1,721,260 research outputs found
fhaegner/Mak-h-ro: Mak-h-ro ABM v1.0.0
No full textFirst release of the macroeconomic agent-based model Mak-h-ro
NARP augmented mitochondrial dysfunction upon H/RO.
No full text<p>(A) NARP and longer reoxygenation durations augmented H/RO (H: 6 h; RO: 1-4 h)-induced mitochondrial membrane potential (ΔΨm) depolarization. (B) After H/RO with longer reoxygenation duration, mitochondrial reactive oxygen species (mROS) formation increased in both 143B cells and NARP cybrids. NARP augmented mROS formation. (C) After H/RO with longer reoxygenation duration, mitochondrial nitric oxide (mNO) formation increased in both 143B cells and NARP cybrids. NARP augmented the effect of H/RO on mNO formation. (D) Longer reoxygenation durations and NARP augmented cardiolipin depletion. (E) NARP augmented the effect of H/RO on mCa<sup>2+</sup> accumulation. (A′-E′) Quantitative analyses of A-E. Mitochondrial compromised is indicated (#). P-value representing statistically significant differences between NARP cybrids and 143B cells (<i>P</i><0.05) is indicated (*). n=6.</p
Hypoxia/reoxygenation (H/RO) induced apoptotic death in NARP cybrids and 143B cells.
No full text<p>(A) H/RO (H: 6h, RO: 2h) induced apoptosis in NARP cybrids as measured by Annexin V-propidium iodide (PI) staining. (B) H/RO induced cytochrome c release from mitochondria in NARP cybrids and 143B cells as measured by immunocytochemical analysis. Red color: mitochondrial complex II; Green color: cytochrome c. Note that cytochdrome c and complex II co-localized well before H/RO (yellow color). After H/RO, green fluorescent signal was released from mitochondria in NARP cybrids and 143B cells, which suggested that cytochdrome c was released from mitochondria. (C) MTT assay. After H/RO, cell death was noted in NARP cybrids and 143B cells (death ratio: NARP > 143B). (D) Trypan blue exclusion test of cell viability. After H/RO, cell death was noted in NARP cybrids and 143B cells (death ratio: NARP > 143B). *<i>P</i><0.05 as compared with control; <i>n</i>=3.</p
Melatonin significantly improved H/RO-induced retardation of mitochondrial movement in 143B cells and NARP cybrids.
No full text<p>(A, B) Red/green overlay of two consecutive confocal images (Δt = 2min) of 200 nM tetramethylrhodamine methyl ester (TMRM) fluorescence in NARP cybrids and 143B cells in response to H/RO treatment without and with 100 μm melatonin. H/RO (H: 6 h; RO: 2 h) reduced the velocity of mitochondrial movement in both 143B cells and NARP cybrids, so that the percentage of nonmoving mitochondria (overlapping mitochondrial area, in yellow color) to the entire mitochondria were 57 ± 1.4% in 143B cells and 76 ± 1.4% in NARP cybrids as compared to the cells and cybrids, respectively, without H/RO treatment. Adding melatonin 100 μm during H/RO improved mitochondrial movement in both 143B cells and NARP cybrids as compared with the groups without melatonin during H/RO, so that the percentage of nonmoving mitochondria to the all mitochondria was 48 ± 1.2% in 143B cells and 63 ± 2.2% in NARP cybrids. (C) Quantitative analyses of (A). *<i>P</i><0.05. n=6. Mln: melatonin.</p
Effects of melatonin on cell viability in NARP cybrids and 143B cells in response to H/RO.
No full text<p>(A) MTT assay. After H/RO (H: 6h, RO: 2h), apoptotic death was noted in NARP cybrids and 143B cells (death ratio: NARP > 143B) (column 2). Adding melatonin 100μm during H/RO significantly reduced NARP-augmented cell death (column 4). (B) Trypan blue exclusion test of cell viability. Addition of 100 μm melatonin during H/RO treatment reduced the percentage of cell death in both 143B and NARP cells (columns 2 and 4). (C) MTT assay. Administering melatonin 100μm during H<sub>2</sub>O<sub>2</sub> 5 mM-augmented H/RO improved cell survival in both NARP cybrids and 143B cells (column 4 and 5). (D) Trypan blue exclusion test of cell viability. Addition of melatonin during H/RO treatment reduced the percentage of cell death in 143B and NARP cybrids in response to H<sub>2</sub>O<sub>2</sub>-augmented H/RO insults (columns 4 and 5). Each value represents the mean ± S.E. of three independent determinations. P-values representing statistically significant differences between NARP and 143B cells upon H/RO; without melatonin and with melatonin during H/RO (both in the groups with and without secondary H<sub>2</sub>O<sub>2</sub> stress) are indicated (*). Mln: melatonin.</p
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Effects of H/RO (with different hypoxia durations) on mitochondrial functions in NARP cybrids and 143B cells.
No full text<p>(A) After treating 143B cells with H/RO (H: 6, 12, and 18 h; RO: 2 h), no obvious cardiolipin depletion was noted during recording. Mitochondria remained thread-like. (B) Cardiolipin depletion was noted gradually in NARP cybrids receiving H/RO with durations of hypoxia for 12 and 18 h. Mitochondria became swollen and round. (C) In 143B cells, only transient mCa<sup>2+</sup> accumulation was noted (D) Marked and persistent mCa<sup>2+</sup> accumulation was noted in NARP cybrids exposed to H/RO with duration of hypoxia for 18 h. (E) Red/green overlay of two consecutive confocal images (Δt = 2min) of 80 nM nonyl acridine orange (NAO) fluorescence in NARP cybrids and 143B cells upon H/RO with different hypoxia durations. The percentage of nonmoving mitochondria (overlapping mitochondrial area, in yellow color) to total mitochondrial area increased from 45 ± 3.2% to 63 ± 1.4% in 143B cells and 48 ± 5.1% to 77 ± 2.3% in NARP cybrids after the exposure of cells to H/RO with duration of hypoxia for 18 h. P-value representing statistically significant differences between NARP cybrids and 143B cells is indicated (*). (A′-E′) Quantitative analyses of A-E. n=6.</p
Variations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Effects of melatonin on ΔΨm and mROS upon H<sub>2</sub>O<sub>2</sub>-augmented H/RO in 143B cells and NARP cybrids.
No full text<p>(A, B) In both 143B cells and NARP cybrids, ΔΨm depolarization was faster in the group with H<sub>2</sub>O<sub>2</sub> (5mM)-augmented H/RO (H: 6 h; RO: 2 h); NARP augmented this effect. Adding melatonin 100 μm during H<sub>2</sub>O<sub>2</sub>-augmented H/RO effectively protected ΔΨm from depolarization. (C) In 143B cells, more mROS formation was noted in the group of H<sub>2</sub>O<sub>2</sub>-augmented H/RO. Adding melatonin during H<sub>2</sub>O<sub>2</sub>-augmented H/RO effectively suppressed mROS formation. (D) In NARP cybrids, mROS formation was augmented as compared with 143B cells. Adding melatonin during H<sub>2</sub>O<sub>2</sub>-augmented H/RO still effectively suppressed mROS formation. (A′-D′) Quantitative analyses of A-D. n=6. FI: fluorescence intensity. Mln : melatonin.</p
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