Controlled NiOx Defect Engineering to Harnessing Redox Reactions in Perovskite Photovoltaic Cells via Atomic Layer Deposition.

Albeit the undesirable attributes of NiOx, such as low conductivity, unmanageable defects, and redox reactions occurring at the perovskite/NiOx interface, which impede the progress in inverted perovskite solar cells (i-PSCs), it is the most favorable choice of technology for industrialization of PSCs. In this study, we propose a novel Ni vacancy defect modulate approach to leverage the conformal growth and surface self-limiting reaction characteristics of the atomic layer deposition (ALD)-fabricated NiOx by varying the O2 plasma injection time (tOE) to induce self-doping. Consequently, NiOx thin films with enhanced conductivity, an appropriate Ni3+/Ni2+ ratio, stable surface states, and ultrathinness are realized as hole-transporting layers (HTLs) in p-i-n PSCs. As a result of these improvements, ALD-NiOx-based devices exhibit the highest power conversion efficiency (PCE) of 19.86% and a fill factor (FF) of 81.86%. Notably, the optimal interfacial defects effectively suppressed the severe reaction between the perovskite and NiOx. This suppression is evidenced by the lowest decay rate observed in a harsh environment, lasting for 500 consecutive hours. The proposed approach introduces the possibility of a hierarchical distribution of defects and offers feasibility for the fabrication of large-area, uniform, and high-quality films.

Genomic Basis of Adaptive Divergence in Leg Length between Ground- and Tree-Dwelling Species within a Bird Family.

Hind limbs of tetrapods vary greatly in length and the variability can be associated with locomotor adaptation. Although the phenotypic evolution has been well documented, the underlying genetic basis remains poorly understood. We address this issue by integrating comparative genomics and functional prediction with a study system consisting of ground-dwelling, long-legged and tree-dwelling, short-legged species within the avian family Paridae. Genome-wide divergence and phenotypic correlation analyses jointly identified five highly divergent genomic regions that are significantly related with the difference in leg length between these two groups. Gene annotation for these regions detected three genes involved in skeletal development, that is, PTPA, BRINP1, and MIGA2, with the first one being under the strongest selection. Furthermore, four single nucleotide polymorphisms (SNPs) in the coding region of PTPA can well distinguish the two groups with distinct leg length. Among the four SNPs, one is non-synonymous mutation, and according to the prediction for protein structure and function, it can affect the 3D structure of the encoded protein by altering the corresponding amino acid's position. The alleles of PTPA were found in all sequenced species of the orders Palaeognathae and Psittaciformes, which typically take a ground locomotion style. A whole-genome scanning across bird species uncovered that the four SNPs are more likely to be present in resident passerines with increased leg length/wing length ratios (a proxy of leg-dependent locomotion efficiency). Our findings provide insight into the molecular evolution of locomotion performance based on leg morphology in birds.

An updated review of the new hadron states.

The past decades witnessed the golden era of hadron physics. Many excited open heavy flavor mesons and baryons have been observed since 2017. We shall provide an updated review of the recent experimental and theoretical progresses in this active field. Besides the conventional heavy hadrons, we shall also review the recently observed open heavy flavor tetraquark statesX(2900) andTcc+(3875)as well as the hidden heavy flavor multiquark statesX(6900),Pcs(4459)0,Zcs(3985)-,Zcs(4000)+, andZcs(4220)+. We will also cover the recent progresses on the glueballs and light hybrid mesons, which are the direct manifestations of the non-AbelianSU(3) gauge interaction of the Quantum Chromodynamics in the low-energy region.

The illness perception and health promotion behaviour of young and middle-aged patients with hyperuricaemia: A qualitative study.

AIM: The purpose of this qualitative study was to describe the health-promoting behaviours of patients with hyperuricaemia and influencing factors. DESIGN: A descriptive qualitative design was used to gain insight into the personal experience of health promotion behaviour in patients with hyperuricaemia. METHODS: Sixteen patients were sampled in face-to-face interviews with maximum variation, and the data were transcribed verbatim. The data analysis was based on the phrases of thematic analysis outlined by Braun and Clarke (2006). RESULTS: Four main themes were identified in the data: (a) Perception of disease; (b) Motivation to change health-promoting behaviour; (c) Strategies for health-promoting behaviour; and (d) Encounter obstacles to change health-promoting behaviour.

Multigenerational maternal obesity increases the incidence of HCC in offspring via miR-27a-3p.

BACKGROUND & AIMS: Obesity is an independent risk factor for malignancies, including hepatocellular carcinoma (HCC). However, it remains unknown whether maternal obesity affects the incidence of HCC in offspring. Thus, we aimed to investigate this association and its underlying mechanisms. METHODS: Diethylnitrosamine (DEN) was used to induce HCC in a high-fat diet (HFD)-induced multigenerational obesity model. RNA-sequencing was performed to identify the genes and microRNAs (miRNAs) that were altered over generations. The role of the miR-27a-3p-Acsl1/Aldh2 axis in HCC was evaluated in cell lines and HCC-bearing nude mice, and its intergenerational impact was studied in pregnant mice and their offspring. RESULTS: Under HFD stress, maternal obesity caused susceptibility of offspring to DEN-induced HCC, and such susceptibility was cumulative over generations. We identified that Acsl1 and Aldh2, direct targets of miR-27a-3p, were gradually changed over generations. Under hyperlipidemic conditions, downregulation of Acsl1 and Aldh2 increased cell proliferation (in vitro) or tumor growth (in vivo) in synergy. Intratumor injection of an miR-27a-3p agomir exacerbated tumor growth by downregulating Acsl1 and Aldh2; while intratumor injection of an miR-27a-3p antagomir had the opposite effect. Moreover, serum miR-27a-3p levels gradually increased in the HFD-fed maternal lineage over generations. Injecting pregnant mice with an miR-27a-3p agomir not only upregulated hepatic miR-27a-3p and downregulated Acsl1/Aldh2 in offspring (fetus, young and adult stages), but also exacerbated HCC development in DEN-treated offspring. In human HCC, upregulated miR-27a-3p and downregulated Acsl1/Aldh2 were negatively correlated with survival on TCGA analysis; while, hepatic miR-27a-3p was negatively correlated with Acsl1/Aldh2 expression in tumor/non-tumor tissues from fatty/non-fatty livers. CONCLUSIONS: Maternal obesity plays a role in regulating cumulative susceptibility to HCC development in offspring over multiple generations through the miR-27a-3p-Acsl1/Aldh2 axis. LAY SUMMARY: It is not currently known how maternal obesity affects the incidence of liver cancer in offspring. In this study, we identified a microRNA (miR-27a-3p) that was upregulated in obese mothers and could be passed on to their offspring. This microRNA enhanced the risk of liver cancer in offspring by regulating 2 genes (Acsl1 and Aldh2). This mechanism could be a future therapeutic target.

A review of the open charm and open bottom systems.

Since the discovery of the first charmed meson in 1976, many open-charm and open-bottom hadrons were observed. In 2003 two narrow charm-strange states [Formula: see text] and D s1(2460) were discovered by the BaBar and CLEO Collaborations, respectively. After that, more excited heavy hadrons were reported. In this work, we review the experimental and theoretical progress in this field.

A novel electrochemical sensor based on a molecularly imprinted polymer for the determination of epigallocatechin gallate.

A novel electrochemical sensor based on the molecularly imprinted polymer (MIP) was fabricated by electrochemical polymerization of ß-cyclodextrins (ß-CD) and epigallocatechin-gallate (EGCG) on the graphene oxide (GO) modified glassy carbon (GO/GC) electrode for the first time. The MIP/GO/GC electrode exhibits an excellent ability of specific binding of EGCG and a rapid electrochemical response, high sensitivity and selectivity for determination of EGCG. This prepared MIP sensor presents distinct advantages over conventional electrochemical methods for EGCG determination because it is a one-step preparation and the template molecule can be easily removed by cyclic voltammetry scans, and no elution reagent is required. Under the optimal experimental conditions, the linear response range for EGCG concentrations by the sensor was 3×10-8mol/L to 1×10-5mol/L and the detection limit was 8.78×10-9mol/L(S/N=3). The results demonstrate that the proposed MIP sensor can be a potential alternative for the determination of EGCG in tea samples.

TGF-ß1/FGF-2 signaling mediates the 15-HETE-induced differentiation of adventitial fibroblasts into myofibroblasts.

BACKGROUND: Pulmonary adventitial fibroblasts (PAFs) are activated under stress stimuli leading to their differentiation into myofibroblasts, which is involved in vessel remodeling. 15-HETE is known as an important factor in vessel remodeling under hypoxia; however, the role of 15-HETE in PAF phenotypic alteration is not clear. RESULTS: The effect of 15-HETE on PAF phenotypic alterations was investigated in the present study. PAFs were treated with 15-HETE (0.5 µM) for 24 h, and the myofibroblast marker α-smooth muscle actin (α-SMA) was analyzed. The 15-HETE induced α-SMA expression and cell morphology. 15-HETE upregulated FGF-2 levels in PAFs, and knockdown FGF-2 by siRNAs blocked the enhanced α-SMA expression induced by 15-HETE. p38 kinase was activated, and blocked depressed 15-HETE-induced FGF-2 expression. The downstream of p38 pathway, Egr-1 activation, was also raised by 15-HETE treatment, and silenced Egr-1 suppressed the 15-HETE-induced upregulation of FGF-2. TGF-ß1 was upregulated with FGF-2 treatment, and α-SMA expression induced by FGF-2 was inhibited after the cell was transferred with TGF-ß1 siRNA. Meanwhile, FGF-2 increased α-SMA expression and improved proliferation, which was associated with p27(kip1) and cyclin E variation. CONCLUSIONS: The above results suggest that p38/Egr-1 pathway-mediated FGF-2 is involved in 15-HETE-induced differentiation of PAFs into myofibroblasts and cell proliferation.