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  1. Article ; Online: Decreased temperature as a signal for regulation of heat shock protein expression in anoxic brain and heart: focus on "Expression of heat shock proteins in anoxic crucian carp (Carassius carassius): support for cold as a preparatory cue for anoxia".

    Prentice, Howard M

    American journal of physiology. Regulatory, integrative and comparative physiology

    2010  Volume 298, Issue 6, Page(s) R1496–8

    MeSH term(s) Animals ; Carps/metabolism ; Cold Temperature ; Heart/physiology ; Heat-Shock Proteins/metabolism ; Hypoxia/metabolism
    Chemical Substances Heat-Shock Proteins
    Language English
    Publishing date 2010-04-21
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 603839-6
    ISSN 1522-1490 ; 0363-6119
    ISSN (online) 1522-1490
    ISSN 0363-6119
    DOI 10.1152/ajpregu.00237.2010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Book: The brain without oxygen

    Lutz, Peter L. / Nilsson, Göran E. / Prentice, Howard M.

    causes of failure-physiological and molecular mechanisms for survival

    2003  

    Author's details by Peter L. Lutz ; Göran E. Nilsson and Howard M. Prentice
    Keywords Cerebral Anoxia / physiopathology ; Brain / physiopathology ; Hypoxia, Brain / physiopathology
    Language English
    Size VIII, 252 S. : Ill., graph. Darst.
    Edition 3. ed.
    Publisher Kluwer
    Publishing place Dordrecht u.a.
    Publishing country Netherlands
    Document type Book
    HBZ-ID HT013668285
    ISBN 1-4020-1165-2 ; 978-1-4020-1165-8
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2003 A 2017 order for loan Magazin

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  3. Article ; Online: The major contribution of brain GABAergic function to anoxic survival.

    Prentice, Howard M

    Physiological genomics

    2009  Volume 36, Issue 2, Page(s) 59–60

    MeSH term(s) Animals ; Brain/metabolism ; Carps/metabolism ; Cell Hypoxia ; Receptors, GABA-A/metabolism ; gamma-Aminobutyric Acid/metabolism
    Chemical Substances Receptors, GABA-A ; gamma-Aminobutyric Acid (56-12-2)
    Language English
    Publishing date 2009-01-08
    Publishing country United States
    Document type Comment ; Editorial
    ZDB-ID 2038823-8
    ISSN 1531-2267 ; 1094-8341
    ISSN (online) 1531-2267
    ISSN 1094-8341
    DOI 10.1152/physiolgenomics.90380.2008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: The Role of NMDA Receptor Partial Antagonist, Carbamathione, as a Therapeutic Agent for Transient Global Ischemia.

    Modi, Jigar Pravinchandra / Shen, Wen / Menzie-Suderam, Janet / Xu, Hongyuan / Lin, Chun-Hua / Tao, Rui / Prentice, Howard M / Schloss, John / Wu, Jang-Yen

    Biomedicines

    2023  Volume 11, Issue 7

    Abstract: Carbamathione (Carb), an NMDA glutamate receptor partial antagonist, has potent neuroprotective functions against hypoxia- or ischemia-induced neuronal injury in cell- or animal-based stroke models. We used PC-12 cell cultures as a cell-based model and ... ...

    Abstract Carbamathione (Carb), an NMDA glutamate receptor partial antagonist, has potent neuroprotective functions against hypoxia- or ischemia-induced neuronal injury in cell- or animal-based stroke models. We used PC-12 cell cultures as a cell-based model and bilateral carotid artery occlusion (BCAO) for stroke. Whole-cell patch clamp recording in the mouse retinal ganglion cells was performed. Key proteins involved in apoptosis, endoplasmic reticulum (ER) stress, and heat shock proteins were analyzed using immunoblotting. Carb is effective in protecting PC12 cells against glutamate- or hypoxia-induced cell injury. Electrophysiological results show that Carb attenuates NMDA-mediated glutamate currents in the retinal ganglion cells, which results in activation of the AKT signaling pathway and increased expression of pro-cell survival biomarkers, e.g., Hsp 27, P-AKT, and Bcl2 and decreased expression of pro-cell death markers, e.g., Beclin 1, Bax, and Cleaved caspase 3, and ER stress markers, e.g., CHOP, IRE1, XBP1, ATF 4, and eIF2α. Using the BCAO animal stroke model, we found that Carb reduced the brain infarct volume and decreased levels of ER stress markers, GRP 78, CHOP, and at the behavioral level, e.g., a decrease in asymmetric turns and an increase in locomotor activity. These findings for Carb provide promising and rational strategies for stroke therapy.
    Language English
    Publishing date 2023-07-03
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines11071885
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  5. Article: New science, drug regulation, and emergent public health issues: The work of FDA's division of applied regulatory science.

    Chiu, Kimberly / Racz, Rebecca / Burkhart, Keith / Florian, Jeffry / Ford, Kevin / Iveth Garcia, M / Geiger, Robert M / Howard, Kristina E / Hyland, Paula L / Ismaiel, Omnia A / Kruhlak, Naomi L / Li, Zhihua / Matta, Murali K / Prentice, Kristin W / Shah, Aanchal / Stavitskaya, Lidiya / Volpe, Donna A / Weaver, James L / Wu, Wendy W /
    Rouse, Rodney / Strauss, David G

    Frontiers in medicine

    2023  Volume 9, Page(s) 1109541

    Abstract: The U.S. Food and Drug Administration (FDA) Division of Applied Regulatory Science (DARS) moves new science into the drug review process and addresses emergent regulatory and public health questions for the Agency. By forming interdisciplinary teams, ... ...

    Abstract The U.S. Food and Drug Administration (FDA) Division of Applied Regulatory Science (DARS) moves new science into the drug review process and addresses emergent regulatory and public health questions for the Agency. By forming interdisciplinary teams, DARS conducts mission-critical research to provide answers to scientific questions and solutions to regulatory challenges. Staffed by experts across the translational research spectrum, DARS forms synergies by pulling together scientists and experts from diverse backgrounds to collaborate in tackling some of the most complex challenges facing FDA. This includes (but is not limited to) assessing the systemic absorption of sunscreens, evaluating whether certain drugs can convert to carcinogens in people, studying drug interactions with opioids, optimizing opioid antagonist dosing in community settings, removing barriers to biosimilar and generic drug development, and advancing therapeutic development for rare diseases. FDA tasks DARS with wide ranging issues that encompass regulatory science; DARS, in turn, helps the Agency solve these challenges. The impact of DARS research is felt by patients, the pharmaceutical industry, and fellow regulators. This article reviews applied research projects and initiatives led by DARS and conducts a deeper dive into select examples illustrating the impactful work of the Division.
    Language English
    Publishing date 2023-01-19
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2775999-4
    ISSN 2296-858X
    ISSN 2296-858X
    DOI 10.3389/fmed.2022.1109541
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  6. Article ; Online: A novel sulindac derivative protects against oxidative damage by a cyclooxygenase-independent mechanism.

    Allani, Shailaja Kesaraju / Rayala, Ramanjaneyulu / Rivera, Oscar / Prentice, Howard M / Chen, Xi / Ramírez-Alcántara, Veronica / Canzoneri, Joshua / Menzie-Suderam, Janet / Huang, Xupei / Georgescu, Constantin / Wren, Jonathan D / Piazza, Gary A / Weissbach, Herbert

    The Journal of pharmacology and experimental therapeutics

    2022  

    Abstract: Oxidative damage is believed to play a major role in the etiology of many age-related diseases and the normal aging process. We previously reported that sulindac, a cyclooxygenase (COX) inhibitor and FDA approved anti-inflammatory drug, has ... ...

    Abstract Oxidative damage is believed to play a major role in the etiology of many age-related diseases and the normal aging process. We previously reported that sulindac, a cyclooxygenase (COX) inhibitor and FDA approved anti-inflammatory drug, has chemoprotective activity in cells and intact organs by initiating a pharmacological preconditioning response, similar to ischemic preconditioning (IPC). The mechanism is independent of its COX inhibitory activity as suggested by studies on the protection of the heart against oxidative damage from ischemia/reperfusion and retinal pigmented endothelial (RPE) cells against chemical oxidative and UV damage
    Language English
    Publishing date 2022-06-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3106-9
    ISSN 1521-0103 ; 0022-3565
    ISSN (online) 1521-0103
    ISSN 0022-3565
    DOI 10.1124/jpet.122.001086
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  7. Article: Key contributions of the Na+/H+ exchanger subunit 1 and HCO3- transporters in regulating neuronal cell fate in prolonged hypoxia.

    Prentice, Howard M

    American journal of physiology. Regulatory, integrative and comparative physiology

    2007  Volume 294, Issue 2, Page(s) R448–50

    MeSH term(s) Animals ; Bicarbonates/metabolism ; Cation Transport Proteins/metabolism ; Cell Death/physiology ; Hypoxia, Brain/metabolism ; Hypoxia, Brain/pathology ; Membrane Proteins/metabolism ; Neurons/metabolism ; Neurons/pathology ; Sodium-Bicarbonate Symporters/metabolism ; Sodium-Hydrogen Exchanger 1 ; Sodium-Hydrogen Exchangers/metabolism
    Chemical Substances Bicarbonates ; Cation Transport Proteins ; Membrane Proteins ; Slc9a1 protein, mouse ; Sodium-Bicarbonate Symporters ; Sodium-Hydrogen Exchanger 1 ; Sodium-Hydrogen Exchangers
    Language English
    Publishing date 2007-12-05
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 603839-6
    ISSN 1522-1490 ; 0363-6119
    ISSN (online) 1522-1490
    ISSN 0363-6119
    DOI 10.1152/ajpregu.00846.2007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Lessons from nature: signalling cascades associated with vertebrate brain anoxic survival.

    Nayak, Gauri / Prentice, Howard M / Milton, Sarah L

    Experimental physiology

    2016  Volume 101, Issue 9, Page(s) 1185–1190

    Abstract: New findings: What is the topic of this review? Although the mammalian brain is exquisitely sensitive to hypoxia, some turtles survive complete anoxia by decreasing metabolic demand to match reduced energy supply. These animal models may help to ... ...

    Abstract New findings: What is the topic of this review? Although the mammalian brain is exquisitely sensitive to hypoxia, some turtles survive complete anoxia by decreasing metabolic demand to match reduced energy supply. These animal models may help to elucidate neuroprotective mechanisms and reveal novel therapeutic targets for diseases of oxygen deprivation. What advances does it highlight? The mitogen-activated protein kinases (MAPKs) are part of the suite of adaptive responses to anoxia that are modulated by adenosine, a 'retaliatory metabolite' released in early anoxia. In anoxic turtle neurons, upregulation of pro-survival Akt and extracellular signal-regulated kinase 1/2 and suppression of the p38MAPK and JNK pathways promote cell survival, as does the anoxic- and post-anoxic upregulation of the antioxidant methionine sulfoxide reductase. Mammalian neurons undergo rapid degeneration when oxygen supply is curtailed. Neuroprotective pathways are induced during hypoxia/ischaemia, but their analysis is complicated by concurrent pathological events. Survival mechanisms can be investigated in anoxia-tolerant freshwater turtle species, which survive oxygen deprivation and post-anoxic reoxygenation by entrance into a state of reversible hypometabolism. Many energy-demanding processes are suppressed, including ion flux and neurotransmitter release, whereas cellular protective mechanisms, including certain mitogen-activated protein kinases (MAPKs), are upregulated. This superfamily of serine/threonine kinases plays a significant role in vital cellular processes, including cell proliferation, differentiation, stress adaptation and apoptosis in response to external stimuli. Here, we report that neuronal survival relies on robust co-ordination between the major signalling cascades, with upregulation of the pro-survival Akt and extracellular signal-regulated kinase 1/2 and suppression of the p38MAPK and JNK pathways. Other protective responses, including the upregulation of heat shock proteins and antioxidants, allow the turtle brain to abrogate potential oxidative stress upon reoxygenation.
    Language English
    Publishing date 2016-04-28
    Publishing country England
    Document type Journal Article
    ZDB-ID 1016295-1
    ISSN 1469-445X ; 0958-0670
    ISSN (online) 1469-445X
    ISSN 0958-0670
    DOI 10.1113/EP085673
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  9. Article: Sensing and responding to hypoxia, molecular and physiological mechanisms.

    Lutz, Peter L / Prentice, Howard M

    Integrative and comparative biology

    2011  Volume 42, Issue 3, Page(s) 463–468

    Abstract: In order to adapt to low oxygen it is necessary first to be able to detect hypoxia, then to initiate the appropriate defense mechanisms. There are two basic detectors: molecular sensors that are directly linked to gene regulation and metabolic indicators ...

    Abstract In order to adapt to low oxygen it is necessary first to be able to detect hypoxia, then to initiate the appropriate defense mechanisms. There are two basic detectors: molecular sensors that are directly linked to gene regulation and metabolic indicators that are triggered when the cell goes into a state of energy imbalance. The molecular responses to oxygen deprivation are characterized in a variety of cell types and include activation of oxygen sensors, signaling through specific promoter elements and subsequent downstream adaptations. Many of the components are highly conserved across species. In the brain, the most hypoxic vulnerable of all vertebrate tissues, low oxygen quickly results in a fall in ATP and a consequent increase in adenosine. Both changes act as metabolic indicators of cellular energy crisis and effect mechanisms to reduce metabolic demand. Important lessons on the potential scope of such mechanisms can be provided by the anoxic tolerant turtle brain. Anoxia provokes an early release of adenosine which mediates channel arrest, causes a reduction in K(+) efflux and Ca(2+) influx, and inhibits excitatory neurotransmitter release. There is a differential expression between normoxic and anoxic turtle brains of transcripts encoding the immediate early gene products c-fos and c-jun, the HSP-70 and the apoptosis regulators bcl-2 and bax.
    Language English
    Publishing date 2011-06-28
    Publishing country England
    Document type Journal Article
    ZDB-ID 201481-6
    ISSN 1540-7063 ; 0003-1569
    ISSN 1540-7063 ; 0003-1569
    DOI 10.1093/icb/42.3.463
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  10. Article ; Online: Protein arginine methyltransferase 4 modulates nitric oxide synthase uncoupling and cerebral blood flow in Alzheimer's disease.

    Clemons, Garrett A / Silva, Alexandre Couto E / Acosta, Christina H / Udo, Mariana Sayuri Berto / Tesic, Vesna / Rodgers, Krista M / Wu, Celeste Yin-Chieh / Citadin, Cristiane T / Lee, Reggie Hui-Chao / Neumann, Jake T / Allani, Shailaja / Prentice, Howard / Zhang, Quanguang / Lin, Hung Wen

    Journal of cellular physiology

    2022  

    Abstract: Alzheimer's disease (AD) is the leading cause of mortality, disability, and long-term care burden in the United States, with women comprising the majority of AD diagnoses. While AD-related dementia is associated with tau and amyloid beta accumulation, ... ...

    Abstract Alzheimer's disease (AD) is the leading cause of mortality, disability, and long-term care burden in the United States, with women comprising the majority of AD diagnoses. While AD-related dementia is associated with tau and amyloid beta accumulation, concurrent derangements in cerebral blood flow have been observed alongside these proteinopathies in humans and rodent models. The homeostatic production of nitric oxide synthases (NOS) becomes uncoupled in AD which leads to decreased NO-mediated vasodilation and oxidative stress via the production of peroxynitrite (ONOO-∙) superoxide species. Here, we investigate the role of the novel protein arginine methyltransferase 4 (PRMT4) enzyme function and its downstream product asymmetric dimethyl arginine (ADMA) as it relates to NOS dysregulation and cerebral blood flow in AD. ADMA (type-1 PRMT product) has been shown to bind NOS as a noncanonic ligand causing enzymatic dysfunction. Our results from RT-qPCR and protein analyses suggest that aged (9-12 months) female mice bearing tau- and amyloid beta-producing transgenic mutations (3xTg-AD) express higher levels of PRMT4 in the hippocampus when compared to age- and sex-matched C57BL6/J mice. In addition, we performed studies to quantify the expression and activity of different NOS isoforms. Furthermore, laser speckle contrast imaging analysis was indicative that 3xTg-AD mice have dysfunctional NOS activity, resulting in reduced production of NO metabolites, enhanced production of free-radical ONOO-, and decreased cerebral blood flow. Notably, the aforementioned phenomena can be reversed via pharmacologic PRMT4 inhibition. Together, these findings implicate the potential importance of PRMT4 signaling in the pathogenesis of Alzheimer's-related cerebrovascular derangement.
    Language English
    Publishing date 2022-08-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3116-1
    ISSN 1097-4652 ; 0021-9541
    ISSN (online) 1097-4652
    ISSN 0021-9541
    DOI 10.1002/jcp.30858
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