Enhancing CZTSSe solar cells through electric field induced ion migration

Solar cells made from Cu 2 ZnSn(S,Se) 4 (CZTS)-derived materials have been widely studied for their favourable material properties utilized in photovoltaic energy conversion. Drawbacks of the materials are associated with low open circuit voltage (V oc) resulting from non-radiative recombination at grain boundaries and interfaces. Considerable work has focused on the incorporation of sodium (Na), which is found to passivate trap states and reduce electronic losses. Here we present evidence that Na + as well as several ionic species (Se 2À and Zn 2+), do not remain stationary after device fabrication, but in fact migrate under electrical biasing. Furthermore, this ionic migration can be manipulated at room temperature by exposing the device to an external electric forming field. We outline a novel procedure that can effectively control and adjust ionic movement and associated local distribution in fully fabricated devices. Our results show that this simple treatment leads to favourable improved device performance and provides insight into light-induced reduction in performance which may be partially reversible

Engineering of Interface and Bulk Properties in Cu2ZnSn(S,Se)4 Thin-Film Solar Cells with Ultrathin CuAlO2 Intermediate Layer and Ge Doping

Recently, kesterite-based absorbers and related compounds have been considered as promising eco-friendly light absorber materials for thin-film solar cells (TFSCs). However, the device performances of kesterite-based TFSCs are limited because of the formation of defects and poor interfacial properties. In this study, we developed a strategic approach to improve the device performances of Cu2ZnSn­(S,Se)4 (CZTSSe) solar cells using back-interface passivation of the absorber layer and further reduced the formation of defects through Ge doping. The application of CuAlO2 (CAO) as an intermediate layer near the back interface efficiently improves the grain growth and minimizes the detrimental Mo­(S,Se)2 thickness. In addition, the Ge nanolayer deposited over the CAO layer improves the absorber bulk quality, effectively suppresses the defect density, and reduces the nonradiative carrier recombination losses. As a result, the short-circuit current density, fill factor, and power conversion efficiency of the champion device with the CAO and Ge nanolayer improved from 31.91 to 36.26 mA/cm2, 0.55 to 0.61, and 8.58 to 11.01%, respectively. This study demonstrates a potential approach to improve the performances of CZTSSe TFSCs using a combination of back-interface passivation and doping

Nanoscale Rear-Interface Passivation in Cu2ZnSn(S,Se)4 Solar Cells through the CuAlO2 Intermediate Layer

The present work demonstrates that the addition of p-type CuAlO2 (CAO) as an intermediate layer between molybdenum (Mo) and the absorber rear interface efficiently improves the Cu2ZnSn(S,Se)4 (CZTSSe) device performance. The efficacy of the intermediate layer is analyzed through sputtering the CAO nanolayer at different deposition times on top of the Mo layer. The addition of an ultrathin CAO nanolayer improved the absorber bulk quality with the formation of compact and larger crystalline grains. Furthermore, the CZTSSe device with an optimum deposition time (154 s) of the CAO nanolayer successfully reduced the Mo(S,Se)2 layer thickness from ∼50 to ∼25 nm. This reduced Mo(S,Se)2 layer thickness results in the reduced series resistance (Rs) in the device providing improvement in the overall device performance. The short-circuit current density (JSC) and the power conversion efficiency of the device with the CAO nanolayer increased from 33.48 to 35.40 mA/cm2 and from 9.61 to 10.54%, respectively, compared to a reference device. © 2021 American Chemical Society.1

Author’s Reply to “Concerns regarding Validity of the Use of Bean Extract-Based Gargle for COVID-19 Diagnosis”

[No abstract available]TRU

Integrative epigenomic and transcriptomic analyses reveal metabolic switching by intermittent fasting in brain

10.1007/s11357-022-00537-zGEROSCIENCE4442171-219

A missense variant in SHARPIN mediates Alzheimer's disease-specific brain damages

Established genetic risk factors for Alzheimer's disease (AD) account for only a portion of AD heritability. The aim of this study was to identify novel associations between genetic variants and AD-specific brain atrophy. We conducted genome-wide association studies for brain magnetic resonance imaging measures of hippocampal volume and entorhinal cortical thickness in 2643 Koreans meeting the clinical criteria for AD (n = 209), mild cognitive impairment (n = 1449) or normal cognition (n = 985). A missense variant, rs77359862 (R274W), in the SHANK-associated RH Domain Interactor (SHARPIN) gene was associated with entorhinal cortical thickness (p = 5.0 × 10-9) and hippocampal volume (p = 5.1 × 10-12). It revealed an increased risk of developing AD in the mediation analyses. This variant was also associated with amyloid-β accumulation (p = 0.03) and measures of memory (p = 1.0 × 10-4) and executive function (p = 0.04). We also found significant association of other SHARPIN variants with hippocampal volume in the Alzheimer's Disease Neuroimaging Initiative (rs3417062, p = 4.1 × 10-6) and AddNeuroMed (rs138412600, p = 5.9 × 10-5) cohorts. Further, molecular dynamics simulations and co-immunoprecipitation indicated that the variant significantly reduced the binding of linear ubiquitination assembly complex proteins, SHPARIN and HOIL-1 Interacting Protein (HOIP), altering the downstream NF-κB signaling pathway. These findings suggest that SHARPIN plays an important role in the pathogenesis of AD

A missense variant in SHARPIN mediates Alzheimer's disease-specific brain damages

Established genetic risk factors for Alzheimer's disease (AD) account for only a portion of AD heritability. The aim of this study was to identify novel associations between genetic variants and AD-specific brain atrophy. We conducted genome-wide association studies for brain magnetic resonance imaging measures of hippocampal volume and entorhinal cortical thickness in 2643 Koreans meeting the clinical criteria for AD (n = 209), mild cognitive impairment (n = 1449) or normal cognition (n = 985). A missense variant, rs77359862 (R274W), in the SHANK-associated RH Domain Interactor (SHARPIN) gene was associated with entorhinal cortical thickness (p = 5.0 x 10(-9)) and hippocampal volume (p = 5.1 x 10(-12)). It revealed an increased risk of developing AD in the mediation analyses. This variant was also associated with amyloid-beta accumulation (p = 0.03) and measures of memory (p = 1.0 x 10(-4)) and executive function (p = 0.04). We also found significant association of other SHARPIN variants with hippocampal volume in the Alzheimer's Disease Neuroimaging Initiative (rs3417062, p = 4.1 x 10(-6)) and AddNeuroMed (rs138412600, p = 5.9 x 10(-5)) cohorts. Further, molecular dynamics simulations and co-immunoprecipitation indicated that the variant significantly reduced the binding of linear ubiquitination assembly complex proteins, SHPARIN and HOIL-1 Interacting Protein (HOIP), altering the downstream NF-kappa B signaling pathway. These findings suggest that SHARPIN plays an important role in the pathogenesis of AD.N