Vaspin alleviates the lncRNA LEF1-AS1-induced osteogenic differentiation of vascular smooth muscle cells via the Hippo/YAP signaling pathway.

Vascular calcification (VC) is closely related to higher cardiovascular mortality and morbidity, and vascular smooth muscle cell (VSMC) switching to osteogenic-like cells is crucial for VC. LncRNA LEF1-AS1 promotes atherosclerosis and dental pulp stem cells calcification, while its role in VC remains unknown. Visceral adipose tissue-derived serine protease inhibitor (vaspin) is an adipokine regulating bone metabolism. However, the relationship between vaspin and VC is still unclear. We aimed to explore the role of LEF1-AS1 on VSMC osteogenic transition, whether vaspin inhibited LEF1-AS1-mediated osteogenic differentiation of VSMCs, and the responsible mechanism. In this study, quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting analysis indicated that LEF1-AS1 overexpression significantly upregulated osteogenic marker Runt-related transcription factor-2 (RUNX2) level and downregulated VSMC contractile marker α-smooth muscle actin (α-SMA) level. Alizarin red staining, alkaline phosphatase (ALP) staining, ALP activity assay, and calcium content assay also suggested that LEF1-AS1 overexpression promoted calcium deposition in VSMCs. However, vaspin treatment abolished this phenomenon. Mechanistically, LEF1-AS1 markedly decreased phosphorylated YAP level, while vaspin reversed LEF1-AS1-induced phosphorylated YAP decline. Our results revealed that LEF1-AS1 accelerated the osteogenic differentiation of VSMCs by regulating the Hippo/YAP pathway, while vaspin eliminated the LEF1-AS1-meditated VSMCs osteogenic phenotype switch.

[Relation analysis of phosphorus removal and BOD5 loading using PHB monitoring in A2/O process].

In a pilot-scale anaerobic-anoxic-oxic experimental system for municipal wastewater treatment, PHB consumption in an oxic tank and PHB production in an anaerobic tank had been monitored overtime, and relations among PHB consumption/production, phosphorus removal/release and BOD5 loading had been analyzed. The results indicated that the consumption of PHB was positively related with phosphorus removal, and about 140 mg PHB consumption could result in 1 mg P removal. In the anaerobic tank, about 1.17 mg P release could result in 100 mg PHB production. The PHB production at the loading of 0.176 g/(g x d) was 4 mg/g MLSS less than that at 0.413 g/(g x d). No significant relevance was observed between PHB and BOD5 removal. The PHB of microorganism synthesizes was increased with the increase of temperature. Compared with the lowest temperature (17.1 degrees C), 20% of the total PHB content was increased at the maximum temperature (33.2 degrees C) in active sludge.

[Experimental investigation of shear bond strength on orthodontic bonding on dental fluorosis after air abrading surface preparation technique].

OBJECTIVE: To find a way to having higher bond strength on mottled enamel. METHODS: Sixty mottled enamel first bicuspid teeth extracted from fifteen patients needing orthodontic force were prepared and divided into four groups. Group A was routine acid etched, group B was air abraded, group C was etched by clearfil liner self-etching primer, group D was air abraded and then etched by clearfil liner self-etching primer. Next the bond and resin were used. The shear bond strength was observed and compared. The data were analysed by SPSS 11.5 statistical package. RESULTS: The shear bonding strength of group A was (2.247 +/- 0.261) MPa, group B was (5.374 +/- 0.469) MPa, group C was (4.345 +/- 0.401) MPa, group D was (5.791 +/- 0.636) MPa. The strengths of four groups were significantly different (P < 0.01). The adhesive remnant index (ARI) scores of the four groups had no significant difference. CONCLUSION: In clinic, using air abrasion surface preparation technique is an acceptable way to enhancing the shear bond strength before sticking the orthodontic bonding on dental fluorosis.