidelines for Pharmacists Performing Clinical Interventions
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(12) United States Patent (10) Patent No.: US 7,074,961 B2 Wang Et Al
US007074961B2 (12) United States Patent (10) Patent No.: US 7,074,961 B2 Wang et al. (45) Date of Patent: Jul. 11, 2006 (54) ANTIDEPRESSANTS AND THEIR 6.211,171 B1 4/2001 Sawynok et al. ANALOGUES AS LONG-ACTING LOCAL 6,545,057 B1 4/2003 Wang et al. ANESTHETCS AND ANALGESCS 2001/0036943 A1 11/2001 Coe et al. (75) Inventors: Ging Kuo Wang, Westwood, MA (US); FOREIGN PATENT DOCUMENTS Peter Gerner, Weston, MA (US); Donald K. Verrecchia, Winchester, MA CH 534124 A 2, 1973 (US) WO WO95/17903 A1 7, 1995 WO WO95/1818.6 A1 7, 1995 (73) Assignee: The Brigham and Women's Hospital, WO WO 99.59.598 A1 11, 1999 Inc., Boston, MA (US) WO WO O2/060870 A2 8, 2002 (*) Notice: Subject to any disclaimer, the term of this OTHER PUBLICATIONS patent is extended or adjusted under 35 U.S.C. 154(b) by 451 days. Luo et al., Xenobiotica, vol. 25, No. 3, pp. 291-301, 1995.* (21) Appl. No.: 10/117,708 Ehlert et al., The Interaction of Amitriptyline, Doxepin, Imipramine and Their N-Methyl Quaternary Ammonium (22) Filed: Apr. 4, 2002 Derivatives with Subtypes of Muscarinic Receptors in Brain (65) Prior Publication Data and Heart, The Journal of Pharmacology and Experimental Therapeutics, Apr. 1990, vol. 253, No. 1, pp. 13–19. US 2003/00968.05 A1 May 22, 2003 Gerner, P., et al., Anesthesiology (2002) 96:1435–42. Related U.S. Application Dat e pplication Uata Khan, M.A., et al., Anesthesiology (2002) 96:109–16. (63) stripps'965,138, filed on Sep. -
Curriculum Vitae: Daniel J
CURRICULUM VITAE: DANIEL J. WALLACE, M.D., F.A.C.P., M.A.C.R. Up to date as of January 1, 2019 Personal: Address: 8750 Wilshire Blvd, Suite 350 Beverly Hills, CA 90211 Phone: (310) 652-0010 FAX: (310) 360-6219 E mail: [email protected] Education: University of Southern California, 2/67-6/70, BA Medicine, 1971. University of Southern California, 9/70-6/74, M.D, 1974. Postgraduate Training: 7/74-6/75 Medical Intern, Rhode Island (Brown University) Hospital, Providence, RI. 7/75-6/77 Medical Resident, Cedars-Sinai Medical Center, Los Angeles, CA. 7/77-6/79 Rheumatology Fellow, UCLA School of Medicine, Los Angeles, CA. Medical Boards and Licensure: Diplomate, National Board of Medical Examiners, 1975. Board Certified, American Board of Internal Medicine, 1978. Board Certified, Rheumatology subspecialty, 1982. California License: #G-30533. Present Appointments: Medical Director, Wallace Rheumatic Study Center Attune Health Affiliate, Beverly Hills, CA 90211 Attending Physician, Cedars-Sinai Medical Center, Los Angeles, 1979- Clinical Professor of Medicine, David Geffen School of Medicine at UCLA, 1995- Professor of Medicine, Cedars-Sinai Medical Center, 2012- Expert Reviewer, Medical Board of California, 2007- Associate Director, Rheumatology Fellowship Program, Cedars-Sinai Medical Center, 2010- Board of Governors, Cedars-Sinai Medical Center, 2016- Member, Medical Policy Committee, United Rheumatology, 2017- Honorary Appointments: Fellow, American College of Physicians (FACP) Fellow, American College of Rheumatology (FACR) -
Testosterone, Myocardial Function, and Mortality
Heart Failure Reviews https://doi.org/10.1007/s10741-018-9721-0 Testosterone, myocardial function, and mortality Vittorio Emanuele Bianchi1 # Springer Science+Business Media, LLC, part of Springer Nature 2018 Abstract The cardiovascular system is particularly sensitive to androgens, but some controversies exist regarding the effect of testosterone on the heart. While among anabolic abusers, cases of sudden cardiac death have been described, recently it was reported that low serum level of testosterone was correlated with increased risk of cardiovascular diseases (CVD) and mortality rate. This review aims to evaluate the effect of testosterone on myocardial tissue function, coronary artery disease (CAD), and death. Low testosterone level is associated with increased incidence of CAD and mortality. Testosterone administration in hypogonadal elderly men and women has a positive effect on cardiovascular function and improved clinical outcomes and survival time. Although at supraphysiologic doses, androgen may have a toxic effect, and at physiological levels, testosterone is safe and exerts a beneficial effect on myocardial function including mechanisms at cellular and mitochondrial level. The interaction with free testosterone and estradiol should be considered. Further studies are necessary to better understand the interaction mechanisms for an optimal androgen therapy in CVD. Keywords Testosterone . Coronary artery disease . Heart failure . Cardiovascular disease . Cardiomyocytes . Cardiac mitochondria . Cardiovascular mortality Introduction essential role [20]. Asymptomatic hypogonadism is observed in men 30–79 years old with an incidence of about 5.6% [21] The effects of testosterone on myocardial function have gen- and is more relevant in aging subjects. In recent years, pre- erated a great deal of discussion in the literature but remain scriptions for testosterone replacement therapy have increased controversial. -
Genome-Wide Identification of Brain Mirnas in Response to High
Zhao et al. BMC Molecular Biol (2019) 20:3 https://doi.org/10.1186/s12867-019-0120-4 BMC Molecular Biology RESEARCH ARTICLE Open Access Genome‑wide identifcation of brain miRNAs in response to high‑intensity intermittent swimming training in Rattus norvegicus by deep sequencing Yanhong Zhao1*†, Anmin Zhang2,3*†, Yanfang Wang4, Shuping Hu3, Ruiping Zhang2 and Shuaiwei Qian2 Abstract Background: Physical exercise can improve brain function by altering brain gene expression. The expression mecha- nisms underlying the brain’s response to exercise still remain unknown. miRNAs as vital regulators of gene expres- sion may be involved in regulation of brain genes in response to exercise. However, as yet, very little is known about exercise-responsive miRNAs in brain. Results: We constructed two comparative small RNA libraries of rat brain from a high-intensity intermittent swim- ming training (HIST) group and a normal control (NC) group. Using deep sequencing and bioinformatics analysis, we identifed 2109 (1700 from HIST, 1691 from NC) known and 55 (50 from HIST, 28 from NC) novel candidate miRNAs. Among them, 34 miRNAs were identifed as signifcantly diferentially expressed in response to HIST, 16 were up- regulated and 18 were down-regulated. The results showed that all members of mir-200 family were strongly up- regulated, implying mir-200 family may play very important roles in HIST response mechanisms of rat brain. A total of 955 potential target genes of these 34 exercise-responsive miRNAs were identifed from rat genes. Most of them are directly involved in the development and regulatory function of brain or nerve. -
Growth Cone Responses to Growth and Chemotropic Factors
European Journal of Neuroscience European Journal of Neuroscience, Vol. 28, pp. 268–278, 2008 doi:10.1111/j.1460-9568.2008.06327.x Growth cone responses to growth and chemotropic factors Staci D. Sanford,1 Jesse C. Gatlin,1,* Tomas Ho¨kfelt2 and Karl H. Pfenninger1 1Departments of Pediatrics, and of Cell and Developmental Biology, and Neuroscience Program, University of Colorado School of Medicine, and University of Colorado Cancer Center, Aurora, CO 80045, USA 2Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden Keywords: attractants, axonal pathfinding, growth cone, growth promotion, neuropeptides, repellents Abstract During nervous system development axons reach their target areas under the influence of numerous guidance cues that affect rate and direction of growth. This report addresses the unsettled question of whether and to what extent growth velocity and turning responses (attraction, repulsion) are interdependent. We exposed individual growth cones of fetal rat dorsal root ganglion neurons in culture asymmetrically to gradients of seven different factors and recorded their growth rates and turning angles. Growth cones exhibited divergent patterns of turning and growth responses. For example, hepatocyte growth factor (HGF), insulin-like growth factor-1 (IGF-1) and thrombin all promoted growth, but HGF was a powerful attractant, thrombin a potent repellent and IGF-1 did not elicit turning. Galanin and neuropeptide Y also affected growth and ⁄ or turning differentially. Finally, nerve growth factor in the culture -
BDNF Genotype Modulates Resting Functional Connectivity in Children
ORIGINAL RESEARCH ARTICLE published: 24 November 2009 HUMAN NEUROSCIENCE doi: 10.3389/neuro.09.055.2009 BDNF genotype modulates resting functional connectivity in children Moriah E. Thomason1*, Daniel J. Yoo1, Gary H. Glover 2 and Ian H. Gotlib1 1 Department of Psychology, Stanford University, Stanford, CA, USA 2 Department of Radiology, Stanford University School of Medicine, Stanford, CA, USA Edited by: A specifi c polymorphism of the brain-derived neurotrophic factor (BDNF) gene is associated Elizabeth D. O’Hare, University of with alterations in brain anatomy and memory; its relevance to the functional connectivity of California at Berkeley, USA brain networks, however, is unclear. Given that altered hippocampal function and structure Reviewed by: Damien Fair, Oregon Health and has been found in adults who carry the methionine (met) allele of the BDNF gene and the Science University, USA molecular studies elucidating the role of BDNF in neurogenesis and synapse formation, we Naftali Raz, Wayne State University, examined the association between BDNF gene variants and neural resting connectivity in USA children and adolescents. We observed a reduction in hippocampal and parahippocampal to *Correspondence: cortical connectivity in met-allele carriers within both default-mode and executive networks. Moriah E. Thomason, Department of Psychology, Stanford University, Jordan In contrast, we observed increased connectivity to amygdala, insula and striatal regions in Hall, Bldg. 420, Stanford, met-carriers, within the paralimbic network. Because of the known association between the CA 94305-2130, USA. BDNF gene and neuropsychiatric disorder, this latter fi nding of greater connectivity in circuits e-mail: [email protected] important for emotion processing may indicate a new neural mechanism through which these gene-related psychiatric differences are manifest. -
Phase II Study of Dehydroepiandrosterone in Androgen Receptor-Positive Metastatic Breast Cancer
Published Ahead of Print on December 27, 2018 as 10.1634/theoncologist.2018-0243. Clinical Trial Results Phase II Study of Dehydroepiandrosterone in Androgen Receptor-Positive Metastatic Breast Cancer a b c c c b ELISABETTA PIETRI, ILARIA MASSA, SARA BRAVACCINI, SARA RAVAIOLI, MARIA MADDALENA TUMEDEI, ELISABETTA PETRACCI, d a e f g h i CATERINA DONATI, ALESSIO SCHIRONE, FEDERICO PIACENTINI, LORENZO GIANNI, MARIO NICOLINI, ENRICO CAMPADELLI, ALESSANDRA GENNARI, j j b b c a a ALESSANDRO SABA, BEATRICE CAMPI, LINDA VALMORRI, DANIELE ANDREIS, FRANCESCO FABBRI, DINO AMADORI, ANDREA ROCCA aDepartment of Medical Oncology, bUnit of Biostatistics and Clinical Trials, cBiosciences Laboratory, and dOncology Pharmacy Unit, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy; eDivision of Medical Oncology, Department of Medical and Surgical Sciences for Children & Adults, University Hospital of Modena, Modena, Italy; fDepartment of Oncology, Infermi Hospital, Rimini, Italy; gOncology Day Hospital Unit, Cervesi Hospital, Cattolica, Italy; hOncology Unit, Faenza Hospital, Faenza, Italy; iMedical Oncology, Department of Translational Medicine, University of Eastern Piedmont, Novara, Italy; jDepartment of Surgical, Medical and Molecular Pathology and Critical Care Medicine, University of Pisa, Pisa, Italy Downloaded from TRIAL INFORMATION http://theoncologist.alphamedpress.org/ • ClinicalTrials.gov Identifier: NCT02000375 • Principal Investigator: Elisabetta Pietri • Sponsor(s): None • IRB Approved: Yes LESSONS LEARNED • The androgen receptor (AR) is present in most breast cancers (BC), but its exploitation as a therapeutic target has been limited. • This study explored the activity of dehydroepiandrosterone (DHEA), a precursor being transformed into androgens within BC cells, in combination with an aromatase inhibitor (to block DHEA conversion into estrogens), in a two-stage phase II study in patients with AR-positive/estrogen receptor-positive/human epidermal growth receptor 2-negative metastatic BC. -
Permeability Due to Drug Binding Kinetics and Reactivation Among
Differential Risk of Tuberculosis Reactivation among Anti-TNF Therapies Is Due to Drug Binding Kinetics and Permeability This information is current as of September 26, 2021. Mohammad Fallahi-Sichani, JoAnne L. Flynn, Jennifer J. Linderman and Denise E. Kirschner J Immunol 2012; 188:3169-3178; Prepublished online 29 February 2012; doi: 10.4049/jimmunol.1103298 Downloaded from http://www.jimmunol.org/content/188/7/3169 Supplementary http://www.jimmunol.org/content/suppl/2012/02/29/jimmunol.110329 http://www.jimmunol.org/ Material 8.DC1 References This article cites 59 articles, 21 of which you can access for free at: http://www.jimmunol.org/content/188/7/3169.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 26, 2021 • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2012 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Differential Risk of Tuberculosis Reactivation among Anti-TNF Therapies Is Due to Drug Binding Kinetics and Permeability Mohammad Fallahi-Sichani,*,1 JoAnne L. -
The Role of the Small Gtpase Rap in Drosophila R7 Photoreceptor Specification
The role of the small GTPase Rap in Drosophila R7 photoreceptor specification Yannis Emmanuel Mavromatakis and Andrew Tomlinson1 Department of Genetics and Development, College of Physicians and Surgeons, Columbia University, New York, NY 10032 Edited* by Richard Axel, Columbia University, New York, NY, and approved January 25, 2012 (received for review September 13, 2011) The Drosophila R7 photoreceptor provides an excellent model sys- and R7 precursors differ dramatically in their levels of RTK tem with which to study how cells receive and “decode” signals signaling: it is mild in the former and robust in the latter. that specify cell fate. R7 is specified by the combined actions of the RTK signaling typically activates the small GTPase Ras, which receptor tyrosine kinase (RTK) and Notch (N) signaling pathways. recruits Raf to the plasma membrane and initiates the phos- These pathways interact in a complex manner that includes antag- phorylation cascade that leads to the translocation of MAPK to onistic effects on photoreceptor specification: RTK promotes the the nucleus. Rap is another member of the Ras GTPase super- photoreceptor fate, whereas N inhibits. Although other photore- family; it was initially considered a Ras antagonist because it sup- ceptors are subject to only mild N activation, R7 experiences a high- pressed Ki-Ras oncogenesis (17) and inhibited Ras-dependent level N signal. To counter this effect and to ensure that the cell is activation of MAPK (18). Roughened is a dominant mutant of specified as a photoreceptor, a high RTK signal is transduced in the Drosophila rap in which R7 photoreceptors are frequently absent cell. -
REVIEW Estrogens and Atherosclerosis
R13 REVIEW Estrogens and atherosclerosis: insights from animal models and cell systems Jerzy-Roch Nofer1,2 1Center for Laboratory Medicine, University Hospital Mu¨nster, Albert Schweizer Campus 1, Geba¨ude A1, 48129 Mu¨nster, Germany 2Department of Medicine, Endocrinology, Metabolism and Geriatrics, University of Modena and Reggio Emilia, Modena, Italy (Correspondence should be addressed to J-R Nofer at Center for Laboratory Medicine, University Hospital Mu¨nster; Email: [email protected]) Abstract Estrogens not only play a pivotal role in sexual development but are also involved in several physiological processes in various tissues including vasculature. While several epidemiological studies documented an inverse relationship between plasma estrogen levels and the incidence of cardiovascular disease and related it to the inhibition of atherosclerosis, an interventional trial showed an increase in cardiovascular events among postmenopausal women on estrogen treatment. The development of atherosclerotic lesions involves complex interplay between various pro- or anti-atherogenic processes that can be effectively studied only in vivo in appropriate animal models. With the advent of genetic engineering, transgenic mouse models of atherosclerosis have supplemented classical dietary cholesterol- induced disease models such as the cholesterol-fed rabbit. In the last two decades, these models were widely applied along with in vitro cell systems to specifically investigate the influence of estrogens on the development of early and advanced atherosclerotic lesions. The present review summarizes the results of these studies and assesses their contribution toward better understanding of molecular mechanisms underlying anti- and/or pro-atherogenic effects of estrogens in humans. Journal of Molecular Endocrinology (2012) 48, R13–R29 Introduction circumstances, these hormones promote the develop- ment of atherosclerosis. -
Network-Based Characterization of Drug-Protein Interaction Signatures
Tabei et al. BMC Systems Biology 2019, 13(Suppl 2):39 https://doi.org/10.1186/s12918-019-0691-1 RESEARCH Open Access Network-based characterization of drug-protein interaction signatures with a space-efficient approach Yasuo Tabei1*, Masaaki Kotera2, Ryusuke Sawada3 and Yoshihiro Yamanishi3,4 From The 17th Asia Pacific Bioinformatics Conference (APBC 2019) Wuhan, China. 14–16 January 2019 Abstract Background: Characterization of drug-protein interaction networks with biological features has recently become challenging in recent pharmaceutical science toward a better understanding of polypharmacology. Results: We present a novel method for systematic analyses of the underlying features characteristic of drug-protein interaction networks, which we call “drug-protein interaction signatures” from the integration of large-scale heterogeneous data of drugs and proteins. We develop a new efficient algorithm for extracting informative drug- protein interaction signatures from the integration of large-scale heterogeneous data of drugs and proteins, which is made possible by space-efficient representations for fingerprints of drug-protein pairs and sparsity-induced classifiers. Conclusions: Our method infers a set of drug-protein interaction signatures consisting of the associations between drug chemical substructures, adverse drug reactions, protein domains, biological pathways, and pathway modules. We argue the these signatures are biologically meaningful and useful for predicting unknown drug-protein interactions and are expected to contribute to rational drug design. Keywords: Drug-protein interaction prediction, Drug discovery, Large-scale prediction Background similar drugs are expected to interact with similar pro- Target proteins of drug molecules are classified into a pri- teins, with which the similarity of drugs and proteins are mary target and off-targets. -
Q3D(R1) Elemental Impurities
Q3D(R1) Elemental Impurities Guidance for Industry U. S. Department of Health and Human Services Food and Drug Administration Center for Drug Evaluation and Research (CDER) Center for Biologics Evaluation and Research (CBER) March 2020 ICH Revision 1 Q3D(R1) Elemental Impurities Guidance for Industry Additional copies are available from: Office of Communications, Division of Drug Information Center for Drug Evaluation and Research Food and Drug Administration 10001 New Hampshire Ave., Hillandale Bldg., 4th Floor Silver Spring, MD 20993-0002 Phone: 855-543-3784 or 301-796-3400; Fax: 301-431-6353 Email: [email protected] https://www.fda.gov/drugs/guidance-compliance-regulatory-information/guidances-drugs and/or Office of Communication, Outreach and Development Center for Biologics Evaluation and Research Food and Drug Administration 10903 New Hampshire Ave., Bldg. 71, Room 3128 Silver Spring, MD 20993-0002 Phone: 800-835-4709 or 240-402-8010 Email : [email protected] https://www.fda.gov/vaccines-blood-biologics/guidance-compliance-regulatory-information-biologics/biologics-guidances U.S. Department of Health and Human Services Food and Drug Administration Center for Drug Evaluation and Research (CDER) Center for Biologics Evaluation and Research (CBER) March 2020 ICH Revision 1 Contains Nonbinding Recommendations TABLE OF CONTENTS I. INTRODUCTION (1) ....................................................................................................... 1 II. SCOPE (2).........................................................................................................................