Bandgap Engineering and Doping in ZnCdO Thin Films

佐賀大学博士(工学)学位論文(Thesis)doctoral thesi

Temporal and Spatial Variations of Total Electron Content Enhancements During a Geomagnetic Storm on 27 and 28 September 2017

Temporal and spatial evolutions of total electron content (TEC) and electron density in the ionosphere during a geomagnetic storm that occurred on 27 and 28 September 2017 have been investigated using global TEC data obtained from many Global Navigation Satellite System stations together with the ionosonde, geomagnetic field, Jicamarca incoherent scatter and Super Dual Auroral Radar Network (SuperDARN) radar data. Our analysis results show that a clear enhancement of the ratio of the TEC difference (rTEC) first occurs from noon to afternoon at high latitudes within 1 hr after a sudden increase and expansion of the high‐latitude convection and prompt penetration of the electric field to the equator associated with the southward excursion of the interplanetary magnetic field. Approximately 1–2 hr after the onset of the hmF2 increase in the midlatitude and low‐latitude regions associated with the high‐latitude convection enhancement, the rTEC and foF2 values begin to increase and the enhanced rTEC region expands to low latitudes within 1–2 hr. This signature suggests that the ionospheric plasmas in the F2 region move at a higher altitude due to local electric field drift, where the recombination rate is smaller, and that the electron density increases due to additional production at the lower altitude in the sunlit region. Later, another rTEC enhancement related to the equatorial ionization anomaly appears in the equatorial region approximately 1 hr after the prompt penetration of the electric field to the equator and expands to higher latitudes within 3–4 hr.ファイル公開：2021-01-01journal articl

Temporal and Spatial Variations of Total Electron Content Enhancements During a Geomagnetic Storm on 27 and 28 September 2017

Temporal and spatial evolutions of total electron content (TEC) and electron density in the ionosphere during a geomagnetic storm that occurred on 27 and 28 September 2017 have been investigated using global TEC data obtained from many Global Navigation Satellite System stations together with the ionosonde, geomagnetic field, Jicamarca incoherent scatter and Super Dual Auroral Radar Network (SuperDARN) radar data. Our analysis results show that a clear enhancement of the ratio of the TEC difference (rTEC) first occurs from noon to afternoon at high latitudes within 1 hr after a sudden increase and expansion of the high‐latitude convection and prompt penetration of the electric field to the equator associated with the southward excursion of the interplanetary magnetic field. Approximately 1–2 hr after the onset of the hmF2 increase in the midlatitude and low‐latitude regions associated with the high‐latitude convection enhancement, the rTEC and foF2 values begin to increase and the enhanced rTEC region expands to low latitudes within 1–2 hr. This signature suggests that the ionospheric plasmas in the F2 region move at a higher altitude due to local electric field drift, where the recombination rate is smaller, and that the electron density increases due to additional production at the lower altitude in the sunlit region. Later, another rTEC enhancement related to the equatorial ionization anomaly appears in the equatorial region approximately 1 hr after the prompt penetration of the electric field to the equator and expands to higher latitudes within 3–4 hr.ファイル公開：2021-01-01journal articl

Glucose diffusion through microwell scaffolds.

<p>(A)Typical glucose diffusion graphs for thin film and electrospun microwell scaffolds. For the thin film microwell scaffold, the concentration of glucose in the acceptor compartment is represented as a dashed line, because only the last time-point was within analytical range of the Vitros DT60 II chemistry system. (B) Maximum glucose flux through dense and electrospun microwell scaffolds. Data represents mean ± SD (n = 3), **<i>p</i><0.01.</p

Insulin, glucagon and type 2 diabetes susceptibility gene expression in diabetic sorted islet cells.

<p>A: Differential expression of beta cell insulin and alpha cell glucagon in non-diabetic (white bars) compared to diabetic (black bars) islet cells. B: Expression levels of type 2 diabetes susceptibility gene in diabetic alpha cells (white bars) and beta cells (black bars). C: Differential expression of <i>FTO</i> in both cell fractions from non-diabetic (white bars) compared to diabetic (black bars) islet cells. Statistical comparison of diabetic to non-diabetic samples was by unpaired T test assuming unequal variance. n = 16 non-diabetic and 3 diabetic samples.</p

PEOT/PBT wettability and water uptake.

<p>(A) Contact angle measurements of non heat-treated and heat-treated 4000PEOT30PBT70 block copolymer films using the captive bubble method. Data represents mean ± SD of 20 measurements (<i>N</i> = 3 per condition). (B) Water uptake of non-treated and heat-treated 4000PEOT30PBT70 block copolymer films. Data represents mean ± SD, (<i>N</i> = 3 per condition), *<i>p</i><0.05, **<i>p</i><0.01.</p

Beta cell adaptation in islets grafts from different pancreatic regions transplanted in syngeneic diabetic mice.

<p>A. Average islet size per transplant. B. Blood glucose concentrations of STZ-induced diabetic mice followed up to 10 days after transplantation (n = 6–8 mice per region) of DR, GR or SR islets. C. AUC blood glucose concentrations post-transplantation corrected for pre-transplantation glucose concentration (n = 6–8 mice per region). D. Image of proliferating beta-cells, positive for both BrdU (brown) and insulin (red) in islets transplanted under the kidney capsule of diabetic mice. Scale bar = 20 µm. E. Beta cell proliferation in the islet grafts 10 days after transplantation, BrdU labeling during the final 7 days (n = 6–7 mice per region). DR  =  duodenal region, GR  =  gastric region, SR  =  splenic region, AUC  =  area under the curve.</p

Nampt and NMN potentiate glucose stimulated insulin secretion (GSIS) in human islets.

<p>GSIS from human islets cultured on extracellular matrix coated dishes and chronically (<b>A–D</b>) or acutely (E–I) exposed to NMN (100 µM) and Nampt (2.5 ng/ml). (<b>A–D</b>) Islets were chronically exposed to the treatment conditions for 72 h (<b>A,B</b>: 5.5 mM glucose; <b>C,D</b>: 5.5 mM glucose, the mixture of 22.2 mM glucose/0.5 mM palmitate or 2 ng/ml IL-1β/1000 IU IFN-γ), medium was changed and GSIS performed in the absence of the treatment conditions. Basal and stimulated insulin secretion indicate the amount secreted during 1 h incubations at 2.8 (basal) and 16.7 mM (stimulated) glucose following the 72 h culture period and normalized to insulin content. The stimulatory index was calculated (<b>B,D</b>). (<b>E,F</b>) Islets were pre-cultured for 48h and then exposed to 2.8 mM glucose for 1 h (basal), to 2.8 mM glucose including the adipocytokines for 1 h (basal+adipokine) and another subsequent hour to 16.7 mM glucose including the adipocytokines (stim+adipokine). The stimulatory index was calculated (<b>F</b>). (<b>G, H</b>) Islets were pre-cultured for 48 h and then exposed to 2.8 mM glucose for 1 h (basal), to 16.7 mM glucose for 1 h (stimulated) and another subsequent hour to 16.7 mM glucose including the adipocytokines (stim+adipokine). The stimulatory index was calculated (<b>H</b>). (<b>I</b>) Stimulatory index from human islets exposed to 2.8 mM glucose (basal) and subsequently to 1 h exposure to IBMX (100 mM)/Forskolin (10 mM) with or without Nampt or NMN was calculated. Results are means ±SEM from triplicates from three independent experiments from three donors. *p<0.05 to the respective untreated control, ⁺p<0.05 to 2.8 mM basal glucose.</p

Glucose-induced insulin secretion from isolated islets of control and HFD mice.

<p>Insulin secretion was corrected for DNA content. A. Insulin secretion during 2 mM and 20 mM glucose stimulation from islets in the entire pancreas (n = 24). B. Insulin secretion from islets by pancreatic region during incubation in 2 mM glucose buffer (n = 8 per region) and C. 20 mM glucose buffer (n = 8 per region) for control and HFD mice. D. Insulin mRNA expression by pancreatic region, control = 1. DR  =  duodenal region, GR  =  gastric region, SR  =  splenic region, HFD  =  high-fat diet. *<i>p</i><0.05, **<i>p</i><0.01, ***<i>p</i><0.001.</p

Islet function in microwell scaffolds.

<p>(A) Insulin secretory response to glucose stimulation of human islets cultured for 7 days in thin film and electrospun microwell scaffolds. Free-floating islets served as a control. Data represent mean ± SD (n = 3 per condition). (B) Insulin content of human islets cultured in thin film and electrospun microwell scaffold or under free-floating conditions. Data represent mean ± SD (n = 3 per condition).</p