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Laser scribing technology is a straightforward technique to fabricate porous graphene, yet only conducted with polymeric precursors. Compared to polymers, molecular engineering of small organic molecules is much easier, which can be used to modify the graphene with tailored performance. Here we report the first employment of a laser to respectively transform small organic molecules, pentacene quinone and tetraazapentacene quinone (TAPQ), into graphene (P‐LIG and N‐LIG) as high‐performance lithium‐ion battery anodes. The TAPQ, as the N‐fused molecular precursor, produces nitrogen‐doped graphene. Both N‐LIG and P‐LIG exhibit significant self‐enhancement of capacity upon cycling; the N‐LIG anode delivers reversible capacities of 5863 mAh g‐1 at 0.2 A g‐1 and retains 1970 mAh g‐1 at 2 A g‐1 after another 500 cycles, which is the best performance for the graphene‐type anode. Kinetics studies and structural characterizations verify that the surface‐ and diffusion‐controlled processes are both progressively optimized, providing extra lithium storage upon cycling. It is also supported by small‐angle X‐ray scattering that the disordering level of micropores is increased upon cycling for N‐LIG, corresponding to the enhancement of microporous level. Our work successfully develops a novel facile approach to fabricating heteroatom‐doped microporous graphene exhibiting high performance and provides new insight into the lithium storage mechanism. [ABSTRACT FROM AUTHOR]

The rising global population and improved living standards have led to an alarming increase in non‐communicable diseases, notably cardiovascular and chronic respiratory diseases, posing a severe threat to human health. Wearable sensing devices, utilizing micro‐sensing technology for real‐time monitoring, have emerged as promising tools for disease prevention. Among various sensing platforms, graphene‐based sensors have shown exceptional performance in the field of micro‐sensing. Laser‐induced graphene (LIG) technology, a cost‐effective and facile method for graphene preparation, has gained particular attention. By converting polymer films directly into patterned graphene materials at ambient temperature and pressure, LIG offers a convenient and environmentally friendly alternative to traditional methods, opening up innovative possibilities for electronic device fabrication. Integrating LIG‐based sensors into health monitoring systems holds the potential to revolutionize health management. To commemorate the tenth anniversary of the discovery of LIG, this work provides a comprehensive overview of LIG's evolution and the progress of LIG‐based sensors. Delving into the diverse sensing mechanisms of LIG‐based sensors, recent research advances in the domain of health monitoring are explored. Furthermore, the opportunities and challenges associated with LIG‐based sensors in health monitoring are briefly discussed. [ABSTRACT FROM AUTHOR]

The molecule of the title compound, C16H22N4S2, has a center of symmetry. The crystal packing is mainly stabilized by van der Waals forces. [ABSTRACT FROM AUTHOR]

The study was conducted between 2018 and 2020. From a cohort of 113 hearing impaired (HI), five non‐DFNB12 probands identified with heterozygous CDH23 variants were subjected to exome analysis. This resolved the etiology of hearing loss (HL) in four South Indian assortative mating families. Six variants, including three novel ones, were identified in four genes: PNPT1 p.(Ala46Gly) and p.(Asn540Ser), MYO15A p.(Leu1485Pro) and p.(Tyr1891Ter), PTPRQ p.(Gln1336Ter), and SLC12A2 p.(Pro988Ser). Compound heterozygous PNPT1 variants were associated with DFNB70 causing prelingual profound sensorineural hearing loss (SNHL), vestibular dysfunction, and unilateral progressive vision loss in one family. In the second family, MYO15A variants in the myosin motor domain, including a novel variant, causing DFNB3, were found to be associated with prelingual profound SNHL. A novel PTPRQ variant was associated with postlingual progressive sensorineural/mixed HL and vestibular dysfunction in the third family with DFNB84A. In the fourth family, the SLC12A2 novel variant was found to segregate with severe‐to‐profound HL causing DFNA78, across three generations. Our results suggest a high level of allelic, genotypic, and phenotypic heterogeneity of HL in these families. This study is the first to report the association of PNPT1, PTPRQ, and SLC12A2 variants with HL in the Indian population. [ABSTRACT FROM AUTHOR]

Abstract: Background: AnWj is a high‐incidence blood group antigen associated with three clinical disorders: lymphoid malignancies, immunologic disorders, and autoimmune hemolytic anemia. The aim of this study was to determine the genetic basis of an inherited AnWj‐negative phenotype. Methods: We identified a consanguineous family with two AnWj‐negative siblings and 4 additional AnWj‐negative individuals without known familial relationship to the index family. We performed exome sequencing in search for rare homozygous variants shared by the two AnWj‐negative siblings of the index family and searched for these variants in the four non‐related AnWj‐negative individuals. Results: Exome sequencing revealed seven candidate genes that showed complete segregation in the index family and for which the two AnWj‐negative siblings were homozygous. However, the four additional non‐related AnWj‐negative subjects were homozygous for only one of these variants, rs114851602 (R320Q) in the SMYD1 gene. Considering the frequency of the minor allele, the chance of randomly finding 4 consecutive such individuals is 2.56 × 10−18. Conclusion: We present genetic and statistical evidence that the R320Q substitution in SMYD1 underlies an inherited form of the AnWj‐negative blood group phenotype. The mechanism by which the mutation leads to this phenotype remains to be determined. [ABSTRACT FROM AUTHOR]

Abstract: In this study, we aimed to investigate the anti‐melanoma effects and the JAK2/STAT3 pathway‐related mechanism of action of atractylenolide I in human melanoma cells. Our results showed that atractylenolide I effectively reduced viability, induced apoptosis and inhibited migration of melanoma cells. Meanwhile, atractylenolide I decreased the protein expression levels of phospho‐JAK2 and phospho‐STAT3, and in turn downregulated the mRNA levels of STAT3‐targeted genes, including Bcl‐xL, MMP‐2 and MMP‐9. Furthermore, the cytotoxic effect of atractylenolide I was attenuated in STAT3‐overactivated A375 cells. These findings indicate that inhibition of JAK2/STAT3 signalling contributes to the anti‐melanoma effects of atractylenolide I. [ABSTRACT FROM AUTHOR]