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  1. Article ; Online: Comment on: "Safety of Marketed Cancer Supportive Care Biosimilars in the U.S.: A Disproportionality Analysis Using the Food and Drug Administration Adverse Event Reporting System (FAERS) Database".

    Putzke, Joerg / Haughie, Scott / Zou, Kelly H / Ranganna, Gopinath M

    BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy

    2021  Volume 35, Issue 3, Page(s) 373–374

    MeSH term(s) Adverse Drug Reaction Reporting Systems ; Biosimilar Pharmaceuticals/adverse effects ; Databases, Factual ; Humans ; Neoplasms/drug therapy ; United States ; United States Food and Drug Administration
    Chemical Substances Biosimilar Pharmaceuticals
    Language English
    Publishing date 2021-04-16
    Publishing country New Zealand
    Document type Letter ; Comment
    ZDB-ID 1364202-9
    ISSN 1179-190X ; 1173-8804
    ISSN (online) 1179-190X
    ISSN 1173-8804
    DOI 10.1007/s40259-021-00476-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Book ; Thesis: Tierexperimentelle Studien zur Änderung der Genexpression während verschiedener Phasen der Alkoholabhängigkeit

    Putzke, Jörg

    1997  

    Author's details vorgelegt von Jörg Putzke
    Language German
    Size III, 117 S., S. IV - V, Ill., graph. Darst
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Univ., Diss.--München, 1997
    Database Former special subject collection: coastal and deep sea fishing

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  3. Book ; Thesis: Tierexperimentelle Studien zur Änderung der Genexpression während verschiedener Phasen der Alkoholabhängigkeit

    Putzke, Jörg

    1997  

    Author's details vorgelegt von Jörg Putzke
    Language German
    Size III, 117 S., S. IV - V, Ill., graph. Darst
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Univ., Diss.--München, 1997
    Database Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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  4. Article ; Online: Altered postsynaptic-density-levels of caldendrin in the para-chloroamphetamine-induced serotonin syndrome but not in the rat ketamine model of psychosis.

    Smalla, Karl-Heinz / Sahin, Jale / Putzke, Jörg / Tischmeyer, Wolfgang / Gundelfinger, Eckart D / Kreutz, Michael R

    Neurochemical research

    2009  Volume 34, Issue 8, Page(s) 1405–1409

    Abstract: Caldendrin is a synaptic calcium sensor protein that is tightly associated with the postsynaptic density (PSD). Previous work has shown that the association of the protein with the synapse is highly dynamic and is increased in an activity-dependent ... ...

    Abstract Caldendrin is a synaptic calcium sensor protein that is tightly associated with the postsynaptic density (PSD). Previous work has shown that the association of the protein with the synapse is highly dynamic and is increased in an activity-dependent manner. In the present study the caldendrin-association with the postsynaptic cytomatrix was analyzed in animal models of psychosis and drug abuse induced neurotoxicity. Subchronic administration of the N-methyl-D-aspartate (NMDA)-receptor antagonist ketamine, serving as a model of NMDA-receptor hypofunction and schizophrenia showed no significant effect on the PSD-levels of caldendrin, indicating that NMDA-receptor activity is not required to keep caldendrin at the synapse. However, administration of high doses of the serotonergic neurotoxin p-chloroamphetamine (PCA) lead to significant changes in the association of caldendrin with the PSD. These results underscore the dynamic association of caldendrin with the PSD and suggest a role of this synaptic calcium sensor in the PCA-induced serotonin syndrome.
    MeSH term(s) Animals ; Blotting, Western ; Calcium-Binding Proteins/metabolism ; Excitatory Amino Acid Antagonists ; Ketamine ; Male ; Nerve Tissue Proteins/metabolism ; Psychoses, Substance-Induced/metabolism ; Rats ; Rats, Sprague-Dawley ; Serotonin Agents ; Serotonin Syndrome/chemically induced ; Serotonin Syndrome/metabolism ; Synapses/drug effects ; Synapses/metabolism ; p-Chloroamphetamine
    Chemical Substances Calcium-Binding Proteins ; Excitatory Amino Acid Antagonists ; Nerve Tissue Proteins ; Serotonin Agents ; p-Chloroamphetamine (64-12-0) ; Ketamine (690G0D6V8H) ; Ca2+-binding protein-1 (EC 5.3.4.-)
    Language English
    Publishing date 2009-02-18
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 199335-5
    ISSN 1573-6903 ; 0364-3190
    ISSN (online) 1573-6903
    ISSN 0364-3190
    DOI 10.1007/s11064-009-9925-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: The effects of p-chloroamphetamine, methamphetamine and 3,4-methylenedioxymethamphetamine (ecstasy) on the gene expression of cytoskeletal proteins in the rat brain.

    Putzke, Jörg / Spina, Mariarosa G / Büchler, Jochen / Kovar, Karl-Artur / Wolf, Gerald / Smalla, Karl-Heinz

    Addiction biology

    2007  Volume 12, Issue 1, Page(s) 69–80

    Abstract: Repeated administration of beta-phenylalkylamines is known to produce neuronal changes in the central and peripheral nervous systems of mammals. It is suggested that various components of the cytoskeleton undergo profound alterations after amphetamine ... ...

    Abstract Repeated administration of beta-phenylalkylamines is known to produce neuronal changes in the central and peripheral nervous systems of mammals. It is suggested that various components of the cytoskeleton undergo profound alterations after amphetamine use and misuse, contributing to behavioral changes and neurotoxicity. Here we studied the expression of microtubule-associated protein 2 (MAP2) and beta-actin after repeated intraperitoneal applications with equimolar doses of p-chloroamphetamine (PCA), methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA) in the brain of male Wistar rats. Effective (molecular) pharmacological doses (ED) were derived and used for the calculation of (molecular) pharmacological indices (PI). Besides clear but different dose-response curves on the toxicity of the drugs, in situ hybridization and Western blot analysis revealed that repeated administration of these compounds resulted in different substance- and dose-dependent changes in MAP2 gene expression, e.g. in the frontoparietal somatosensoric cortex. In contrast, the expression of beta-actin was not influenced by any of the compounds at the dose levels tested. Lethal doses were determined with 2.1 (PCA), >5.1 (METH) and 8.4 mg/kg/day (MDMA). Linear and non-linear repeat-dose lethality was observed for MDMA and PCA, respectively, whereas METH was non-lethal in the dose range used. Values for ED(MAP2) were 0.3, 0.52 and >16.8 mg/kg/day, and therefore those for PI(MAP2) were 20, 4, and 0.5 for METH, PCA and MDMA, respectively. Although the results on mortality did not reflect changes in MAP2 gene expression, they suggest a remarkable difference for those amphetamines without substituents or with a halogen atom at the paraposition of the benzene ring, such as METH or PCA, when compared with MDMA-like substances.
    MeSH term(s) Actins/genetics ; Animals ; Blotting, Western ; Brain Mapping ; Central Nervous System Stimulants/toxicity ; Cerebral Cortex/drug effects ; Cerebral Cortex/metabolism ; Cerebral Cortex/pathology ; Cytoskeletal Proteins/genetics ; Dose-Response Relationship, Drug ; Gene Expression/drug effects ; In Situ Hybridization ; Injections, Intraperitoneal ; Male ; Methamphetamine/toxicity ; Microtubule-Associated Proteins/genetics ; N-Methyl-3,4-methylenedioxyamphetamine/toxicity ; Rats ; Rats, Wistar ; Survival Analysis ; p-Chloroamphetamine/toxicity
    Chemical Substances Actins ; Central Nervous System Stimulants ; Cytoskeletal Proteins ; Microtubule-Associated Proteins ; Methamphetamine (44RAL3456C) ; p-Chloroamphetamine (64-12-0) ; N-Methyl-3,4-methylenedioxyamphetamine (KE1SEN21RM)
    Language English
    Publishing date 2007-03
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1324314-7
    ISSN 1369-1600 ; 1355-6215
    ISSN (online) 1369-1600
    ISSN 1355-6215
    DOI 10.1111/j.1369-1600.2006.00047.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: The neuronal nitric oxide synthase gene is critically involved in neurobehavioral effects of alcohol.

    Spanagel, Rainer / Siegmund, Sören / Cowen, Michael / Schroff, Karl-Christian / Schumann, Gunter / Fiserova, Magdalena / Sillaber, Inge / Wellek, Stefan / Singer, Manfred / Putzke, Jörg

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2002  Volume 22, Issue 19, Page(s) 8676–8683

    Abstract: In the present study, we describe a new role of the neuronal nitric oxide synthase (nNOS) gene in the regulation of alcohol drinking behavior. Mice deficient in the nNOS gene (nNOS -/-) and wild-type control mice were submitted to a two-bottle free- ... ...

    Abstract In the present study, we describe a new role of the neuronal nitric oxide synthase (nNOS) gene in the regulation of alcohol drinking behavior. Mice deficient in the nNOS gene (nNOS -/-) and wild-type control mice were submitted to a two-bottle free-choice procedure with either water or increasing concentrations of alcohol (2-16%) for 6 weeks. nNOS -/- mice did not differ in consumption and preference for low alcohol concentrations from wild-type animals; however, nNOS -/- mice consumed sixfold more alcohol from highly concentrated alcohol solutions than wild-type mice. Taste studies with either sucrose or quinine solutions revealed that alcohol intake in nNOS -/- and wild-type mice is associated, at least in part, with sweet solution intake but not with the taste of bitterness. When compared with wild-type mice, the nNOS -/- mice were found to be less sensitive to the sedative effects of ethanol as measured by shorter recovery time from ethanol-induced sleep and did not develop rapid tolerance to ethanol-induced hypothermia, although plasma ethanol concentrations were not significantly different from those of controls. Our findings contrast with previous reports that showed that nonselective NOS inhibitors decrease alcohol consumption. However, because alcohol consumption was suppressed in wild-type as well as nNOS -/- mice by the NOS inhibitor N(G)-nitro-L-arginine methyl ester, we conclude that the effect of nonselective NOS inhibitors on alcohol drinking is not mediated by nNOS. Other NOS isoforms, most likely in the periphery or other splice variants of the NOS gene, might contribute to the effect of nonselective NOS inhibitors on alcohol drinking. In summary, the nNOS gene is critically involved in the regulation of neurobehavioral effects of alcohol.
    MeSH term(s) Administration, Oral ; Alternative Splicing ; Animals ; Behavior, Animal/drug effects ; Brain/drug effects ; Brain/enzymology ; Choice Behavior/drug effects ; Choice Behavior/physiology ; Dose-Response Relationship, Drug ; Drug Tolerance/physiology ; Enzyme Inhibitors/pharmacology ; Ethanol/blood ; Ethanol/pharmacology ; Homozygote ; Hypothermia/chemically induced ; In Situ Hybridization ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide Synthase/antagonists & inhibitors ; Nitric Oxide Synthase/genetics ; Nitric Oxide Synthase/metabolism ; Nitric Oxide Synthase Type I ; Quinine/administration & dosage ; RNA, Messenger/metabolism ; Reflex/drug effects ; Self Administration ; Sucrose/administration & dosage ; Taste/drug effects
    Chemical Substances Enzyme Inhibitors ; RNA, Messenger ; Ethanol (3K9958V90M) ; Sucrose (57-50-1) ; Quinine (A7V27PHC7A) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Nitric Oxide Synthase Type I (EC 1.14.13.39) ; Nos1 protein, mouse (EC 1.14.13.39) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
    Language English
    Publishing date 2002-09-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    Database MEDical Literature Analysis and Retrieval System OnLINE

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