Supplemental Material - Similarity as a safe haven: Similarity leads to satisfaction in prevention focus

Supplemental Material for Similarity as a safe haven: Similarity leads to satisfaction in prevention focus by Jeong Eun Cheon and Young-Hoon Kim in Journal of Social and Personal Relationships</p

Engineering Colloidal Perovskite Nanocrystals and Devices for Efficient and Large-Area Light-Emitting Diodes

ConspectusColloidal metal halide perovskite nanocrystals (PNCs) have high color purity, solution processability, high luminescence efficiency, and facile color tunability in visible wavelengths and therefore show promise as light emitters in next-generation displays. The external quantum efficiency (EQE) of PNC light-emitting diodes (LEDs) has been rapidly increased to reach 24.96% by using colloidal PNCs and 28.9% using on-substrate in situ synthesized PNCs. However, high operating stability and a further increase of EQE in PNC-LEDs have been impeded for three reasons: (1) Colloidal PNCs consist of ionic crystal structures in which ligands bind dynamically and therefore easily agglomerate in colloidal solution and films; (2) Long-alkyl-chain organic ligands that adhere to the PNC surface improve the photoluminescence quantum efficiency and colloidal stability of PNCs in solution but impede charge transport in PNC films and limit their electroluminescence efficiency in LEDs; (3) Unoptimized device structure and nonuniform PNC films limit the charge balance and reduce the device efficiency in PNC-LEDs.In this Account, we summarize strategies to solve the limitations in PNCs and PNC-LEDs as consequences of photoluminescence quantum efficiency in PNCs and the charge-balance factor and out-coupling factor in LEDs, which together determine the EQE of PNC-LEDs. We introduce the fundamental photophysical properties of colloidal PNCs related to effective mass of charge carriers and surface stoichiometry, requirements for PNC surface stabilization, and subsequent research strategies to demonstrate highly efficient colloidal PNCs and PNC-LEDs with high operating stability.First, we present various ligand-engineering strategies that have been used to achieve both efficient carrier injection and radiative recombination in PNC films. In situ ligand engineering reduces ligand length and concentration during synthesis of colloidal PNCs, and it can achieve size-independent high color purity and high luminescent efficiency in PNCs. Postsynthesis ligand engineering such as optimized purification, replacement of organic ligands with inorganic ligands or strongly bound ligands can increase charge transport and coupling between PNC dots in films. The luminescence efficiency of PNCs and PNC-LEDs can be further increased by various postsynthesis ligand-engineering methods or by sequential treatment with different ligands. Second, we present methods to modify the crystal structure in PNCs to have alloy- or core/shell-like structure. Such crystal engineering is performed by the correlation between entropy and enthalpy in PNCs and result in increased carrier confinement (increased radiative recombination) and reduced defects (decreased nonradiative recombination). Third, we present strategies to boost the charge-balance factor and out-coupling factor in PNC-LEDs such as modification of thickness of each layer and insertion of additional interlayers, and out-coupling hemispherical lens are discussed. Finally, we present the advantages, potential, and remaining challenges to be solved to enable use of colloidal PNCs in commercialized industrial displays and solid-state lighting. We hope this Account will help its readers to grasp the progresses and perspectives of colloidal PNCs and PNC-LEDs, and that our insights will guide future research to achieve efficient PNC-LEDs that have high stability and low toxicity

Proteasome inhibitor MG132 extends the ZFN half-life.

<p>After transfection of ZFN-encoding plasmids (<b>A</b> and <b>C</b>, myc-ZFN-224; <b>B</b> and <b>D</b>, HA-K230) into 293T cells and treatment with CHX (200 µg/mL) for different time intervals, the ZFN levels in these cells were analyzed. The duration of CHX treatment is indicated above the blot. Experiments were performed either in the absence or presence of MG132 (5 µM) as indicated on the figure. Each experiment was repeated at least three times.</p

MG132 enhances ZFN function.

<p>(<b>A</b>) Schematic of the surrogate reporters used for quantifying the effect of MG132 on ZFN function. The reporter was constructed by introducing the mRFP gene (in-frame), a ZFN target sequence, and eGFP gene (out-of-frame) into pRGS vector. Frame shift mutations created by non-homologous DNA repair of ZFN-induced breaks can render the eGFP gene in-frame with mRFP, resulting in the expression of a mRFP-eGFP fusion protein. eGFP expression was quantified using flow cytometry. (<b>B</b>) A schematic representation of the experimental procedure: After transfection with the ZFN and reporter plasmids, 293T cells were treated with various concentrations of MG132 and subjected to flow cytometry. (<b>C</b>) Flow cytometry of the cells: MG132 increased the percentage of GFP+RFP+ cells, suggesting that MG132 enhanced ZFN function. Untransfected cells and cells transfected with reporters alone were used as analysis controls. n = 3. *<i>P</i><0.05.</p

Proteasome inhibitor MG132 increases ZFN protein levels.

<p>293T cells were transfected with equal concentrations of ZFN-encoding plasmids (<b>A</b>, myc-ZFN-224; <b>B</b>, HA-K230) and treated with various concentrations of MG132 for 16 hours. The ZFN levels were determined by Western blot. As an internal control, β-actin was used. n = 3. *<i>P</i><0.05, ***<i>P</i><0.001.</p

<i>In vivo</i> ubiquitination of a ZFN.

<p>293T cells were transfected with pcDNA3-myc-ZFN-224 and pEFIRES-HA-ubiquitin separately and together. ZFN ubiquitination was confirmed by co-immunoprecipitation with an anti-myc antibody and immunoblotting with an anti-HA antibody. To cross confirm, co-immunoprecipitation was performed using anti-HA antibody and immunoblotting with an anti-myc antibody. MG132 treatment further increased ZFN ubiquitination, as shown by the increased amounts of the high molecular weight smear, which represents polyubiquitin coupled with the ZFN.</p

Transferrin-mediated increase of labile iron Pool following simulated ischemia causes lipid peroxidation during the early phase of reperfusion

Heart ischemia/reperfusion (I/R) injury is related to iron content. However, the occurrence and mechanism of changes in labile iron pool (LIP) during I/R is debatable. Moreover, the identity of the iron form dominant in LIP during I/R is unclear. Herein, we measured changes of LIP during simulated ischemia (SI) and reperfusion (SR), in which ischemia was simulated in vitro with lactic acidosis and hypoxia. Total LIP did not change in lactic acidosis, whereas LIP, especially Fe3+, increased in hypoxia. Under SI, accompanied by hypoxia with acidosis, both Fe2+ and Fe3+ were significantly increased. Increased total LIP was maintained at 1 h post-SR. However, the Fe2+ and Fe3+ portion was changed. The increased Fe2+ was decreased, and conversely the Fe3+ was increased. BODIPY oxidized signal increased and through the time-course these changes correlated with blebbing of cell membrane and SR-induced LDH release. These data suggested lipid peroxidation occurred via Fenton’s reaction. The experiments using bafilomycin A1 and zinc protoporphyrin suggested no role of ferritinophagy or heme oxidation in the increase of LIP during SI. The extracellular source, transferrin assessed using serum transferrin bound iron (TBI) saturation showed that the depletion of TBI reduced SR-induced cell damages and additive saturation of TBI accelerated SR-induced lipid peroxidation. Furthermore, Apo-Tf dramatically blocked the increase of LIP and SR-induced damages. In conclusion, Tf-mediated iron induces the increase of LIP during SI, and it causes Fenton reaction-mediated lipid peroxidation during the early phase of SR.</p

MG132 increases the frequency of ZFN-driven mutations.

<p>After transfection of plasmids encoding ZFNs (<b>A</b>: ZFN-224; <b>B</b>: K230), 293T cells were treated with various concentrations of MG132. Genomic DNA was isolated and ZFN-driven mutations were analyzed by the T7E1 assay. Arrows indicate the expected positions of DNA bands cleaved by T7E1. (<b>A</b>) ZFN-224: Because the target site lies in the center of the amplicon (780 bp), T7E1 treatment of the heteroduplexed DNA gave rise to two DNA bands with almost same size (387 bp and 389 bp), which appear as a single band. (<b>B</b>) K230: Because the target site does not lie in the center of the ampicon, T7E1 treatment of the heteroduplexed DNA gave rise to two DNA bands (493 bp and 311 bp), observed as two separate bands. The numbers at the bottom of the gel denote mutation percentages calculated by band intensities. n = 3. *<i>P</i><0.05, ***<i>P</i><0.001.</p

Regression coefficients as a function of gender and task framing.

<p>Regression coefficients as a function of gender and task framing.</p

The unskilled and unaware phenomenon.

<p>The unskilled and unaware phenomenon.</p