Formation of in-volume nanogratings with sub-100 nm periods in glass by femtosecond laser irradiation

We present direct experimental observation of the morphological evolution during the formation of nanogratings with sub-100-nm periods with the increasing number of pulses. Theoretical simulation shows that the constructive interference of the scattering light from original nanoplanes will create an intensity maximum located between the two adjacent nanoplanes, resulting in shortening of the nanograting period by half. The proposed mechanism enables explaining the formation of nanogratings with periods beyond that predicted by the nanoplasmonic model.Comment: 4 pages, 3 figure

Case report: identification of one frameshift variant and two in cis non-canonical splice variants of NEB gene in prenatal arthrogryposis

NEB mutation is associated with congenital nemaline myopathies. Here, we report a family with recurrent prenatal arthrogryposis. Trio whole exome sequencing (WES) disclosed three novel NEB (NM_001271208.2) variants including one paternal frameshift c.19049_19050delCA (p.Thr6350Argfs*14) and two double maternal variants in cis c. [24871G>T;24871-10C>G] (p. [Val8291Phe;?]). They are evaluated as “likely pathogenic (LP)”, “variant of uncertain of significance (VUS)”, and “VUS”, respectively. After further prediction, the c.24871G>T, c.24871-10C>G, and c.[24871G>T;24871-10C>G] were respectively genetically engineered into the three plasmids. Compared with their wild-type counterparts, the three plasmids all produced truncated transcripts, and also a significant proportion of the full-length transcripts, which allowed us to reclassify NEB c.24871G>T and c.24871-10C>G variants as LP. As far as we know, this is the first case carrying NEB allele-specific function of partial loss. This result helped the couple make informed reproductive choices and opt for assisted reproduction for future pregnancies. This study also increased awareness to the phenotype of prenatal nemaline myopathy and expanded the variant spectrum of NEB

Cytoprotective Effects of Cell-Permeable Bifunctional Antioxidant Enzyme, GST-TAT-SOD, against Cisplatin-Induced Cell Damage

GST-TAT-SOD, a cell-permeable bifunctional antioxidant enzyme, is a potential selective radioprotector. This study aimed to investigate the cytoprotective activity of GST-TAT-SOD against cisplatin-induced damage. The current study showed that cisplatin induced the formation of reactive oxygen species in normal L-02 cells. GST-TAT-SOD (2000 U/mL) executed its antioxidant role by directly scavenging excess intracellular free radicals and augmenting cellular antioxidant defense such as reducing MDA level, enhancing the SOD activity, GST activity, and T-AOC. Thus, it suppressed the growth inhibition and apoptosis of cisplatin-treated normal cells. Meanwhile, the growth inhibition of tumor cells (SMMC-7721) caused by cisplatin was unaffected by GST-TAT-SOD pretreatment. GST-SOD, as a comparison, seemed to be powerless for related indicators as it could not enter into cells without cell-permeating peptide. These results suggest that GST-TAT-SOD might be a potential cytoprotective agent for cisplatin-induced side effects

Whole-genome sequencing reveals genomic characterization of Listeria monocytogenes from food in China

IntroductionListeria monocytogenes is a foodborne bacterium that could persist in food and food processing environments for a long time. Understanding the population structure and genomic characterization of foodborne L. monocytogenes is essential for the prevention and control of listeriosis.MethodsA total of 322 foodborne L. monocytogenes isolates from 13 geographical locations and four food sources in China between 2000 and 2018 were selected for whole-genome sequencing.ResultsIn silico subtyping divided the 322 isolates into five serogroups, 35 sequence types (STs), 26 clonal complexes (CCs) and four lineages. Serogroup IIa was the most prevalent serogroup and ST9 was the most prevalent ST of foodborne L. monocytogenes strains isolated in China. The in-depth phylogenetic analysis on CC9 revealed that ST122 clone might be original from ST9 clone. Furthermore, 23 potentially relevant clusters were identified by pair-wised whole-genome single nucleotide polymorphism analysis, indicating that persistent- and/or cross-contamination had occurred in markets in China. ST8 and ST121 were the second and third top STs of L. monocytogenes in China, which had heterogeneity with that of L. monocytogenes isolates from other countries. The antibiotic resistance genes aacA4, tetM, tetS, dfrG carried by different mobile elements were found in L. monocytogenes strains. One lineage II strain carrying Listeria Pathogenicity Island 3 was first reported. In addition, a novel type of premature stop codon in inlA gene was identified in this study.DiscussionThese findings revealed the genomic characteristics and evolutionary relationship of foodborne L. monocytogenes in China on a scale larger than previous studies, which further confirmed that whole-genome sequencing analysis would be a helpful tool for routine surveillance and source-tracing investigation

Sestrin2 protects against hypoxic nerve injury by regulating mitophagy through SESN2/AMPK pathway

Hypoxia induced by high altitude can lead to severe neurological dysfunction. Mitophagy is known to play a crucial role in hypoxic nerve injury. However, the regulatory mechanism of mitophagy during this injury remains unclear. Recent studies have highlighted the role of Sestrin2 (SESN2), an evolutionarily conserved stress-inducible protein against acute hypoxia. Our study demonstrated that hypoxia treatment increased SESN2 expression and activated mitophagy in PC12 cells. Furthermore, the knock-out of Sesn2 gene led to a significant increase in mitochondrial membrane potential and ATP concentrations, which protected the PC12 cells from hypoxic injury. Although the AMPK/mTOR pathway was significantly altered under hypoxia, it does not seem to participate in mitophagy regulation. Instead, our data suggest that the mitophagy receptor FUNDC1 plays a vital role in hypoxia-induced mitophagy. Moreover, SESN2 may function through synergistic regulation with other pathways, such as SESN2/AMPK, to mediate cellular adaptation to hypoxia, including the regulation of mitophagy in neuron cells. Therefore, SESN2 plays a critical role in regulating neural cell response to hypoxia. These findings offer valuable insights into the underlying molecular mechanisms governing the regulation of mitophagy under hypoxia and further highlight the potential of SESN2 as a promising therapeutic target for hypoxic nerve injury