Search

Taking full advantage of interface engineering to strengthen interface polarization is an effective strategy to improve microwave absorption. Therefore, constructing the mixed-dimensional heterostructures and/or three-dimensional (3D) interconnected network structures should be attractive pathways to create the abundant interfaces for enhanced interfacial effect. Herein, mixed-dimensional framework structure carbon foam (CF)/carbon nanotubes (CNTs)@Fe 3 C@Fe 3 O 4 samples consisting of 3D CF, one-dimensional (1D) CNTs and zero-dimensional (0D) Fe 3 C@Fe 3 O 4 nanoparticles were elaborately designed and produced through a simple catalytic chemical vapor deposition process. The as-prepared CF/CNTs@Fe 3 C@Fe 3 O 4 heterostructures with the different contents of CNTs could be selectively produced by regulating the pyrolysis time. Owing to the unique structure and excellent synergistic effects, the obtained mixed-dimensional CF/CNTs@Fe 3 C@Fe 3 O 4 samples presented the excellent comprehensive electromagnetic wave absorption performances (EMWAPs) including strong absorption capabilities, broad absorption bandwidths, thin matching thicknesses and low densities. Furthermore, the obtained results demonstrated that the enhanced content of CNTs greatly boosted their conduction and polarization loss abilities, which resulted in the enhanced comprehensive EMWAPs. Therefore, our findings not only offered a simple strategy to produce the mixed-dimensional framework structure magnetic CF/CNTs-based heterostructures as excellent lightweight high-efficiency microwave absorbers, but also provided an effective pathway to make the best of interface engineering for enhancing interface polarization. Constructing mixed-dimensional lightweight flexible CF/CNTs@Fe 3 C@Fe 3 O 4 heterostructures: an effective strategy to achieve tunable and boosted microwave absorption. [Display omitted] • Mixed-dimensional framework structure CF/CNTs@Fe 3 C@Fe 3 O 4 heterostructures were produced through a simple process. • The CF/CNTs@Fe 3 C@Fe 3 O 4 with different contents of CNTs were produced by regulating the pyrolysis time. • The enhanced content of CNTs greatly boosted their conduction and polarization loss abilities. • Owing to the abundant interfaces, the designed CF/CNTs@Fe 3 C@Fe 3 O 4 presented the excellent EMWAPs. • Our findings provided an effective pathway to make the best of interface engineering for enhanced interface polarization. [ABSTRACT FROM AUTHOR]

A novel and versatile approach to the preparation of multitype polymers brushes on the quantum dots surface is reported. In this method, an azo initiator is first immobilized covalently onto CdSe/CdS particle surface by reacting with the 4,4′-Azobis (4-cyanovaleric acid) through an ester linkage. CdSe/CdS nanoparticles with polymer brushes (CdSe/CdS-polymers) of different properties, including hydrophilic polyacrylamide, poly(acrylic acid), and poly(vinyl pyrrolidone); hydrophobic oleophilic poly(vinyl acetate), poly(methyl acrylate), and poly(methyl methacrylate); polystyrene with conjugate group; and polyacrylonitrile with strong polarity group, are synthesized by one approach (the surface-initiated radical poly­merization technique), respectively. The structures and properties of CdSe/CdS-polymers reveal that the CdSe/CdS-azo initiator has excellent ability to initiate various kinds of vinyl monomers and these synthetic CdSe/CdS-polymers exhibit good stability and can emit multiple colors from the emission 405 to 569 nm. Moreover, CdSe/CdS-polymers brushes show characteristic micromorphologies. Such strategy provides a platform to achieve nanocomposites with different properties by a new CdSe/CdS-azo initiator through the simple conventional radical polymerization technique. Besides, the synthetic approach gives access to multitype modification of different nanoparticles with polymers. [ABSTRACT FROM AUTHOR]

Aim: To characterize the different phenotypes of GABRB2-related epilepsy and to establish a genotype-phenotype correlation.Method: We used next-generation sequencing to identify GABRB2 variants in 15 patients.Results: Eleven GABRB2 variants were novel and 12 were de novo. The age at the onset of seizures ranged from 1 day to 26 months. Nine patients had multiple seizure types, including focal seizures, generalized tonic-clonic seizures, myoclonic seizures, epileptic spasms, and atonic seizures. Seizures were fever-sensitive in 13 out of the 15 patients. Eleven patients displayed developmental delay, while 11 had abnormal video electroencephalography. Abnormalities in the brain images included dysplasia of the frontal and temporal cortex, dysplasia of the corpus callosum, and delayed myelination in four patients. One patient was diagnosed with febrile seizures, three with febrile seizures plus, three with Dravet syndrome, three with West syndrome, one with Ohtahara syndrome, three with developmental delays and epilepsy, and one with non-specific early-onset epileptic encephalopathy.Interpretation: The most common phenotypes of patients with GABRB2 variants include early onset of seizure and fever sensitivity. Febrile seizures and febrile seizures plus are new phenotypes of GABRB2 variants. The phenotypic spectrum of GABRB2 variants ranges from mild febrile seizures to severe epileptic encephalopathy. [ABSTRACT FROM AUTHOR]

Leptin has been found to be involved in the ovarian granulosa cell apoptosis and steroidogenesis. Loss of neuropeptide Y (NPY) can correct the obesity syndrome of mutant mice lacking of leptin (ob/ob). However, the association of NPY and leptin in ovarian granulosa cells and ovarian steroidogenesis has not been investigated. Here, C57BL/6J ob/ob mice and C57BL/6J (control) mice were intraperitoneally injected with PBS, leptin (0.4 μg/g bodyweight) or BIIE0246 (NPY2 receptor [NPY2R] antagonist, 30 μg/kg bodyweight) every day for 15 days. We found that NPY2R mRNA expression in mouse ovary was suppressed by leptin treatment, but increased by leptin deficiency. Leptin or BIIE0246 treatment significantly increased E2, but notably decreased progesterone in both mice. A lower level of E2 and a higher level of progesterone was observed in ob/ob mice than in control mice. Further, we then knocked down leptin expression in human ovarian granulosa cells by siRNA transfection and treated the cells with DMSO or BIIE0246. In vitro experiments confirmed the findings in mice. siLeptin treatment decreased the secretion of E2, anti-Mullerian hormone (AMH), insulin-like growth factor (IGF)-1 and transforming growth factor (TGF)-β, and the cell proliferation, but increased the secretion of progesterone and cell apoptosis. Western blotting analysis of PCNA, Bcl-2 and Bax confirmed the results of cell proliferation and apoptosis. Activation of JAK2 and STAT3 was also suppressed by knocking down leptin. All the effects of siLeptin on ovarian granulosa cells were partially reversed by BIIE0246. In conclusion, knockdown of leptin significantly affected ovarian steroidogenesis and ovarian function through NPY. siLeptin transfection impaired the activation of JAK2/STAT3 and contributed to ovarian granulosa cell apoptosis partially through up-regulating NPY2R expression. [ABSTRACT FROM AUTHOR]

Mental retardation-40 (MRD40) is a rare autosomal dominant neurodevelopmental disorder with a poor prognosis that is caused by a heterozygous mutation in chromosome alignment maintaining phosphoprotein 1 (CHAMP1). It was previously considered a non-syndromic disease due to the lack of specific external features. Only limited international reports describing CHAMP1 mutations are currently available. The present case study was the first to report on a Chinese patient with MRD40. The patient presented with severe global development delay with significant craniofacial dysmorphia. Using trio whole-exome sequencing, a novel de novo frameshift mutation in CHAMP1, NM_032436.2: c.530delCinsTTT, was identified, which expands the spectrum of the known pathogenic variants. The present case report helps to improve the syndromic profile of the rare MRD40 disorder and provides an example for the clinical diagnosis of MRD40. [ABSTRACT FROM AUTHOR]