PMC

a Age-adjusted changes in lifestyle and psychosocial factors by degree of housing damage^† in men (n = 679). ^†Degree of housing damage: extensive damage (solid line); partial damage (dashed line); and no damage (dotted line). All factors a) through i), p < .001 by Cochran–Mantel–Haenszel tests for trends adjusted for age. A significant result on this test means that after controlling for age and time of year, the proportion of people who reported a certain factor was different depending on the degree of housing damage. b Age-adjusted changes in lifestyle and psychosocial factors by degree of housing damage^† in women (n = 850). ^†Degree of housing damage: extensive damage (solid line); partial damage (dashed line); and no damage (dotted line). Factors c) through i), p < .001 by Cochran–Mantel–Haenszel tests for trends adjusted for age. A significant result on this test means that after controlling for age and time of year, the proportion of people who reported a certain factor was different depending on the degree of housing damage

Ice sheet model with damage feedback result (see Movie S6 for animated version). (A) Initial ice thickness in BISICLES ice sheet model with initial grounding line (black dotted line). Grounding lines after 100 y model simulation for different model forcings are illustrated in colors corresponding to key in B. Dashed lines are used for no initial damage and solid lines for damage via introduction of crevasses at the location of star in C on both sides of the shear margin, while the red dotted-dashed line corresponds to channelized melting scenario. Black dashed-dotted lines illustrate location of profile in B. (B) Profile showing the geometries and grounding lines locations for different model forcing corresponding to different colors (see key) where dashed lines represent no initial damage, solid lines show runs for damage via introduction of crevasses at the location of the star in C, and the red dotted-dashed line corresponds to a channelized melting scenario. (C) Integrated damage for 25 m/y oceanic melt at grounding line with 20 m enhanced damage. Upper half shows simulation without the local damage enhancement at the grounding line, whereas Lower half shows simulation with damage enhancement at the grounding (at location of star) via introduction of crevasses. (D) Integrated damage for 25 m/y oceanic melt at grounding line with 20 m enhanced channelized melting in the lower shear zone. Gray values represent areas where the ice thickness is 0. (E) Maximum (Max) strain rate for simulation without/with (Upper/Lower half) enhanced damage at the grounding line. (F) Max strain rate for simulation with channelized melting. (G–L) Changes in damage fraction (G and H), thickness (I and J), and velocity (K and L) in 25 m/y melt run without/with 20 m vertically integrated crevasse depths implemented in the shear zone at grounding line (G, I, and K) and without/with channelized melting (H, J, and L), respectively, where negative/positive values represent thinning/thickening/increased values or slowdown/speedup/decreased values due to damage introduction and channelized melting, respectively.

Changes in mitotic phase chromosome compaction during DNA damage response. (A) Mitotic HeLa cell expressing EGFP with the chromatin marked by Hoechst 33342, scale bar equals 3 μm. The line scan selected for pair correlation analysis of EGFP molecular flow with respect to damaged and undamaged chromatin superimposed at position 1 and 2, respectively. DNA damage is induced along the line scan at position 1 by microirradiation and then the chromatin is measured 0–10 min afterward. (B) Intensity profile of free EGFP (green) and DNA (blue) along the line scan at position 1 before DNA damage shows a high-density chromatin region between pixels 10 and 46 to exclude EGFP from this environment. Pair correlation analysis along this line scan reveals this chromatin density region to cause delayed molecular flow (as indicated by double-arc feature). (C) Intensity profile of free EGFP (green) and DNA (blue) along the line scan at position 2 before DNA damage shows a high-density chromatin region between pixels 10 and 50 to exclude EGFP from this environment. Pair correlation analysis along this line scan reveals this chromatin density region to cause delayed molecular flow (as indicated by double-arc feature). (D) The average time delay for EGFP molecular flow inside, outside, and in-between mitotic chromosome before DNA damage (representative data shown in panel B) and how these times are changed after DNA damage (representative data shown in panel E). (E) Intensity profile of free EGFP (green) and DNA (blue) along the line scan at position 1 at 0 min after DNA damage shows the high-density chromatin region between pixels 10 and 46 to no longer exclude EGFP from this environment. Pair correlation analysis along this line scan reveals this chromatin density region to no longer cause delayed molecular flow but instead free diffusion in and out of this environment. (F) Intensity profile of free EGFP (green) and DNA (blue) along the line scan at position 2 at 0 min after DNA damage shows the high-density chromatin region between pixels 10 and 50 to still exclude EGFP from this environment. Pair correlation analysis along this line reveals no change in chromatin accessibility. (G) Intensity profile of free EGFP (green) and DNA (blue) along the line scan at position 1 at 10 min after DNA damage shows the high-density chromatin region between pixels 10 and 46 to again exclude EGFP from this environment. Pair correlation analysis along this line scan reveals this chromatin density region to again cause a delay in molecular flow in and out of this environment. (H) Intensity profile of free EGFP (green) and DNA (blue) along the line scan at position 2 at 10 min after DNA damage shows the high-density chromatin region between pixels 10 and 50 to still exclude EGFP from this environment. Pair correlation analysis along this line reveals no change in chromatin accessibility. To see this figure in color, go online.

(A) Evolution of mitochondrial mass (grey lines) over time subjected to four different damage signals (black line). Line graphs display mean value and standard deviation (shaded regions) of 100 simulations for an initial total mitochondrial mass of 300 normalized to the total mass at time point 0. Parameter values obtained from the optimization were used, in particular, fusion probability = fission probability = 50%, fusion frequency = fission frequency = 5 minutes, biogenesis probability = 22.1%, biogenesis frequency = 28.9 minutes, receptor threshold = 12 minutes, damage threshold = 12.4 minutes, degradation frequency = 5.7 minutes and damage probabilities: 0%, 10%, 30% and 50%. Simulations were performed for a total of 12 hours. Blue region indicates the area in which biogenesis is dominant while red region indicates the area in which degradation is dominant. (B) Schematic representation of the link between the number of healthy and damaged mitochondria with the energetic stress (E_S) of the cell. (C) Schematic representation of the connection between energetic (red line) stress and fission (dark green line) and biogenesis (orange line) probabilities. (D) Line graphs display mean value and standard deviation (shaded regions) of 100 simulations of probabilities of fusion (dark green line), fission (light green line), biogenesis (orange line) and damage signal (black line). Initial values assigned to the model: fusion probability = fission probability = 50%, fusion frequency = fission frequency = 5 minutes, biogenesis probability = 22.1%, biogenesis frequency = 28.9 minutes, receptor threshold = 12 minutes, damage threshold = 12.4 minutes, degradation frequency = 5.7 minutes. All the simulations were performed for a total time of 24 hours. (E) Line graphs display mean value and standard deviation (shaded area) of 100 simulations for an initial mitochondrial mass of 300 of the total mitochondrial mass (grey line) and three mitochondria subpopulations: small mass (orange line), medium mass (blue line) and big mass (green line) subjected to five different damage signals (10% and 20%) every two hours for one hour. The plot represents the evolution of the total mass and of three mitochondrial subpopulations normalized to the total mass at time point 0. Initial values assigned to the model: fusion probability = fission probability = 50%, fusion frequency = fission frequency = 5 minutes, biogenesis probability = 22.1%, biogenesis frequency = 28.9 minutes, receptor threshold = 12 minutes, damage threshold = 12.4 minutes, degradation frequency = 5.7 minutes. All the simulations were performed for a total time of 24 hours. (F) Line graphs display mean value and standard deviation (shaded regions) of 100 simulations of bioenergetics stress (red line). Initial values assigned to the model: fusion probability = fission probability = 50%, fusion frequency = fission frequency = 5 minutes, biogenesis probability = 22.1%, biogenesis frequency = 28.9 minutes, receptor threshold = 12 minutes, damage threshold = 12.4 minutes, degradation frequency = 5.7 minutes. All the simulations were performed for a total time of 24 hours. (G) Same as (D) but with mitochondria subjected to five different damage signals (40%) every two hours for one hour. (H) Same as (E) but with mitochondria subjected to five different damage signals (40%) every two hours for one hour. (I) Same as (F) but with mitochondria subjected to five different damage signals (40%) every two hours for one hour.