New progress in the pathogenesis of traumatic temporomandibular joint ankylosis / 口腔疾病防治

@#Traumatic temporomandibular joint ankylosis refers to fibrous or bony fusion between the condyle and the glenoid fossa. It can cause problems with mouth-opening limitations, mastication difficulties, obstructive sleep apnea and hypopnea syndrome. When traumatic temporomandibular joint ankylosis occurs during childhood, it can cause facial asymmetry, micrognathia, and malocclusion, which significantly affect the physical and mental health. Once temporomandibular joint ankylosis occurs, it will be refractory and recurrent. The pathogenesis of temporomandibular joint ankylosis has not been completely elucidated and has always been a research hotspot in the oral and maxillofacial fields. In this paper, worldwide research was conducted, and the pathogenesis of traumatic temporomandibular joint ankylosis was clarified, such as “damage of condyle”,“disc displacement or rupture”,“damage to the glenoid fossa” and “lateral pterygoid muscle distraction”. The relative pathogenesis hypotheses were summarized, such as “hematoma organization” and “lateral pterygoid muscle distraction osteogenesis”. The related pathogenesis of traumatic temporomandibular joint ankylosis was discussed based on the latest cytology and molecular biology research.

Effect of risperidone on proliferation and apoptosis of MC3T3-E1 cells

This aim of this study was to assess the molecular mechanism of osteoporosis in schizophrenia patients with risperidone use. Here, we investigated the effects of risperidone on cellular proliferation and apoptosis of a preosteoblast cell line, MC3T3-E1. Cell viability and apoptotic rate of MC3T3-E1 were detected by cell counting kit-8 and flow cytometry at a serial dose of risperidone and at different time points, respectively. Bone transformation relevant gene serum osteocalcin (BGP), collagen 1, tumor necrosis factor-α (TNF-α), osteoprotegerin (OPG), and receptor activator of nuclear factor-κB ligand (RANKL) mRNA levels were determined by real-time PCR (qPCR). Their protein expression patterns were evaluated using western blot. The results revealed that risperidone dramatically inhibited MC3T3-E1 cell proliferation in a dose-dependent manner. It also significantly induced MC3T3-E1 cell apoptosis. TNF-α gene and protein levels were greatly enhanced after risperidone treatment. In contrast, BGP, collagen 1, OPG, and RANKL gene and protein levels were markedly downregulated. Our study indicated that risperidone suppressed MC3T3-E1 cell proliferation and induced apoptosis. It also regulated BGP gene and protein expression.

Individual Health Risk and Ethics of Health Care / 中国医学伦理学

By reviewing relevant literatures in bioethics and clinical medicine,this thesis explores a series of issues including the ethics education of health risk factors,carrier ethics,ethics of family health care,information property right and file clarification,genotyping ethics,individual decision-making,informed consent,and consent contract.