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848 Treffer

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  1. Detailansicht für Treffer 81 öffnen
    Figure 5. PKA inhibition reduces the size of the RRP. ; (A) Representative EPSCs recorded in response to CF stimulation at 50 Hz for 500 ms in control (black) and KT5720-treated (blue) slices. To relieve receptor saturation, 3 mM KYN was added in a recording solution with 2.5 mM Ca2+; Vm = −60 mV). (B) Superimposed train responses from control (black) and KT5720-treated (blue) slices, normalized to the first EPSC. Inset1: Average EPSC1 amplitude in control and KT5720-treated slices. Inset2: Normalized EPSC amplitude plotted as a function of stimulus number. The time constants were similar between control (23.3 ± 0.6 ms, n = 7) and KT5720-treated slices (22.9 ± 0.4 ms, n = 5, p=0.6, unpaired t-test). (C, left) Cumulative EPSC amplitude plotted as a function of stimulus number for control (black) and KT5720-treated (blue) slices. A line was fit to the final 5 EPSCs in each condition. (C, right) The RRPtrain (15.8 ± 1.0 nA and 7.5 ± 1.0 nA, n = 7 and 5; p=0.0002, unpaired t-test) and Prtrain (0.78 ± 0.03 and 0.80 ± 0.05, n = 7 and 5; p=0.61, unpaired t-test) were calculated from this plot. (D, left) Representative plots of EPSC amplitude versus the cumulative EPSC in control (black) and KT5720-treated (blue) recording with linear regressions to the initial portion of each data set. (D, right) The RRPeq (13.7 ± 0.7 nA and 6.6 ± 0.9 nA, n = 7 and 5; p=0.0001, unpaired t-test) and Preq (0.90 ± 0.02 and 0.90 ± 0.01, n = 7 and 5; p=0.85, unpaired t-test) were calculated from this plot.
    2019
    unknown
    Wie komme ich dran?
  2. Detailansicht für Treffer 82 öffnen
    Figure 7. Electrophysiological analysis of the functional effects of mutations in the putative membrane-binding loops of the Munc13-1 C2C domain. ; (A–C) Representative mEPSCs (A), EPSCs (B), and postsynaptic currents evoked by 0.5 M sucrose (C) in Munc13-1/2 DKO neurons expressing WT (black), R1598E mutant (blue), F1658E mutant (green) or R1598E/F1658E mutant (red) Munc13-1. (D–G) Mean mEPSC frequencies (D), EPSC amplitudes (E), RRP charges (F) and Pvr (G), measured in the Munc13-1/2 DKO neurons rescued with WT Munc13-1 and the indicated Munc13-1 mutants. (H) Paired-pulse ratios of Munc13-1/2 DKO neurons rescued with the WT Munc13-1 and the indicated Munc13-1 mutants. (I) Normalized EPSC amplitudes in response to a 10 Hz AP train in Munc13-1/2 DKO neurons rescued with WT (black), R1598E mutant (blue), F1658E mutant (green) or R1598E/F1658E mutant (red) Munc13-1. Numbers above the bars represent number of neurons pooled together of each group. Numbers in parentheses represent number of cultures or replicates used. All data are mean ±SEM. Significance and p values were determined by Kruskal Wallis test followed by a multiple comparison. *p
    2019
    unknown
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  3. Detailansicht für Treffer 83 öffnen
    Figure 8. Electrophysiological analysis of the functional effects of mutations in the polybasic region of the Munc13-1 C2C domain. ; (A–C) Examples of mEPSC (A), EPSCs (B) and sucrose induced currents (C) recorded from DKO neurons expressing WT Munc13-1 (black) or a Munc13-1 with a double point mutation at the polybasic stretch within the C2C domain, Munc13-1 K1613A/K1616A (grey). (D–F) Plots showing the average mEPSC frequencies (D), EPSC amplitudes (E) and RRP charges (F), obtained from the DKO neurons rescued with WT or K1613A/K1616A mutant Munc13-1. (G) Calculated Pvr in % for Munc13-1 WT and for the polybasic mutant K1613A/K1616A. (H) Graph showing the average paired-pulse ratios calculated from 2 APs with ISI of 25 ms (40 Hz) of DKO rescued with WT or K1613A/K1616A mutant Munc13-1. (I) Analysis of EPSC amplitudes in response to a train of 50 AP with an ISI of 100 ms (10 Hz) normalized to the first EPSC and plotted over time for the WT or K1613A/K1616A mutant Munc13-1 rescues. Numbers within the bars represent the number of neurons pooled together of each group. Numbers in parentheses represent the number of cultures or replicates used. All data are mean ± SEM. Significance and p values were determined by Mann Whitney test. *p
    2019
    unknown
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  4. Detailansicht für Treffer 84 öffnen
    Monitoring Public Health Impact of HPV Vaccination on RRP
    Singh, Vidisha ; Meites, Elissa ; et al.
    In: Recurrent Respiratory Papillomatosis ; page 33-44 ; ISBN 9783319638225 9783319638232; (2017)
    Buch
    Wie komme ich dran?
  5. Detailansicht für Treffer 85 öffnen
    Adherence of a high-speed RRP LDMOS characterization setup to JESD 24-10 standard
    Bernal, Carlos ; Jimenez, Manuel
    In: 2017 IEEE 8th Latin American Symposium on Circuits & Systems (LASCAS, 2017
    Online Konferenz
    Zugriff:
    Volltext
    Wie komme ich dran?
  6. Detailansicht für Treffer 86 öffnen
    A. David Moody, Thomas Stearns Eliot, Poet. 2nd Ed. Cambridge, Cambridge University press, 1994. pp. xxi + 387. RRP $31.95 (paper); The Cambridge Companion to T.S. Eliot, ed A. David Moody. Cambridge: Cambridge University Press, 1994. pp. xix + 259. RRP $27.50 (paper). [ Book Review]
    Tankard, Paul
    2017
    academicJournal
    Wie komme ich dran?
  7. Detailansicht für Treffer 87 öffnen
    John Leonard, 100 Elegies for Modernity, Hale and Iremonger (Sydney, 1997). pp. 79. RRP $16.95 (paper). Geoff Page, Mrs Schnell Arrives in Heaven and Other Light Verse, Polonius Press(Canberra, 1995). pp.53. RRP $16.95 (paper). Doris Brett, In the Constellation of the Crab, Hale and Iremonger (Melbourne, 1996). pp. 64. RRP $16.95 (paper). Alan Gould, Mermaid, William Heinemann (Melbourne, 1996). pp.77. RRP $16.95 (paper). [Book review]
    Hollier, Nathan
    2017
    academicJournal
    Wie komme ich dran?
  8. Detailansicht für Treffer 88 öffnen
    Controlling Cu–Sn mixing so as to enable higher critical current densities in RRP ® Nb 3 Sn wires
    Sanabria, Charlie ; Field, Michael ; et al.
    In: Superconductor Science and Technology ; volume 31, issue 6, page 064001 ; ISSN 0953-2048 1361-6668, 2018
    Online academicJournal
    Zugriff:
    Volltext
    Wie komme ich dran?
  9. Detailansicht für Treffer 89 öffnen
    Effect of subelement spacing in RRP Nb3Sn strands
    Barzi, E. ; Turrioni, D. ; et al.
    2022
    unknown
    Wie komme ich dran?
  10. Detailansicht für Treffer 90 öffnen
    Development and test of Nb3Sn cos-theta magnets based on RRP and PIT strands
    Feher, S. ; Ambrosio, G. ; et al.
    2022
    unknown
    Wie komme ich dran?
  11. Detailansicht für Treffer 91 öffnen
    Performance of Nb3Sn RRP strands and cables based on a 108/127 stack design
    Barzi, E. ; Ambrosio, G. ; et al.
    2022
    unknown
    Wie komme ich dran?
  12. Detailansicht für Treffer 92 öffnen
    Jacques Derrida, Points.: Interviews 1974 - 1994, ed. Elisabeth Weber, trans. Peggy Kamuf and others. (Meridian: Crossing Aesthetics) Stanford University Press (Stanford, California, 1995). pp. xii + 499. RRP $35.00 (paper). [Book review]
    Johnson, Andrew
    2017
    academicJournal
    Wie komme ich dran?
  13. Detailansicht für Treffer 93 öffnen
    Maurice Blanchot, The Work of Fire. trans. Charlotte Mandell. (Meridian Crossing Aesthetics.) Stanford: Stanford University Press, 1995. pp. xii + 344. RRP $32.50. [Book Review]
    Madder, Clive
    2017
    academicJournal
    Wie komme ich dran?
  14. Detailansicht für Treffer 94 öffnen
    C.W.E. Bigsby, Modern American Drama: 1945-1990, Cambridge and New York: Cambridge University Press, 1992, pb rpt 1995. pp. ix + 362. RRP $37.50. [Book Review]
    Pulford, Donald
    2017
    academicJournal
    Wie komme ich dran?
  15. Detailansicht für Treffer 95 öffnen
    G.J. Barker-Benfield, The Culture of Sensibility: Sex and Society in Eighteenth-Century Britain. Chicago and London: The University of Chicago Press, 1992, pb rpt 1995, pp. xxxiv + 520 RRP $47.50. [Book Review]
    Rechter, Deborah
    2017
    academicJournal
    Wie komme ich dran?
  16. Detailansicht für Treffer 96 öffnen
    Figure 2—figure supplement 1. Oxytocin receptor antagonist atosiban abolishes the oxytocin-induced effects on glutamatergic synaptic transmission. ; (a and b) Representative traces of evoked EPSCs (a) and postsynaptic currents induced by the application of 0.5 M sucrose solution (b) in glutamatergic autaptic control neurons (Ctrl) and neurons treated with 100 nM atosiban alone (ATO), or with 100 nM atosiban plus 100 nM Oxt (ATO + Oxt) for 1 day (1d) or 3 days (3d). (c–e) Average values of evoked EPSC amplitudes (c), apparent RRP size (d), and Pvr (e). The RRP was measured as the net charge transferred during application of 0.5 M sucrose solution. Pvr was calculated by dividing the charge transferred during the evoked PSC by the charge transferred during sucrose application. (f) Change in EPSC amplitudes during a 10 Hz stimulation train in glutamatergic autaptic control neurons (Ctrl) and neurons treated with 100 nM atosiban alone (ATO), or with 100 nM atosiban plus 100 nM Oxt (ATO + Oxt) for 1 day (1d) or 3 days (3d). Data were normalized to the first response in the respective train (Ctrl, n = 42; ATO 1d, n = 30; ATO+Oxt 1d, n = 38; ATO 3d, n = 37; ATO+Oxt 3d, n = 34). (g) Representative traces of responses to exogenous glutamate (100 μM) in a glutamatergic autaptic control neuron (Ctrl) and neurons treated with 100 nM atosiban alone (ATO), or with 100 nM atosiban plus 100 nM Oxt (ATO + Oxt) for 1 day (1d) or 3 days (3d). (h) Representative traces of mEPSCs in a glutamatergic autaptic control neuron (Ctrl) and neurons treated with 100 nM atosiban alone (ATO), or with 100 nM atosiban plus 100 nM Oxt (ATO + Oxt) for 1 day (1d) or 3 days (3d). (i) Average amplitudes of EPSCs induced by 100 μM glutamate in glutamatergic autaptic control neurons and neurons treated with 100 nM atosiban alone (ATO), or with 100 nM atosiban plus 100 nM Oxt (ATO + Oxt) for 1 day (1d) or 3 days (3d). (j and k) Average mEPSC amplitudes (j) and mEPSC frequencies (k) in glutamatergic autaptic control neurons (Ctrl) and neurons treated with 100 nM atosiban alone (ATO), or with 100 nM atosiban plus 100 nM Oxt (ATO + Oxt) for 1 day (1d) or 3 days (3d). Data are shown as mean ± SEM. Numbers of analyzed cells are indicated in the histogram bars. See also Supplementary file 1.
    2017
    unknown
    Wie komme ich dran?
  17. Detailansicht für Treffer 97 öffnen
    Figure 2—figure supplement 2. Oxytocin affects early stages of glutamatergic neuron develpment. ; (a–b) Representative traces of evoked EPSCs (a) and postsynaptic currents induced by the application of 0.5 M sucrose solution (b) from glutamatergic autaptic control neurons (Ctrl, black) and from glutamatergic autaptic neurons treated with Oxt at 7 day (Oxt 7d, light grey) or 7–9 days (Oxt 7-9d, dark grey). (c–e) Average values of evoked EPSC amplitudes (c), apparent RRP size (d), and Pvr (e). The RRP was measured as the net charge transferred during application of 0.5 M sucrose solution. Pvr was calculated by dividing the charge transferred during the evoked PSC by the charge transferred during sucrose application. (f) Change in EPSC amplitudes during a 10 Hz stimulation train in glutamatergic autaptic control neurons (Ctrl, dark n = 28) glutamatergic autaptic neurons treated with Oxt at 7 day (Oxt 7d, light grey, n = 27) or 7–9 days (Oxt 7-9d, dark grey, n = 30). Data were normalized to the first response in the respective train. (g) Representative traces of EPSCs induced by 100 μM glutamate in a glutamatergic autaptic control neuron (Ctrl, black) and neurons treated with Oxt at 7 day (Oxt 7d, light grey) or 7–9 days (Oxt 7-9d, dark grey). (h) Average amplitudes of EPSCs induced by 100 μM glutamate in glutamatergic autaptic control neurons and neurons and neurons treated with Oxt at 7 day (Oxt 7d) or 7–9 days (Oxt 7-9d). (i) Representative traces of mEPSCs in a glutamatergic autaptic control neuron (Ctrl, black) and neurons treated with Oxt at 7 day (Oxt 7d, light grey) or 7–9 days (Oxt 7-9d, dark grey). (j–k) Average mEPSC amplitudes (J) and mPSC frequencies (K) in glutamatergic autaptic control neurons (Ctrl) and neurons treated with Oxt at 7 day (Oxt 7d) or 7–9 days (Oxt 7-9d). Ctrl, control. Data are shown as mean ± SEM. Numbers of analyzed cells are indicated in the histogram bars. See Supplementary file 1 and 2 for further details.
    2017
    unknown
    Wie komme ich dran?
  18. Detailansicht für Treffer 98 öffnen
    Figure 5. Ca2+-dependence of the RRP vesicle fusion defect in Otof C2C/C2C IHCs. ; (A1) Protocol used to depolarize IHCs from −95 mV to potentials between −65 to +35 mV (top). Examples of Ca2+ currents (ICa) (middle) and corresponding Cm traces (bottom) for P15-P18 Otof C2C/+ and Otof C2C/C2C IHCs after 20 ms of depolarization to −10 mV. (A2) Mean Ca2+ current amplitudes (ICa) (top) and ΔCm (bottom) for P15-P18 Otof C2C/+ and Otof C2C/C2C IHCs after 20 ms of depolarization to potentials between −65 mV to +35 mV. The vertical dashed line indicates the −30 mV voltage point. (A3) Mean ΔCm values plotted against the Ca2+ currents elicited by depolarizing steps to potentials underlying the falling segment of the ICa/Vm curve (−65 mV to −10 mV), corresponding to increasing Ca2+ currents. The vertical dashed line indicates the −30 mV voltage point. The Otof C2C/+ and Otof C2C/C2C ΔCm data were fitted with a power function, yielding an exponent of 0.94 and 0.83, respectively. (B1) Protocol used to depolarize IHCs from −95 mV to −10 mV for voltage steps of different durations from 2 ms to 50 ms (top). Corresponding example Cm traces from P15-P18 Otof C2C/+ and Otof C2C/C2C IHCs (bottom). The example traces for each genotype come from the same patch-clamped IHC. (B2) Kinetics of Ca2+-dependent exocytosis in P15-P18 Otof C2C/+ and Otof C2C/C2C IHCs for voltage steps of 2 ms to 50 ms. Mean ΔCm is plotted against the duration of the depolarization to −10 mV (Δt). The inset shows the detail for Δt values between 2 ms and 10 ms. For the 2 ms and 5 ms depolarizations, five repetitions of the recordings were averaged, to increase the signal-to-noise ratio. The decrease in Ca2+-sensitivity of RRP vesicle fusion was evaluated by fitting the ΔCm versus Δt plots with a line for Δt between 2 and 10 ms in Otof C2C/+ IHCs and for Δt between 2 and 20 ms in Otof C2C/C2C IHCs. The Otof C2C/+ fit was plotted for durations greater than 10 ms, to illustrate the onset of the second component of release corresponding to the initiation of vesicle pool replenishment. (B3) We evaluated the coupling of voltage-gated Ca2+ channels to RRP vesicles, by setting the intracellular EGTA concentration to 5 mM in Otof C2C/+ IHCs (gray, n = 9) and in Otof C2C/C2C IHCs (light blue, n = 10). The data for an intracellular EGTA concentration of 0.5 mM are as in (B2). (C1) Protocol used to depolarize IHCs from −95 mV to −10 mV for 20 ms with different extracellular Ca2+ concentrations (top). Example Cm traces from P15-P18 Otof C2C/+ and Otof C2C/C2C IHCs for different extracellular Ca2+ concentrations (bottom). Each example Cm trace for a given genotype was obtained from a different IHC. (C2) ΔCm values plotted against the Ca2+ currents elicited at different extracellular Ca2+ concentrations ([Ca2+]e) in Otof C2C/+ and Otof C2C/C2C P15-P18 IHCs. Dashed lines show linear fits to the data. Data information: In (A2, B2–B3), data are presented as the mean ± SEM. ***p
    2017
    unknown
    Wie komme ich dran?
  19. Detailansicht für Treffer 99 öffnen
    Figure 5—figure supplement 1. Blocking PI(4,5)P2-degradation to DAG augments recovery of the RRP. ; These experiments measure exocytosis (capacitance changes) induced by sudden intracellular Ca2+ elevations. (a) Ca2+ uncaging (at arrow) stimulates fast and slow components of exocytosis. The response to a second Ca2+ uncaging (Stimulation 2, 100 s after Stimulation 1) is smaller. We reasoned that Ca2+ not only triggers the release of secretory vesicles from chromaffin cells, but also activates PLC, leading to PI(4,5)P2 hydrolysis. To test whether the lack of full recovery after the first stimulation might be due to an induction of PLC activity, we blocked PLC pharmacologically. Top panel: intracellular [Ca2+] (mean) following uncaging (at 0.5 s, see arrow). Bottom panel: average capacitance traces. Black traces are the first stimulation, red traces a second stimulation delivered 100 s later. Shown are mean traces from all measured cells. The inactive analog U73343 of the PLC inhibitor was present in the pipette (concentration 10 μM). (b) Similar experiment, but including the active PLC inhibitor (U73122, 10 μM) in the patch-clamp pipette. (c) The preflash (before uncaging) [Ca2+] (mean ±SEM) was unchanged between experiments performed with the active and the inactive compound (blue and green bars, respectively, a two-tailed Student’s t-test was used to test for differences between means, Stimulation 1: p=0.733; Stimulation 2: p=0.936). (d) Kinetic analysis of capacitance traces was used to identify the Readily-Releasable Pool (RRP) and the Slowly-Releasable Pool (SRP). The fractional recovery of the RRP (mean ±SEM) was significantly augmented by the active PLC-inhibitor (tested by a Student’s t-test p=0.0379 for RRP and p=0.323 for SRP). Number of cells, n = 36 (U73343), n = 36 (U73122). *p
    2017
    unknown
    Wie komme ich dran?
  20. Detailansicht für Treffer 100 öffnen
    Figure 11. A mass action model of synaptic release reproduces Ca2+ sensitivity defects in Otof C2C/C2C IHCs. ; (A) Diagram of the synaptic vesicle pools described by the model: the RRP (red), the recycling pool (violet), the reserve pool (green), and the distant pool (yellow). The process of synaptic exocytosis is governed by four rate constants, for RRP vesicle fusion (k1), replenishment of the RRP from the recycling pool (k2), replenishment of the recycling pool from the reserve pool (k3), and replenishment of the reserve pool from the distant pool (k4). The vesicle numbers indicated for each pool are the results obtained by least-squares fitting to the experimental data for Otof C2C/+ IHCs. (B) Original Ca2+ current (ICa) trace (recorded without the sine wave variation of the holding potential used to determine Cm) elicited by a train of 50 successive 5 ms depolarizations in an Otof C2C/+ IHC (upper panel), and the corresponding integrated charge QCa as a function of time (lower panel). (C) Experimental mean ΔCm data as in Figure 8F, converted into the number of fused vesicles (black and blue circles) during a train of 50 successive 5 ms depolarizations, superimposed onto the best least-squares fits (black and blue lines) of the model for Otof C2C/+ and Otof C2C/C2C IHCs (see Table 1). (D) Corresponding simulation of changes in vesicle numbers for each vesicle pool in Otof C2C/+ and Otof C2C/C2C IHCs.
    2017
    unknown
    Wie komme ich dran?
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