Entity

Time filter

Source Type


Yu H.,Dalian Medical University | Yu H.-G.,South Branch of Yantaishan Hospital | Xu S.,Yantai Stomatological Hospital | Liu Z.-H.,Yantai Stomatological Hospital
Journal of Dalian Medical University | Year: 2010

[Objective] To study the effect of maxillary sinus floor lifting by bone graft with instant ITI implants placement. [Methods] Eighty - seven patients suffered the loss of up posterior teeth, sixty - six cases whose bone height of maxillary sinus floor was between 6-10 mm underwent internal sinus floor elevation, and other 21 cases whose bone height between 2-5 mm underwent maxillary sinus lift with bone graft. All cases were simultaneously placed implants. The implants were restored 3 to 6 months later by using digital panoramic. Evaluate the osseointegration during a follow - up period of 6 to 52 months. [Results] There were no clinical complaints of maxillary sinusitis for all cases. Only one implant lost in total 98 implants. The rest 97 implants were stable and had well osseointegration on X - ray film. [Conclusion] It is practical to take maxillary sinus lift with bone graft or internal sinus floor elevation with simultaneous placement of implants according to different height of alveolar ridges. Two approaches with bone graft and simultaneous placement of ITI implants show desirable clinical results. Source


Wang B.,South Branch of Yantaishan Hospital | Zhu L.,Zhucheng City Peoples Hospital | Sui S.,YanTai Development Zone Hospital | Sun C.,Yantaishan Hospital | And 2 more authors.
Biochemical and Biophysical Research Communications | Year: 2014

Cilostazol is a drug licensed for the treatment of intermittent claudication. Its main action is to elevate intracellular levels of cyclic monophosphate (cAMP) by inhibiting the activity of type III phosphodiesterase, a cAMP-degrading enzyme. The effects of cilostazol on fatty acid oxidation (FAO) are as yet unknown. In this study, we report that cilostazol can elevate complete FAO and decrease both triacylglycerol (TAG) accumulation and TAG secretion. This use of cilostazol treatment increases expression of PGC-1α and, subsequently, its target genes, such as ERRα, NOR1, CD36, CPT1, MCAD, and ACO. Expression of these factors is linked to fatty acid β-oxidation but this effect is inhibited by H-89, a specific inhibitor of the PKA/CREB pathway. Importantly, knockdown of PGC-1α using siRNA abolished the effects of cilostazol in fatty acid oxidation (FAO) and TAG metabolism. These findings suggested that the PKA/CREB/PGC-1α pathway plays a critical role in cilostazol-induced fatty acid oxidation and TAG metabolism. © 2014 Elsevier Inc. Source

Discover hidden collaborations