Rational Design of Nanosheet Array-Like Layered-Double-Hydroxide-Derived NiCo2O4 In Situ Grown on Reduced-Graphene-Oxide-Coated Nickel Foam for High-Performance Solid-State Supercapacitors.

The investigation of high-performance supercapacitors is essential for accelerating the development of energy storage devices. In this work, a 3D hierarchical nanosheet array-like nickel cobaltite/reduced graphene oxide/nickel foam composite (NiCo2O4/rGO/NF) was assembled via an aqueous coprecipitation-hydrothermal strategy assisted by citric acid. Benefiting from a NiCo layered-double-hydroxide precursor with an atomic-level lattice confinement effect of metal ions and effective hybridization with rGO, the NiCo2O4/rGO/NF composite is featured as thin NiCo2O4 nanosheets (∼113.6 nm × 11.2 nm) composed of NiCo2O4 nanoparticles (∼10.9 nm) vertically staggered on the surface of a rGO-modified NF skeleton, leading to high surface area, abundant mesoporous structure, and active site exposure. The as-obtained NiCo2O4/rGO/NF was directly used as a binder-free integrated electrode for supercapacitors, achieving an excellent specific capacitance of 2863.4 F g-1 (1503.3 C g-1) at 1 A g-1, a superior rate performance of 2335.2 F g-1 at 20 A g-1, and a stability retention of 91.7% after 5000 cycles. More impressively, a solid-state asymmetric supercapacitor assembled by the present NiCo2O4/rGO/NF integrated electrode as the positive electrode and commercial activated carbon as the negative electrode achieved a high energy density of 69.2 Wh kg-1 at a power density of 800 W kg-1, and the energy density at a peak power density of 20004 W kg-1 still remained at 48.9 Wh kg-1, also showing a good cycling stability of 87.2% retention over 10000 cycles. The present facile synthesis strategy of the as-obtained NiCo2O4/rGO/NF nanosheet array composite can be used for the design and construction of many other transition-metal oxide/graphene/NF composite materials with excellent structural stability and performance in energy storage and other related areas.

Prenatal ultrasound-assisted identification of multiple malformations caused by a deletion in the long-arm end of chromosome 7 and review of the literature.

Clinical cases of chromosome 7 long-arm end deletion are rare. Generally, 7q terminal deletion syndrome results in complex clinical phenotypes, such as microcephaly, growth and development retardation, holoprosencephaly, and sacral hypoplasia. Herein, we report the genetic and clinical features of a fetus with multiple malformations observed by prenatal ultrasound. The results showed that there was a large fragment deletion of approximately 27.7 Mb in 7q32.3-qter. The induced fetus showed facial abnormalities of cleft lip and palate, and some organ structural abnormalities (such as diaphragmatic hernia and polycystic renal dysplasia) were observed by autopsy and pathology. To provide more reliable information for disease diagnosis and genetic counseling, we reviewed and analyzed the reported cases of isolated 7q terminal syndrome.

Knockdown of long non-coding RNA plasmacytoma variant translocation 1 inhibits cell proliferation while promotes cell apoptosis via regulating miR-486-mediated CDK4 and BCAS2 in multiple myeloma.

AIMS: This study aimed to investigate the effect of long non-coding RNA-plasmacytoma variant translocation 1 (lnc-Pvt1) knockdown on regulating cell proliferation and apoptosis, and to explore its molecular mechanism in multiple myeloma (MM). METHODS: Lnc-Pvt1 expression was detected in MM cell lines (NCI-H929, U-266, LP-1 and RPMI-8226 cell lines) and human normal plasma cells. In U-266 cells and LP-1 cells, control shRNA and lnc-Pvt1 shRNA plasmids were transferred. Rescue experiments were further performed by transfection of lnc-Pvt1 shRNA alone and lnc-Pvt1 shRNA and miR-486 shRNA plasmids. Cells proliferation, apoptosis, RNA expression, and protein expression were determined by cell counting kit-8, annexin V-FITC-propidium iodide, quantitative polymerase chain reaction, and Western blot assays, respectively. RESULTS: Lnc-Pvt1 expression was increased in MM cell lines (NCI-H929, U-266 and LP-1 cell lines) compared with human normal plasma cells. In U-266 cells, lnc-Pvt1 shRNA suppressed cell proliferation while enhanced cell apoptosis compared with control shRNA. Also, lnc-Pvt1 shRNA increased miR-486 expression compared with control shRNA. Further rescue experiment revealed that miR-486 shRNA did not change lnc-Pvt1 level, but increased CDK4 and BCAS2 expressions in lnc-Pvt1 knockdown-treated cells. In addition, miR-486 shRNA promoted cell proliferation while inhibited cell apoptosis in lnc-Pvt1 knockdown-treated cells. These results were further validated in LP-1 cells. CONCLUSIONS: Lnc-Pvt1 knockdown inhibits cell proliferation and induces cell apoptosis through potentially regulating miR-486-mediated CDK4 and BCAS2 in MM.