No abstract available.

This is to report the histo-pathologic findings of the degenerated inferior alveolar nerves(IAN) causing uncontrollable neuralgia persisted for over 3 years. The patients had sufferred from frequent attack of unbearable pain along the mandibular branches of the Vth nerve. The pain arised spontaneously 5-10 times a day and lasted for 2-5 minutes. The medications including Tegretol were neither so effective to alleviate the pain level, nor enough to keep free from pain all days. The peripheral neurectomies were preceded by diagnostic nerve block, and partial resection of the IAN in the mandibular canals were approached by sagittal split osteomy of the ramus. The histopathologic findings of the resected IAN were as follows ; 1. Special staining with Luxol Fast Blue (LFB) and Masson Trichrome (MT) disclosed marked degeneration of the axons, decreased in number and fibrosis between the nerve fibers. 2. EM study revealed destruction of myelin continuity surrounding axons, degeneration of Schwann cell and endoneureal sheath, and coarse collagen between the destructed axons. 3. The 3 of 6 patients presented again with recurred pain in 2-3 years after the peripheral neurectomies. Excisional biopsy of the retromolarpterygomandibular softtissues disclosed the collateralization neuropathy beside the long-buccal nerves and their neuromatous findings.
Axons ; Biopsy ; Carbamazepine ; Collagen ; Fibrosis ; Humans ; Mandibular Nerve* ; Myelin Sheath ; Nerve Block ; Nerve Fibers ; Neuralgia ; Trigeminal Neuralgia*

No abstract available.

From mechanocardiography and echocardiography, the systolic time intervals and the ejection phase indices were measured with determination of serum digoxin concentration(SDC) to elucidate the value of oral maintenance digoxin therapy on patients with heart failure in sinus rhythm. The drug interactions of digoxin with quinidine in heart failure, with verapamil in atrial fibrillation, and with aluminium hydroxide gel in healthy volunteers were observed with concomitant changes of SDCs. The results obtained are as follows. 1. After 10 days of treatment with digoxin 0.25 mg/day in 21 patients with heart failure there was a significant decrease in electromechanical systole(QS2), pre-ejection period(PEP) and PEP/left ventricular ejection time(LVET) ratio. There was also and equivocal decrease in LVET and an equivocal increase in mean velociy of circumferential fiber shortening(Vcf). However there was no significant change in ejection fraction(EF) and heart rate. The steadystate SDC was 1.20+/-0.12(S.E.M.)ng/ml. 2. Excellent correlation of the systolic time interval sand ejection phase indices measured from mechanocardiography and those determined from echocardiography was demonstrated. 3. SDCs were measured before and following quinidine therapy in 20 patients receiving maintenance digoxin for heart failure and who require quinidine for suppression of ventricular premature beats. Steady-state SDC following quinidine(Y) could be estimated form steady-state SDC before quinidine(X) as expressed by regression equation, Y=-0.394+2.309 X with correlation coeffcient, r=0.927(p<0.01). 4. In 12 patients with atrial fibrillation receving maintenance digoxin 0.25 mg/day, SDC before and following coadministration fo first 160 mg/day and later 240 mg/day of verapamil for 7days on each occasion was 0.85+/-0.07(S.E.M.) ng/ml, 1.00+/-0.09(S.E.M.)ng/ml and 1.33+/-0.13(S.E.M.)ng/ml, respectively. The difference of SDC between at control and under 240mg/day of verapamil was significant statistically(p<0.05). 5. Digoxin 0.75mg single-dose studies of bioavailability in 11 healthy volunteers showed a statistically significant difference(p<0.05) of the area under the 8-hour SDC curve between the digoxin only group and the digoxin plus aluminium hydroxide gel group. The area under the curve was 680+/-25(S.E.M.) min*ng/ml and 509+/-29(S.E.M.) min*ng/ml, respectively.
Atrial Fibrillation ; Biological Availability ; Cardiac Complexes, Premature ; Digoxin* ; Drug Interactions ; Echocardiography ; Healthy Volunteers ; Heart Failure ; Heart Rate ; Humans ; Quinidine ; Silicon Dioxide ; Systole ; Verapamil

The mechanism of cytolysis by complement attack of nucleated cells(NC) is of special interest in comparison to that of red blood cells. It is known that NC death by membrane attack comples, C5b-9, is caused by many factors, i.e., efficiency of complex assembly, activation of intrinsic metabolic pathway by signal transduction, cytotoxic effect of the channel itself and natural repair ability. These factors suggest that colloid osmotic lysis, known in red blood cells, does not fully explain the complement-mediated cell death of NC. In this study, the authors investigated correlation between biochemical and morphological changes to prove "Ca2+-mediated metabolic death"8~13) representing a mechanism of NC death caused by C5b-9 attack. The L1210 cells, mouse leukemic cell line carrying small complement channel(TAC5b-91) were used in the experiments. The amounts of intracellular adenine nucleotides to extracellular Ca2+, ouabain, KC1 and dextran were analyzed by bioluminescence method using luminometer. Cell viability was checked by 0.4% trypan blue dye and LDH release. Morphological observation of TAC5b-91 was done by immunocytochemical staining and electron microscope. The results were as follows: 1) The release of ATP, ADP and AMP followed by cell death was rapid and progressive along the incubation time at 37 degrees C and it was accelerated in 1.5 mM of [Ca2+]0. 2) There was no evidence of ATP repairment in the TAC5b-91. 3) Extracellular KC1(150 mM), dextran(0.66 mM) and ATP supplement(0.2 microM) could not effectively inhibit ATP depletion and cell death. Ouabain(27 and 100 microM) enhanced cell death and could not completely prevent ATP loss. 4) Most of the mitochondria showed swelling, loss of cristae and Ca2+ deposit in matrix in the electron microscopic observation. Rapid, sustained and irreversible depletion of adenine nucleotides was due to Ca2+ deposit with destruction of mitochondria and also the leakage through transmembrane channels. Moreover this energy depletion was accelerated by high extracellular Ca2+ concentration. These results indicate that Ca2+-mediated, energy exhaustion is one of the mechanisms of the metabolic cell death by C5b-9 attack of NC.
Mice ; Animals

No abstract available.
Epithelium* ; Humans* ; Larynx*

No abstract available.
Orthognathic Surgery

14 cases of femoral shaft fractures were treated with cast-brace for two years from June, 1974 to June, 1976 at the Department of Orthopedic Surgery, College of Medicine, Seoul National University Hospital. The results were as followings; 1. Of the 14 cases, eleven cases were male and three were female, and they were between 18 to 51 years of ages. 2. The fracture site was accounted that three of 14 cases were at the distal one third of the femur and the other eleven at the mid one third with four cases being comminuted. 3. 7 cases were treated with cast-brace initially, and the other 7 cases were secondarily treated, because of being complicated. 4. The average time of fracture healing was 14 weeks in the cases with cast-brace which is compared with 20 weeks of spica-cast control group in the same period. 5. One of 7 cases treated primarily developed shortening and angulation, which was corrected by open reduction and internal fixation.
Clinical Study ; Female ; Femoral Fractures ; Femur ; Fracture Healing ; Humans ; Male ; Orthopedics ; Seoul

No abstract available in English.
Arm

Fat embolism is one of a rare catastrophic complication after multiple fraetures and extensive soft tissue injury. Many hypothesis on its pathogenesis has been postulated by many writers, still its exact pathogenesis, definite diagnostic criteria and treatment is not established. Nowadays fat embolism is considered as a respiratory insufficiency syndrome, even disseminated intravascular coagulation rather than isolated phenomena after extensive trauma of musculoakeletal system. Respiratory failure associated with fat embolism is a major cause of death, but is usually seIf-limited and is responsive to intensive treatment. Monitoring of blood gas is required for early diagnosis and respiratory supportive treatment with continued monitoring is necessary until resolution. The writers experienced six cases of fat embolism, at the Department of Orthopedic Surgery, Seoul National University Hospital for the period of three years from June 1974 till May 1977. Respiratory support, parenteral steroid and low molecular weight dextran with other supportive measure was a mainstay of treatment. Of six cases, five was recovered without sequalae and one was expired four days after trauma.
Cause of Death ; Dextrans ; Disseminated Intravascular Coagulation ; Early Diagnosis ; Embolism, Fat ; Molecular Weight ; Orthopedics ; Respiratory Insufficiency ; Seoul ; Soft Tissue Injuries