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  • 1
    Online Resource
    Online Resource
    The Distinction between Pattern and Process in Evolutionary Biology: The Use and Abuse of the Term 'Strategy'
    JSTOR ; 1988
    In:  Oikos Vol. 53, No. 1 ( 1988-07), p. 136-
    Details
    In: Oikos, JSTOR, Vol. 53, No. 1 ( 1988-07), p. 136-
    Type of Medium: Online Resource
    ISSN: 0030-1299
    URL: Article
    DOI: 10.2307/3565673
    Language: Unknown
    Publisher: JSTOR
    Publication Date: 1988
    detail.hit.zdb_id: 2025658-9
    detail.hit.zdb_id: 207359-6
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Morphological Differentiation of Etheostoma olmstedi and E. nigrum (Pisces: Percidae) in Canada
    JSTOR ; 1985
    In:  Copeia Vol. 1985, No. 4 ( 1985-12-10), p. 855-
    Details
    In: Copeia, JSTOR, Vol. 1985, No. 4 ( 1985-12-10), p. 855-
    Type of Medium: Online Resource
    ISSN: 0045-8511
    URL: Article
    DOI: 10.2307/1445233
    Language: Unknown
    Publisher: JSTOR
    Publication Date: 1985
    detail.hit.zdb_id: 217256-2
    detail.hit.zdb_id: 2198974-6
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Phylogenetic Status of Paralichthodes algoensis (Pleuronectiformes: Paralichthodidae)
    JSTOR ; 1998
    In:  Copeia Vol. 1998, No. 2 ( 1998-05-01), p. 477-
    Details
    In: Copeia, JSTOR, Vol. 1998, No. 2 ( 1998-05-01), p. 477-
    Type of Medium: Online Resource
    ISSN: 0045-8511
    URL: Article
    DOI: 10.2307/1447445
    Language: Unknown
    Publisher: JSTOR
    Publication Date: 1998
    detail.hit.zdb_id: 217256-2
    detail.hit.zdb_id: 2198974-6
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Paraplagusia sinerama (Pleuronectiformes: Cynoglossidae), a New Indo-Pacific Tongue Sole with a Revised Key to Species of the Genus
    JSTOR ; 1993
    In:  Copeia Vol. 1993, No. 3 ( 1993-08-18), p. 798-
    Details
    In: Copeia, JSTOR, Vol. 1993, No. 3 ( 1993-08-18), p. 798-
    Type of Medium: Online Resource
    ISSN: 0045-8511
    URL: Article
    DOI: 10.2307/1447245
    Language: Unknown
    Publisher: JSTOR
    Publication Date: 1993
    detail.hit.zdb_id: 217256-2
    detail.hit.zdb_id: 2198974-6
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    The immune system and hypertension
    Springer Science and Business Media LLC ; 2014
    In:  Immunologic Research Vol. 59, No. 1-3 ( 2014-8), p. 243-253
    Details
    In: Immunologic Research, Springer Science and Business Media LLC, Vol. 59, No. 1-3 ( 2014-8), p. 243-253
    Type of Medium: Online Resource
    ISSN: 0257-277X , 1559-0755
    URL: Article
    DOI: 10.1007/s12026-014-8548-6
    RVK:
    YC 5122
    RVK:
    YC 5187
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2014
    detail.hit.zdb_id: 2079303-0
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  • 6
    Online Resource
    Online Resource
    Abstract 20340: Defect of Ca 2+ -activated Cl - Channel in Intestinal Nodose Neurons Contributes to Impaired Satiety Signal in High-Fat Diet Induced Obesity
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Vol. 130, No. suppl_2 ( 2014-11-25)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 130, No. suppl_2 ( 2014-11-25)
    Abstract: High fat diet inhibits the cholecystokinin (CCK) induced satiety signal in vagal afferents, which may contribute to the associated increased food intake. We hypothesized that a defect of Ca 2+ -activated chloride channel (CaCC) in high fat (HFD) fed mice leads to the reduction of CCK responses in intestinal vagal afferent nodose neurons. By using the whole cell patch-clamp in cultured nodose ganglia neurons isolated from C57BL/6 mice, we found that CCK (10nM) induced large inward chloride (Cl - ) currents (36.0±11pA/pF) that were eliminated with the fast Ca 2+ chelator BAPTA (1.0±0.5pA/pF, n=7), and reduced significantly by the CaCC channel inhibitor niflumic acid (100 μM, 13.6±2.0pA/pF, p 〈 0.05, n=8). The response to CCK in DiI-labeled proximal intestinal nodose neurons from obese mice fed a 60% HFD for 10 weeks was reduced significantly (6.1±2.9pA/pF, n=7, p 〈 0.01) relative to control lean mice (24.8±4.9pA/pF, n=7). The underlying molecular mechanism of the reduced CCK response in mice fed a HFD did not involve altered expression of CCK receptors in nodose neurons. We found that the relative mRNA (qPCR) of CCK receptor B was not significantly changed (1.01±0.13 in control vs. 1.18±0.31 in HFD nodose ganglia, n=4, p 〉 0.05) and the mRNA of CCK receptor A was even increased from 1.06±0.37 in control to 1.54±0.41 in HFD ganglia (n=4, p 〈 0.05). In contrast, the CaCC channel mRNA (Ano I) was decreased to 0.61±0.09 relative to 1.01±0.20 (n=4, p 〈 0.001), and Ano II mRNA was decreased to 0.31±0.07 relative to 1.02±0.22 (n=4, p 〈 0.001) in nodose ganglia from HFD fed vs. control lean mice. Since the maximum current induced by a saturation level of ligand reflects the level of protein expressed on the cytoplasmic membrane, we tested the CaCC current induced by a high level of intracellular Ca 2+ (20μM). We found that the maximum current was smaller in DiI labeled intestinal nodose neurons from HFD fed mice (13.7±2.9 pA/pF vs. 26.9±3.6 pA/pF in control mice, n=10, p 〈 0.05). Our results indicate that CCK-activated currents recorded from intestinal vagal afferent nodose neurons are reduced in mice fed a HFD, and are associated with reduced expression of a CCK-activated Ca 2+ -dependent Cl - channel. This mechanism may contribute significantly to HFD-induced suppression of the satiety reflex.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.130.suppl_2.20340
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 1466401-X
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  • 7
    Online Resource
    Online Resource
    Non–Voltage-Gated Ca 2+ Influx Through Mechanosensitive Ion Channels in Aortic Baroreceptor Neurons
    Ovid Technologies (Wolters Kluwer Health) ; 1997
    In:  Circulation Research Vol. 80, No. 6 ( 1997-06), p. 861-867
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 80, No. 6 ( 1997-06), p. 861-867
    Abstract: Abstract The mechanisms underlying mechanotransduction in baroreceptor neurons (BRNs) are undefined. In this study, we specifically identified aortic baroreceptor neurons in primary neuronal cell cultures from nodose ganglia of rats. Aortic baroreceptor neurons were identified by labeling their soma with the fluorescent dye 1,1′-dioleyl-3,3,3′,3′-tetramethylindocarbocyanine (DiI) applied to the aortic arch. Using Ca 2+ imaging with fura 2, we examined these BRNs for evidence of Ca 2+ influx and determined its mechanosensitivity and voltage dependence. Mechanical stimuli were produced by ejecting buffer from a micropipette onto the cell surface with a pneumatic picopump, producing a shift in the center of mass of the cell that was related to intensity of stimulation. Ninety-three percent of DiI-labeled neurons responded to mechanical stimulation with an increase in [Ca 2+ ] i . The magnitude of the increases in [Ca 2+ ] i was directly related to the intensity of the stimulus and required the presence of external Ca 2+ . The trivalent cations Gd 3+ or La 3+ in equimolar concentrations (20 μmol/L) eliminated the K + -induced rises in [Ca 2+ ] i , demonstrating that both trivalent cations are equally effective at blocking voltage-gated Ca 2+ channels in these baroreceptor neurons. In contrast, the mechanically induced increases in [Ca 2+ ] i were blocked by Gd 3+ (20 μmol/L) only and not by La 3+ (20 μmol/L). Stretch-activated channels (SACs) have been shown in other preparations to be blocked by Gd 3+ specifically. Our data demonstrate that (1) BRNs, specifically identified as projecting to the aortic arch, have ion channels that are sensitive to mechanical stimuli; (2) mechanically induced Ca 2+ influx in these cells is mediated by a Gd 3+ -sensitive ion channel and not by voltage-gated Ca 2+ channels; (3) the magnitude of the Ca 2+ influx is dependent on the intensity of the stimulus and the degree and duration of deformation; and (4) repeated stimuli of the same intensity result in comparable increases in [Ca 2+ ] i . We conclude that mechanical stimulation increases Ca 2+ influx into aortic BRNs independent of voltage-gated Ca 2+ channels. The results suggest that Gd 3+ -sensitive SACs are the mechanoelectrical transducers in baroreceptors.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.80.6.861
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1997
    detail.hit.zdb_id: 1467838-X
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  • 8
    Online Resource
    Online Resource
    Nicotine Mediates CD161a + Renal Macrophage Infiltration and Premature Hypertension in the Spontaneously Hypertensive Rat
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Circulation Research Vol. 119, No. 10 ( 2016-10-28), p. 1101-1115
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 119, No. 10 ( 2016-10-28), p. 1101-1115
    Abstract: Renal inflammation contributes to the pathophysiology of hypertension. CD161a + immune cells are dominant in the (SHR) spontaneously hypertensive rat and expand in response to nicotinic cholinergic activation. Objective: We aimed to phenotype CD161a + immune cells in prehypertensive SHR after cholinergic activation with nicotine and determine if these cells are involved in renal inflammation and the development of hypertension. Methods and Results: Studies used young SHR and WKY (Wistar–Kyoto) rats. Splenocytes and bone marrow cells were exposed to nicotine ex vivo, and nicotine was infused in vivo. Blood pressures, kidney, serum, and urine were obtained. Flow cytometry, Luminex/ELISA, immunohistochemistry, confocal microscopy, and Western blot were used. Nicotinic cholinergic activation induced proliferation of CD161a + /CD68 + macrophages in SHR-derived splenocytes, their renal infiltration, and premature hypertension in SHR. These changes were associated with increased renal expression of MCP-1 (monocyte chemoattractant protein-1) and VLA-4 (very-late antigen-4). LLT1 (lectin-like transcript 1), the ligand for CD161a, was overexpressed in SHR kidney, whereas vascular cellular and intracellular adhesion molecules were similar to those in WKY. Inflammatory cytokines were elevated in SHR kidney and urine after nicotine infusion. Nicotine-mediated renal macrophage infiltration/inflammation was enhanced in denervated kidneys, not explained by angiotensin II levels or expression of angiotensin type-1/2 receptors. Moreover, expression of the anti-inflammatory α7-nAChR (α7-nicotinic acetylcholine receptor) was similar in young SHR and WKY rats. Conclusions: A novel, inherited nicotinic cholinergic inflammatory effect exists in young SHR, measured by expansion of CD161a + /CD68 + macrophages. This leads to renal inflammation and premature hypertension, which may be partially explained by increased renal expression of LLT-1, MCP-1, and VLA-4.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.116.309402
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 1467838-X
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  • 9
    Online Resource
    Online Resource
    Oxygen-Derived Free Radicals Contribute to Baroreceptor Dysfunction in Atherosclerotic Rabbits
    Ovid Technologies (Wolters Kluwer Health) ; 1996
    In:  Circulation Research Vol. 79, No. 4 ( 1996-10), p. 802-811
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 79, No. 4 ( 1996-10), p. 802-811
    Abstract: The goal of the present study was to determine whether oxygen-derived free radicals contribute to baroreceptor dysfunction in atherosclerosis. Baroreceptor activity was measured from the carotid sinus nerve during pressure ramps in isolated carotid sinuses of anesthetized rabbits. Rabbits fed a 0.5% to 1.0% cholesterol diet for 7.9±0.4 months (mean±SE; range, 5.5 to 10) developed atherosclerotic lesions in the carotid sinuses. Maximum baroreceptor activity measured at 140 mm Hg and the slope of the pressure-activity curve were reduced in atherosclerotic (n=15) compared with normal (n=13) rabbits (425±34 versus 721±30 spikes per second and 6.2±0.6 versus 10.8±0.8 spikes per second per mm Hg, respectively, P 〈 .05). The level of activity was inversely related to plasma cholesterol concentration ( r =.86, P 〈 .001) and total cholesterol load (plasma concentration×duration of diet, r =.92). Mean arterial pressure was normal in both groups. Exposure of the carotid sinus to the free-radical scavengers superoxide dismutase (SOD) and catalase significantly increased maximum baroreceptor activity by 25±4% in atherosclerotic rabbits (n=6) but caused only small and irreversible changes in activity in normal rabbits (n=8). Catalase alone but not SOD also increased baroreceptor activity in atherosclerotic rabbits (n=7). Exposure of the carotid sinus of normal rabbits to exogenous free radicals generated from the reaction between xanthine and xanthine oxidase inhibited baroreceptor activity in a dose-dependent and reversible manner (n=8, P 〈 .05). The inhibition of activity was attenuated by SOD and catalase but was not attenuated by the inhibitor of hydroxyl radical formation, deferoxamine. Neither restoration of baroreceptor activity in atherosclerotic rabbits by catalase nor inhibition of activity by xanthine/xanthine oxidase could be explained by changes in the carotid pressure-diameter relation or prostacyclin formation. These results indicate that oxidant stress inhibits baroreceptor activity and that endogenous oxyradicals produced in atherosclerotic carotid sinuses contribute to baroreceptor dysfunction.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.79.4.802
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1996
    detail.hit.zdb_id: 1467838-X
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  • 10
    Online Resource
    Online Resource
    Abstract P341: Renal Denervation Prevents Cholinergic Mediated Hypertension and Renal Macrophage Infiltration
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Hypertension Vol. 70, No. suppl_1 ( 2017-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 70, No. suppl_1 ( 2017-09)
    Abstract: In vivo cholinergic activation with nicotine induces renal infiltration of M1 inflammatory CD161a+/CD68+ macrophages and the development of hypertension. Renal denervation has been proposed as a treatment for essential hypertension. Based on this we hypothesized that the renal sympathetic nerves play a role in these processes. Bilateral renal denervation was performed surgically in 3-4 week old Spontaneously Hypertensive Rats (SHR), a genetic model of essential hypertension. Following one week recovery, animals received subcutaneous infusion of nicotine (15mg/kg/day) via osmotic pumps for 2 weeks. Blood pressure was measured by tail-cuff and kidneys harvested on completion of infusion. Prior to nicotine infusion, at baseline, there was no difference between the systolic blood pressures of the sham treated (n=7) and renal denervation (n=10) groups, 132 ± 4 vs 128 ± 3 mmHg, respectively (p 〉 0.05). In contrast, nicotine infusion significantly raised the systolic blood pressure in the sham treated group (159 ± 3mmHg), but not in the renal denervation group (135 ± 5 mmHg) (p 〈 0.001). Moreover, nicotine infusion induced a significantly greater infiltration of inflammatory CD161a+ immune cells and CD161a+/CD68+ inflammatory macrophages into the renal medulla of the sham treated group (n=4) (13 ± 2 cells/hpf and 5 ±1 cells/hpf, respectively), compared to renal denervation(n=4) (2 ± 1 cells/hpf and 2 ± 1 cells/hpf) (p 〈 0.001). We conclude that renal sympathetic innervation is required for the nicotine-induced migration of inflammatory CD161a+ immune cells and CD161a+/CD68+ inflammatory macrophages into the renal medulla and that renal denervation prevents the cholinergic-induced renal inflammation and hypertension in this model.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.70.suppl_1.p341
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 2094210-2
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