BACKGROUND: Standard treatments may provide adequate containment in mild to moderate Legg-Calve-Perthes disease (LCPD), but they can be problematic in more severe cases. The purpose of this study was to report the results of combined shelf acetabuloplasty with femoral varus osteotomy in severe LCPD. METHODS: We reviewed 12 patients who had undergone combined shelf acetabuloplasty with femoral varus osteotomy. The indications for this type of operation were: (1) above 8 years of age at clinical onset; (2) massive femoral epiphysis involvement (Catterall group 4, lateral pillar C); (3) femoral head lateral subluxation on the anteroposterior radiograph; and (4) impending hinged abduction on preoperative magnetic resonance imaging or arthrography. The mean age was 9.3 years (range, 8 to 10.8 years). The patients were clinically evaluated with Iowa hip score and leg length discrepancy at the final follow-up. Radiographic outcome was assessed using the Stulberg classification to evaluate femoral head sphericity. The presence of osteoarthritis was evaluated by the Tonnis classification. Correlation analysis was conducted to analyze the preoperative factors that were strongly associated with patients' outcomes. RESULTS: The mean follow-up period was 10.1 years (range, 7.1 to 13.2 years). Functional grade was excellent in all patients at last follow-up (mean, 92; range, 82 to 99). The mean leg length discrepancy after skeletal maturity was 0.9 cm (range, 0 to 1.7 cm). There were no significant complications or need for additional surgery. Radiographically, 92% of patients reached satisfactory outcomes: Stulberg grade I, 0 cases; Stulberg grade II, 4 cases (34%); Stulberg III, 7 cases (58%), Stulberg IV, 1 case (8%); and Stulberg V, 0 cases. There was no osteoarthritis by Tonnis classification. CONCLUSIONS: The surgical outcomes for combined shelf acetabuloplasty with femoral varus osteotomy in severe LCPD patients over 8 years old are comparable with other advanced surgical methods. In the cases of severe disease that match our inclusion criteria, our containment method could be another treatment option.
Acetabuloplasty/adverse effects/*methods ; Child ; Female ; Humans ; Leg Length Inequality ; Legg-Calve-Perthes Disease/radiography/*surgery ; Male ; Osteotomy/adverse effects/*methods ; Pain ; Postoperative Complications ; Retrospective Studies ; Treatment Outcome

No abstract available.
Hemorrhage*

No abstract available.
Hemorrhage*

Prospective study of gallbladder wall thickness by utrasonography was performed in 38 patients of acute viral hepatitis and 50 normal subjects as a control group from June 1983 to April 1984. The results were as follows; 1.In normal population, the range of gallbladder wall thickness is from 1mm to 3mm with peak incidence in 2mm(66%,33 case). Mean thickness of gallbladder wall is about 1.9±0.6mm. 2. In acute viral hepatitis, the range of gallbladder wall thickness is from 2mm to 8mm with peak incidence in 3mm(34%, 13 case), second peak in 4mm (29%,11 case). Mean thickness of gallbladder wall is about 3.6±1.6mm, which is thicker than normal with statistical signifiance. (p<0.005) 3, In acute viral hepatitis , the mean thickness of glabladder wall is about 4.4±1.8mm in the group of SGOT/ SGPT level above 400 IU, and 2.8±0.8mm in the group of SGOT/SGPT level below 400 IU. This difference is significant statistically. (p<0.05).
Alanine Transaminase ; Gallbladder ; Hepatitis ; Humans ; Incidence ; Prospective Studies

No abstract available.
Fetal Death*

The T cell antigen receptor (TcR) in combination with costimulatory signals triggered by accessory molecules present on the surface of the antigen-presenting cells (APC) regulates the activation and growth of T lymphocytes. Calyculin A and Okadaic acid is known to be an inhibitor of serine/threonine phosphatase and RK-682 specifically blocks functions of tyrosine phosphatase. To investigate roles of these inhibitors in TcR-mediated signaling cascade, chimeric molecule CD8-5 which contains the extracellular and transmembrane domains of the human CD8a molecule and the cytoplasmic tail of TcR 5 chain were stably expressed in Jurkat cell line. CD8-5 chimeric protein induced tyrosine phosphorylation of various cytoplasmic substrates and IL-2 gene expression in a NFAT dependent manner by stimulation with anti-CD8 mAb OKT8 as seen in TcR stimulation. When CD8-5 transfectants were preincubated with Okadaic acid, Calyculin or RK682, they differentially affected tyrosine phosphorylation of signaling mediators including CD8-5 molecule. When Jurkat Tag cell line was used where SV40 T antigen is stably expressed and the expression of p-galactosidase is driven by the multiple NFAT binding sites plus minimal IL-2 promoter, these phosphatase inhibitors -RK682, Calyculin A, Okadaic acid- effectively inhibited IL-2 gene expression at the concentration of 1.2832 x 10 ' M, 3.9924 x 10 M, 7.2707 x 10 M respectively. These results suggested that Okadaic acid, Calyculin or RK682 modulate TcR-proximal as well as TcR-distal signaling events during T cell activation.
Antigen-Presenting Cells ; Antigens, Viral, Tumor ; Binding Sites ; Cell Line ; Cytoplasm ; Gene Expression ; Humans ; Interleukin-2 ; Jurkat Cells ; Okadaic Acid* ; Phosphorylation ; Receptors, Antigen, T-Cell ; T-Lymphocytes ; Tyrosine

The earliest reports of the use of electrical energy to directly stimulate bone healing seem to be in 1853 from England, the techniques involved the introduction of direct current into the non-united fracture site percutaneously via metallic needles, with subsequent healing of the defect. One endpoint of the periodontal therapy is to generate structure lost by periodontal diseases. Several procedural advances may support regeneration of attachment, however, regeneration of alveolar bone does not occur consistently. Therefore, factors which stimulate bone repair are areas for research in periodontal reconstructive therapy. Effects of cytokines or growth factors on bone repair are examples of such areas. Another one is electrical current which occurs in bone naturally, so that such bone may be particularly susceptible to electrical therapy. The purposes of this study were to observe the effects of electrical stimulation on the normal periodontium, to determine whether the electricity is the useful means for periodontal regeneration or not. Forty rats weighted about 100 gram were used and divided into 4 groups, the first group, there was no electrical stimulation with the connection of electrodes only. In the second group, there was stimulated by the 10 mA during 10 minutes per a day, in the third group was stimulated by the 25 mA , and the fourth by the 50 mA. At 3, 5, 10 and 15 days post-appliance , two rats in each group were serially sacrificed. and the maxillae and the mandible processed to paraffin, and the specimens were prepared with Hematoxylin-Eosin stain for the light microscopic evaluation. The results of this study were as follows : 1. There was the distinct reversal line on the lingual alveolar crest, whereas a little changes in the labial alveolar crest to the duration and amount of currents. 2. In 50 mA group, the cells were highly concentrated at the apex of anterior teeth, and was observed the necrotic tissue. In posterior root apex, the hypercementosis was appeared, and newly formed cementum layer has been increased continuously with the time. 3. The periodontal ligament fiber and Sharpey's fiber were arranged in order, and the bone trabeculae were increased as the experiment proceeded by, relatively the bone marrows were decreased. 4. In the pulp tissue, the blood vessels were increased with blood congestion in the experimetal specimens remarkably, and the dentinal tubules were obstructed . 5. The osteoblasts in alveolar bone proper had been showed highly activity, and also observed the formation of bone trabeculea. In the conclusion, it was suggested that the electrical stimulation has influence on the periodontium and the pulp tissue. However, there might be the injurious effects.
Animals ; Blood Vessels ; Bone Marrow ; Cytokines ; Dental Cementum ; Dentin ; Electric Stimulation* ; Electricity ; Electrodes ; England ; Estrogens, Conjugated (USP) ; Hypercementosis ; Intercellular Signaling Peptides and Proteins ; Mandible ; Maxilla ; Needles ; Osteoblasts ; Osteogenesis ; Paraffin ; Periodontal Diseases ; Periodontal Ligament ; Periodontium* ; Rats ; Regeneration ; Tooth

PURPOSE: To evaluate the use of stereotactic navigation during orbital decompression surgery. METHODS: We conducted a retrospective analysis of 27 patients (48 orbits) with thyroid-associated orbitopathy who underwent orbital decompression. Stereotactic navigation was performed on 28 orbits of 15 patients, and orbital decompression surgery without navigation was performed on 20 orbits of 12 patients. The changes in medial wall, lateral wall and inferior wall orbital volume in CT scans and horizontal and vertical eyeball deviation after surgery were analyzed in the 2 patient groups. RESULTS: The mean decompressed volume of orbits was significantly increased in the lateral wall decompression with stereotactic navigation patient group than without stereotactic navigation (p < 0.05, p = 0.025). However, in the inferior wall and the medial wall decompression, there was no significant difference between the 2 groups. The changes of horizontal and vertical deviation were not significant between the 2 groups and no patient experienced neural damage. CONCLUSIONS: The stereotactic navigation during lateral orbital wall decompression is a safe and effective method for inducing greater decompressed volume.
Decompression* ; Humans ; Orbit* ; Retrospective Studies ; Tomography, X-Ray Computed

A major limiting factor in the use of cyclosporine A (CsA) is nephrotoxicity, but the mechanisms of nephrotoxicity are not fully understood. In order to elucidate the pathogenesis of CsA tubulotoxicity, we examined mechanisms (DNA synthesis, necrosis and apoptosis) of cellular injury induced by CsA in cultured LLC-PK1 renal tubular cell line. The possible role of Fas antigen in the mediation of CsA-induced cell death and the hypothesis that CsA-mediated injury activates the glucose transporter GLUT1, a stress response gene in renal tubular cells were also investigated. CsA treatment for 24 hours in LLC-PK1 cells showed significantly decreased 3H-thymidine uptake in a dose dependent manner (0.1 microgram/ml to 1 mg/ml), indicating that DNA damage is a sensitive indicator of CsA induced nephrotoxicity. A dose of 10 microgramml CsA caused a significant increase in LDH release (M+/-S.D., 11.0+/-3.0% vs 27.0+/-9.8, p<0.05). On flow cytometric analysis, 9.9 4.2% of control cells appeared in a region of decreased forward light scatter and increased side scatter, respectively. Both indices representing characteristics of apoptotic cell death. Compared to control, treatment with 10 ng/ml of CsA for 24 hours significantly increased the proportion of cells in apoptotic region to 38.9 13.5%. This finding was supported by electrophoretic analysis of the DNA extracted from CsA-treated cells, where a series of bands corresponding to integer multiples of 180 to 200 base pairs was visualized. CsA (0.1 microgram/ml) treatment for 24 hours was seen to cause a significant elevation in the expression of the 45 kD Fas protein by Western blot analysis. In addition, the exposure to CsA was also associated with an increase of GLUT1 protein levels up to 2.2 fold (mean) on Western blot analysis. In conclusion, CsA is directly toxic to tubular cells with inhibiting DNA synthesis and inducing cell death in the form of necrosis or apoptosis. Fas antigen-ligand system and glucose transporter GLUT1 may play roles in mediating CsA induced tubular cytotoxicity.
Animals ; Antigens, CD95 ; Apoptosis* ; Base Pairing ; Blotting, Western ; Cell Death ; Cell Line ; Cyclosporine* ; DNA ; DNA Damage ; Epithelial Cells* ; Glucose Transport Proteins, Facilitative ; Glucose Transporter Type 1 ; LLC-PK1 Cells ; Necrosis ; Negotiating ; Swine

A major limiting factor in the use of cyclosporine A (CsA) is nephrotoxicity, but the mechanisms of nephrotoxicity are not fully understood. In order to elucidate the pathogenesis of CsA tubulotoxicity, we examined mechanisms (DNA synthesis, necrosis and apoptosis) of cellular injury induced by CsA in cultured LLC-PK1 renal tubular cell line. The possible role of Fas antigen in the mediation of CsA-induced cell death and the hypothesis that CsA-mediated injury activates the glucose transporter GLUT1, a stress response gene in renal tubular cells were also investigated. CsA treatment for 24 hours in LLC-PK1 cells showed significantly decreased 3H-thymidine uptake in a dose dependent manner (0.1 microgram/ml to 1 mg/ml), indicating that DNA damage is a sensitive indicator of CsA induced nephrotoxicity. A dose of 10 microgramml CsA caused a significant increase in LDH release (M+/-S.D., 11.0+/-3.0% vs 27.0+/-9.8, p<0.05). On flow cytometric analysis, 9.9 4.2% of control cells appeared in a region of decreased forward light scatter and increased side scatter, respectively. Both indices representing characteristics of apoptotic cell death. Compared to control, treatment with 10 ng/ml of CsA for 24 hours significantly increased the proportion of cells in apoptotic region to 38.9 13.5%. This finding was supported by electrophoretic analysis of the DNA extracted from CsA-treated cells, where a series of bands corresponding to integer multiples of 180 to 200 base pairs was visualized. CsA (0.1 microgram/ml) treatment for 24 hours was seen to cause a significant elevation in the expression of the 45 kD Fas protein by Western blot analysis. In addition, the exposure to CsA was also associated with an increase of GLUT1 protein levels up to 2.2 fold (mean) on Western blot analysis. In conclusion, CsA is directly toxic to tubular cells with inhibiting DNA synthesis and inducing cell death in the form of necrosis or apoptosis. Fas antigen-ligand system and glucose transporter GLUT1 may play roles in mediating CsA induced tubular cytotoxicity.
Animals ; Antigens, CD95 ; Apoptosis* ; Base Pairing ; Blotting, Western ; Cell Death ; Cell Line ; Cyclosporine* ; DNA ; DNA Damage ; Epithelial Cells* ; Glucose Transport Proteins, Facilitative ; Glucose Transporter Type 1 ; LLC-PK1 Cells ; Necrosis ; Negotiating ; Swine