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  • 1
    Online Resource
    Online Resource
    Increased protein synthesis is necessary for the development of late preconditioning against myocardial stunning
    American Physiological Society ; 1999
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 277, No. 3 ( 1999-09-01), p. H874-H884
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 277, No. 3 ( 1999-09-01), p. H874-H884
    Abstract: In phase I of this study, the rate of protein synthesis was measured by the incorporation of [ 3 H]leucine into the protein pool in the heart of conscious rabbits. At 2 h after ischemic preconditioning (PC) with six 4-min occlusion/4-min reperfusion (O/R) cycles ( group II), the [ 3 H]leucine content in the ischemic-reperfused region was increased by 82% compared with that in controls ( group I), indicating increased protein synthesis. This increase was completely abrogated by pretreatment with cycloheximide (CH; group III). In phase II, rabbits underwent six O/R cycles for three consecutive days ( days 1–3). Controls ( group IV) exhibited late PC against myocardial stunning on days 2 and 3. In group V, which received CH 30 min before the 1st O/R cycle on day 1 (same dose as group III), late PC against stunning on day 2 was completely abrogated. In group VI, pretreatment with CH 24 h before the 1st sequence of O/R cycles had no effect on myocardial stunning on day 1, indicating that the absence of late PC on day 2 in group V cannot be ascribed to delayed toxicity of CH. Taken together, these results demonstrate that, in the conscious rabbit, ischemic PC causes a rapid increase in myocardial protein synthesis and that this increased protein synthesis (or at least a fraction of it) is necessary for the development of the protection against myocardial stunning 24 h later. The late phase of ischemic PC is therefore dependent on the formation of new proteins in intact animals.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.1999.277.3.H874
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    The late phase of ischemic preconditioning is abrogated by targeted disruption of the inducible NO synthase gene
    Proceedings of the National Academy of Sciences ; 1999
    In:  Proceedings of the National Academy of Sciences Vol. 96, No. 20 ( 1999-09-28), p. 11507-11512
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 96, No. 20 ( 1999-09-28), p. 11507-11512
    Abstract: The goal of this study was to interrogate the role of inducible NO synthase (iNOS) in the late phase of ischemic preconditioning (PC) in vivo . A total of 321 mice were used. Wild-type mice preconditioned 24 h earlier with six cycles of 4-min coronary occlusion/4-min reperfusion exhibited a significant ( P 〈 0.05) increase in myocardial iNOS protein content, iNOS activity (assessed as calcium-independent l -citrulline formation), and nitrite + nitrate tissue levels. In contrast, endothelial NOS protein content and calcium-dependent NOS activity remained unchanged. No immunoreactive neuronal NOS was detected. When wild-type mice were preconditioned 24 h earlier with six 4-min occlusion/4-min reperfusion cycles, the size of the infarcts produced by a 30-min coronary occlusion followed by 24 h of reperfusion was reduced markedly (by 67%; P 〈 0.05) compared with sham-preconditioned controls, indicating a late PC effect. In contrast, when mice homozygous for a null iNOS allele were preconditioned 24 h earlier with the same protocol, infarct size was not reduced. Disruption of the iNOS gene had no effect on early PC or on infarct size in the absence of PC. These results demonstrate that ( i ) the late phase of ischemic PC is associated with selective up-regulation of iNOS, and ( ii ) targeted disruption of the iNOS gene completely abrogates the infarct-sparing effect of late PC (but not of early PC), providing unequivocal molecular genetic evidence for an obligatory role of iNOS in the cardioprotection afforded by the late phase of ischemic PC. Thus, this study identifies a specific protein that mediates late PC in vivo .
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.96.20.11507
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 1999
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 3
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    Online Resource
    Bifunctional Role of Protein Tyrosine Kinases in Late Preconditioning Against Myocardial Stunning in Conscious Rabbits
    Ovid Technologies (Wolters Kluwer Health) ; 1999
    In:  Circulation Research Vol. 85, No. 12 ( 1999-12-03), p. 1154-1163
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 85, No. 12 ( 1999-12-03), p. 1154-1163
    Abstract: Abstract —Although protein tyrosine kinases (PTKs) have been implicated in late preconditioning (PC) against infarction, their role in late PC against stunning is unknown. Furthermore, it is unknown whether PTK signaling is necessary only to trigger late PC on day 1 or also to mediate it on day 2. Thus, conscious rabbits underwent a sequence of six 4-minute coronary occlusion/4-minute reperfusion cycles for 3 consecutive days (days 1, 2, and 3). In the control group (group I, n=7), the recovery of systolic wall thickening after the 6 occlusion/reperfusion cycles was markedly improved on days 2 and 3 compared with day 1, indicating the development of late PC against stunning. Administration of the PTK inhibitor lavendustin-A (LD-A, 1 mg/kg IV) before the first occlusion on day 1 (group II, n=7) completely prevented the late PC effect against stunning on day 2. Late PC against stunning was also abrogated when LD-A was given before the first occlusion on day 2 (group III, n=7); however, in these rabbits, the late PC effect became apparent on day 3, indicating that LD-A itself did not have any delayed deleterious actions on myocardial stunning. In group V (n=5), the sequence of 6 occlusion/reperfusion cycles resulted in a robust increase in the activity of inducible NO synthase (iNOS [assessed as Ca 2+ -independent l -citrulline formation]) and nitrite+nitrate (NO x ) tissue levels 24 hours later (on day 2), with no concomitant change in Ca 2+ -dependent NO synthase (endothelial NO synthase and/or neuronal NO synthase) activity. Similar results were obtained on day 3 (group VIII, n=6), indicating sustained upregulation of iNOS. Administration of LD-A either on day 1 (group VI, n=5) or on day 2 (group VII, n=6) abrogated the increase in iNOS activity and NO x levels on day 2. LD-A had no effect on iNOS activity or NO x levels in the absence of PC (group X, n=5). This study demonstrates that in conscious rabbits, PTK activity is necessary not only to trigger late PC against stunning on day 1 but also to mediate the protection on day 2. This investigation also provides the first direct evidence that cardiac iNOS activity is upregulated during the late phase of ischemic PC in rabbits. Furthermore, the data indicate that PTK signaling is essential for the augmentation of iNOS activity and that PTKs modulate this enzyme at two distinct levels: at an early stage on day 1 and at a late stage on day 2. This bifunctional role of PTKs in late PC has broad implications for the signaling mechanisms that underlie the response of the heart to ischemic stress and, possibly, other stresses.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.85.12.1154
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1999
    detail.hit.zdb_id: 1467838-X
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  • 4
    Online Resource
    Online Resource
    Nuclear Factor-κB Plays an Essential Role in the Late Phase of Ischemic Preconditioning in Conscious Rabbits
    Ovid Technologies (Wolters Kluwer Health) ; 1999
    In:  Circulation Research Vol. 84, No. 9 ( 1999-05-14), p. 1095-1109
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 84, No. 9 ( 1999-05-14), p. 1095-1109
    Abstract: Abstract —Although it is recognized that late preconditioning (PC) results from upregulation of cardioprotective genes, the specific transcription factor(s) that govern this genetic adaptation remains unknown. The aim of this study was to test the hypothesis that the development of late PC is mediated by nuclear factor-κB (NF-κB) and to elucidate the mechanisms that control the activation of NF-κB after an ischemic stimulus in vivo. A total of 152 chronically instrumented, conscious rabbits were used. A sequence of six 4-minute coronary occlusion/4-minute reperfusion cycles, which elicits late PC, induced rapid activation of NF-κB, as evidenced by a marked increase in p65 content (+164%; Western immunoblotting) and NF-κB DNA binding activity (+306%; electrophoretic mobility shift assay) in nuclear extracts isolated 30 minutes after the last reperfusion. These changes were attenuated 2 hours after ischemic PC and resolved by 4 hours. Competition and supershift assays confirmed the specificity of the NF-κB DNA complex signals. The mobility of the NF-κB DNA complex was shifted by anti-p65 and anti-p50 antibodies but not by anti–c-Rel antibodies, indicating that the subunits of NF-κB involved in gene activation after ischemic PC consist of p65-p50 heterodimers. Pretreatment with the NF-κB inhibitor diethyldithiocarbamate (DDTC; 150 mg/kg IP 15 minutes before ischemic PC) completely blocked the nuclear translocation and increased DNA binding activity of NF-κB. The same dose of DDTC completely blocked the cardioprotective effects of late PC against both myocardial stunning and myocardial infarction, indicating that NF-κB activation is essential for the development of this phenomenon in vivo. The ischemic PC-induced activation of NF-κB was also blocked by pretreatment with N ω -nitro- l -arginine (L-NA), a nitric oxide synthase (NOS) inhibitor, N -2-mercaptopropionyl glycine (MPG), a reactive oxygen species (ROS) scavenger, chelerythrine, a protein kinase C (PKC) inhibitor, and lavendustin A, a tyrosine kinase inhibitor (all given at doses previously shown to block late PC), indicating that ischemic PC activates NF-κB via formation of NO and ROS and activation of PKC- and tyrosine kinase–dependent signaling pathways. A subcellular redistribution and increased DNA binding activity of NF-κB quantitatively similar to those induced by ischemic PC could be reproduced pharmacologically by giving the NO donor diethylenetriamine/NO (DETA/NO) (at a dose previously shown to elicit late PC), demonstrating that NO in itself can activate NF-κB in the heart. Taken together, these results provide direct evidence that activation of NF-κB is a critical step in the signal transduction pathway that underlies the development of the late phase of ischemic PC in conscious rabbits. The finding that four different pharmacological manipulations (L-NA, MPG, chelerythrine, and lavendustin A) produced similar inhibition of NF-κB suggests that this transcription factor is a common downstream pathway through which multiple signals elicited by ischemic stress (NO, ROS, PKC, tyrosine kinases) act to induce gene expression. To our knowledge, this is the first demonstration that NO can promote NF-κB activation in the heart, a finding that identifies a new biological function of NO and may have important implications for various pathophysiological conditions in which NO is involved and for nitrate therapy.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.84.9.1095
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1999
    detail.hit.zdb_id: 1467838-X
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  • 5
    Online Resource
    Online Resource
    DEEP LEVELS AND FREE-CARRIER COMPENSATION IN NITROGEN-IMPLANTED GaAs
    Acta Physica Sinica, Chinese Physical Society and Institute of Physics, Chinese Academy of Sciences ; 1996
    In:  Acta Physica Sinica Vol. 45, No. 3 ( 1996), p. 491-
    Details
    In: Acta Physica Sinica, Acta Physica Sinica, Chinese Physical Society and Institute of Physics, Chinese Academy of Sciences, Vol. 45, No. 3 ( 1996), p. 491-
    Abstract: This work presents a detailed study of deep and shallow level defects in nitrogen implanted n-type GaAs. Deep-level transient spectroscopy (DLTS) measurements show four electron traps and one hole trap in 140 keV nitrogen implanted GaAs after a dose of 1×1013cm-2 and a thermal annealing at 800℃ for 30 min: E1(0.111) ,E2(0.234) ,E3(0.415) ,E4(0.669) ,and H(0.545). Meanwhile,only E4 and H(0.545) defects are observed in 10 keV nitrogen-implanted GaAs after a dose of 5×1014cm-2 and the same annealing treatment. It oncluded that E2 and E3 correspond to the damages due to the high-energy implantation, E4 may be complex of intrinsic defect and implantation damage, H(0.545)is a nitrogen-related deep-level and may contribute to the free-carrier compensation in the nitrogen-implanted n-type GaAs.
    Type of Medium: Online Resource
    ISSN: 1000-3290 , 1000-3290
    URL: Journal
    URL: Article
    DOI: 10.7498/aps
    DOI: 10.7498/aps.45.491
    Language: Unknown
    Publisher: Acta Physica Sinica, Chinese Physical Society and Institute of Physics, Chinese Academy of Sciences
    Publication Date: 1996
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  • 6
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    Modification test of staged pulse tube refrigerator for temperatures below 4 K
    Elsevier BV ; 1997
    In:  Cryogenics Vol. 37, No. 9 ( 1997-9), p. 529-532
    Details
    In: Cryogenics, Elsevier BV, Vol. 37, No. 9 ( 1997-9), p. 529-532
    Type of Medium: Online Resource
    ISSN: 0011-2275
    URL: Article
    DOI: 10.1016/S0011-2275(97)00079-9
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1997
    detail.hit.zdb_id: 1501356-X
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