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This study examined the effects of Stmn2 on phenotype transformation of vascular smooth muscle in vascular injury via RNA sequencing and experimental validation. Total RNA was extracted for RNA sequencing after 1, 3 and 5 days of injury to screen the differentially expressed genes (DEGs). Western blot was used to detect the protein expression of Stmn2 and its associated targets. The morphological changes of carotid arteries in rats were examined by hematoxylin and eosin (HE Stmn2 overexpression significantly up-regulated the expression of osteopontin and α-SMA and vimentin in VSMCs. The results of morphology analysis and immunostaining also showed that Stmn2 overexpression promoted the intima thickening and enhanced the proliferating cell nuclear antigen expression in the injured vascular tissues. In conclusion, our results implied that Stmn2 may play a potential role in vascular injury, which may be associated with VSMC phenotype transformation. Further studies are warranted to determine detailed molecular mechanisms of Stmn2 in vascular injury.

While one subspecies of chestnut tiger butterfly (Parantica sita, Lepitoptera: Nymphalidae) undertakes seasonal migration between Taiwan and Japan, it is still unknown whether the nominate subspecies, P. s. sita, migrates seasonally in southwest China. To understand the potential migration of P. s. sita, it is necessary to investigate the genetic differentiation among populations. In our study, we developed 18 novel microsatellite markers from the transcriptome using next-generation sequencing methods. These polymorphic markers were tested on 89 individuals from 4 populations of P. sita. The allele numbers ranged from 2 to 19. The average polymorphism information content values in each population ranged from 0.34 to 0.40. The observed (Ho) and expected (He) heterozygosity of each locus in each population ranged from 0.043 to 0.870 and 0.043 to 0.833, respectively. These informative microsatellite markers would be helpful for discovering the facts of P. sita long-distance migration in China.

Hepatocellular carcinoma (HCC) is a heterogeneous tumor with an increased incidence worldwide accompanied by high mortality and dismal prognosis. Emerging evidence indicates that mesenchymal stem cells (MSCs)-derived exosomes possess protective effects against various human diseases by transporting microRNAs (miRNAs or miRs). We aimed to explore the role of exosomal miR-15a derived from MSCs and its related mechanisms in HCC. Exosomes were isolated from transduced MSCs and co-incubated with Hep3B and Huh7 cells. miR-15a expression was examined by RT-qPCR in HCC cells, MSCs, and secreted exosomes. CCK-8, transwell, and flow cytometry were used to detect the effects of miR-15a or spalt-like transcription factor 4 (SALL4) on cell proliferative, migrating, invasive, and apoptotic properties. A dual-luciferase reporter gene assay was performed to validate the predicted targeting relationship of miR-15a with SALL4. Finally, in vivo experiments in nude mice were implemented to assess the impact of exosome-delivered miR-15a on HCC. The exosomes from MSCs restrained HCC cell proliferative, migrating, and invasive potentials, and accelerated their apoptosis. miR-15a was expressed at low levels in HCC cells and could bind to SALL4, thus curtailing the proliferative, migrating, and invasive abilities of HCC cells. Exosomes successfully delivered miR-15a to HCC cells. Exosomal miR-15a depressed tumorigenicity and metastasis of HCC tumors in vivo. Overall, exosomal miR-15a from MSCs can downregulate SALL4 expression and thereby retard HCC development.

Purpose The present study aimed to explore the clinical characteristics of heparin-induced thrombocytopenia (HIT) after surgery for acute type A aortic dissection and perform a relevant prognostic analysis. Methods After continuous observation and analysis of 204 patients who underwent acute type A aortic dissection, we found that blood platelets decreased significantly after surgery and that these patients can be suspected to suffer HIT based on relevant 4Ts scores. For these suspected HIT patients, a latex particle-enhanced immunoturbidimetric assay was conducted to detect heparin-induced antibodies. Perioperative clinical data of patients in HIT and non-HIT groups were recorded as were blood platelet counts, HIT antibody test results, 4Ts scores, thromboembolic complications, clinical prognosis and outcomes. Results In the present study, 38 suspected HIT patients, 16 HIT patients and 188 non-HIT patients were selected in the clinical setting. Among them, HIT patients were found to have prolonged cardiopulmonary bypass time (223 min on average vs. 164 min) and delayed aortic cross-clamp time (128 min on average vs. 107 min), and these differences between HIT patients and non-HIT patients were significant (P P > 0.05). The transfusions of blood platelets in the HIT group and non-HIT group were 18.7 ± 5.0u and 15.6 ± 7.34 u, respectively. In the HIT group, the mechanic ventilation time and the length of ICU stay were longer comparing the non-HIT group(P P > 0.05). The incidence of continuous renal replacement therapy in HIT group was higher than the non-HIT group (P P > 0.05). However, the HIT antibody titer in the HIT group was significantly higher than that in the Suspected HIT group (2.7 ± 0.8 U/mL vs. 0.3 ± 0.2 U/mL) (P Conclusions After surgery for acute type A aortic dissection, HIT patients developed postoperative complications, the duration of ventilatory support and length of ICU stay were extended, and the incidence of thromboembolism increased. HIT antibody detection and risk classification should be implemented for high-risk patients showing early clinical characteristics.

A major obstacle to achieving reasonable strength prediction of a composite only from its constituent information is in the determination of in situ strengths of the matrix. One can measure only the original strengths of the pure matrix, on the basis of which the predicted transverse strengths of a unidirectional (UD) composite are far from reality. It is impossible to reliably measure matrix in situ strengths. This paper focuses on the correlation between in situ and original strengths. Stress concentrations in a matrix owing to the introduction of fibers are attributed to the strength variation. Once stress concentration factors (SCFs) are obtained, the matrix in situ strengths are assigned as the original counterparts divided by them. Such an SCF cannot be defined following a classical approach. All of the relevant issues associated with determining it are systematically addressed in this paper. Analytical expressions for SCFs under transverse tension, transverse compression, and transverse shear are derived. Closed-form and compact formulas for all of the uniaxial strengths of a UD composite are first presented in this paper. Their application to strength predictions of a number of typical UD composites demonstrates the correctness of these formulas.

This review summarizes the recent developments in topological string theory from the author's perspective, mostly focused on aspects of research in which the author is involved. After a brief overview of the theory, we discuss two aspects of these developments. First, we discuss the computational progress in the topological string partition functions on a class of elliptic Calabi-Yau manifolds. We propose to use Jacobi forms as an ansatz for the partition function. For non-compact models, the techniques often provide complete solutions, while for compact models, though it is still not completely solvable, we compute to higher genus than previous works. Second, we explore a remarkable connection of refined topological strings on a class of non-compact toric Calabi-Yau threefolds with non-perturbative effects in quantum-mechanical systems. The connections provide rarely available exact quantization conditions for quantum systems and new insights on non-perturbative formulations of topological string theory., A review article of the author's recent research, 16 pages, 2 figures. Journal version for "Science China Physics, Mechanics & Astronomy"

Deafness or hearing loss is a major issue in human health. Inner ear hair cells are the main sensory receptors responsible for hearing. Defects in hair cells are one of the major causes of deafness. A combination of induced pluripotent stem cell (iPSC) technology with genome-editing technology may provide an attractive cell-based strategy to regenerate hair cells and treat hereditary deafness in humans. Here, we report the generation of iPSCs from members of a Chinese family carrying MYO15A c.4642G>A and c.8374G>A mutations and the induction of hair cell-like cells from those iPSCs. The compound heterozygous MYO15A mutations resulted in abnormal morphology and dysfunction of the derived hair cell-like cells. We used a CRISPR/Cas9 approach to genetically correct the MYO15A mutation in the iPSCs and rescued the morphology and function of the derived hair cell-like cells. Our data demonstrate the feasibility of generating inner ear hair cells from human iPSCs and the functional rescue of gene mutation-based deafness by using genetic correction.