The concurrent photocatalytic synthesis of hydrogen gas and high-valued chemicals over two-dimensional semiconductors is extremely attractive to alleviate global energy and environmental concerns ...through directly using sunlight. Herein, a novel layered In
4/3
P
2
Se
6
nanosheet is synthesized by a space confined chemical vapor conversion method, and it acts as a dual-functional photocatalyst to deliver the co-production of hydrogen gas and
N
-benzylidenebenzylamine from water reduction and selective benzylamine oxidation. The simultaneous yield of hydrogen gas and
N
-benzylidenebenzylamine is 895 μmol g
−1
and 681 μmol g
−1
, respectively, within 16-hour continuous reaction involving a small amount of water in acetonitrile solvent. Moreover, 97.4%
N
-benzylidenebenzylamine selectivity from benzylamine oxidation can be achieved with continuous 10 hour-reaction only in acetonitrile solvent under ambient conditions. Further
in situ
electron paramagnetic resonance measurements and reaction optimization tests reveal that the reaction mechanism strongly relies on the conditions over the In
4/3
P
2
Se
6
nanosheet photocatalyst.
Herein, a novel 2D layered In
4/3
P
2
Se
6
nanosheet was developed as dual-functional photocatalyst for the co-production of H
2
and
N
-benzylidenebenzylamine through water reduction and benzylamine oxidation under light illumination.
The high incidence of metastasis accounts for most of the lethality of ovarian cancer. Invadopodia are small, specialized types of machinery that degrade the extracellular matrix and are thus ...involved in the invasion and metastasis of cancer cells. The formation of invadopodia is regulated by both genetic and epigenetic factors. However, the ways by which methylation/demethylation regulates the dynamics of invadopodia in ovarian cancer are largely unknown. In this study, we found that the inhibition of methylation by 5-AZ (5-Azacytidine) increased the formation of invadopodia and enhanced degradation of the extracellular matrix in ovarian cancer cells. In mouse xenograft models, treatment with 5-AZ increased the number of metastatic nodules, which suggests an elevated potential for metastasis by demethylation. Further investigation indicated that the inhibition of methylation elevated the transcription of PIK3CA and upregulated genes involved in the PI3K-AKT signaling pathway. In addition, this induction likely occurs though the epigenetic regulation of PIK3CA because analyses of the DNA methylation level of the PIK3CA promoter region found that 5-AZ treatment decreased the methylation of CpG islands in SKOV3 and A2780 cells. Our study demonstrated that epigenetic factors regulate the metastatic potential of ovarian cancer cells and provide rationale for therapies that inhibit PI3K- invadopodia-mediated metastasis.
Primary familial brain calcification (PFBC) is a rare calcifying disorder of the brain with extensive clinical and genetic heterogeneity. Its prevalence is underestimated due to clinical selection ...bias (compared with symptomatic PFBC patients, asymptomatic ones are less likely to undergo genetic testing).
A total of 273 PFBC probands were enrolled in a multicenter retrospective cohort study by two different approaches. In Group I (nonsystematic approach), 37 probands diagnosed at our clinic were enrolled. In Group II (systematic approach), 236 probands were enrolled by searching the medical imaging databases of 50 other hospitals using specific keywords. Genetic testing of four genes known to be causative of autosomal dominant PFBC was performed in all probands using cDNA. All identified variants were further confirmed using genomic DNA and classified according to ACMG-AMP recommendations.
Thirty-two variants including 22 novel variants were detected in 37 probands. Among these probands, 83.8% (31/37) were asymptomatic. Two probands with homozygous pathogenic SLC20A2 variants presented more severe brain calcification and symptoms. Based on the variant detection rate of probands in Group II, we extrapolated an overall minimal prevalence of PFBC of 6.6 per 1,000, much higher than previously reported (2.1 per 1000).
We identified a higher proportion of genetically confirmed PFBC probands who were asymptomatic. These patients would be overlooked due to clinical selection bias, leading to underestimation of the disease prevalence. Considering that PFBC patients with biallelic variants had more severe phenotypes, this specific condition should be focused on in genetic counseling.
•A high proportion of asymptomatic PFBC patients remain undiagnosed in the clinic.•We extrapolated an overall minimal disease prevalence of PFBC to 6.6 p. 1000.•Biallelic mutations in SLC20A2 caused severe symptoms and brain calcification.
PDF
