The Waltons method-a method of dynamic reconstruction of old ligament injuries of the knee and a combination procedure of O'Donoghue, Bosworth, and Slocum-was introduced with one case experience. This method seemed to be better than other reconstructive procedures, especially in the aspect of rotatory and valgus instability of the knee.
Knee ; Ligaments ; Methods

A young metastatic lung cancer patient developed empyema due to an infection with carbapenem-resistant Acinetobacter baumannii. Hydropneumothorax was detected and managed by a tube thoracotomy. However, persistent air leakage through the chest tube was observed due to the presence of a bronchopleural fistula (BPF). As hypercapnic respiratory failure had progressed and the large air leak did not diminish by conservative management, a pumpless extracorporeal lung assist (pECLA) device was inserted. The pECLA allowed the patient to be weaned from mechanical ventilation and the BPF to heal. The present case shows the effective application of pECLA in a patient with empyema complicated with BPF and severe hypercapnic respiratory failure. pECLA enabled us to minimize airway pressure to aid in the closure of the BPF in the mechanically ventilated patient.
Acinetobacter baumannii ; Bronchial Fistula ; Carbon Dioxide* ; Carbon* ; Chest Tubes ; Empyema* ; Fistula ; Humans ; Hydropneumothorax ; Hypercapnia ; Lung ; Lung Neoplasms ; Respiration, Artificial ; Respiratory Insufficiency ; Thoracotomy

No abstract available.

Fibrous Dysplasia of bone is a relatively rare condition characterized by fibrous tissue replacement of skeleton. It may be monostotic (confined to one bone) or polyostotic (situated in many bones). Here, six cases of fibrous dysplasia and, among them, typical three groups classified by Lichtenstein & Jaffe were experienced and treated during past one year. Three cases were monostotic lesion, which is more common, and usually mild and asymptomatic. And another three cases were polyostotic lesion, two of which were not associated with extraskeletal symptoms, and one case was associated with extraskeletal symptoms, so called Albrights disease. These six cases of fibrous dysplasia are reported with a review of the literatures.
Fibrous Dysplasia of Bone ; Skeleton

Recently, it has been postulated that diabetic autonomic neuropathy is caused by reduction in availability of nerve growth factor (NGF) in enteric nervous system. This experiments were performed to determine the changes of the distribution of enteric neuropeptide by diabetes and these changes could be prevented by administration of NGF. Sprague Dawley rats (200~250gm) were made diabetic by a single intraperitoneal injection of streptozotocin 65 mg/kg in saline. Recombinant human NGF (Sigma, Co., Ltd.) were administered at a dose of 500ng/kg subcutaneously every day for consecutive 4 weeks after streptozotocin administration. After 4 weeks, rats were anesthetized with ether and perfused with 4% paraformaldehyde. ileum was dissected and prepared by whole mount preparation method. Prepared segments were immunostained for substance p, calcitonin gene-related peptide, vasoactive intestinal peptide, and galanin by PAP technique. For the observation of the interstitial cells of Cajal, segments were immersed in Champy-Maillet solution for 2 days Results obtained were as follows: 1. In myenteric plexus of diabetic rats, substance P-like and VIP-like immunoreactivity were not changed compared with that of the control group. CGRP-like and galanin-like immunoreactivity were decreased in diabetic group and immunoreactive cells for CGRP and galanin were also decreased 18.1% (P<0.01) and 43.7% (P<0.01) respectively. 2. In NGF administerd diabetic group, immunoreactivity of substance p, VIP, galanin in myenteric plexus were slightly increased and immunoreactive cells for substancre p, VIP, galanin were almost the same as that of the control group. However, immunoreactive cells for CGRP of myenteric plexus were not changed by NGF. 3. In submucous plexus of diabetic rats, immunoreactivity of all four neuropeptides(substance p, CGRP, VIP, galanin) were decreased compared with that of the control group. Immunoreactive cells for substance p, CGRP, VIP, and galanin were also decreased in 38.8%, 77.6%, 33.0%, and 35.7%, respectively (P<0.01). 4. In NGF administered diabetic group, immunoreactivities of substance p, VIP and galanin in submucous plexus were increased and the immunoreactive cells were increased significantly compared to diabetic group. However, immunoreactive cells for CGRP of submucous plexus were not changed by NGF. 5. Interstitial cells of Cajal of diabetic group were decreased 7.4% ovoidal cells (A type) and 28.3% round cells (B type) In NGF administered group, the morphology and the number of ICC were not different to the control group. With the above results, it could be assumed that NGF prevent the damage of neurotransmitter and ICC in enteric nervous system.
Animals ; Calcitonin Gene-Related Peptide ; Diabetic Neuropathies ; Enteric Nervous System ; Ether ; Galanin ; Humans ; Ileum ; Injections, Intraperitoneal ; Interstitial Cells of Cajal ; Myenteric Plexus ; Nerve Growth Factor* ; Neuropeptides ; Neurotransmitter Agents ; Peristalsis* ; Rats* ; Rats, Sprague-Dawley ; Streptozocin ; Submucous Plexus ; Substance P ; Vasoactive Intestinal Peptide

No abstract available.
Lymphangioma, Cystic* ; Turner Syndrome* ; Ultrasonography*

No abstract available.
Child* ; Humans ; Lung Diseases, Interstitial*

Macrodactyly is one of the most difficult congenital anomalies to treat. Treatment of macrodactyly requires surgical intervention because it gives rise to esthetic, social, and functional disability including difficulty in wearing shoes. A myriad of surgical techniques has been introduced to reduce the size of macrodactyly. However, treatment of toe macrodactyly has not been spotlighted due to less significant functional and social issues compared with finger macrodactyly. We treated two patients with toe macrodactyly by single stage reduction operation.
Fingers ; Humans ; Shoes ; Toes*

BACKGROUND: The tumor suppressor gene p53 is one of the most frequently altered genes in human tumors, including those of the lung. There is now a compelling evidence that wild-type p53 can negatively influence cell growth by causing G1 arrest or by inducing apoptosis. The possibilities of using p53 for gene therapy are also gathering much interest. MATERIAL AND METHOD: Our approach towards understanding p53 function would be to study the biological consequences of overexpression of wild-type p53 in normal and tumor cells by using adenovirus vectors capable of giving high levels of the p53 gene product in cells. We have used this vector containing wild-type p53 to infect tumor cells with different p53 status (null, mutant, or wild-type) to confirm that expression of p53 in null or mutant cell lines becomes possible by Adenovirus-p53 transduction, to examine the effects of high levels of p53 expression on the growth properties of tumor cells, to evaluate the role of apoptosis in p53-mediated biological effects, and to examine the effect of Adenovirus-p53 on the tumorigenicities of the lung cancer cell lines in vitro. RESULT: The results of our study showed that cells expressing endogenous mutant p53 and those devoid of p53 expression altogether were significantly more sensitive to Adenovirus-p53-mediated cytotoxicity compared to tumor cells expressing endogenous wild-type p53 and that overexpression of wild-type p53 induced programmed cell death. Also we knew that Adenovirus-p53 significantly reduced tumor colony formation of human non-small cell lung cancer cell lines, and decreased the growth of preformed colonies in vitro. CONCLUSION: These results suggest that adenovirus is an efficient vector for mediating transfer and expression of tumor suppressor genes in human non-small cell lung cancer cells and that the tumor cells null for p53 or expressing mutant p53 readily undergo apoptosis by Adenovirus-p53.
Adenoviridae ; Apoptosis ; Carcinoma, Non-Small-Cell Lung* ; Cell Death ; Cell Line* ; Genes, p53 ; Genes, Tumor Suppressor ; Genetic Therapy ; Humans ; Lung ; Lung Neoplasms ; Negotiating

No abstract available.
Lymphangioma*