Controllable Circularly Polarized Luminescence with High Dissymmetry Factor via Co-Assembly of Achiral Dyes in Liquid Crystal Polymer Films.

Circularly polarized luminescence (CPL) materials are highly demanded due to their great potential in optoelectronic and chiroptical elements. However, the preparation of CPL films with high luminescence dissymmetry factors (glum ) remains a formidable task, which impedes their practical application in film-based devices. Herein, a facile strategy to prepare solid CPL film with a high glum through exogenous chiral induction and amplification of liquid crystal polymers is proposed. Amplification and reversion of the CPL appear when the films are annealed at the chiral nematic liquid crystalline temperature and the maximal glum up to 0.30 due to the enhancement of selective reflection. Thermal annealing treatment at different liquid crystalline states facilitates the formation of the chiral liquid phase and adjusts the circularly polarized emission. This work not only provides a straightforward and versatile platform to construct organic films capable of exhibiting strong circularly polarized emission but also is helpful in understanding the exact mechanism for the liquid crystal enhancement of CPL performance.

SpTNF regulates apoptosis and antimicrobial peptide synthesis in mud crab (Scylla paramamosain) during white spot syndrome virus infection.

Tumor necrosis factor (TNF) is an inflammatory cytokine that is important in cell survival, proliferation, differentiation, and death. However, the functions of TNF in the innate immune responses of invertebrates have been less studied. In this study, SpTNF was cloned and characterized from mud crab (Scylla paramamosain) for the first time. SpTNF contains an open reading frame of 354 bp encoding 117 deduced amino acids, with a conserved C-terminal TNF homology domain (THD) domain. RNAi knockdown of SpTNF reduced hemocyte apoptosis and antimicrobial peptide (AMP) synthesis. Expression of SpTNF was initially down-regulated but subsequently up-regulated after 48 h in hemocytes of mud crabs after WSSV infection. Results of RNAi knockdown and overexpression showed that SpTNF inhibits the WSSV infection through activating apoptosis, NF-κB pathway, and AMP synthesis. Furthermore, the lipopolysaccharide-induced TNF-α factor (SpLITAF) can regulate the expression of SpTNF, induction of apoptosis, and activation of the NF-κB pathway and AMP synthesis. The expression and nuclear translocation of SpLITAF were found to be regulated by WSSV infection. Knocking down of SpLITAF increased the WSSV copy number and expression of VP28 gene. Taken together, these results proved the protective function of SpTNF, which is regulated by SpLITAF, in the immune response of mud crabs against WSSV through the regulation of apoptosis and activation of AMP synthesis.

A Modified Technique in Rhinoplasty: A Septal Extension Graft Complex Using Septal Cartilage, Ethmoid Bone, and Auricular Cartilage.

BACKGROUND: Due to the small and weak septal cartilage of Asians, it is a challenge to obtain ideal tip projection and nose lengthening in this population by performing septal extension grafts with only septal cartilage. OBJECTIVES: The aim of this study was to introduce a septal extension graft complex incorporating nasal septal cartilage, the perpendicular plate of the ethmoid bone, and bilateral auricular cartilage, and to examine its effectiveness in terms of morphological and mechanical support. METHODS: Septal cartilage was harvested under an endoscope according to standard techniques. Two pieces of the perpendicular plate of the ethmoid bone, placed on either side of the "L" strut, served as 2 spreader grafts. A double layer of auricular cartilage was fixed as columellar strut grafts. Three-dimensional facial scanning was used to examine the change of 3 parameters. Nasal tip resistance was evaluated by a digital Newton meter. RESULTS: In total, 25 patients were followed up postoperatively for a mean of 25.9 months. The analysis showed significant differences in both contour parameters and nasal resistance: nasal length (mean [standard deviation], 41.4 [4.0] vs 46.2 [3.4] mm, P < 0.05) and nasal tip projection (21.3 [3.2] vs 24.4 [2.7] mm, P < 0.05) appeared to increase postoperatively, whereas nasolabial angle (117.6° [5.9°] vs 109.5° [5.3°], P < 0.05) showed a significant decrease after surgery. The resistance of the nasal tip also increased significantly (P < 0.05) at displacements of 1, 2, and 3 mm. All patients were satisfied with the aesthetic results, and no serious complications occurred. CONCLUSIONS: This kind of modified septal extension graft technique can effectively adjust nasal morphology for short-nose East Asians.

SpBNIP3 regulates apoptosis and autophagy in mud crab (Scylla paramamosain) during white spot syndrome virus infection.

BNIP3 (BCL2 and adenovirus E1B 19-kDa-interacting protein 3), which is a pro-apoptotic protein in the BCL-2 family involves a variety of cell signaling pathways, including mitochondrial dysfunction, mitochondrial autophagy, and apoptosis in vertebrates. However, the role of BNIP3 in the regulation of apoptosis and/or autophagy in crustaceans suffering virus infection is still limited. In this study, the mud crab (Scylla paramamosain) BNIP3 (SpBNIP3) was identified and studied to elucidate its association with the white spot syndrome virus (WSSV) infection. SpBNIP3 was widely expressed in all tested tissues and significantly down-regulated in the hemocytes of mud crab after WSSV infection. Knockdown of SpBNIP3 using RNA interference increased the apoptosis rate and Caspase 3 activity but decreased the mitochondrial membrane potential and autophagy levels, as well as viral copy number in mud crabs infected with WSSV. Additionally, the relationship between the viral infection and the autophagy of hemocytes was observed. The level of autophagy was reduced upon WSSV infection, and the activation of autophagy enriched the viral copy number. Taken together, the results of this study provide a new finding on the mechanism that SpBNIP3 may participate in the WSSV infection through the regulation of apoptosis and autophagy processes in mud crabs.