On the basis of the preliminary study of the prevention and treatment of Bohai Sea divers' dermatitis from 1983 to 1987, the morphological characteristic of 5. rosea (see section I ), the pathogenic organism of the divers' dermatitis, was studied in the field of systematic zoology, some aspect concerning medical pathogenic characteristic of the nematocysts from the red sea anemone (section I ) was studied from the point of view of pathophysiology,a preliminary study on active proteins from 5. rosea (section I ) was studied according to toxicology. The article further stated the pathogenic mechanism of the sea anemones' dermatitis, in order to go further into the new ways and methods for preventing and treating the divers' dermatitis.

Objective To observe the effect on Foxg1 gene expression in the subgranular zone (SGZ) of cerebral tissue from neonatal rats with hypoxic-ischemic brain damage (HIBD) after transplantation of neural stem cells (NSCs) derived from umbilical cord blood.Methods Mononuclear cells separated from umbilical cord blood by density gradient centrifugation were cultured with orientated induction to differentiate the NSCs.The neuronal phenotype was identified using immunocytochemical methods.A total of 150 Sprague-Dawley rats were randomly divided into a sham-operation group,an HIBD group and an HIBD-NSCs group.Rats in the HIBD group and the HIBD-NSCs group were subject to ligation of the left carotid artery and then kept in a box under 8％ oxygen and 92％ nitrogen for 2.5 hours to establish the HIBD animal model.The artery was separated but not ligated in the sham operation group,which was not subjected to hypoxia.Twenty-four hours after the operation,the cultivated NSCs were transplanted by caudal vein injection into the rats in the HIBD-NSCs group.Rats were then sacrificed on the 3rd,7th,14th,21st and 28th days after the operation.Foxg1 gene expression in the SGZ was examined using in-situ hybridization methods.Results The number of Nestin-positive cells peaked on the 6th day of cultivation and then decreased by the 9th day.The Foxg1 gene was expressed in the SGZs of each group.The expression increased by the 3rd day after surgery in the HIBD and HIBD-NSCs groups,and peaked on 7th day after the operation,then declined gradually.The average expression level of Foxg1 in the HIBD group was significantly lower than that in the HIBD-NSCs group on the 7th day and thereafter.Conclusions Human umbilical cord blood mesenchymal stem cells can be induced and differentiated into neural stem cells.Foxg1 genes can still be present in the SGZ after birth.HIBD can induce the expression of Foxg1 genes.Transplanting NSCs can promote the expression of Foxg1 genes and improve morphological and functional recovery after HIBD,at least in neonatal rats.

Osteosarcoma is the most common primary sarcoma of bone, and it is a leading cause of cancer death among adolescents and young adults. However, the molecular mechanism underlying osteosarcoma carcinogenesis remains poorly understood. Recently, cyclin-dependent kinase 6 (CDK6) was identified as an important oncogene. We found that CDK6 protein level, rather than CDK6 mRNA level, is much higher in osteosarcoma tissues than in normal adjacent tissues, which indicates a post-transcriptional mechanism involved in CDK6 regulation in osteosarcoma. MiRNAs are small non-coding RNAs that repress gene expression at the post-transcriptional level and have widely been shown to play important roles in many human cancers. In this study, we investigated the role of miR-29b as a novel regulator of CDK6 using bioinformatics methods. We demonstrated that CDK6 can be downregulated by miR-29b via binding to the 3'-UTR region in osteosarcoma cells. Furthermore, we identified an inverse correlation between miR-29b and CDK6 protein levels in osteosarcoma tissues. Finally, we examined the function of miR-29b-driven repression of CDK6 expression in osteosarcoma cells. The results revealed that miR-29b acts as a tumor suppressor of osteosarcoma by targeting CDK6 in the proliferation and migration processes. Taken together, our results highlight an important role for miR-29b in the regulation of CDK6 in osteosarcoma and may open new avenues for future osteosarcoma therapies.
3' Untranslated Regions ; Animals ; Base Sequence ; Bone Neoplasms ; metabolism ; pathology ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Cyclin-Dependent Kinase 6 ; antagonists & inhibitors ; genetics ; metabolism ; Humans ; Mice ; MicroRNAs ; metabolism ; Osteosarcoma ; metabolism ; pathology ; RNA Interference ; RNA, Messenger ; metabolism ; RNA, Small Interfering ; metabolism ; Rats ; Sequence Alignment ; Up-Regulation