This study was investigated to compare the bond strength of polysulfide adhesive between tray resin and border molding materials and to evaluate the effect of saliva contamination on them. We made the 135 resin tray secimens with a dimension of 1 X 1 X 1cm and divided them into 3 groups by the materials 1) Quicky group, 2) Compound group, and 3) Impregum group Each group was subdivided by saliva contimination. Group S I: applied adhesive without saliva contamination Group S2: applied adhesive after drying 15seconds after saliva contamination Group S3: applied adhesive no after saliva contamination. Tensile tests were performed with a Universal Load testing machine. Results showed Impregum group significantly higher bond strength than Quicky group, but there was no significant difference in adhesive bond strength between Compound group and Quicky group in experimental group by materials In experimental group by saliva contamination, S1 group is signifiantly higher bond strength than S2 group and S2 group is signifiantly higher bond strength than S3 group in Quicky group and S1, S2 group is signifiantly higher bond strength than S3 group in Compoud group and ImpregLun group. Impression compound and Impregum F which are usually used as an individual tray border molding material can be said to be satisfied in adhesive bond strength to polysulfide impression materials. After try-in and clinical adjustment are performed, a custom tray should be properly rinsed and air dried before tray adhesive was placed.
Adhesives* ; Fungi* ; Saliva

No abstract available.

No abstract available.

Extracapsular cataract extraction(ECCE) with posterior chamber intraocular lens(PC-IOL) implantation is now favorable surgery to improye decreased visual acuity due to cataract. But this surgical method often causes secondary glaucoma, hyphema, uveitis, and macular edema, which result in poor visual outcome. We studied the causes of elevated intraocular pressure(IOP) retrospectively in 15 eyes of 14 patients among 1,657 cases undergone with the implantation of PC-IOL, in recent 5 years. As the preoperative causes, preexisting uveitis(5 eyes, 33%) and underlying glaucoma(3 eyes, 20%) were important factors. Postoperative causes were newly developed uveitis(1 eye, 6.7%), steroid responder(2 eyes, 13.3%) and idiopathy(4 eyes, 27%). From the above results, We should take more meticulous care in intraoperative and postopertive management in cases of preexisting uveitis and glaucoma.
Cataract Extraction* ; Cataract* ; Glaucoma ; Humans ; Hyphema ; Intraocular Pressure* ; Lenses, Intraocular* ; Macular Edema ; Retrospective Studies ; Uveitis ; Visual Acuity

No abstract available.

STUDY DESIGN: Establishment of a multipotent neural stem cell line from the adult mouse cerebrum. OBJECTIVES: To establish a daughter cell line, B2A1, from B2 cells through the limiting dilution method, and to determine if the cells have the characteristics of neural stem cell (NSCs) using immunocytochemistry and RT-PCR methods. SUMMARY AND LITERATURE REVIEW: In the development of NSCs, differentiated organ or tissue-derived multipotent stem cells have attracted considerable interest because of the lack of ethical issues. Previously, a glial precursor cell line (B2 cells) was generated from the primary cultures of oligodendrocytes/ astrocytes in an adult BALB/c mouse brain. These cells exhibited the cell-type specific markers for immature neuroectodermal cells, astrocytes, and oligodendrocytes in serum-contained media. MATERIALS AND METHODS: The primary cultures of oligodendrocytes/astrocytes were established from the whole brains of 12 to 16-week-old BALB/c mice from either gender. After 6 months with 25 serial passages, the culture consisted of a morphologically homogeneous cell population, which was designated as B2 cells. A subclone, B2A1, was isolated from B2 cells through two consecutive limiting dilutions. RESULTS: More than 90% of B2A1 cells showed immunopositivity for nestin, a specific marker for NSC. The cells also showed immunopositivity for the neuronal, astrocytic and oligodendroglial markers. These cells expressed the genotypic mRNA messages for both neural progenitor cells and differentiated neuronoglial cells. These positive immunocytochemical reactions and mRNA messages for neuronoglial cells varied according to the extrinsic growth factors used. However, the treatment of extrinsic growth factors did not produce any significant differences in the nestin-immunopositive cells. CONCLUSIONS: B2A1 cells have the immunocytochemical and cytogenetic properties of NSCs, and the capacity to differentiate into neuronoglial cells.
Adult* ; Animals ; Astrocytes ; Brain ; Cell Line ; Cerebrum* ; Cytogenetics ; Ethics ; Humans ; Immunohistochemistry ; Intercellular Signaling Peptides and Proteins ; Mice* ; Multipotent Stem Cells ; Nestin ; Neural Plate ; Neural Stem Cells* ; Neurons ; Nuclear Family ; Oligodendroglia ; RNA, Messenger ; Serial Passage ; Stem Cells

No abstract available.
DNA* ; Ploidies* ; Stomach Neoplasms*

BACKGROUND: Enhanced lipogenesis plays a critical role in cell senescence via induction of expression of the mature form of sterol regulatory element binding protein 1 (SREBP1), which contributes to an increase in organellar mass, one of the indicators of senescence. We investigated the molecular mechanisms by which signaling molecules control SREBP1-mediated lipogenesis and senescence. METHODS: We developed cellular models for stress-induced senescence, by exposing Chang cells, which are immortalized human liver cells, to subcytotoxic concentrations (200 microM) of deferoxamine (DFO) and H2O2. RESULTS: In this model of stress-induced cell senescence using DFO and H2O2, the phosphorylation profile of glycogen synthase kinase 3alpha (GSK3alpha) and beta corresponded closely to the expression profile of the mature form of SREBP-1 protein. Inhibition of GSK3 with a subcytotoxic concentration of the selective GSK3 inhibitor SB415286 significantly increased mature SREBP1 expression, as well as lipogenesis and organellar mass. In addition, GSK3 inhibition was sufficient to induce senescence in Chang cells. Suppression of GSK3 expression with siRNAs specific to GSK3alpha and beta also increased mature SREBP1 expression and induced senescence. Finally, blocking lipogenesis with fatty acid synthase inhibitors (cerulenin and C75) and siRNA-mediated silencing of SREBP1 and ATP citrate lyase (ACL) significantly attenuated GSK3 inhibition-induced senescence. CONCLUSION: GSK3 inactivation is an important upstream event that induces SREBP1-mediated lipogenesis and consequent cell senescence.
Aging* ; Aminophenols ; ATP Citrate (pro-S)-Lyase ; Carrier Proteins* ; Cell Aging ; Deferoxamine ; Fatty Acid Synthetase Complex ; Glycogen Synthase Kinase 3* ; Glycogen Synthase Kinases* ; Glycogen Synthase* ; Glycogen* ; Humans ; Lipogenesis* ; Liver ; Maleimides ; Multienzyme Complexes ; Oxo-Acid-Lyases ; Phosphorylation ; RNA, Small Interfering ; Sterol Regulatory Element Binding Protein 1

BACKGROUND: Enhanced lipogenesis plays a critical role in cell senescence via induction of expression of the mature form of sterol regulatory element binding protein 1 (SREBP1), which contributes to an increase in organellar mass, one of the indicators of senescence. We investigated the molecular mechanisms by which signaling molecules control SREBP1-mediated lipogenesis and senescence. METHODS: We developed cellular models for stress-induced senescence, by exposing Chang cells, which are immortalized human liver cells, to subcytotoxic concentrations (200 microM) of deferoxamine (DFO) and H2O2. RESULTS: In this model of stress-induced cell senescence using DFO and H2O2, the phosphorylation profile of glycogen synthase kinase 3alpha (GSK3alpha) and beta corresponded closely to the expression profile of the mature form of SREBP-1 protein. Inhibition of GSK3 with a subcytotoxic concentration of the selective GSK3 inhibitor SB415286 significantly increased mature SREBP1 expression, as well as lipogenesis and organellar mass. In addition, GSK3 inhibition was sufficient to induce senescence in Chang cells. Suppression of GSK3 expression with siRNAs specific to GSK3alpha and beta also increased mature SREBP1 expression and induced senescence. Finally, blocking lipogenesis with fatty acid synthase inhibitors (cerulenin and C75) and siRNA-mediated silencing of SREBP1 and ATP citrate lyase (ACL) significantly attenuated GSK3 inhibition-induced senescence. CONCLUSION: GSK3 inactivation is an important upstream event that induces SREBP1-mediated lipogenesis and consequent cell senescence.
Aging* ; Aminophenols ; ATP Citrate (pro-S)-Lyase ; Carrier Proteins* ; Cell Aging ; Deferoxamine ; Fatty Acid Synthetase Complex ; Glycogen Synthase Kinase 3* ; Glycogen Synthase Kinases* ; Glycogen Synthase* ; Glycogen* ; Humans ; Lipogenesis* ; Liver ; Maleimides ; Multienzyme Complexes ; Oxo-Acid-Lyases ; Phosphorylation ; RNA, Small Interfering ; Sterol Regulatory Element Binding Protein 1

no abstract available.