Enhancing brown fat activity and promoting white fat browning are attractive therapeutic strategies for treating obesity and associated metabolic disorders. To provide a comprehensive picture of the gene regulatory network in these processes, we conducted a series of transcriptome studies by RNA sequencing (RNA-seq) and quantified the mRNA and long noncoding RNA (lncRNA) changes during white fat browning (chronic cold exposure, beta-adrenergic agonist treatment, and intense exercise) and brown fat activation or inactivation (acute cold exposure or thermoneutrality, respectively). mRNA–lncRNA coexpression networks revealed dynamically regulated lncRNAs to be largely embedded in nutrient and energy metabolism pathways. We identified a brown adipose tissue–enriched lncRNA, lncBATE10, that was governed by the cAMP-cAMP response element-binding protein (Creb) axis and required for a full brown fat differentiation and white fat browning program. Mechanistically, lncBATE10 can decoy Celf1 from Pgc1α, thereby protecting Pgc1α mRNA from repression by Celf1. Together, these studies provide a comprehensive data framework to interrogate the transcriptomic changes accompanying energy homeostasis transition in adipose tissue.

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Absolute geostrophic currents in the North Pacific Ocean are calculated from the newly gridded Argo profiling float data using the P-vector method for the period of 2004-11. The zonal geostrophic currents based on the Argo profile data are found to be stronger than those based on the traditional World Ocean Atlas 2009 (WOA09) data. A westward mean geostrophic flow underneath the North Equatorial Countercurrent is identified using the Argo data, which is evidenced by sporadic direct current measurements and geostrophic calculations in history. This current originates east of the date line and transports more than 4 3 10 6 m 3 s 21 of water westward in the subsurface northwestern tropical Pacific Ocean. The authors name this current the North Equatorial Subsurface Current. The transport in the geostrophic currents is compared with the Sverdrup theory and found to differ significantly in several locations. Analyses have shown that errors of wind stress estimation cannot account for all of the differences. The largest differences are found in the area immediately north and south of the bifurcation latitude of the North Equatorial Current west of the date line and in the recirculation area of the Kuroshio and its extension, where nonlinear activities are vigorous. It is, therefore, suggested that the linear dynamics of the Sverdrup theory is deficient in explaining the geostrophic transport of the tropical northwestern Pacific Ocean.

Instead of individually aligned along the external electric field, the carbon nanotubes (CNTs) were electrically induced into aligned chains in a shape memory polymer (SMP)/carbon black (CB) composite, which would serve as long-distance conductive channels to bridge the CB aggregations. Compared with SMP composites with randomly filled CNTs, the electrical resistivity in those with chained CNTs was reduced for more than 100 times. The fabricated conductive SMP composites could be actuated by a low electrical power.

Shape memory fibrous membranes (SMFMs) are an emerging class of active polymers, which are capable of switching from a temporary shape to their permanent shape upon appropriate stimulation. Quintuple-shape memory membranes based on the thermoplastic polymer Nafion, with a stable fibrous structure, are achieved via electrospinning technology, and possess a broad transition temperature. The recovery of multiple temporary shapes of electrospun membranes can be triggered by heat in a single triple-, quadruple-, quintuple-shape memory cycle, respectively. The fiber morphology and nanometer size provide unprecedented design flexibility for the adjustable morphing effect. SMFMs enable complex deformations at need, having a wide potential application field including smart textiles, artificial intelligence robots, bio-medical engineering, aerospace technologies, etc in the future.

Obesity induces profound transcriptome changes in adipocytes, and recent evidence suggests that long-noncoding RNAs (lncRNAs) play key roles in this process. We performed a comprehensive transcriptome study by RNA sequencing in adipocytes isolated from interscapular brown, inguinal, and epididymal white adipose tissue in diet-induced obese mice. The analysis revealed a set of obesity-dysregulated lncRNAs, many of which exhibit dynamic changes in the fed versus fasted state, potentially serving as novel molecular markers of adipose energy status. Among the most prominent lncRNAs is , which is transcribed from an enhancer region upstream of leptin (). Expression of is sensitive to insulin and closely correlates to expression across diverse pathophysiological conditions. Functionally, induction of is essential for adipogenesis, and its presence is required for the maintenance of expression in vitro and in vivo. Direct interaction was detected between DNA loci of and in mature adipocytes, which diminished upon knockdown. Our study establishes as a new regulator of .

Mutation of distal-less homeobox 3 (DLX3) is responsible for human tricho-dento-osseous syndrome (TDO) with amelogenesis imperfecta, indicating a crucial role of DLX3 in amelogenesis. However, the expression pattern of DLX3 and its specific function in amelogenesis remain largely unknown. The aim of this study was to investigate the effects of DLX3 on enamel matrix protein (EMP) genes. By immunohistochemistry assays of mouse tooth germs, stronger immunostaining of DLX3 protein was identified in ameloblasts in the secretory stage than in the pre-secretory and maturation stages, and the same pattern was found for Dlx3 mRNA using Realtime PCR. In a mouse ameloblast cell lineage, forced expression of DLX3 up-regulated the expression of the EMP genes Amelx, Enam, Klk4, and Odam, whereas knockdown of DLX3 down-regulated these four EMP genes. Further, bioinformatics, chromatin immunoprecipitation, and luciferase assays revealed that DLX3 transactivated Enam, Amelx, and Odam through direct binding to their enhancer regions. Particularly, over-expression of mutant-DLX3 (c.571_574delGGGG, responsible for TDO) inhibited the activation function of DLX3 on expression levels and promoter activities of the Enam, Amelx, and Odam genes. Together, our data show that DLX3 promotes the expression of the EMP genes Amelx, Enam, Klk4, and Odam in amelogenesis, while mutant-DLX3 disrupts this regulatory function, thus providing insights into the molecular mechanisms underlying the enamel defects of TDO disease.