PURPOSE: . The present study compared the accuracy between digital and conventional implant impressions. MATERIALS AND METHODS: . The experimental models were divided into six groups depending on the implant location and the scanning span. Digital impressions were captured using the intraoral optical scanner TRIOS (3Shape, Copenhagen, Denmark). Conventional impressions were taken with the monophase impression material based on addition-cured silicones, Honigum-Mono (DMG, Hamburg, Germany). A highprecision laboratory scanner D900 (3Shape, Copenhagen, Denmark) was used to obtain digital data of resin models and stone casts. Surface tessellation language (STL) datasets from scanner were imported into the analysis software Geomagic Qualify 14 (3D Systems, Rock Hill, SC, USA), and scan body deviations were determined through two-dimensional and three-dimensional analyses. Each scan body was measured five times. The Sidak t test was used to analyze the experimental data. RESULTS: . Implant position and scanning distance affected the impression accuracy. For a unilateral arch implant and the mandible models with two implants, no significant difference was observed in the accuracy between the digital and conventional implant impressions on scan bodies; however, the corresponding differences for trans-arch implants and mandible with six implants were extremely significant (P <.001). CONCLUSION . For short-span scanning, the accuracy of digital and conventional implant impressions did not differ significantly. For long-span scanning, the precision of digital impressions was significantly inferior to that of the traditional impressions.

Polycystic ovary syndrome (PCOS) is the most common endocrine disease in reproductive-aged women, which is characterized by polycystic ovary changes, hyperandrogenism and anovulation. A large number of studies have confirmed that miRNAs play an important role in the pathophysiology of PCOS. The miRNA-17-92 gene cluster is a family of miRNAs containing multiple cistron clusters. It was initially considered to be an oncogene, but it can trigger a variety of physiological and pathological processes in many diseases. In recent years, more and more evidence has showed that miRNA-17-92 gene cluster plays an important role in the development of PCOS. In this study, we reviewed the roles of miRNA-17-92 gene cluster in the development of PCOS.

Recurrent spontaneous abortion (RSA) is a common adverse pregnancy outcome in women of childbearing age and its etiology is complex and still not clear. The maternal-fetal interface microenvironment plays a key role in maintaining pregnancy. There are trophoblast cells, decidual stromal cells and immune cells in the maternal-fetal interface microenvironment. The abnormal number or function of these cells may induce changes in the microenvironment of maternal-fetal interface, such as spiral artery remodeling disorder and abnormal decidualization, which may lead to RSA. This review discusses the role and mechanism of these three main cells in RSA.

Polycystic ovary syndrome (PCOS) is the most common endocrine disease in reproductive-aged women, which is characterized by polycystic ovary changes, hyperandrogenism and anovulation. A large number of studies have confirmed that miRNAs play an important role in the pathophysiology of PCOS. The miRNA-17-92 gene cluster is a family of miRNAs containing multiple cistron clusters. It was initially considered to be an oncogene, but it can trigger a variety of physiological and pathological processes in many diseases. In recent years, more and more evidence has showed that miRNA-17-92 gene cluster plays an important role in the development of PCOS. In this study, we reviewed the roles of miRNA-17-92 gene cluster in the development of PCOS.

Recurrent spontaneous abortion (RSA) is a common adverse pregnancy outcome in women of childbearing age and its etiology is complex and still not clear. The maternal-fetal interface microenvironment plays a key role in maintaining pregnancy. There are trophoblast cells, decidual stromal cells and immune cells in the maternal-fetal interface microenvironment. The abnormal number or function of these cells may induce changes in the microenvironment of maternal-fetal interface, such as spiral artery remodeling disorder and abnormal decidualization, which may lead to RSA. This review discusses the role and mechanism of these three main cells in RSA.