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Change in soft tissue in relation to that in hard tissue following orthognathic surgery was evaluated. Twenty-five patients were enrolled in the study. The diagnosis in all was jaw deformity (maxillary retrusion and mandibular protrusion) and all underwent a Le Fort I osteotomy and bilateral sagittal splitting ramus osteotomy. Three-dimensional (3D) computer-aided design (CAD) models (polygon models) of the hard and soft tissue of the maxilla and mandible were constructed and superimposed. Reference points were established on the pre- and postoperative hard and soft tissues. Specific elements of each reference point were divided into X, Y, and Z components, respectively, and the distances in each direction and 3D distance (normal distance) measured. The Wilcoxon signed-rank test was used to determine differences in the mean values for the distance moved of each element as the error between pre- and postoperatively. The results revealed statistically significant differences in the Y-direction in the maxilla and the X- and Z-directions in the mandible. A significant difference was also observed in the 3D distances of the maxilla and mandible. Little evidence was found of linearity between the amount of hard and soft tissue movement in the X- and Z-directions in the maxilla. This means that 3D movement in the maxilla was masked more by changes in the morphology of the soft tissue than in the mandible, making it less evident. The results of this study suggest that the 3D analysis method used enables changes in hard and soft tissues to be understood qualitatively, and that it can be used in diagnosis and treatment in orthognathic surgery. It may also be useful in simulation of morphological change in soft tissue.

Objectives: This study explores clinical and laboratory abnormalities that contribute to the prevalence of bone fractures in frail and control elderly patients, to ascertain factors that relate to bone strength and fragility., Methods: Patients were selected as free from renal failure and not taking supplements or medications that affect their magnesium status, and categorized according to their underlying diseases, sex and age, and evaluated by tests of bone strength., Results: Findings, differentiating elderly patients on the basis of their magnesium, calcium, serum albumin, body mass, bone mineral density and their fracture occurrence were tabulated., Conclusion: Evidence is presented of low magnesium and albumin serum levels, especially in women with low bone density, as well as of low calcium and trace minerals.

Erythropoietic protoporphyria (EPP) is an inherited disorder of heme biosynthesis caused by cellular decreases in ferrochelatase (FECH) activity. Clinical expression of this disorder usually requires coinheritance of a mutant FECH allele and a normal FECH allele expressed at a low level. In this study, we investigated the methylation status of a normal, but poorly expressed, FECH gene in a single Japanese family with EPP. In this family, the proband died from liver failure, whereas the mother and sister exhibited overt EPP with mild liver dysfunction. A splicing mutation (IVS9+1g-->a) in the FECH gene, which produces a mutant FECH transcript lacking exon 9, was detected in the maternal allele of the proband and his sister. All subjects, including the father, who did not exhibit EPP, possessed the IVS3-48c/c genotype. This allele increases the proportion of aberrantly spliced mRNA, resulting in reduced FECH activity. Normal FECH transcripts were, however, detected in the mother and sister, but not in the proband. The CpG sites in the region from bases -78 to -31 were partially methylated in the proband and his father, but not in his mother or sister. Additionally, CpG methylation within this region reduced transcription of the FECH gene. These results suggest that whereas the combination of a maternal IVS9+1a allele and a paternal IVS3-48c allele results in overt EPP, CpG methylation of the FECH gene promoter, likely inherited from the father, increases the severity of EPP, leading to fatal liver failure, as seen in the proband.

Cyclin D1, one of the G(1) cyclins, is frequently overexpressed in several types of carcinomas and is thought to play an important role in tumorigenesis and tumor progression including hepatocellular carcinoma. We constructed a retrovirus vector-carrying rat cyclin D1 cDNA in the reverse orientation, resulting in expression of antisense (AS) cyclin D1 mRNA. For efficient transduction of this recombinant retrovirus, two-step gene transfer was performed. The rat hepatoma cell line (dRLh84) was infected with this recombinant retrovirus after preinfection with adenovirus expressing the retrovirus receptor. In the rat hepatoma cells, AS cyclin D1 mRNA was expressed, inducing a decrease in the expression of endogenous cyclin D1 mRNA and an inhibition of cell growth. Moreover, two-step gene transfer of AS cyclin D1 into s.c. hepatoma xenografts resulted in inhibition of tumor growth and prolonged animal survival. In the virus-infected tumor xenografts, expression of cyclin D1 was immunohistochemically inhibited, and apoptosis of hepatoma cells was detected. These findings suggest that transduction of AS cyclin D1 is useful as an adjunct to standard treatments for hepatocellular carcinoma.

We previously reported that the retroviral vector expressing the herpes simplex virus-thymidine kinase gene under the control of 0.3-kb human alpha-fetoprotein (AFP) gene promoter (AF0.3) provided the cytotoxicity to ganciclovir (GCV) in high-AFP-producing human hepatoma cells but not in low-AFP-producing cells. Therefore, specific enhancement of AFP promoter activity is likely to be required to induce enough cytotoxicity in low-AFP-producing hepatoma cells. In this study, we constructed a hybrid promoter, [HRE]AF, in which a 0.4-kb fragment of human vascular endothelial growth factor 5'-flanking sequences containing hypoxia-responsive element (HRE) was fused to AF0.3 promoter. By means of the reporter gene transfection assay, hypoxia-inducible transcriptions that were mediated by [HRE]AF promoter were detected in low- and non-AFP-producing human hepatoma cells, but not in nonhepatoma cells. When the herpes simplex virus-thymidine kinase gene controlled by [HRE]AF promoter was transduced into hepatoma and nonhepatoma cells by a retroviral vector, the exposure to 1% O2 induced GCV cytotoxicity specifically in the hepatoma cells. Moreover, in nude mice bearing solid tumor xenografts, only the tumors consisting of the virus-infected hepatoma cells gradually disappeared by GCV administration. These results indicate that the hypoxia-inducible enhancer of the human vascular endothelial growth factor gene, which is directly linked to human AFP promoter, involves selective and enhanced tumoricidal activity in gene therapy for hepatocellular carcinoma.