Optical optimization of double-side-textured monolithic perovskite–silicon tandem solar cells for improved light management

Tandem configuration-containing perovskite and silicon solar cells are promising candidates for realizing a high power conversion efficiency of 30% at reasonable costs. Silicon solar cells with planar front surfaces used in tandem devices cause high optical losses, which significantly affects their efficiency. Moreover, some studies have explored the fabrication of perovskites on textured silicon cells. However, due to improper texturing, light trapping is not ideal in these devices, which reduces the efficiency. In this work, we optimized the pyramid height of textured silicon cells and efficiently characterized them to achieve enhanced light trapping. Two different kinds of perovskites, namely, Cs_0.17FA_0.6Pb(Br_0.17I_0.7)₃ and Cs_0.25FA_0.6Pb(Br_0.20I_0.7)₃ with wide bandgaps were conformally deposited on textured silicon cells, and the performance of these flat and fully textured tandem devices was numerically analyzed. The thickness of each layer in the tandem cell was optimized in a way to ensure a perfect current match between the top perovskite and bottom silicon subcells. The results indicated that the textured tandem configuration enhances light absorption over a broad spectral range due to the optimized pyramid height compared to flat surfaces. Eventually, the photovoltaic parameters of the proposed tandem cell were compared with the already existing structures, and our design supports large values of open circuit voltage (V_oc) = 1.78 V, short circuit current density (J_sc) = 20.09 mA cm⁻², fill factor (FF) = 79.01%, and efficiency (η) = 28.20% compared to other kinds of tandem solar cells.

Tandem configuration-containing perovskite and silicon solar cells are promising candidates for realizing a high power conversion efficiency of 30% at reasonable costs.     

mTORC2 regulates renal tubule sodium uptake by promoting ENaC activity

The epithelial Na⁺ channel (ENaC) is essential for Na⁺ homeostasis, and dysregulation of this channel underlies many forms of hypertension. Recent studies suggest that mTOR regulates phosphorylation and activation of serum/glucocorticoid regulated kinase 1 (SGK1), which is known to inhibit ENaC internalization and degradation; however, it is not clear whether mTOR contributes to the regulation of renal tubule ion transport. Here, we evaluated the effect of selective mTOR inhibitors on kidney tubule Na⁺ and K⁺ transport in WT and Sgk1^–/– mice, as well as in isolated collecting tubules. We found that 2 structurally distinct competitive inhibitors (PP242 and AZD8055), both of which prevent all mTOR-dependent phosphorylation, including that of SGK1, caused substantial natriuresis, but not kaliuresis, in WT mice, which indicates that mTOR preferentially influences ENaC function. PP242 also substantially inhibited Na⁺ currents in isolated perfused cortical collecting tubules. Accordingly, patch clamp studies on cortical tubule apical membranes revealed that mTOR inhibition markedly reduces ENaC activity, but does not alter activity of K⁺ inwardly rectifying channels (ROMK channels). Together, these results demonstrate that mTOR regulates kidney tubule ion handling and suggest that mTOR regulates Na⁺ homeostasis through SGK1-dependent modulation of ENaC activity.     

Hyperresponsiveness of the mucosal barrier in Crohn's disease is not tumor necrosis factor-dependent

BACKGROUND: Crohn's disease (CD) is associated with gut barrier dysfunction. Besides the baseline barrier defect, a subgroup of patients also expresses an intestinal barrier hyperresponsiveness to nonsteroidal anti-inflammatory drugs. We studied whether reducing inflammation and restoring gut barrier dysfunction with anti-tumor necrosis factor (TNF) antibody treatment also antagonizes the permeability increase by oral nonsteroidal anti-inflammatory drug intake in patients with CD. METHODS: Thirty-one healthy control subjects and 25 patients with active CD were studied. The 31 controls performed intestinal permeability testing for Cr-EDTA before (baseline) and after oral intake of indomethacin (50 + 75 mg). Twenty-five patients carried out a baseline and indomethacin-mediated permeability test before infliximab infusion. The patients repeated either the indomethacin test (12/25) or baseline and indomethacin tests (13/25), 1 month after this treatment. Intestinal permeability was studied by measurement of urinary excretion of Cr-EDTA after oral intake. RESULTS: Increased whole gut permeation before treatment (3.16%; interquartile range [IQR], 2.92-5.72) was restored to normal values (2.47%; IQR, 1.97-2.78) by anti-TNF treatment. Indomethacin increased whole gut permeability significantly more in patients with CD (before anti-TNF: 6.50%; IQR, 4.84-10.38; after anti-TNF: 5.50%; IQR, 3.97-10.09) compared with the healthy subjects (4.66%; IQR, 3.51-5.64). Eleven of 25 patients (44%) had an abnormal whole gut permeability response to indomethacin before anti-TNF, and 9 of them remained hyperresponsive after infusion, despite clinical remission. CONCLUSIONS: Although anti-TNF treatment suppresses inflammation and restores gut barrier function in patients with CD, it does not antagonize the barrier hyperresponsiveness to indomethacin. These data support the notion of an underlying intestinal mucosal barrier hyperresponsiveness in a subset of patients with CD, independent of inflammation.     

Correlation between genotype,metabolic data,and clinical presentation in carnitine palmitoyltransferase 2 (CPT2) deficiency

Carnitine palmitoyltransferase 2 (CPT2) deficiency, the most common inherited disease of the mitochondrial long-chain fatty acid (LCFA) oxidation, may result in distinct clinical phenotypes, namely a mild adult muscular form and a severe hepatocardiomuscular disease with an onset in the neonatal period or in infancy. In order to understand the mechanisms underlying the difference in severity between these phenotypes, we analyzed a cohort of 20 CPT2-deficient patients being affected either with the infantile (seven patients) or the adult onset form of the disease (13 patients). Using a combination of direct sequencing and denaturing gradient gel electrophoresis, 13 CPT2 mutations were identified, including five novel ones, namely: 371G>A (R124Q), 437A>C (N146T), 481C>T (R161W), 983A>G (D328G), and 1823G>C (D608H). After updating the spectrum of CPT2 mutations (n=39) and genotypes (n=38) as well as their consequences on CPT2 activity and LCFA oxidation, it appears that both the type and location of CPT2 mutations and one or several additional genetic factors to be identified would modulate the LCFA flux and therefore the severity of the disease.     

Synthesis and Antitubercular Activity Evaluation of Novel Unsymmetrical Cyclohexane‐1,2‐diamine Derivatives

A library of unsymmetrical cyclohexane‐1,2‐diamine derivatives were synthesized and evaluated for their activity against Mycobacterium tuberculosis H37Rv in vitro. Out of the 46 compounds synthesized, eight compounds ( 11h , 13a , 13e , 13f , 14a , 14c , 14d , and 15d ) were found to be active at or below 6.25 µM concentration, with negligible toxicity to human red blood cells at a concentration much higher than the MIC₉₉. Compound 13a was the best active compound showing inhibition at 3.125–6.25 µM, and was found to be non‐hemolytic up to 500 µg/mL concentration.     

Potential of endogenous estrogen receptor beta to influence the selective ER modulator ERbeta complex

The ratio of estrogen receptor beta (ERbeta) to ERalpha can alter the estrogen-like properties of tamoxifen. Transient transfection of ERbeta cDNA into cells can decrease the estrogen-like properties of the ERalpha:tamoxifen complex, whereas an increase in the amount of ERbeta is associated with tamoxifen-resistant breast cancer. We have addressed each of these hypotheses by examining well characterized laboratory models. We determined whether changes in endogenous ERbeta are responsible for the estrogen-like or antiestrogenic properties of tamoxifen or raloxifene in MDA-MB-231 cells transfected with cDNAs for ERalpha or mutants D351G, D351Y. We found that the amount of ERbeta mRNA in separate, stable transfectants of mutant ERalpha cDNA was always < 2% of ERalpha. Since at least a 50:50 mixture of ERalpha:ERbeta is needed to silence the tamoxifen:ERalpha complex, we conclude that insufficient ERbeta mRNA is available for selective ER modulation in stable transfectants of D351G and D351Y ERalpha. Similarly, to test the hypothesis that ERbeta is up-regulated and plays an important role during the development of tamoxifen-stimulated tumor growth, we quantitatively analyzed ERbeta and ERalpha mRNA in tamoxifen-na?ve (MCF-7:E2, ECC1:E2) and tamoxifen-stimulated tumors (MCF-7:TAM, EnCa 101:TAM). We found that ERbeta mRNA levels were not significantly elevated in tamoxifen-stimulated tumors and the ERalpha mRNA remained over 99% out of all ER species for all the tumors tested. The same results were also obtained when mRNA levels of ERbeta and ERalpha in a series of tamoxifen-na?ve and tamoxifen-resistant breast cancer was analyzed. We conclude that endogenous ERbeta may not play a dominant role in the modulation of the tamoxifen ERalpha complex, or in the development of tamoxifen-stimulated resistant tumor growth.     

Does distillery yeast sludge ameliorate moldy feed toxic effects in White Leghorn hens?

Aflatoxin and ochratoxin are important mycotoxins formed by different species of Aspergillus and Penicillium. The purpose of this study was to check the toxic pathological effects of moldy feed in White Leghorn (WLH) hens and to estimate the amelioration by distillery yeast sludge (DYS) against mycotoxins. For this purpose, 100, 40-weeks old WLH hens were procured and kept under standard management conditions. Birds were divided in five equal groups. Birds were kept on moldy feed (ochratoxin A (OTA): 56?μg/kg and aflatoxin B1 (AFB1): 136?μg/kg) mixed with 0, 0.5, 1 and 2% DYS/kg moldy feed. Group A served as control. The birds of the control group were active, with normal feed intake and feathers as compared to moldy feed and in combination with DYS. The attraction toward feed and water, feed intake, body weight gain, egg production (%) and egg weight significantly (p?≤?0.05) decreased in the moldy group as compared to control group. The relative weight of liver, kidney, heart and spleen increased significantly in groups B (moldy feed) and C (moldy feed?+?0.5% DYS) as compared to control group. Total erythrocyte count (TEC), total leukocyte count (TLC), hemoglobin (Hb) and hematocrit lowered significantly in B and C groups. Moldy feed in liver, kidney and spleen produced pathological changes like enlargement, ecchymotic hemorrhages on the surface, vacuolar degeneration, cellular infiltration, congestion, etc. Almost all parameters studied were normal compared to control group with the addition of 2% DYS in moldy feed while 1% DYS partially ameliorated the toxic effects of mycotoxins.     

Diagnostic value of integrin alpha3, beta4, and beta5 gene expression levels for the clinical outcome of tongue squamous cell carcinoma

BACKGROUND: The objective of the current study was to identify biomarkers that reflect the clinical course of squamous cell carcinoma of the tongue (TSCC). METHODS: TSCC tissue samples from 66 patients were subjected to gene expression analysis by real-time polymerase chain reaction. Eleven integrin family genes and 14 genes used for normalization, including housekeeping genes and genes that encode desmosomal, cytoskeletal, and extracellular matrix molecules, were considered. Multivariate statistical analysis was performed on 154 expression ratios of integrin genes with clinical parameters. RESULTS: In principal-component analysis, the first principal component was related to the outcome of death, and the second principal component mainly reflected the tendency for cervical lymph node (LN) metastasis. The former axis consisted of the variance of the integrin beta4 gene (ITGB4) and ITGB5 expression levels, and the latter axis agreed with the expression level of the integrin alpha3 gene (ITGA3). Multivariate logistic regression analysis with cervical LN metastasis as the response variable concordantly identified ITGA3/junction plakoglobin gene (JUP) expression (P=.02) and ITGB5/paxillin gene (PXN) expression (P=.04) as significant factors. Only ITGB4/JUP expression was identified as a significant factor in terms of the outcome of death (P<.00049) by a Cox proportional hazards model. The group with high ITGB4/JUP levels exhibited a significantly high death rate on a Kaplan-Meier curve (P<.0001; Wilcoxon and log-rank tests). CONCLUSIONS: The expression levels of ITGA3, ITGB4, and ITGB5 with functional normalization by desmosomal or cytoskeletal molecule genes were selected as candidate biomarkers for cervical LN metastasis or for the outcome of death in TSCC.