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Mitochondrial oxidative injury can result in many cardiovascular diseases including cardiac ischemia-reperfusion (I/R) injury. This study was designed to investigate whether microRNA-34a (miR-34a) influences cardiac I/R or hypoxia/reoxygenation (H/R) injury by regulating the mitochondrial apoptotic pathway from oxidative injury.

Endometrial carcinoma is a common gynecological malignant tumor, small nucleolar RNAs (snoRNAs) are involved in cancer development. However, researches on the roles of snoRNAs in endometrial carcinoma are limited. The expression levels of snoRNAs in endometrial cancer tissues were analyzed using The Cancer Genome Atlas (TCGA) database. Antisense oligonucleotides (ASOs) and plasmids were used for transfection. Moreover, CCK-8, EdU, wound-healing assay, transwell, cell apoptosis, western blotting, and xenograft model were employed to examine the biological functions of related molecules. real-time reverse transcription polymerase chain reaction and western blotting were performed to detect messenger RNA (mRNA) and protein levels. Including bioinformatics, fluorescence in situ hybridization, RNA pulldown, actinomycin D and RTL-P assays were also carried out to explore the molecular mechanism. Analysis of data from TCGA showed that the expression level of small nucleolar RNA, C/D box 60 (SNORD60) in endometrial cancer tissues is observably higher than that in normal endometrial tissues. Further research suggested that SNORD60 played a carcinogenic role both in vitro and in vivo, and significantly upregulated the expression of PIK3CA. However, the carcinogenic effects can be reversed by knocking down fibrillarin (FBL) or PIK3CA. SNORD60 forms complexes by binding with 2'-O-methyltransferase fibrillarin, thus catalyzes the 2'-O-methylation (Nm) modification of PIK3CA mRNA and modulates the PI3K/AKT/mTOR signaling pathway, so as to promote the development of endometrial cancer. In short, SNORD60 might become a new biomarker for the therapy of endometrial cancer in the future and provide new strategies for diagnosis and treatment.

A new arylene ethynylene macrocycle (AEM) molecule bearing endo-acetamide groups was obtained by a Pd/Cu mediated homo-coupling reaction. Introducing tetraethylene glycol ether as a linkage between two C-shaped fragments substantially improved the final cyclization yield (30%). Concentration-dependent 1HNMR experiments indicated that strong aggregates formed through H-bonds were observed for this new macrocycle with amide groups in solution. And also, this macrocycle was fluorescent in solution and showed a highly selective fluorescence quenching response toward the highly toxic Hg2+. More importantly, this macrocycle could induce gelation of several solvents. Significantly, an interesting aggregation-induced enhanced emission (AIEE) behavior was observed for this macrocycle upon gelation. Both SEM and TEM investigations revealed that nanoporous structures existed in the xerogels. This study offers a new molecular design approach to develop fluorescent gels from planar AEM molecules with a functional cavity.

Figure-eight (lemniscular) shaped macrocycles, besides their esthetic beauty, often have interesting chiroptical properties. However, only limited figure-eight carbocyclic frameworks have been reported as yet and most of them have been acquired by dimerizing helicenes with inherently helical structures. Herein a novel figure-eight carbocyclic framework, lemniscular arylene ethynylene macrocycle (AEM), was firstly synthesized from non-helical precursors. By simply increasing the reactant concentration, intramolecular cyclization was effectively suppressed, while intermolecular cyclization was significantly increased to obtain figure-eight macrocycles in acceptable yields. Scanning tunneling microscopy (STM) investigation was firstly employed to confirm the figure-eight shape through molecular imaging. Furthermore, the figure-eight cyclization mechanism was systematically discussed. Interestingly, macrocycles bearing inner –NH2 groups (SPM-Q6-NH2 and SPM-Q12-NH2) showed a specific sensing behavior toward highly toxic Hg2+. Even more intriguing is that, compared to planar macrocycle SPM-Q6-NH2, its figure-eight dimer (SPM-Q12-NH2) exhibited much stronger complexation with Hg2+. This study opens up a new way to construct figure-eight conjugated carbocyclic macrocycles from an inherently non-helical precursor. More importantly, with this figure-eight AEM as a molecular platform, further structural derivations can be achieved through simple cycloaddition reactions with unsaturated bonds (ethynylene bonds and diyne bonds) or introducing donor–acceptor (D–A) structures.

In terms of high-efficiency PM6:Y6 binary systems, there is still room to narrow the lowest unoccupied molecular orbital (LUMO) level offset (0.36 eV) between PM6 and Y6 to further mitigate energy loss through introducing a second acceptor in the construction of ternary organic solar cells (OSCs). In this study, we designed and synthesized a new slightly twisted perylene diimide (PDI)-tetramer with a large, planar coronene unit as the core, Cor-T-PDI, which has four quasi molecular orbitals that have little energy difference between them. Although the pairing of Cor-T-PDI with PM6 gives a fairly low photovoltaic performance, interestingly, when Cor-T-PDI is used as a second acceptor, an obvious increase in open-circuit voltage (Voc) was achieved for a PM6:Y6 base ternary system due to the creation of a cascade energy level alignment by Cor-T-PDI. After tuning the PM6 : Y6 : Cor-T-PDI ratio to 1 : 1.0 : 0.1, the Voc value was significantly increased to 0.854 V without sacrificing the short-circuit current density (Jsc) and fill factor (FF), resulting in a high PCE of 16.88% with a low energy loss (0.47 eV), which are among the best values for single-junction OSCs. This preliminary study shows that for a binary system with a high Jsc value but low or moderate Voc values, such as the PM6:Y6 blend, producing a cascade energy level alignment is a more efficient strategy to enhance the PCE by introducing a third component with an appropriate structure. It is believed that lowering the highest unoccupied molecular orbital level of this PDI derivative to fall between that of Y6 and PM6 or tailoring the absorption to achieve a complementary absorption profile with that of the PM6:Y6 blend will further improve the efficiency.

Macrocyclic molecule [3]C 12 TT-TPA was synthesized by stille-coupling reaction though alternately connecting 4,7-bisthienyl-2,1,3-thienothiazole (B) unit and triphenylamine (A) unit. The concentration-dependent self-assembly structures of [3]C 12 TT-TPA were explored in liquid/solid interface by scanning tunneling microscopy and density functional theory. Increasing the solution concentration, five different nanostructures were constructed and the molecular packing densities were gradually enhanced. Those structural transformations from loose structures to compact structures are thermodynamically favourable because those transformations are accompanied by the adsorption of more [3]C 12 TT-TPA molecules from liquid phase, which increases the molecule-molecule interactions and molecule-substrate interactions considerably. This study of fundamental exploration is important to understand the basic formation mechanisms and the stability of two-dimensional functional materials.

To construct and identify adenovirus vector co-expressing hBMP2 and hVEGF165 fusion protein which labeled with green fluorescence protein, and laying the foundtion of the effect of hBMP2 and hVEGF165 gene inducing BMMSCs differentiation to osteoblast and bone defect repaired in the body.BMP2 and VEGF165 gene was amplified from cDNA library by PCR and inserted to the polyclonal site of adenovirus shuttle plasmid pAd-MCMV-GFP. Ad-BMP2- VEGF165 was recombinated and propagated in HEK293 cells by co-transfecting with the constructed recombinant shuttle plasmid pAd-MCMV-BMP2-VEGF165 and adenovirus helper plasmid pBHGloxΔ E1, 3Cre. The recombinant adenovirus was purified and virustiter was determined, and then to research GFP expression and to calculate the adenovirus transfection rate in rabbit BMMSCs.The recombinant adenovirus vector Ad-BMP2-VEGF165 was successfully constructed by the methods of gene analyzing, colony PCR, Western blotting and observing GFP expression, and the titer of the adenovirus was 1×10Recombinant adenovirus vector containing hBMP2 and hVEGF165 gene was successfully constructed and its high titer was obtained.

This project aimed to explore the protective effect of ginsenoside Rg_1 on hypoxia/reoxygenation(H/R)-induced H9 c2 cardiomyocyte injury and its underlying signaling pathway. The H/R model of H9 c2 cardiomyocytes was established and then the cells were divided into different treatment groups. CCK-8(cell counting kit-8) was used to detect the activity of cardiomyocytes; Brdu assay was used to detect the proliferation of H9 c2 cells; the caspase-3 activity was tested, and then the protein expression was assessed by Western blot. Flow cytometry was used to evaluate the apoptosis level of cardiomyocytes. Ginsenoside Rg_1 inhibited H/R-induced cardiomyocyte apoptosis and caspase-3 activity, promoted nuclear transcription of nuclear factor erythroid-2 related factor 2(Nrf2), and enhanced the expression of the downstream heme oxygenase-1(HO-1). Ginsenoside Rg_1 could increase Nrf2 nuclear transcription and HO-1 expression with the increase of concentration(10, 20, 40, 60 μmol·L~(-1)). However, the protective effect of ginsenoside Rg_1 on cardiomyocytes was significantly weakened after the transfection of Nrf2-siRNA. Ginsenoside Rg_1 could protect cardiomyocytes by activating the Nrf2/HO-1 pathway.

The study aims to explore the effects of miR-135b-5p on myocardial ischemia/reperfusion (I/R) injuries by regulating Janus protein tyrosine kinase 2 (JAK2)/signal transducer and activator of transcription (STAT) signaling pathway by mediating inhalation anesthesia with sevoflurane. A sum of 120 healthy Wistar male mice was assigned into six groups. Left ventricular ejection fraction (LVEF) and left ventricular shortening fraction (LVSF) were detected. Cardiomyocyte apoptosis was determined by terminal dexynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL) assay. MiR-135b-5p expression, mRNA and protein expression of p-STAT3, p-JAK2, STAT3, JAK2, B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein B (Bax) were detected by quantitative real-time PCR (qRT-PCR) and Western blotting. Target relationship between miR-135b-5p and JAK2 was confirmed by dual-luciferase reporter assay. The other five groups exhibited increased cardiomyocyte necrosis, apoptosis, miR-135b-5p and Bax expression, mRNA expression of JAK2 and STAT3, and protein expression of p-STAT3 and p-JAK2 compared with the sham group, but showed decreased LVEF, LVFS, and Bcl-2 expression. Compared with the model and AG490 + Sevo groups, the Sevo, inhibitor + Sevo and inhibitor + AG490 + Sevo groups displayed reduced cardiomyocyte necrosis, apoptosis, miR-135b-5p and Bax expression, but displayed elevated mRNA expression of JAK2 and STAT3, protein expression of p-STAT3 and p-JAK2, LVEF, LVFS and Bcl-2 expression. Compared with the Sevo and inhibitor + AG490 + Sevo groups, the AG490 + Sevo group showed decreased LVEF, LVFS, Bcl-2 expression, mRNA expressions of JAK2 and STAT3, and protein expressions of p-STAT3 and p-JAK2, but increased cardiomyocyte necrosis, apoptosis, and Bax expressions. MiR-135b-5p negatively targetted JAK2. Inhibition of miR-135b-5p can protect against myocardial I/R injury by activating JAK2/STAT3 signaling pathway through mediation of inhalation anesthesia with sevoflurane.

Esophageal squamous cell carcinoma (ESCC) is the most common histologic subtype of esophageal cancer and is characterized by a poor prognosis. Determining gene changes in ESCCs should improve understanding of putative risk factors and provide potential targets for therapy. We sequenced about 55 million pair-end reads from a pair of adjacent normal and ESCC samples to identify the gene expression level and gene fusion. Sanger sequencing was used to verify the result. About 17 thousand genes were expressed in the tissues, of which approximately 2400 demonstrated significant differences between tumor and adjacent non tumor tissue. GO and KEGG pathway analysis revealed that many of these genes were associated with cellular adherence and movement, simulation responses and immune responses. Notably we identified and validated one fusion gene, HLA-E and HLA-B, located 1 MB apart. We also identified thousands of remarkably expressed transcripts. In conclusion, a novel fusion gene HLA-E and HLA-B was identified in ESCC via whole transcriptome sequencing, which would be a biomarker for ESCC diagnosis and target for therapy, shedding new light for better understanding of ESCC tumorigenesis.

To observe the protective effect of electroacupuncture (EA) intervention on the expression of brain-derived-neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) proteins and genes in the hippocampus areas in myocardial ischemia (MI) rats, so as to reveal its underlying mechanisms in protecting hippocampal cells under MI.Eighty healthy male SD rats were randomized into sham-operation (sham), MI model, Shenmen (HT 7), HT 7-Zhizheng (SI 7) and HT 7-Xinshu (BL 15) groups (n = 15 in each group). The MI model was established by occlusion of the anterior descending branch of the left coronary artery. EA (2 Hz, 2 mA) was applied to bilateral HT 7, HT 7-SI 7, and HT 7-BL 15, respectively for 15 min, once per day for a week. The number of BDNF and its receptor TrkB positive cells in the left hippocampus and that of mRNAs in the right hippocampus tissue were determined by immunohistochemistry and real-time fluorescence quantitative PCR, respectively.In comparison with the sham group, the numbers of both BDNF and TrkB positive cells in the left hippocampus and the expression levels of BDNF mRNA and TrkB mRNA in the right hippocampus were increased slightly (P0.05). After EA intervention, the numbers of hippocampal BDNF and TrkB positive cells and the expression levels of BDNF mRNA and TrkB mRNA were evidently up-regulated (P0.05, P0.01), and the effects of HT 7-SI 7 and HT 7-BL 15 were obviously superior to those of simple HT 7 in up-regulating BDNF and TrkB expression (P0.01, P0.05). No significant differences were found between the HT 7-SI 7 and HT 7-BL 15 groups in increasing the number of hippocampal BDNF and TrkB positive cells and in up-regulating expression of both BDNF mRNA and TrkB mRNA (P0.05).EA intervention is effective in increasing the expression of hippocampal BDNF and TrkB in MI rats, which may contribute to its effect in protecting hippocampal cells from injury under MI condition. The effect of EA stimulation of HT 7-SI 7 and HT 7-BL 15 was obviously superior to that of simple HT 7 in up-regulating BDNF and TrkB expression.