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Two-dimensional (2D) covalent organic framework (COF) membranes featuring well-aligned and programmable vertical nanochannels have emerged as a promising candidate for advanced nanofluidic devices and showcased vast potential in the fields of smart-gating, ion-separation, and energy-harvesting. However, the transverse interlayer nanochannels with a height of sub-nanometer-scale in 2D-COF membranes have scarcely been studied in comparison. Here, we report the ion transport characteristics in 2D interlayer nanochannels of protonated COF membranes. The distinct surface-charge-governed ionic conductance in domination of electrolyte concentration below 10−3 M as well as the exceptional anion/cation (Cl−/K+) selectivity is revealed due to the pronounced charge and nano-confinement effects. Additionally, evident ion current rectification is witnessed when incorporating asymmetric geometry into the system, which is attributed to the dynamic process of ion enrichment and dissipation within the protonated nanochannels. This work offers immense prospects for 2D-COF membranes in the fields of biomimetic nanofluidic devices and cutting-edge electronic devices. [ABSTRACT FROM AUTHOR]

Objective: This study focused on casual sex motivation to explore why some users tend to have more sexual partners and are more likely to take risks in sexual practices, thereby raising their chances of contracting sexually transmitted infections (STIs). Methods: We recruited Chinese heterosexual dating app users (N = 582) online to investigate the serial mediation model. Results: Casual sex motivation for dating app use was not directly related to the diagnoses of STIs. Number of sexual partners and frequency of risky sexual behavior serially mediated the relationship between casual sex motivation and STI diagnoses. Conclusions: Using dating apps for casual sex motivation is not necessarily associated with higher incidences of STIs, provided that users do not engage in risky sexual practices. [ABSTRACT FROM AUTHOR]

The development and repair of dentin are strictly regulated by hundreds of genes. Abnormal dentin development is directly caused by gene mutations and dysregulation. Understanding and mastering this signal network is of great significance to the study of tooth development, tissue regeneration, aging, and repair and the treatment of dental diseases. It is necessary to understand the formation and repair mechanism of dentin in order to better treat the dentin lesions caused by various abnormal properties, whether it is to explore the reasons for the formation of dentin defects or to develop clinical drugs to strengthen the method of repairing dentin. Molecular biology of genes related to dentin development and repair are the most important basis for future research. [ABSTRACT FROM AUTHOR]

Acute kidney injury (AKI) and chronic kidney disease (CKD) are posing great threats to global health within this century. Studies have suggested that estrogen and estrogen receptors (ERs) play important roles in many physiological processes in the kidney. For instance, they are crucial in maintaining mitochondrial homeostasis and modulating endothelin-1 (ET-1) system in the kidney. Estrogen takes part in the kidney repair and regeneration via its receptors. Estrogen also participates in the regulation of phosphorus homeostasis via its receptors in the proximal tubule. The ERα polymorphisms have been associated with the susceptibilities and outcomes of several renal diseases. As a consequence, the altered or dysregulated estrogen/ERs signaling pathways may contribute to a variety of kidney diseases, including various causes-induced AKI, diabetic kidney disease (DKD), lupus nephritis (LN), IgA nephropathy (IgAN), CKD complications, etc. Experimental and clinical studies have shown that targeting estrogen/ERs signaling pathways might have protective effects against certain renal disorders. However, many unsolved problems still exist in knowledge regarding the roles of estrogen and ERs in distinct kidney diseases. Further research is needed to shed light on this area and to enable the discovery of pathway-specific therapies for kidney diseases. [ABSTRACT FROM AUTHOR]

Accumulative studies showed that tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) was up-regulated in the blood and urine from patients diagnosed with lupus nephritis (LN) and that it might be used as a novel biomarker for active LN. This meta-analysis aimed to determine the diagnostic value of TWEAK in active LN. We searched the Cochrane Library, Embase, PubMed, Springer, Wanfang and CNKI databases for articles published up to 20 August 2020. The diagnostic capacity of TWEAK for active LN was assessed using pooled sensitivity and specificity, positive and negative likelihood ratios (PLR and NLR), diagnostic odds ratio (DOR), and area under the receiver operating characteristic curve (AUC). Quality assessment and publication bias were also evaluated. STATA 11.0 and Meta-Disc 1.4 were used to perform these analyses. Nine cross-sectional studies were included in this meta-analysis. The overall pooled sensitivity of TWEAK for the diagnosis of active LN was 0.69 (95% CI, 0.63–0.75), and specificity was 0.77 (95% CI, 0.71–0.82). The overall pooled PLR and NLR were 3.31 (95% CI, 2.05–5.35) and 0.38 (95% CI, 0.26–0.55), respectively, with a DOR of 10.89 (95% CI, 6.73–17.63) and AUC (SE) of 0.8276 (0.0289). Deeks' funnel plot revealed that the publication bias was insignificant in the study (p =.32). Our results suggest that TWEAK might be a potential biomarker for patients with active LN. Future cross-sectional and longitudinal studies are needed to confirm its diagnostic value, as well as to establish more definite cutoff for active LN. [ABSTRACT FROM AUTHOR]

The NOVA (neuro-oncological ventral antigen) protein family, composed of two paralogs, NOVA1 and NOVA2, consists of RNA-binding proteins involving in processes such as alternative splicing and transport of some target mRNAs. The function of NOVA has been well studied, and increasing evidence has shown that NOVA proteins may be important contributors to carcinogenesis. However, the molecular mechanisms underlying the roles of NOVA proteins in carcinogenesis remain to be determined. Here, we have identified both NOVA1 and NOVA2 as novel β-catenin RNA-binding proteins. The NOVA1/NOVA2 heterodimer positively regulates β-catenin expression by enhancing β-catenin mRNA stability. Furthermore, we demonstrated that NOVA1 and NOVA2 promote epithelial-mesenchymal transition via β-catenin in breast cancer cells, as NOVA-induced upregulation of epithelial and mesenchymal marker expression was attenuated by restoring β-catenin expression. Our results advance the current understanding of β-catenin post-transcriptional regulation and shed light on the role of NOVA proteins in cancer, suggesting that NOVA proteins are potential therapeutic targets in breast cancer. [ABSTRACT FROM AUTHOR]

N6-methyladenosine (m6A) is considered as a reversible RNA modification occurring more frequently on the GAC than AAC context in vivo, which regulates post-transcriptional gene expression in mammalian cells. m6A 'writers' METTL3 and METTL14 demonstrate a strong preference for binding AC-containing motifs in living cells. However, this evidence is currently lacking for m6A erasers, leaving the dynamics of the internal m6A modification under debate recently. We analysed three recently published FTO CLIP-seq data sets and two generated in this study, one of the two known m6A 'erasers'. FTO binding peaks from all cell lines contain RRACH motifs. Only those from K562, 3T3-L1and HeLa cells were enriched in AC-containing motifs, while those from HEK293 were not. The exogenously overexpressed FTO effectively binds to m6A motif-containing RNA sites. FTO overexpression specifically removed m6A modification from GGACU and RRACU motifs in a concentration-dependent manner. These findings underline the dynamics of FTO in target selection, which is predicted to contribute to both the m6A dynamics and the FTO plasticity in biological functions and diseases. [ABSTRACT FROM AUTHOR]