Two-Dimensional SnS: A Phosphorene Analogue with Strong In-Plane Electronic Anisotropy

We study the anisotropic electronic properties of two-dimensional (2D) SnS, an analogue of phosphorene, grown by physical vapor transport. With transmission electron microscopy and polarized Raman spectroscopy, we identify the zigzag and armchair directions of the as-grown 2D crystals. The 2D SnS field-effect transistors with a cross-Hall-bar structure are fabricated. They show heavily hole-doped (∼1019 cm–3) conductivity with strong in-plane anisotropy. At room temperature, the mobility along the zigzag direction exceeds 20 cm2 V–1 s–1, which can be up to 1.7 times that in the armchair direction. This strong anisotropy is then explained by the effective mass ratio along the two directions and agrees well with previous theoretical predictions. Temperature-dependent carrier density determined the acceptor energy level to be ∼45 meV above the valence band maximum. This value matches a calculated defect level of 42 meV for Sn vacancies, indicating that Sn deficiency is the main cause of the p-type conductivity

Azepine-Embedded Seco-Hexabenzocoronene-Based Helix Nanographenes: Access to Modification of the Core by N–H Functionalization

Contorted polycyclic aromatic hydrocarbons (PAHs) or nanographenes (NGs) have received increasing attention and are mostly prepared by “bottom-up” strategies. Apparently, systematically tuning the properties of NGs for application is important but challenging. Here, a new type of helix, azepine-embedded NGs, were designed and synthesized by the introduction of NH into the hexa-peri-hexabenzocoronene (HBC) core. We demonstrate that this nitrogen-doped NG can be functionalized via N–H derivatization. Through modifications to the NH site with a chiral auxiliary reagent, optical resolution of the chiral NG was achieved. Meanwhile, it was found that by introducing various aryl groups with electron-donating or electron-withdrawing substituents, the emission intensity and the fluorescence mechanism can be modulated. Compared to the original NH-containing NG, the modified derivative exhibited improved fluorescence efficiency and tunable emission wavelength. A functionalized structure of benzoic acid with considerably improved fluorescence efficiency, hydrophilicity, and membrane permeability to stain the live cells was proved

Surface-Functionalized Coating for Lithium-Rich Cathode Material To Achieve Ultra-High Rate and Excellent Cycle Performance

Although the lithium-rich cathode material Li1.2Mn0.54Ni0.13Co0.13O2, as a promising cathode material, has a high specific capacity, it suffers from capacity decay and discharge voltage decay during cycling. In this work, the specific capacity and discharge voltage of Li1.2Mn0.54Ni0.13Co0.13O2 are stabilized by surface-functionalized LiCeO2 coating. We have conducted LiCeO2 coating via a mild synchronous lithium strategy to protect the electrode surface from electrolyte attack. This optimized LiCeO2 coating has high Li+ conductivity and abundant oxygen vacancies. The results demonstrate that 3% LiCeO2-coated Li1.2Mn0.54Ni0.13Co0.13O2 exhibits the highest capacity retention rate at 1, 2, and 5 C after 200 cycles, which were 84.3%, 85.4%, and 86.3%, respectively. The discharge specific capacity was almost 1.3, 1.4, and 1.4 times that of the pristine electrode. In addition, the 3% LiCeO2 electrode exhibited the least voltage decay of 0.409, 0.497, and 0.494 V at 1, 2, and 5 C, which was only about half of the pristine electrode. It should not be overlooked that the 3% LiCeO2 electrode still exhibits a high capacity at high current densities of 1250 mA g–1 (5 C) and 2500 mA g–1 (10 C), and its specific discharge capacities are 190.5 and 160.6 mAh g–1, respectively. These outstanding electrochemical properties benefit from surface-functionalized LiCeO2 coatings. To better understand the mechanism of oxygen loss of lithium-rich materials, we propose the lattice oxygen migration path of the LiCeO2-coated electrodes during the cycle. Our research provides a possible solution to the poor rate capability and cycle performance of cathode materials through surface-functionalized coatings

DataSheet1_Novel Partial Exon 51 Deletion in the Duchenne Muscular Dystrophy Gene Identified via Whole Exome Sequencing and Long-Read Whole-Genome Sequencing.ZIP

Duchenne muscular dystrophy (DMD), one of the most common progressive and severely disabling neuromuscular diseases in children, can be largely attributed to the loss of function of the DMD gene on chromosome Xp21.2-p21.1. This paper describes the case of a 10-year-old boy diagnosed with DMD. Whole exome sequencing confirmed the hypothesized large partial exonic deletion of c.7310-11543_7359del (chrX:g.31792260_31803852del) spanning exon 51 and intron 50 in DMD. This large deletion was verified to be de novo by PCR, and the two breakpoints were further confirmed by Sanger sequencing and long-read whole-genome sequencing. Notably, this partial exonic deletion was the only complex variation in the deep intron regions or intron–exon junction regions in DMD. In addition, the case study demonstrates the clinical importance of using multiple molecular genetic testing methods for the diagnosis of rare diseases.</p

Additional file 1 of Menin orchestrates hepatic glucose and fatty acid uptake via deploying the cellular translocation of SIRT1 and PPARγ

Additional file 1: Table S1. Key resources used in the study. Table S2. The primer information designed for mRNA expressing detection in the liver tissues of dairy cows. Table S3. The primers information used for Menin-ChIP and/or SIRT1-ChIP assays in the mouse hepatocytes, designed in the promoter region of PPARγ targeted genes. Table S4. The primers information used for Menin-ChIP assays in the liver tissues of dairy cows, designed in the promoter region of PPARγ target genes

DataSheet1_Case Report: A Novel Homozygous Mutation in MYF5 Due to Paternal Uniparental Isodisomy of Chromosome 12 in a Case of External Ophthalmoplegia With Rib and Vertebral Anomalies.zip

External ophthalmoplegia with rib and vertebral anomalies (EORVA) is characterized by congenital nonprogressive external ophthalmoplegia, ptosis, scoliosis, torticollis, vertebral, and rib anomalies, caused by homozygous mutations in the myogenic factor 5 gene (MYF5) located on chromosome 12q21.31. Uniparental disomy (UPD) is a rare inheritance of a pair of chromosomes originating from only one parent. This study describes a case of an 8-year-old boy with ptosis, scoliosis, and dysmorphic hypoplastic ribs with fusion anomalies. Trio-based exome sequencing (trio-ES) identified a novel homozygous mutation c.191delC (p.Ala64Valfs*33) in MYF5 in the proband, with the father being heterozygous and the mother wild-type, as verified by Sanger sequencing. UPD identified from trio-ES variant call format data suggested the possibility of paternal UPD of chromosome 12 (UPD12pat) in the proband, further confirmed to be a complete isodisomy type of UPD by genome-wide single nucleotide polymorphism array. MYF5 was significantly downregulated by 69.14% (**p < 0.01) in HeLa cells transfected with mutant MYF5 containing c.191delC compared to those transfected with the wild-type MYF5, resulting in a truncated protein with a size of ∼20 kDa. In conclusion, this study identified a novel homozygous mutation in MYF5, broadening the genetic spectrum of EORVA and further deepening the understanding of this rare disease.</p

Additional file 2 of PKM2/STAT1-mediated PD-L1 upregulation on neutrophils during sepsis promotes neutrophil organ accumulation by serving an anti-apoptotic role

Additional file 2

Additional file 1 of PKM2/STAT1-mediated PD-L1 upregulation on neutrophils during sepsis promotes neutrophil organ accumulation by serving an anti-apoptotic role

Additional file 1: Supplementary Figure 1. Purity of isolated peripheral blood neutrophils, verified by measurement of CD11b, CD16 and CD66b expression through cytometry. Supplementary Figure 2A. Gating strategy for human peripheral blood neutrophils. Supplementary Figure 2B. Gating strategy for dHL-60s

Transcriptome provides insights into bovine mammary regulatory mechanisms during the lactation cycle

The molecular events underlying the lactation curve of dairy animals have long been a biological conundrum for mammary biologists, and a cause of a considerable loss of income for dairy farmers. To better understand the regulatory mechanisms and developmental processes of the mammary gland during the lactation cycle, whole-genome transcriptome profiles of bovine mammary tissues at five different lactation stages were investigated using the RNA-Seq technique. The differentially expressed genes were identified by comparing different lactation stage combinations. Gene expression changes were validated using quantitative reverse-transcription polymerase chain reaction. Some differentially expressed genes were found to locate in the known quantitative trait loci regions that are associated with multiple milk production traits. Proteins of potentially important genes were confirmed to be expressed in the mammary epithelium of dairy cows. An integrated analysis of differential gene expression indicated that internal development regularities underlying the shape of the milk production curve. First, the mammary gland is enriched in similar activities during lactation onset and involution, but in opposite regulatory directions. Second, the lactation stages before and after the milk peak shared similar biological processes that were mainly involved in extracellular matrix remodelling. The discoveries of the study provide information necessary to improve milk production.</p

Additional file 2 of Menin orchestrates hepatic glucose and fatty acid uptake via deploying the cellular translocation of SIRT1 and PPARγ

Additional file 2: Figure S1. Menin was abundently expressed in metabolism-associated tissues in cattle. A. Real-time quantitative PCR results of MEN1 gene in different tissues of calves. The same data with the same letter is not significantly different (P > 0.05), and the different letters are the same (P  0.05), and the different letters with the top is significant (P < 0.05). C. Immunohistochemical staining of Menin in different tissues of calves. The letters A, B, C, D, E and F at lower right corners represents the immunity histochemical staining results from liver, kidney, pancreas, testis, duodenal mucosa and duodenal muscle layer, respectively. Figure S2. Liver-specific fatty acid transporter Fabp1 in hepatocytes was found inhibited upon Menin higher- and/or lower expression. The protein expression of Fabp1 was shown to be suppressed in both conditions of Menin over-expression by transfecting Men1 cds clone (mMen1) and Menin low-expression by transfecting Men1 specific siRNA (si-Men1), compared with their negative controls (Vector and control) transfected cells. Figure S3. Menin knockdown induced inflammation in hepatocytes. The expresssion of inflammation promoting factors Il1α and Il1β were detected to be enhanced in Menin-specific siRNA (si-Men1) treated mouse hepatocytes (NCTC-1469) at 24 h after transfection, compared with that of nonspecific negative control siRNA (Ctrl) treated cells. Figure S4. Optimization of treatment conditions for fatty liver cell model induction using sodium oleate (OA). A. The viability of NCTC-1469 cells was measured under different concentrations of OA, indicating that 0.25 mM OA was the optimum condition; B. Upon treatment of NCTC-1469 cells with 0.25 mM OA for 24 h, 48 h and 72 h, the accumulate TAG (triglyceride) in cells was significantly increased, with lipid droplets appearance. Figure S5. Menin expression was elevated in fatty liver tissues of dairy cows, compared with that in normal livers. A. WB results of Menin protein expression in biopsied normal (Norm) and fatty liver (FL) tissues from different prenatal dairy cows. B. Quantitative results of WB results indicated Menin expression was elevated in biopsied fatty liver tissues. Figure S6. OA induction, producing a fatty cell model, activates insuling pathway and Akt, but inhibites the activity of Ampk, Pparγ and Gsk3β, enhancing fatty acid uptake and adopogenesis, but suppressing glucose uptake and glugluconeogenesis. A. Representative WB results of key mediator factors insulin receptor (activated Irs1 being phosphorylated at S307, and its total protein), Akt (activated Akt being phosphorylated at S437, and its total protein), Ampk (activated Ampk being phosphorylated at T172, and its total protein), Pparγ (activated Pparγ being phosphorylated at S273, and its total protein) and Gsk3β (activated Gsk3β being phosphorylated at T216, and its total protein), upon OA induction in hepatocytes. B. Quantitative results of WB results obtained from OA treated whole cell extracts, indicating that enhanced activity of Irs1, Akt, but inhibited activity of Ampk and Pparγ and/or Gsk3β. C. Representative WB results of down-stream factors involved in Ppar signaling pathway upon OA treatment in hepatocytes, showing increased fatty acid receptor Cd36, but inhibited rate-limit enzyme of glucose uptake Gk and gluconeogenesis Pck, Gsk3β. D. Quantitative results of WB results from OA treated whole cell extracts, indicating that OA induction facilitates fatty acid uptake (Cd36) and lipid synthesis, whileas suppresses gucose uptake (Gk) and glugluconeogenesis (Pck)