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  • 1
    Online Resource
    Online Resource
    Blood Pressure–Independent Effects in Rats With Human Renin and Angiotensinogen Genes
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Hypertension Vol. 35, No. 2 ( 2000-02), p. 587-594
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 35, No. 2 ( 2000-02), p. 587-594
    Abstract: Abstract —The blood pressure–independent effects of angiotensin II (Ang II) were examined in double transgenic rats (dTGR) harboring human renin and human angiotensinogen genes, in which the end-organ damage is due to the human components of the renin angiotensin system. Triple-drug therapy (hydralazine 80 mg/L, reserpine 5 mg/L, and hydrochlorothiazide 25 mg/L in drinking water) was started immediately after weaning. Triple-drug therapy normalized blood pressure and coronary resistance, only partially prevented cardiac hypertrophy, and had no effect on ratio of renal weight to body weight. Although triple-drug therapy delayed the onset of renal damage, severe albuminuria nevertheless occurred. Semiquantitative scoring of ED-1–positive and MIB-5–positive (nuclear cell proliferation–associated antigen Ki-67) cells showed profound perivascular monocyte/macrophage infiltration and cell proliferation in kidneys and hearts of untreated dTGR. Triple-drug therapy had only a minimal effect on local inflammatory response or vascular cell proliferation. In contrast, a novel orally active human renin inhibitor (HRI), 30 mg/kg by gavage for 4 weeks, normalized blood pressure and coronary resistance and also prevented cardiac hypertrophy and albuminuria. ED-1–positive cells and MIB-5–positive cells were decreased by HRI in hearts and kidneys almost to levels observed in normotensive Sprague-Dawley rats. The renoprotective effects of HRI were at least in part due to improved renal hemodynamics and distal tubular function, since HRI shifted renal pressure-diuresis/natriuresis curves leftward by ≈35 mm Hg, increased glomerular filtration rate and renal blood flow, and shifted the fractional water and sodium excretion curves leftward. In untreated dTGR, plasma Ang II was increased by 400% and renal Ang II level was increased by 300% compared with Sprague-Dawley rats. HRI decreased plasma human renin activity by 95% and normalized Ang II levels in both plasma and kidney compared with triple-drug therapy. Our findings indicate that in dTGR harboring human renin and angiotensinogen genes, Ang II causes end-organ damage and promotes inflammatory response and cellular growth largely independent of blood pressure.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.35.2.587
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
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  • 2
    Online Resource
    Online Resource
    Renal and Mesenteric Arterial Tone in Rats with Human Renin and Angiotensinogen Genes
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Hypertension Vol. 36, No. suppl_1 ( 2000-10), p. 694-694
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. suppl_1 ( 2000-10), p. 694-694
    Abstract: P6 The vascular endothelium plays a key role in the control of vasomotor tone, local hemostasis, and vascular wall proliferation processes. We characterized vascular functions in double-transgenic rats (dTGR) harboring human renin and human angiotensinogen. In dTGR, the endothelium-mediated relaxations of noradrenaline (NA)-precontracted renal (large conduit vessel) and mesenteric arterial (smaller conduit vessel) rings to acetylcholine (ACh) were markedly impaired, compared to normotensive Sprague Dawley rats (p 〈 0.05). In contrast, the endothelium-independent relaxation to sodium nitroprusside (SNP) were similar in both strains. Preincubation of the arterial rings with the NOS inhibitor L-NAME and the COX inhibitor diclofenac inhibited relaxations to ACh almost completely in dTGR, suggesting that endothelial dysfunction could be attributed, at least in part, to reduced relaxation via arterial K+ channels. Contractions to Ang II, ET-1, and NA were decreased in dTGR suggesting agonist-dependent down-regulation of the receptors. The vascular media-to-lumen ratio was similar in both strains, indicating that vascular functions were characterized during an early stage of hypertension. 24-hour urinary NOx excretion, a marker of total body NO generation, was markedly decreased in dTGR (p 〈 0.05). AT1 receptor blockade by valsartan (30 mg/kg p.o. for 3 weeks) normalized blood pressure, endothelial dysfunction, and the contractile responses to ET-1 and NA. We also quantified AT1, AT2, neutral endopeptidase (NEP), and ACE expressions in the kidney by autoradiography. In dTGR, AT1, AT2 and NEP expressions were decreased, whereas ACE expression was unchanged. The activity of renal xanthine oxidoreductase (XOR), a hypoxia-inducible enzyme capable of generating reactive oxygen species, was increased by 50 % in dTGR, and normalized by valsartan. Our findings indicate that hypertension in dTGR is associated with endothelial dysfunction, down-regulation of Ang II, ET-1, and NA receptors, as well as increased renal XOR activity. AT1 receptor blockade effectively normalized blood pressure, alterations in arterial function, and renal XOR activity.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.36.suppl_1.694-a
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
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  • 3
    Online Resource
    Online Resource
    3D High-Efficiency Video Coding for Multi-View Video and Depth Data
    Institute of Electrical and Electronics Engineers (IEEE) ; 2013
    In:  IEEE Transactions on Image Processing Vol. 22, No. 9 ( 2013-9), p. 3366-3378
    Details
    In: IEEE Transactions on Image Processing, Institute of Electrical and Electronics Engineers (IEEE), Vol. 22, No. 9 ( 2013-9), p. 3366-3378
    Type of Medium: Online Resource
    ISSN: 1057-7149 , 1941-0042
    URL: Journal
    URL: Article
    DOI: 10.1109/TIP.83
    DOI: 10.1109/TIP.2013.2264820
    Language: Unknown
    Publisher: Institute of Electrical and Electronics Engineers (IEEE)
    Publication Date: 2013
    detail.hit.zdb_id: 2034319-X
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  • 4
    Online Resource
    Online Resource
    NMR and chiroptical examination of the diastereoisomers of (S)-Eu–EOB–DTPA
    Royal Society of Chemistry (RSC) ; 2004
    In:  Dalton Trans. , No. 12 ( 2004), p. 1892-1895
    Details
    In: Dalton Trans., Royal Society of Chemistry (RSC), , No. 12 ( 2004), p. 1892-1895
    Type of Medium: Online Resource
    ISSN: 1477-9226 , 1477-9234
    URL: Article
    DOI: 10.1039/B403863K
    Language: English
    Publisher: Royal Society of Chemistry (RSC)
    Publication Date: 2004
    detail.hit.zdb_id: 1472887-4
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  • 5
    Online Resource
    Online Resource
    Dexamethasone Inhibits Nf-κB, P22phox, and Protects Against Angiotensin Ii-Induced Renal Damage
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Hypertension Vol. 36, No. suppl_1 ( 2000-10), p. 723-723
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. suppl_1 ( 2000-10), p. 723-723
    Abstract: P167 We recently reported that NF-κB activation promotes inflammation in rats harboring both human renin and angiotensinogen genes (dTGR). We now tested the hypothesis that dexamethasone (DEX) inhibits NF-κB and ameliorates renal and cardiac end-organ damage. The dTGR feature moderate hypertension, severe renal, and cardiac damage, as well as over 50% mortality at 7 weeks. Immunohistochemical analysis shows increased infiltration of monocytes and T-cells. Electrophoretic mobility shift assay showed increased NF-κB DNA binding activity in heart and kidney of dTGR. One-week treatment with DEX (1 mg/kg/d i.p.) initially increased blood pressure at week 5, compared to dTGR (191±2 vs.152±6 mm Hg, p 〈 0.01), whereas blood pressure was not different at week 7 (193±15 vs. 182±8 mm Hg, p=0.8). However, DEX reduced 24 h albuminuria by 85 % (2.7±0.5 vs. 18.0±3.4 mg/d, p 〈 0.001) and prevented mortality completely. Vasculopathy was ameliorated in kidney and heart and perivascular fibrosis was reduced. DEX inhibited NF-κB DNA-binding activity and also the NF-κB-regulated adhesion molecule ICAM-1. We also studied localization of NADPH subunit p22phox. Immunostaining of p22phox was detected in the endothelium and also colocalized with monocytes. DEX reduced both infiltration of cells and p22phox expression. Thus, these results demonstrate that DEX suppresses NF-κB binding activity, p22phox expression of infiltrated cells, inflammation, and protects against angiotensin II-induced end-organ damage, all without blood pressure reduction.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.36.suppl_1.723-c
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
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  • 6
    Online Resource
    Online Resource
    Effect of Bosentan on NF-κB, Inflammation, and Tissue Factor in Angiotensin II–Induced End-Organ Damage
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Hypertension Vol. 36, No. 2 ( 2000-08), p. 282-290
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. 2 ( 2000-08), p. 282-290
    Abstract: Abstract —Reports on the effectiveness of endothelin receptor blockers in angiotensin (Ang) II–induced end-organ damage are conflicting, and the mechanisms involved are uncertain. We tested the hypothesis that endothelin (ET) A/B receptor blockade with bosentan (100 mg/kg by gavage after age 4 weeks) ameliorates cardiac and renal damage by decreasing inflammation in rats harboring both human renin and angiotensinogen genes (dTGR). Furthermore, we elucidated the effect of bosentan on tissue factor (TF), which is a key regulator of the extrinsic coagulation cascade. We compared bosentan with hydralazine (80 mg/L in the drinking water for 3 weeks) as a blood pressure control. Untreated dTGR featured hypertension, focal necrosis in heart and kidney, and a 45% mortality rate (9 of 20) at age 7 weeks. Compared with Sprague-Dawley controls, both systolic blood pressure and 24-hour albuminuria were increased in untreated dTGR (203±8 versus 111±2 mm Hg and 67.1±8.6 versus 0.3±0.06 mg/d at week 7, respectively). Bosentan and hydralazine both reduced blood pressure and cardiac hypertrophy. Mortality rate was markedly reduced by bosentan (1/15) and partially by hydralazine (4/15). However, only bosentan decreased albuminuria and renal injury. Untreated and hydralazine-treated dTGR showed increased nuclear factor (NF)-κB and AP-1 expression in the kidney and heart; the p65 NF-κB subunit was increased in the endothelium, vascular smooth muscles cells, infiltrating cells, glomeruli, and tubules. In the heart and kidney, ET A/B receptor blockade inhibited NF-κB and AP-1 activation compared with hydralazine treatment. Macrophage infiltration, ICAM-1 expression, and the integrin expression on infiltrating cells were markedly reduced. Renal vasculopathy was accompanied by increased tissue factor expression on macrophages and vessels of untreated and hydralazine-treated dTGR, which was markedly reduced by bosentan. Thus, ET A/B receptor blockade inhibits NF-κB and AP-1 activation and the NF-κB– and/or AP-1–regulated genes ICAM-1, VCAM-1, and TF, independent of blood pressure–related effects. We conclude that Ang II–induced NF-κB and AP-1 activation and subsequent inflammation and coagulation involve at least in part the ET A/B receptors.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.36.2.282
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
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  • 7
    Online Resource
    Online Resource
    Mixed-layer dynamics and buoyancy transports
    Stockholm University Press ; 1991
    In:  Tellus A Vol. 43, No. 5 ( 1991-10), p. 350-365
    Details
    In: Tellus A, Stockholm University Press, Vol. 43, No. 5 ( 1991-10), p. 350-365
    Type of Medium: Online Resource
    ISSN: 0280-6495 , 1600-0870
    URL: Article
    DOI: 10.1034/j.1600-0870.1991.t01-1-00009.x
    RVK:
    RA 1000
    RVK:
    UA 8382.1
    Language: English
    Publisher: Stockholm University Press
    Publication Date: 1991
    detail.hit.zdb_id: 2026987-0
    SSG: 16,13
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  • 8
    Online Resource
    Online Resource
    Depth Intra Coding for 3D Video Based on Geometric Primitives
    Institute of Electrical and Electronics Engineers (IEEE) ; 2016
    In:  IEEE Transactions on Circuits and Systems for Video Technology Vol. 26, No. 3 ( 2016-3), p. 570-582
    Details
    In: IEEE Transactions on Circuits and Systems for Video Technology, Institute of Electrical and Electronics Engineers (IEEE), Vol. 26, No. 3 ( 2016-3), p. 570-582
    Type of Medium: Online Resource
    ISSN: 1051-8215 , 1558-2205
    URL: Journal
    URL: Article
    DOI: 10.1109/TCSVT.76
    DOI: 10.1109/TCSVT.2015.2407791
    Language: Unknown
    Publisher: Institute of Electrical and Electronics Engineers (IEEE)
    Publication Date: 2016
    detail.hit.zdb_id: 2034312-7
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  • 9
    Online Resource
    Online Resource
    Angiotensin II induced inflammation in the kidney and in the heart of double transgenic rats
    Springer Science and Business Media LLC ; 2002
    In:  BMC Cardiovascular Disorders Vol. 2, No. 1 ( 2002-12)
    Details
    In: BMC Cardiovascular Disorders, Springer Science and Business Media LLC, Vol. 2, No. 1 ( 2002-12)
    Type of Medium: Online Resource
    ISSN: 1471-2261
    URL: Article
    DOI: 10.1186/1471-2261-2-3
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2002
    detail.hit.zdb_id: 2059859-2
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  • 10
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    Online Resource
    Cyclosporin A Protects Against Angiotensin II–Induced End-Organ Damage in Double Transgenic Rats Harboring Human Renin and Angiotensinogen Genes
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Hypertension Vol. 35, No. 1 ( 2000-01), p. 360-366
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 35, No. 1 ( 2000-01), p. 360-366
    Abstract: Abstract —Leukocyte infiltration and adhesion molecule activation play a central role in the pathogenesis of angiotensin II (Ang II)–induced end-organ damage in double transgenic rats (dTGR) harboring human renin and angiotensinogen genes. We tested the hypothesis that the immunosuppressive agent cyclosporine (CsA) protects against the Ang II–induced myocardial and renal damage in dTGR. Furthermore, we investigated the influence of CsA on interleukin-6 (IL-6) and inducible nitric oxide synthase (iNOS) expression and the DNA binding activity of transcription factor necrosis factor-κB (NF-κB). The 4-week-old rats were divided into 4 groups: (1) control dTGR (n=20), (2) dTGR plus CsA (5 mg/kg SC for 3 weeks, n=15), (3) normotensive Sprague-Dawley (SD) rats (n=10), and (4) SD rats plus CsA (n=8). In dTGR, CsA completely prevented cardiovascular death (0 of 15 versus 9 of 20), decreased 24-hour albuminuria by 90% and systolic blood pressure by 35 mm Hg, and protected against the development of cardiac hypertrophy. Whole blood CsA concentrations 24 hours after the last drug treatment were 850±15 ng/mL. Semiquantitative ED-1 and Ki-67 (a nuclear cell proliferation–associated antigen) scoring showed that CsA prevented perivascular monocyte/macrophage infiltration and prevented cell proliferation in the kidneys and hearts of dTGR, respectively. The beneficial effects of CsA were, at least in part, mediated by the suppression of IL-6 and iNOS expression. Electrophoretic mobility shift assay revealed that CsA regulated inflammatory response in part through the NF-κB transcriptional pathway. In contrast to dTGR, CsA increased blood pressure in normotensive SD rats by 10 mm Hg and had no effect on cardiac mass or 24-hour urinary albumin excretion. Perivascular monocyte/macrophage infiltration, IL-6, and iNOS expression or cell proliferation were not affected by CsA in SD rats. Our findings indicate that CsA protects against Ang II–induced end-organ damage and underscore the central role of vascular inflammatory response in the pathogenesis of myocardial and renal damage in dTGR. The beneficial effects of CsA in the kidney and heart are mediated, at least in part, by suppression of IL-6 and iNOS expression via NF-κB transcriptional pathway.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.35.1.360
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
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