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Biomedical subjects

K Hanada

Publications and source records attributed to K Hanada.

At least 379 records · Page 21Linked to original sources
PubMed1976

Orthodontic treatment of malocclusions caused by facial trauma.

Assessment and orthodontic treatment of malocclusions caused by traffic accidents were reported. Different methods were employed to reestablish the harmony of the occlusion with consequent good facial appearance. Appliances like the activator and direct bonding techniques were illustrated. Principles and techniques of orthodontics play an important role in the treatment of the malocclusions left untreated at the time of surgical operation for the facial trauma.

Activator Appliances↗
PubMed1976

Surgical-orthodontic approach to skeletal class III malocclusion.

Twenty-nine adult patients with skeletal Class III malocclusion were treated by combined surgical-orthodontic management. A thorough analysis enabled us to point out the exact location and degree of the deformity and was of great help in determining the appropriate types of treatment. Corrections were made in 12 patients by the mandibular body ostectomy in the premolar region; the curved oblique osteotomy, in which the ascending ramus was cut obliquely on a curved line from the anterior border of the ramus to the angle, was used for the treatment of the remaining 17 patients. The resulting profile and occlusal improvements were satisfactory, Preoperative orthodontic treatment such as leveling of the dental arches, expansion of the upper dental arch to accommodate the maxilla to the mandible, correction of the upper and lower incisal inclinations, extraction of the premolars to decrease horizontal discrepancy or alignment of malpositioned teeth, and postoperative adjustment were effective in providing definite changes in profile and a stable occlusion-an important factor in the prevention of postoperative relapse.

Adult↗
PubMedDate not supplied

In vivo introduction of the interleukin 6 gene into human keratinocytes: induction of epidermal proliferation by the fully spliced form of interleukin 6, but not by the alternatively spliced form.

The achievement of keratinocyte gene therapy in clinical practice requires fundamental experiments using human keratinocytes or skin. We have recently demonstrated that the in vivo introduction of the interleukin 6 (IL-6) gene into rat keratinocytes induces epidermal proliferation and lymphocyte infiltration into the skin. In this study, we first amplified the human IL-6 cDNA from oligo-dT-primed keratinocyte cDNA and then detected the fully spliced (FS) form and the alternatively spliced (AS) form of IL-6 cDNA. Sequence analysis showed that the AS form, which was composed of the IL-6 coding region with all of exon II deleted except for the first guanine, was identical to that reported to be present in lymphocytes. We constructed the expression vectors phIL6 of the FS form and phIL6S of the AS form. We transplanted human skin onto nude rats and introduced phIL6 and phIL6S into the human keratinocytes using the naked DNA method. Keratinocytes prepared 24 h after introduction from the areas treated with them were examined by reverse transcriptase (RT)-PCR and enzyme linked immunosorbent assay (ELISA). RT-PCR showed that the amounts of FS IL-6 mRNA and AS IL-6 mRNA were similar, whereas the ELISA showed that the amount of FS IL-6 peptide was four times that of the AS IL-6 peptide. Histological examination 48 h after introduction showed that the FS form had induced epidermal proliferation, whereas the AS form had not. The epidermal thickening without lymphocyte infiltration induce by the FS form indicates that keratinocyte proliferation is caused by a direct effect of overexpressed IL-6, and not by a secondary effect of infiltrating lymphocytes. This is the first report of the introduction of a human gene into human keratinocytes to produce a biologically active transgenic gene product in human skin using the naked DNA method.

Alternative Splicing↗