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Amylase Release from Rat Parotid Gland Slices C.L
Br. J. P!harmnic. (1981) 73, 517-523 THE EFFECTS OF SUBSTANCE P AND RELATED PEPTIDES ON a- AMYLASE RELEASE FROM RAT PAROTID GLAND SLICES C.L. BROWN & M.R. HANLEY MRC Neurochemical Pharmacology Unit, Medical Research Council Centre, Medical School, Hills Road, Cambridge CB2 2QH 1 The effects of substance P and related peptides on amylase release from rat parotid gland slices have been investigated. 2 Supramaximal concentrations (1 F.M) of substance P caused enhancement of amylase release over the basal level within 1 min; this lasted for at least 40 min at 30°C. 3 Substance P-stimulated amylase release was partially dependent on extracellular calcium and could be inhibited by 50% upon removal of extracellular calcium. 4 Substance P stimulated amylase release in a dose-dependent manner with an ED50 of 18 nm. 5 All C-terminal fragments of substance P were less potent than substance P in stimulating amylase release. The C-terminal hexapeptide of substance P was the minimum structure for potent activity in this system, having 1/3 to 1/8 the potency of substance P. There was a dramatic drop in potency for the C-terminal pentapeptide of substance P or substance P free acid. Physalaemin was more potent than substance P (ED50 = 7 nM), eledoisin was about equipotent with substance P (ED5o = 17 nM), and kassinin less potent than substance P (ED50 = 150 nM). 6 The structure-activity profile observed is very similar to that for stimulation of salivation in vivo, indicating that the same receptors are involved in mediating these responses. -
Digitoxin-Induced Cytotoxicity in Cancer Cells Is Mediated Through Distinct Kinase and Interferon Signaling Networks
Published OnlineFirst August 22, 2011; DOI: 10.1158/1535-7163.MCT-11-0421 Molecular Cancer Therapeutic Discovery Therapeutics Digitoxin-Induced Cytotoxicity in Cancer Cells Is Mediated through Distinct Kinase and Interferon Signaling Networks Ioannis Prassas1,2, George S. Karagiannis1,2, Ihor Batruch4, Apostolos Dimitromanolakis1,2, Alessandro Datti2,3,5, and Eleftherios P. Diamandis1,2,4 Abstract Cardiac glycosides (e.g., digoxin, digitoxin) constitute a diverse family of plant-derived sodium pump inhibitors that have been in clinical use for the treatment of heart-related diseases (congestive heart failure, atrial arrhythmia) for many years. Recently though, accumulating in vitro and in vivo evidence highlight potential anticancer properties of these compounds. Despite the fact that members of this family have advanced to clinical trial testing in cancer therapeutics, their cytotoxic mechanism is not yet elucidated. In this study, we investigated the cytotoxic properties of cardiac glycosides against a panel of pancreatic cancer cell lines, explored their apoptotic mechanism, and characterized the kinetics of cell death induced by these drugs. Furthermore, we deployed a high-throughput kinome screening approach and identified several kinases of the Na-K-ATPase-mediated signal transduction circuitry (epidermal growth factor receptor, Src, pkC, and mitogen-activated protein kinases) as important mediators downstream of cardiac glycoside cytotoxic action. To further extend our knowledge on their mode of action, we used mass-spectrometry–based quantitative proteomics (stable isotope labeling of amino acids in cell culture) coupled with bioinformatics to capture large-scale protein perturbations induced by a physiological dose of digitoxin in BxPC-3 pancreatic cancer cells and identified members of the interferon family as key regulators of the main protein/protein interactions downstream of digitoxin action. -
(12) Patent Application Publication (10) Pub. No.: US 2006/0110428A1 De Juan Et Al
US 200601 10428A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2006/0110428A1 de Juan et al. (43) Pub. Date: May 25, 2006 (54) METHODS AND DEVICES FOR THE Publication Classification TREATMENT OF OCULAR CONDITIONS (51) Int. Cl. (76) Inventors: Eugene de Juan, LaCanada, CA (US); A6F 2/00 (2006.01) Signe E. Varner, Los Angeles, CA (52) U.S. Cl. .............................................................. 424/427 (US); Laurie R. Lawin, New Brighton, MN (US) (57) ABSTRACT Correspondence Address: Featured is a method for instilling one or more bioactive SCOTT PRIBNOW agents into ocular tissue within an eye of a patient for the Kagan Binder, PLLC treatment of an ocular condition, the method comprising Suite 200 concurrently using at least two of the following bioactive 221 Main Street North agent delivery methods (A)-(C): Stillwater, MN 55082 (US) (A) implanting a Sustained release delivery device com (21) Appl. No.: 11/175,850 prising one or more bioactive agents in a posterior region of the eye so that it delivers the one or more (22) Filed: Jul. 5, 2005 bioactive agents into the vitreous humor of the eye; (B) instilling (e.g., injecting or implanting) one or more Related U.S. Application Data bioactive agents Subretinally; and (60) Provisional application No. 60/585,236, filed on Jul. (C) instilling (e.g., injecting or delivering by ocular ion 2, 2004. Provisional application No. 60/669,701, filed tophoresis) one or more bioactive agents into the Vit on Apr. 8, 2005. reous humor of the eye. Patent Application Publication May 25, 2006 Sheet 1 of 22 US 2006/0110428A1 R 2 2 C.6 Fig. -
(12) Patent Application Publication (10) Pub. No.: US 2004/0224012 A1 Suvanprakorn Et Al
US 2004O224012A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2004/0224012 A1 Suvanprakorn et al. (43) Pub. Date: Nov. 11, 2004 (54) TOPICAL APPLICATION AND METHODS Related U.S. Application Data FOR ADMINISTRATION OF ACTIVE AGENTS USING LIPOSOME MACRO-BEADS (63) Continuation-in-part of application No. 10/264,205, filed on Oct. 3, 2002. (76) Inventors: Pichit Suvanprakorn, Bangkok (TH); (60) Provisional application No. 60/327,643, filed on Oct. Tanusin Ploysangam, Bangkok (TH); 5, 2001. Lerson Tanasugarn, Bangkok (TH); Suwalee Chandrkrachang, Bangkok Publication Classification (TH); Nardo Zaias, Miami Beach, FL (US) (51) Int. CI.7. A61K 9/127; A61K 9/14 (52) U.S. Cl. ............................................ 424/450; 424/489 Correspondence Address: (57) ABSTRACT Eric G. Masamori 6520 Ridgewood Drive A topical application and methods for administration of Castro Valley, CA 94.552 (US) active agents encapsulated within non-permeable macro beads to enable a wider range of delivery vehicles, to provide longer product shelf-life, to allow multiple active (21) Appl. No.: 10/864,149 agents within the composition, to allow the controlled use of the active agents, to provide protected and designable release features and to provide visual inspection for damage (22) Filed: Jun. 9, 2004 and inconsistency. US 2004/0224012 A1 Nov. 11, 2004 TOPCAL APPLICATION AND METHODS FOR 0006 Various limitations on the shelf-life and use of ADMINISTRATION OF ACTIVE AGENTS USING liposome compounds exist due to the relatively fragile LPOSOME MACRO-BEADS nature of liposomes. Major problems encountered during liposome drug Storage in vesicular Suspension are the chemi CROSS REFERENCE TO OTHER cal alterations of the lipoSome compounds, Such as phos APPLICATIONS pholipids, cholesterols, ceramides, leading to potentially toxic degradation of the products, leakage of the drug from 0001) This application claims the benefit of U.S. -
United States Patent (19) 11 Patent Number: 4,540,564 Bodor (45) Date of Patent: Sep
United States Patent (19) 11 Patent Number: 4,540,564 Bodor (45) Date of Patent: Sep. 10, 1985 54 BRAIN-SPECIFICDRUG DELIVERY 57 ABSTRACT 75 Inventor: Nicholas S. Bodor, Gainesville, Fla. The subject compounds, which are adapted for the site-specific/sustained delivery of centrally acting drug 73) Assignee: University of Florida, Gainesville, species to the brain, are: Fla. (a) compounds of the formula 21 Appl. No.: 516,382 22 Filed: Jul. 22, 1983 D-DHC) (I) Related U.S. Application Data wherein D is a centrally acting drug species, and 63 Continuation-in-part of Ser. No. 379,316, May 18, DHC is the reduced, biooxidizable, blood-brain 1982, Pat. No. 4,479,932, Ser. No. 461,543, Jan. 27, barrier penetrating lipoidal form of a dihydropyri 1983, , and Ser. No. 475,493, Mar. 15, 1983, , said Ser. dine - pyridinium salt redox carrier, with the No. 46,543, and Ser. No. 475,493, each is a continua proviso that when DHC) is tion-in-part of Ser. No. 379,316. 30 Foreign Application Priority Data O May 12, 1983 WO, PCT Int'l Appl. ......... WO83/00725 May 16, 1983 ICA) Canada ................................... 42892 51) Int. Cl...................... A61K 49/00; A61K 31/58; r’sN CO7J 17/00 52 U.S. Cl. ..................................... 424/9; 260/239.5; R 514/176 58 Field of Search .................. 424/9, 241; 260/239.5 wherein R is lower alkyl or benzyl and D is a drug species containing a single NH2 or OH func 56 References Cited tional group, the single OH group when present U.S. -
Classification of Medicinal Drugs and Driving: Co-Ordination and Synthesis Report
Project No. TREN-05-FP6TR-S07.61320-518404-DRUID DRUID Driving under the Influence of Drugs, Alcohol and Medicines Integrated Project 1.6. Sustainable Development, Global Change and Ecosystem 1.6.2: Sustainable Surface Transport 6th Framework Programme Deliverable 4.4.1 Classification of medicinal drugs and driving: Co-ordination and synthesis report. Due date of deliverable: 21.07.2011 Actual submission date: 21.07.2011 Revision date: 21.07.2011 Start date of project: 15.10.2006 Duration: 48 months Organisation name of lead contractor for this deliverable: UVA Revision 0.0 Project co-funded by the European Commission within the Sixth Framework Programme (2002-2006) Dissemination Level PU Public PP Restricted to other programme participants (including the Commission x Services) RE Restricted to a group specified by the consortium (including the Commission Services) CO Confidential, only for members of the consortium (including the Commission Services) DRUID 6th Framework Programme Deliverable D.4.4.1 Classification of medicinal drugs and driving: Co-ordination and synthesis report. Page 1 of 243 Classification of medicinal drugs and driving: Co-ordination and synthesis report. Authors Trinidad Gómez-Talegón, Inmaculada Fierro, M. Carmen Del Río, F. Javier Álvarez (UVa, University of Valladolid, Spain) Partners - Silvia Ravera, Susana Monteiro, Han de Gier (RUGPha, University of Groningen, the Netherlands) - Gertrude Van der Linden, Sara-Ann Legrand, Kristof Pil, Alain Verstraete (UGent, Ghent University, Belgium) - Michel Mallaret, Charles Mercier-Guyon, Isabelle Mercier-Guyon (UGren, University of Grenoble, Centre Regional de Pharmacovigilance, France) - Katerina Touliou (CERT-HIT, Centre for Research and Technology Hellas, Greece) - Michael Hei βing (BASt, Bundesanstalt für Straßenwesen, Germany). -
Drug Discovery to Counteract Antinociceptive Tolerance with Mu
bioRxiv preprint doi: https://doi.org/10.1101/182360; this version posted August 29, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. Drug discovery to counteract antinociceptive tolerance with mu- opioid receptor endocytosis Po-Kuan Chao1, Yi-Yu Ke1, Hsiao-Fu Chang1, Yi-Han Huang2, Li-Chin Ou1, Jian-Ying Chuang2, Yen- Chang Lin3, Pin-Tse Lee4, Wan-Ting Chang1, Shu-Chun Chen1, Shau-Hua Ueng1, John Tsu-An Hsu1, Pao-Luh Tao5, Ping-Yee Law6, Horace H. Loh6, Chuan Shih1, and Shiu-Hwa Yeh1,2 * 1 Institute of Biotechnology and Pharmaceutical Research, National Health Research Institutes, Zhunan 35053, Taiwan 2 The PhD Program for Neural Regenerative Medicine, Taipei Medical University, Taipei 110, Taiwan 3 Graduate Institute of Biotechnology, Chinese Culture University, Taipei 1114, Taiwan 4 Cellular Pathobiology Section, Intramural Research Program, National Institute on Drug Abuse, NIH/DHHS, Baltimore, MD 21224, USA 5 Center for Neuropsychiatric Research, National Heath Research Institutes, Zhunan 35053, Taiwan 6 Department of Pharmacology, University of Minnesota Medical School, Minneapolis, MN 55455- 0217, USA Competing financial interests: The authors have declared that no conflict of interest exists. *Correspondence to: Shiu-Hwa Yeh Institute of Biotechnology and Pharmaceutical Research, National Health Research Institutes, Zhunan 35053, Taiwan Tel: (886)-37-246166 ext. 35759 Fax: (886)-37-586456 Email: [email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/182360; this version posted August 29, 2017. -
)&F1y3x PHARMACEUTICAL APPENDIX to THE
)&f1y3X PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE )&f1y3X PHARMACEUTICAL APPENDIX TO THE TARIFF SCHEDULE 3 Table 1. This table enumerates products described by International Non-proprietary Names (INN) which shall be entered free of duty under general note 13 to the tariff schedule. The Chemical Abstracts Service (CAS) registry numbers also set forth in this table are included to assist in the identification of the products concerned. For purposes of the tariff schedule, any references to a product enumerated in this table includes such product by whatever name known. Product CAS No. Product CAS No. ABAMECTIN 65195-55-3 ACTODIGIN 36983-69-4 ABANOQUIL 90402-40-7 ADAFENOXATE 82168-26-1 ABCIXIMAB 143653-53-6 ADAMEXINE 54785-02-3 ABECARNIL 111841-85-1 ADAPALENE 106685-40-9 ABITESARTAN 137882-98-5 ADAPROLOL 101479-70-3 ABLUKAST 96566-25-5 ADATANSERIN 127266-56-2 ABUNIDAZOLE 91017-58-2 ADEFOVIR 106941-25-7 ACADESINE 2627-69-2 ADELMIDROL 1675-66-7 ACAMPROSATE 77337-76-9 ADEMETIONINE 17176-17-9 ACAPRAZINE 55485-20-6 ADENOSINE PHOSPHATE 61-19-8 ACARBOSE 56180-94-0 ADIBENDAN 100510-33-6 ACEBROCHOL 514-50-1 ADICILLIN 525-94-0 ACEBURIC ACID 26976-72-7 ADIMOLOL 78459-19-5 ACEBUTOLOL 37517-30-9 ADINAZOLAM 37115-32-5 ACECAINIDE 32795-44-1 ADIPHENINE 64-95-9 ACECARBROMAL 77-66-7 ADIPIODONE 606-17-7 ACECLIDINE 827-61-2 ADITEREN 56066-19-4 ACECLOFENAC 89796-99-6 ADITOPRIM 56066-63-8 ACEDAPSONE 77-46-3 ADOSOPINE 88124-26-9 ACEDIASULFONE SODIUM 127-60-6 ADOZELESIN 110314-48-2 ACEDOBEN 556-08-1 ADRAFINIL 63547-13-7 ACEFLURANOL 80595-73-9 ADRENALONE -
Pdf; Chi 2015 DPP Air in Cars.Pdf; Dodson 2014 DPP Dust CA.Pdf; Kasper-Sonnenberg 2014 Phth Metabolites.Pdf; EU Cosmetics Regs 2009.Pdf
Bouge, Cathy (ECY) From: Nancy Uding <[email protected]> Sent: Friday, January 13, 2017 10:24 AM To: Steward, Kara (ECY) Cc: Erika Schreder Subject: Comments re. 2016 CSPA Rule Update - DPP Attachments: DPP 131-18-0 exposure.pdf; Chi 2015 DPP air in cars.pdf; Dodson 2014 DPP dust CA.pdf; Kasper-Sonnenberg 2014 phth metabolites.pdf; EU Cosmetics Regs 2009.pdf Please accept these comments from Toxic-Free Future concerning the exposure potential of DPP for consideration during the 2016 CSPA Rule update. Regards, Nancy Uding -- Nancy Uding Grants & Research Specialist Toxic-Free Future 206-632-1545 ext.123 http://toxicfreefuture.org 1 JES-00888; No of Pages 9 JOURNAL OF ENVIRONMENTAL SCIENCES XX (2016) XXX– XXX Available online at www.sciencedirect.com ScienceDirect www.elsevier.com/locate/jes Determination of 15 phthalate esters in air by gas-phase and particle-phase simultaneous sampling Chenchen Chi1, Meng Xia1, Chen Zhou1, Xueqing Wang1,2, Mili Weng1,3, Xueyou Shen1,4,⁎ 1. College of Environmental & Resource Sciences, Zhejiang University, Hangzhou 310058, China 2. Zhejiang National Radiation Environmental Technology Co., Ltd., Hangzhou 310011, China 3. School of Environmental and Resource Sciences, Zhejiang Agriculture and Forestry University, Hangzhou 310058, China 4. Zhejiang Provincial Key Laboratory of Organic Pollution Process and Control, Hangzhou 310058, China ARTICLE INFO ABSTRACT Article history: Based on previous research, the sampling and analysis methods for phthalate esters (PAEs) Received 24 December 2015 were improved by increasing the sampling flow of indoor air from 1 to 4 L/min, shortening the Revised 14 January 2016 sampling duration from 8 to 2 hr. -
We Have Reported That the Antibiotics Chloramphenicol, Lincomycin
THE BIOGENESIS OF MITOCHONDRIA, V. CYTOPLASMIC INHERITANCE OF ERYTHROMYCIN RESISTANCE IN SACCHAROMYCES CEREVISIAE* BY ANTHONY W. LINNANE, G. W. SAUNDERS, ELLIOT B. GINGOLD, AND H. B. LUKINS BIOCHEMISTRY DEPARTMENT, MONASH UNIVERSITY, CLAYTON, VICTORIA, AUSTRALIA Communicated by David E. Green, December 26, 1967 The recognition and study of respiratory-deficient mutants of yeast has been of fundamental importance in contributing to our knowledge of the genetic control of the formation of mitochondria. From these studies it has been recognized that cytoplasmic genetic determinants as well as chromosomal genes are involved in the biogenesis of yeast mitochondria.1' 2 Following the recog- nition of the occurrence of mitochondrial DNA,3 4 attention has recently been focused on the relationship between mitochondrial DNA and the cytoplasmic determinant.' However, the information on this latter subject is limited and is derived from the study of a single class of mutant of this determinant, the re- spiratory-deficient cytoplasmic petite. This irreversible mutation is pheno- typically characterized by the inability of the cell to form a number of compo- nents of the respiratory system, including cytochromes a, a3, b, and c1.6 A clearer understanding of the role of cytoplasmic determinants in mitochondrial bio- genesis, could result from the characterization of new types of cytoplasmic mutations which do not result in such extensive biochemical changes. This would thus simplify the biochemical analyses as well as providing additional cytoplasmic markers to assist further genetic studies. We have reported that the antibiotics chloramphenicol, lincomycin, and the macrolides erythromycin, carbomycin, spiramycin, and oleandomycin selec- tively inhibit in vitro amino acid incorporation by yeast mitochondria, while not affecting the yeast cytoplasmic ribosomal system.7' 8 Further, these antibiotics do not affect the growth of S. -
Macrocyclic Antibiotics As Separation Agents
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Missouri University of Science and Technology (Missouri S&T): Scholars' Mine Missouri University of Science and Technology Scholars' Mine Chemistry Faculty Research & Creative Works Chemistry 07 Mar 2006 Macrocyclic Antibiotics as Separation Agents Daniel W. Armstrong Missouri University of Science and Technology Follow this and additional works at: https://scholarsmine.mst.edu/chem_facwork Part of the Chemistry Commons Recommended Citation D. W. Armstrong, "Macrocyclic Antibiotics as Separation Agents," U.S. Patents, Mar 2006. This Patent is brought to you for free and open access by Scholars' Mine. It has been accepted for inclusion in Chemistry Faculty Research & Creative Works by an authorized administrator of Scholars' Mine. This work is protected by U. S. Copyright Law. Unauthorized use including reproduction for redistribution requires the permission of the copyright holder. For more information, please contact [email protected]. USOO70O8533B2 (12) United States Patent (10) Patent No.: US 7,008,533 B2 Armstrong (45) Date of Patent: Mar. 7, 2006 (54) MACROCYCLIC ANTIBIOTICSAS (52) U.S. Cl. ............................... 210/1982; 21.0/502.1; SEPARATION AGENTS 210/635; 210/656 (58) Field of Classification Search ................ 210/635, (75) Inventor: Daniel Armstrong, Rolla, MO (US) 210/656, 198.2, 502.1; 502/.401, 403, 404; 435/174, 176, 178,180 (73) Assignee: Curators of the University of See application file for complete Search history. Missouri, Columbia, MO (US) (*) Notice: Subject to any disclaimer,- 0 the term of this (56) References Cited patent is extended or adjusted under 35 FOREIGN PATENT DOCUMENTS U.S.C. -
Title 16. Crimes and Offenses Chapter 13. Controlled Substances Article 1
TITLE 16. CRIMES AND OFFENSES CHAPTER 13. CONTROLLED SUBSTANCES ARTICLE 1. GENERAL PROVISIONS § 16-13-1. Drug related objects (a) As used in this Code section, the term: (1) "Controlled substance" shall have the same meaning as defined in Article 2 of this chapter, relating to controlled substances. For the purposes of this Code section, the term "controlled substance" shall include marijuana as defined by paragraph (16) of Code Section 16-13-21. (2) "Dangerous drug" shall have the same meaning as defined in Article 3 of this chapter, relating to dangerous drugs. (3) "Drug related object" means any machine, instrument, tool, equipment, contrivance, or device which an average person would reasonably conclude is intended to be used for one or more of the following purposes: (A) To introduce into the human body any dangerous drug or controlled substance under circumstances in violation of the laws of this state; (B) To enhance the effect on the human body of any dangerous drug or controlled substance under circumstances in violation of the laws of this state; (C) To conceal any quantity of any dangerous drug or controlled substance under circumstances in violation of the laws of this state; or (D) To test the strength, effectiveness, or purity of any dangerous drug or controlled substance under circumstances in violation of the laws of this state. (4) "Knowingly" means having general knowledge that a machine, instrument, tool, item of equipment, contrivance, or device is a drug related object or having reasonable grounds to believe that any such object is or may, to an average person, appear to be a drug related object.