Coaxial Wet Spinning of Boron Nitride Nanosheet-Based Composite Fibers with Enhanced Thermal Conductivity and Mechanical Strength.

Hexagonal boron nitride nanosheets (BNNSs) exhibit remarkable thermal and dielectric properties. However, their self-assembly and alignment in macroscopic forms remain challenging due to the chemical inertness of boron nitride, thereby limiting their performance in applications such as thermal management. In this study, we present a coaxial wet spinning approach for the fabrication of BNNSs/polymer composite fibers with high nanosheet orientation. The composite fibers were prepared using a superacid-based solvent system and showed a layered structure comprising an aramid core and an aramid/BNNSs sheath. Notably, the coaxial fibers exhibited significantly higher BNNSs alignment compared to uniaxial aramid/BNNSs fibers, primarily due to the additional compressive forces exerted at the core-sheath interface during the hot drawing process. With a BNNSs loading of 60 wt%, the resulting coaxial fibers showed exceptional properties, including an ultrahigh Herman orientation parameter of 0.81, thermal conductivity of 17.2 W m-1 K-1, and tensile strength of 192.5 MPa. These results surpassed those of uniaxial fibers and previously reported BNNSs composite fibers, making them highly suitable for applications such as wearable thermal management textiles. Our findings present a promising strategy for fabricating high-performance composite fibers based on BNNSs.

Genome-Wide Analysis of Simple Sequence Repeats in Cabbage (Brassica oleracea L.).

Cabbage (Brassica oleracea L. var. capitata) accounts for a critical vegetable crop belonging to Brassicaceae family, and it has been extensively planted worldwide. Simple sequence repeats (SSRs), the markers with high polymorphism and co-dominance degrees, offer a crucial genetic research resource. The current work identified totally 64,546 perfect and 93,724 imperfect SSR motifs in the genome of the cabbage 'TO1000.' Then, we divided SSRs based on the respective overall length and repeat number into different linkage groups. Later, we characterized cabbage genomes from the perspectives of motif length, motif-type classified and SSR level, and compared them across cruciferous genomes. Furthermore, a large set of 64,546 primer pairs were successfully identified, which generated altogether 1,113 SSR primers, including 916 (82.3%) exhibiting repeated and stable amplification. In addition, there were 32 informative SSR markers screened, which might decide 32 cabbage genotypes for their genetic diversity, with level of polymorphism information of 0.14-0.88. Cultivars were efficiently identified by the new strategy designating manual diagram for identifying cultivars. Lastly, 32 cabbage accessions were clearly separately by five Bol-SSR markers. Besides, we verified whether such SSRs were available and transferable in 10 Brassicaceae relatives. Based on the above findings, those genomic SSR markers identified in the present work may facilitate cabbage research, which lay a certain foundation for further gene tagging and genetic linkage analyses, like marker-assisted selection, genetic mapping, as well as comparative genomic analysis.

The gut microbial metabolite phenylacetylglycine protects against cardiac injury caused by ischemia/reperfusion through activating ß2AR.

BACKGROUND: Myocardial ischemia/reperfusion (I/R) injury is closely related to cardiomyocyte apoptosis. Stimulating ß2 adrenergic receptor (ß2AR) can effectively combat cardiomyocyte apoptosis. Previous studies demonstrate that the gut microbial metabolite phenylacetylglycine (PAGly) can stimulate ß2AR. However, the effect of PAGly on myocardial I/R injury remains unknown. METHODS: The hypoxia/reoxygenation (H/R) model was established using the neonatal mouse cardiomyocytes (NMCMs). Different doses of PAGly were used to treat NMCMs, and apoptosis was detected by terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) staining. Additionally, the level of cyclic adenosine monophosphate (cAMP) was examined by using a cAMP detection kit. Mouse model of myocardial I/R injury was established in C57BL/6 mice, and different doses of phenylacetic acid were administrated intraperitoneally. Apoptosis of myocardial cells was detected by TUNEL and α-actin staining. The area at risk and the infarct areas were identified by 2,3,5-triphenyltetrazolium chloride (TTC) and Evans blue staining. Western blotting was used to measure the protein expression levels of phosphorylated phosphatidylinositol 3-kinase (p-PI3K), total Akt (t-Akt), phosphorylated Akt (p-AKT), Bcl-2-associated X protein (Bax), B-cell lymphoma-2 (Bcl-2), cleaved caspase-3. RESULTS: PAGly significantly suppressed H/R injury-induced apoptosis in NMCMs and inhibited apoptosis in myocardial I/R injured mice in vivo. We verified that PAGly activated the anti-apoptotic Gαi/PI3K/AKT signaling cascade in NMCMs via stimulating ß2AR signaling. Continuous administration of PAGly at an appropriate dose could inhibit apoptosis and reduce the infarct size resulting from I/R injury in mice. However, high-dose PAGly treatment was associated with a higher mortality rate. Moreover, we demonstrated that Aspirin reduced the infarct size and the high mortality caused by high doses of PAGly in I/R injured mice. CONCLUSIONS: These findings suggest that treatment with the gut microbial metabolite PAGly could suppress cardiomyocyte apoptosis caused by myocardial I/R injury and reduce the infarct size, which provides a novel therapeutic strategy for patients with myocardial infarction.

Pyrroloquinoline quinone can prevent chronic heart failure by regulating mitochondrial function.

BACKGROUND: Myocardial mitochondrial dysfunction is the leading cause of chronic heart failure (CHF). Increased reactive oxygen species (ROS) levels, disruption of mitochondrial biogenesis and mitochondrial Ca2+([Ca2+]m) homeostasis and reduction of the mitochondrial membrane potential (ΔΨm) cause myocardial mitochondrial dysfunction. Therefore, treating CHF by targeting mitochondrial function is a focus of current research. For the first time, this study investigated the effects of the strong antioxidant pyrroloquinoline quinone (PQQ) on mitochondrial function in a cardiac pressure overload model, and the mechanism by which PQQ regulates [Ca2+]m homeostasis was explored in depth. METHODS: After transaortic constriction (TAC), normal saline and PQQ (0.4, 2 and 10 mg/kg) were administered intragastrically to Sprague Dawley (SD) rats for 12 weeks. In vitro, neonatal rat left ventricle myocytes (NRVMs) were pretreated with 200 nm angiotensin II (Ang II) with or without PQQ (1, 10 and 100 µM). Rat heart remodelling was verified by assessment of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) levels (qRT-PCR), cell surface area (wheat germ agglutinin (WGA) staining in vivo and α-actin in vitro) and echocardiography. Myocardial mitochondrial morphology was assessed by transmission electron microscopy. Western blotting was used to assess mitochondrial biogenesis [peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and transcription factor A, mitochondrial (TFAM)]. The ΔΨm was determined by tetraethyl benzimidazolyl carbocyanine iodide (JC-1) staining and flow cytometry, and ROS levels were measured by dichloro-dihydro-fluorescein diacetate (DCFH-DA) and MitoSOX Red staining. [Ca2+]m was measured by isolating rat mitochondria, and mitochondrial Ca2+ channel proteins [the mitochondrial Na+/Ca2+ exchanger (NCLX) and mitochondrial Ca2+ uniporter (MCU)] were detected by Western blot. RESULTS: In vivo and in vitro, PQQ pretreatment improved pressure overload-induced cardiac remodelling and cell hypertrophy, thus preventing the occurrence of CHF. PQQ also prevented mitochondrial morphology damage and reduced the PGC-1α and TFAM downregulation caused by TAC or Ang II. In addition, in NRVMs treated with Ang II + PQQ, PQQ regulated ROS levels and increased the ΔΨm. PQQ also regulated [Ca2+]m homeostasis and prohibited [Ca2+]m overloading by increasing NCLX expression. CONCLUSIONS: These results show that PQQ can prevent [Ca2+]m overload by increasing NCLX expression and thereby reducing ROS production and protecting the ΔΨm. At the same time, PQQ can increase PGC-1α and TFAM expression to regulate mitochondrial biogenesis. These factors can prevent mitochondrial dysfunction, thereby reducing cardiac damage caused by pressure overload and preventing the occurrence of CHF.

Engineering Graphene Wrinkles for Large Enhancement of Interlaminar Friction Enabled Damping Capability.

Graphene nanoplates are hoped-for solid lubricants to reduce friction and energy dissipation in micro and nanoscale devices benefiting from their interface slips to reach an expected superlubricity. On the contrary, we propose here by introducing engineered wrinkles of graphene nanoplates to exploit and optimize the interfacial energy dissipation mechanisms between the nanoplates in graphene-based composites for enhanced vibration damping performance. Polyurethane (PU) beams with designed sandwich structures have been successfully fabricated to activate the interlaminar slips of wrinkled graphene-graphene, which significantly contribute to the dissipation of vibration energy. These engineered composite materials with extremely low graphene content (∼0.08 wt %) yield a significant increase in quasi-static and dynamic damping compared to the baseline PU beams (by 71% and 94%, respectively). Friction force images of wrinkled graphene oxide (GO) nanoplates detected via an atomic force microscope (AFM) indicate that wrinkles with large coefficients of friction (COFs) indeed play a dominant role in delaying slip occurrences. Reduction of GO further enhances the COFs of the interacting wrinkles by 7.8%, owing to the increased effective contact area and adhesive force. This work provides a new insight into how to design graphene-based composites with optimized damping properties from the microstructure perspective.