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  1. Book: Platelet activating factor receptor

    Shukla, Shivendra D.

    signal mechanisms and molecular biology

    (Pharmacology and toxicology: basic and clinical aspects)

    1993  

    Author's details ed. by Shivendra D. Shukla
    Series title Pharmacology and toxicology: basic and clinical aspects
    Keywords Platelet Activating Factor ; Receptors, Cell Surface ; Signal Transduction ; Platelet activating Factor ; Physiologische Chemie
    Subject Chemische Physiologie ; Biochemische Medizin ; Medizinische Biochemie ; PAF ; Thrombozytenaktivierender Faktor ; Plättchenaktivierender Faktor
    Language English
    Size 184 S. : Ill., graph. Darst.
    Publisher CRC Press
    Publishing place Boca Raton u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT004993456
    ISBN 0-8493-7299-2 ; 978-0-8493-7299-5
    Database Catalogue ZB MED Medicine, Health

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    1993 A 2963 order for loan Magazin

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  2. Article ; Online: Binge Drinking.

    White, Aaron M / Tapert, Susan / Shukla, Shivendra D

    Alcohol research : current reviews

    2019  Volume 39, Issue 1, Page(s) 1–3

    MeSH term(s) Adolescent ; Adult ; Alcohol Drinking in College ; Animals ; Binge Drinking ; Female ; Humans ; Male ; Underage Drinking ; Young Adult
    Language English
    Publishing date 2019-01-15
    Publishing country United States
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 2677485-9
    ISSN 2169-4796 ; 1930-0573 ; 2168-3492 ; 0090-838X
    ISSN (online) 2169-4796 ; 1930-0573
    ISSN 2168-3492 ; 0090-838X
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  3. Article ; Online: A Simple Protocol for Mapping the Plant Root System Architecture Traits.

    Shukla, Devesh / Trivedi, Prabodh Kumar / Sahi, Shivendra

    Journal of visualized experiments : JoVE

    2023  , Issue 192

    Abstract: Comprehensive knowledge of plant root system architecture (RSA) development is critical for improving nutrient use efficiency and increasing crop cultivar tolerance to environmental challenges. An experimental protocol is presented for setting up the ... ...

    Abstract Comprehensive knowledge of plant root system architecture (RSA) development is critical for improving nutrient use efficiency and increasing crop cultivar tolerance to environmental challenges. An experimental protocol is presented for setting up the hydroponic system, plantlet growth, RSA spreading, and imaging. The approach used a magenta box-based hydroponic system containing polypropylene mesh supported by polycarbonate wedges. Experimental settings are exemplified by assessing the RSA of the plantlets under varying nutrient (phosphate [Pi]) supply. The system was established to examine the RSA of Arabidopsis, but it is readily adaptable to study other plants like Medicago sativa (Alfalfa). Arabidopsis thaliana (Col-0) plantlets are used in this investigation as an example to understand the plant RSA. Seeds are surface sterilized by treating ethanol and diluted commercial bleach, and kept at 4 °C for stratification. The seeds are germinated and grown on a liquid half-MS medium on a polypropylene mesh supported by polycarbonate wedges. The plantlets are grown under standard growth conditions for the desired number days, gently picked out from the mesh, and submersed in water-containing agar plates. Each root system of the plantlets is spread gently on the water-filled plate with the help of a round art brush. These Petri plates are photographed or scanned at high resolution to document the RSA traits. The root traits, such as primary root, lateral roots, and branching zone, are measured using the freely available ImageJ software. This study provides techniques for measuring plant root characteristics in controlled environmental settings. We discuss how to (1) grow the plantlets, and collect and spread root samples, (2) obtain pictures of spread RSA samples, (3) capture the images, and (4) use image analysis software to quantify root attributes. The advantage of the present method is the versatile, easy, and efficient measurement of the RSA traits.
    MeSH term(s) Polypropylenes ; Plant Roots ; Phenotype ; Phosphates ; Arabidopsis ; Water
    Chemical Substances Polypropylenes ; Phosphates ; Water (059QF0KO0R)
    Language English
    Publishing date 2023-02-10
    Publishing country United States
    Document type Journal Article ; Video-Audio Media
    ZDB-ID 2259946-0
    ISSN 1940-087X ; 1940-087X
    ISSN (online) 1940-087X
    ISSN 1940-087X
    DOI 10.3791/64876
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  4. Article: Epigenetics--new frontier for alcohol research.

    Shukla, Shivendra D / Zakhari, Samir

    Alcohol research : current reviews

    2013  Volume 35, Issue 1, Page(s) 1–2

    MeSH term(s) Alcohol-Related Disorders/genetics ; Epigenesis, Genetic ; Epigenomics ; Humans
    Language English
    Publishing date 2013-02-07
    Publishing country United States
    Document type Editorial
    ISSN 2168-3492
    ISSN 2168-3492
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  5. Article: Epigenetic effects of ethanol on the liver and gastrointestinal system.

    Shukla, Shivendra D / Lim, Robert W

    Alcohol research : current reviews

    2013  Volume 35, Issue 1, Page(s) 47–55

    Abstract: The widening web of epigenetic regulatory mechanisms also encompasses ethanol-induced changes in the gastrointestinal (GI)-hepatic system. In the past few years, increasing evidence has firmly established that alcohol modifies several epigenetic ... ...

    Abstract The widening web of epigenetic regulatory mechanisms also encompasses ethanol-induced changes in the gastrointestinal (GI)-hepatic system. In the past few years, increasing evidence has firmly established that alcohol modifies several epigenetic parameters in the GI tract and liver. The major pathways affected include DNA methylation, different site-specific modifications in histone proteins, and microRNAs. Ethanol metabolism, cell-signaling cascades, and oxidative stress have been implicated in these responses. Furthermore, ethanol-induced fatty liver (i.e., steatohepatitis) and progression of liver cancer (i.e., hepatic carcinoma) may be consequences of the altered epigenetics. Modification of gene and/or protein expression via epigenetic changes also may contribute to the cross-talk among the GI tract and the liver as well as to systemic changes involving other organs. Thus, epigenetic effects of ethanol may have a central role in the various pathophysiological responses induced by ethanol in multiple organs and mediated via the liver-GI axis.
    MeSH term(s) Carcinoma, Hepatocellular/chemically induced ; Carcinoma, Hepatocellular/genetics ; Central Nervous System Depressants/adverse effects ; Epigenesis, Genetic/drug effects ; Ethanol/adverse effects ; Gastrointestinal Tract/drug effects ; Gastrointestinal Tract/metabolism ; Humans ; Liver/drug effects ; Liver/metabolism ; Liver Diseases, Alcoholic/genetics ; Liver Neoplasms/chemically induced ; Liver Neoplasms/genetics ; Oxidative Stress
    Chemical Substances Central Nervous System Depressants ; Ethanol (3K9958V90M)
    Language English
    Publishing date 2013-11-07
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2168-3492
    ISSN 2168-3492
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  6. Article ; Online: Binge alcohol alters PNPLA3 levels in liver through epigenetic mechanism involving histone H3 acetylation.

    Restrepo, Ricardo J / Lim, Robert W / Korthuis, Ronald J / Shukla, Shivendra D

    Alcohol (Fayetteville, N.Y.)

    2017  Volume 60, Page(s) 77–82

    Abstract: The human PNPLA3 (patatin-like phospholipase domain-containing 3) gene codes for a protein which is highly expressed in adipose tissue and liver, and is implicated in lipid homeostasis. While PNPLA3 protein contains regions homologous to functional ... ...

    Abstract The human PNPLA3 (patatin-like phospholipase domain-containing 3) gene codes for a protein which is highly expressed in adipose tissue and liver, and is implicated in lipid homeostasis. While PNPLA3 protein contains regions homologous to functional lipolytic proteins, the regulation of its tissue expression is reflective of lipogenic genes. A naturally occurring genetic variant of PNPLA3 in humans has been linked to increased susceptibility to alcoholic liver disease. We have examined the modulatory effect of alcohol on PNPLA3 protein and mRNA expression as well as the association of its gene promoter with acetylated histone H3K9 by chromatin immunoprecipitation (ChIP) assay in rat hepatocytes in vitro, and in vivo in mouse and rat models of acute binge, chronic, and chronic followed by acute binge ethanol administration. Protein expression of PNPLA3 was significantly increased by alcohol in all three models used. PNPLA3 mRNA also increased, albeit to a varying degree. ChIP assay using H3AcK9 antibody showed increased association with the promoter of PNPLA3 in hepatocytes and in mouse liver. This was less evident in rat livers in vivo except under chronic treatment. It is concluded for the first time that histone acetylation plays a role in the modulation of PNPLA3 levels in the liver exposed to binge ethanol both in vitro and in vivo.
    Language English
    Publishing date 2017-05
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 605912-0
    ISSN 1873-6823 ; 0741-8329
    ISSN (online) 1873-6823
    ISSN 0741-8329
    DOI 10.1016/j.alcohol.2017.01.009
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  7. Article ; Online: Erratum to: Epigenetic histone modifications in a clinically relevant rat model of chronic ethanol-binge-mediated liver injury.

    Aroor, Annayya R / Restrepo, Ricardo J / Kharbanda, Kusum K / Shukla, Shivendra D

    Hepatology international

    2014  Volume 8 Suppl 2, Page(s) 431

    Language English
    Publishing date 2014-09
    Publishing country United States
    Document type Journal Article ; Published Erratum
    ZDB-ID 2270316-0
    ISSN 1936-0541 ; 1936-0533
    ISSN (online) 1936-0541
    ISSN 1936-0533
    DOI 10.1007/s12072-014-9564-2
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  8. Article ; Online: Binge Alcohol Is More Injurious to Liver in Female than in Male Rats: Histopathological, Pharmacologic, and Epigenetic Profiles.

    Shukla, Shivendra D / Restrepo, Ricardo / Aroor, Annayya R / Liu, Xuanyou / Lim, Robert W / Franke, Jacob D / Ford, David A / Korthuis, Ronald J

    The Journal of pharmacology and experimental therapeutics

    2019  Volume 370, Issue 3, Page(s) 390–398

    Abstract: Binge alcohol consumption is a health problem, but differences between the sexes remain poorly defined. We have examined the in vivo effects of three acute, repeat binge alcohol administration on the liver in male and female rats. Sprague-Dawley rats ... ...

    Abstract Binge alcohol consumption is a health problem, but differences between the sexes remain poorly defined. We have examined the in vivo effects of three acute, repeat binge alcohol administration on the liver in male and female rats. Sprague-Dawley rats were gavaged with alcohol (5 g/kg body weight) three times at 12-hour intervals. Blood and liver tissues were collected 4 hours after the last binge ethanol. Subsequently, several variables were analyzed. Compared with male rats, females had higher levels of blood alcohol, alanine aminotransferase, and triglycerides. Liver histology showed increased lipid vesicles that were larger in females. Protein levels of liver cytochrome P4502E1 were higher in the liver of females than in the liver of males after binge. Hepatic phospho-extracellular signal-regulated kinase 1/2 and phosph-p38 mitogen-activated protein kinase levels were lower in females compared with males after binge alcohol, but no differences were found in the phospho-C-jun N-terminal kinase levels. Peroxisome proliferator-activated receptor
    MeSH term(s) Animals ; Binge Drinking/genetics ; Binge Drinking/metabolism ; Binge Drinking/pathology ; Binge Drinking/physiopathology ; Cytochrome P-450 CYP2E1/metabolism ; Diacylglycerol Kinase/metabolism ; Epigenesis, Genetic ; Ethanol/adverse effects ; Female ; Glycerophospholipids/metabolism ; Liver/drug effects ; Liver/pathology ; MAP Kinase Signaling System/drug effects ; Male ; Rats ; Rats, Sprague-Dawley ; Sex Factors ; Transcription, Genetic/drug effects
    Chemical Substances Glycerophospholipids ; phosphatidylethanol ; Ethanol (3K9958V90M) ; Cytochrome P-450 CYP2E1 (EC 1.14.13.-) ; Diacylglycerol Kinase (EC 2.7.1.107)
    Language English
    Publishing date 2019-07-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3106-9
    ISSN 1521-0103 ; 0022-3565
    ISSN (online) 1521-0103
    ISSN 0022-3565
    DOI 10.1124/jpet.119.258871
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  9. Article ; Online: Binge ethanol intake in chronically exposed rat liver decreases LDL-receptor and increases angiotensinogen gene expression.

    Aroor, Annayya R / Shukla, Shivendra D

    World journal of hepatology

    2011  Volume 3, Issue 9, Page(s) 250–255

    Abstract: Aim: To investigated the status of low-density lipoprotein (LDL)-receptor and angiotensionogen gene expression in rats treated chronically with ethanol followed by binge administration, a model that mimics the human scenario.: Methods: Rats were ... ...

    Abstract Aim: To investigated the status of low-density lipoprotein (LDL)-receptor and angiotensionogen gene expression in rats treated chronically with ethanol followed by binge administration, a model that mimics the human scenario.
    Methods: Rats were chronically treated with ethanol in liquid diet for 4 wk followed by a single binge mode of ethanol administration (5 mg/kg body weight). Samples were processed 4 h after binge ethanol administration (chronic ethanol binge). Control rats were fed isocaloric diet. In the control for binge, ethanol was replaced by water. Expression of mRNA for angiotensinogen, c-fos and LDL-receptor, and nuclear accumulation of phospho-extracellular regulated kinases (ERK)1/2 and ERK1/2 protein were examined.
    Results: Binge ethanol administration in chronically treated rats caused increase in steatosis and necrosis. Chronic ethanol alone had negligible effect on mRNA levels of LDL-receptor, or on the levels of nuclear ERK1/2 and phospho-ERK1/2. But, chronic ethanol followed by binge caused a decrease in LDL-receptor mRNA, and also decreased the levels of ERK1/2 and phospho-ERK1/2 in the nuclear compartment. On the other hand, chronic ethanol-binge increased mRNA expression of angiotensinogen and c-fos.
    Conclusion: Binge ethanol after chronic exposure, causes transcriptional dysregulation of LDL-receptor and angiotensinogen genes, both cardiovascular risk factors.
    Language English
    Publishing date 2011-09-28
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2573703-X
    ISSN 1948-5182 ; 1948-5182
    ISSN (online) 1948-5182
    ISSN 1948-5182
    DOI 10.4254/wjh.v3.i9.250
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  10. Article ; Online: Epigenetic histone modifications in a clinically relevant rat model of chronic ethanol-binge-mediated liver injury.

    Aroor, Annayya R / Restrepo, Ricardo J / Kharbanda, Kusum K / Shukla, Shivendra D

    Hepatology international

    2014  Volume 8 Suppl 2, Page(s) 421–430

    Abstract: Purpose: Ethanol binge augments liver injury after chronic ethanol consumption in humans, but the mechanism behind the enhanced liver injury by ethanol binge is not known. In this study we used a clinically relevant rat model in which liver injury is ... ...

    Abstract Purpose: Ethanol binge augments liver injury after chronic ethanol consumption in humans, but the mechanism behind the enhanced liver injury by ethanol binge is not known. In this study we used a clinically relevant rat model in which liver injury is amplified by binge after chronic ethanol treatment and investigated the importance of histone modifications.
    Methods: Eight-week-old Sprague-Dawley rats were fed ethanol in a liquid diet for 4 weeks. Control rats were fed an isocaloric liquid diet. This was followed by three binge administrations of ethanol (intragastric 5 g/kg body weight, 12 h apart). In the control, ethanol was replaced by water. Four hours after the last binge administration, liver samples were analyzed for histone modifications and parameters of liver injury.
    Results: Chronic ethanol administration alone caused an increase in histone H3 ser10 and ser28 (H3S10 or S28) phosphorylation, and binge ethanol reduced their levels. Levels of dually modified phosphoacetylated histone H3 (H3AcK9/PS10) increased after acute binge ethanol and remained same after chronic ethanol binge. In contrast, histone H3 lysine-9 acetylation (H3AcK9) was not increased after chronic ethanol but increased significantly after acute binge and chronic ethanol binge. Increase in histone acetylation was accompanied by increased phospho-ERK1/2 in the nuclear extracts. Increased acetylation after chronic ethanol binge was also accompanied by increased protein levels of GCN5 histone acetyl transferase and a modest increase in HDAC3 in the nucleus. Histone lysine-9 dimethylation was significantly increased after chronic ethanol binge. Chronic ethanol binge also resulted in a decrease in the SAM:SAH ratio with a relative decrease of SAM levels and a corresponding increase in SAH levels.
    Conclusions: Ethanol binge after chronic ethanol altered the profile of site-specific histone modifications and may underlie the mechanism of augmented liver injury by chronic-ethanol-binge-treated rats.
    Language English
    Publishing date 2014-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2270316-0
    ISSN 1936-0541 ; 1936-0533
    ISSN (online) 1936-0541
    ISSN 1936-0533
    DOI 10.1007/s12072-014-9546-4
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