The muscle glycogen is an important energy source for muscle contraction especially in prolonged exercise. One of the important factors for improvement of physical performance in athletes is the storage of extra-amount of glycogen (supercompensation) in liver and muscles. During 120 minutes treadmill exercise (intensity of exercise was approximatly 80% VO2max), the glycogen concentration was significantly decreased to 36% in liver and 46% in muscles after 60 minutes exercise. At 90 and 120 minutes of exercise, the level of glycogen concentration of liver and muscles statistically were not different from the levels of the 60 minutes exercise. The repletions of glycogen in the liver and muscles in overnight fasted control(C) and 120 minutes treadmill exercise(E) groups during l80minutes after glucose ingestion were investigatect. ln the liver, the concentration of glycogen in C and E groups were markdly increased till 120 minutes after zlucose ingestion, hut the levels of concentration at 180 minutes were decreased comparing to the levels of 120 minutes in both groups. In the muscles, the repletion of glycogen at 60, 120 and 180 minutes of C and E groups were significantly increased comparing to 0 minute of respective groups in the soleus and plantaris muscles. In soleus(SOL), the repletion of glycogen in all of the E groups was significantly higher than that of the respective C groups. However, the repletion of glycogen in all of the E groups of plantaris was revealed higher tendency comparing to respective C groups. Mean repletion rates of glycogen in liver and muscles after glucose ingestion were highest during the first 60 minutes in all groups and the rates of E groups were 2-3 times than those of respective C groups. These results suggest that the glycogen supercompensation in the muscle be provided with decrement of glycogen concentration by exercise, increment of glucose uptake by muscuiar contraction itself and increased insuJin level, and the activation of glycogen synthetase by insulin.
Animals ; Athletes ; Eating* ; Glucose* ; Glycogen Synthase ; Glycogen* ; Humans ; Insulin ; Liver* ; Muscle Contraction ; Muscles ; Rats*

No abstract available.
Anxiety* ; Depression* ; Headache*

Papular elastorrhexis is a connective tissue nevus that occurs in the second decade of life as asymptomatic small white-creamy papules scattered over the chest, shoulder, abdomen, or back Histopathologically, there is a decrease in elastic fibers with focal homogenization of collagen. Recognition of this entity is important to prevent use of unnecessary diagnostic procedures and therapy. We present three cases of papular elastorrhexis. All of them occurred in children under the age 10 years.
Abdomen ; Child ; Collagen ; Connective Tissue ; Elastic Tissue ; Humans ; Nevus ; Shoulder ; Thorax

No Abstract Available.
Patellar Ligament*

Glycopyrrolate(Robinul) is a potent anticholinergic drug. Being a quaternary ammonium compound, it dose not cross the blood-brain barrier and thus dose not have the central effects. It has been shown that glycopyrrolate has a pharmacologic properties similar to that of atropine, belladonna alkaloid, but it has lesser effect on the heart rate than that of atropine. The author administered a small dose of glycopyrrolate intravenously to 18 people who were awake, 21 compatous cases and 17 halothane anesthetized cases. The effect on the heart rate in these 3 groups was compared. The results are as follows: 1) In the awake state, glycopyrrolate(0.1mg) produced a slight decrease in the heart rate. 2) In the comatose state, glycopyrrolate(0.1mg) produced a slight increase in the heart rate. 3) In the halothane anesthetized state, glycopyrrolate(0.1mg) produced a significant increase in the heart rate. 4) In the comatose state, the absence of bradycardia after a small dose of glycopyrrolate is similar to a small dose of atropine. Therefore we suggest that bradycardia after glycopyrrolate and atropine is caused by sympathetic ganglion block.

Mauriac syndrome consists of a triad of poorly controlled diabetes, profound growth retardation and hepatomegaly. We experienced a case of Mauriac syndrome in an 18-year-old girl who had poorly controlled diabetes mellitus, short stature, hepatomegaly and central obesity. Also at the time of examination, she had complications of diabetic cataract and nephropathy. Fourteen years prior to admission, she was diagnosed as diabetes mellitus at a hospital. Thereafter, she had been managed with irregular insulin injection. On physical examination at admission, her height was 135cm(<3 percentile) and her weight was 39kg(<3 percetile). She was short and obese. The liver was 5 cm palpable below the right subcostal margin. Her sexual maturation was Tanner stage I. On ophthalmologic examination, the cataracts were observed on both eyes and diabetic retinopathy was absent. Diabetic nephropathy could not be confirrned by kidney biopsy due to her mother's refusal. We studied the hormonal, radiographic and histological abnormalities. The hormonal study was normal and the bone age was by delayed as much as 10 years. The liver biopsy revealed glycogen accumulation in hepatocyte. She was consistent with Mauriac syndrome. She was managed by strict diabetic control with insulin therapy, diabetic diet and intensive education. She was discharged with well controlled blood glucose. Five months later, growth acceleration and sexual maturation have not been observed, but hepatomegaly subsided. (J Korean Pediatr Soc 2000;43-837-841)
Acceleration ; Adolescent ; Biopsy ; Blood Glucose ; Cataract ; Diabetes Mellitus* ; Diet, Diabetic ; Diabetic Nephropathies ; Diabetic Retinopathy ; Disulfiram ; Education ; Female ; Glycogen ; Hepatocytes ; Hepatomegaly ; Humans ; Insulin ; Kidney ; Liver ; Obesity, Abdominal ; Physical Examination ; Sexual Maturation

The nfa1 gene was cloned from a cDNA library of pathogenic Naegleria fowleri by immunoscreening; it consisted of 360 bp and produced a 13.1 kDa recombinant protein (rNfa1) that showed the pseudopodia-specific localization by immunocytochemistry in the previous study. Based on the idea that the pseudopodia-specific Nfa1 protein mentioned above seems to be involved in the pathogenicity of N. fowleri, we observed the effect of an anti-Nfa1 antibody on the proliferation of N. fowleri trophozoites and the cytotoxicity of N. fowleri trophozoites on the target cells. The proliferation of N. fowleri trophozoites was inhibited after being treated with an anti-Nfa1 polyclonal antibody in a dose-dependent manner for 48 hrs. By a light microscope, CHO cells co-cultured with N. fowleri trophozoites (group I) for 48 hrs showed severe morphological destruction. On the contrary, CHO cells co-cultured with N. fowleri trophozoites and anti-Nfa1 polyclonal antibody (1: 100 dilution) (group II) showed less destruction. In the LDH release assay results, group I showed 50.6% cytotoxicity, and group II showed 39.3%. Consequently, addition of an anti-Nfa1 polyclonal antibody produced a decreasing effect of in vitro cytotoxicity of N. fowleri in a dosedependent manner.
Animals ; Antibodies, Protozoan/*immunology ; Antigens, Protozoan/genetics/*immunology ; CHO Cells ; Dose-Response Relationship, Immunologic ; Female ; Hamsters ; Mice ; Mice, Inbred BALB C ; Naegleria fowleri/growth & development/immunology/*pathogenicity ; Protozoan Proteins/genetics/*immunology ; Recombinant Proteins/immunology ; Support, Non-U.S. Gov't

Glycopyrrolate and propantheline, being synthetic quaternary ammonium compounds that cannot cross the blood-brain barrier, will not have the vagal center stimulation. The author administered each small dose of glycopyrrolate and propantenline intravenously to normal human volunteers, and compared its effect on the heart rate. The result were as follows. 1) Glycopyrrolate(0.1mg) produced a slight decrease on the heart rate. 2) Propantheline (0.5mg) produced no detectable change on the heart rate. 3) Glycopyrrolate(0.1mg) 10min. after pretreatment with propantheline(0.5mg) produced a significant increase on the heart rate. 4) Propantheline(0.5mg) 10 minutes after pretreatment with glycopyrrolate(0.1mg) produced more significant increase on the heart rate than glycopyrrolate after propantheline. 5) From the above results, it is suggested that the depressive effect of sympathetic ganglion by propantheline may be less than by glycopyrrolate.
Blood-Brain Barrier ; Ganglia, Sympathetic ; Glycopyrrolate* ; Healthy Volunteers ; Heart Rate* ; Heart* ; Propantheline* ; Quaternary Ammonium Compounds

PURPOSE: We studied to determine whether the degenerative spondylolisthesis has rotary deformity in addition to forward displacement. MATERIALS AND METHODS: We have made an analysis of difference of rotary deformity between the 31 study groups of symptomatic degenerative spondylolisthesis and 31 control groups without any symptom,statistically. We also reviewed CT findings in 15 study groups. RESULTS: The mean rotary deformity in study groups was 6.1 degree(the standard deviation is 5.20), and the mean rotary deformity in control groups was 2.52 degree(the standard deviation is 2.16)(p <0.01) CONCLUSION: The rotary deformity can be accompanied with degenerative spondylolisthesis. We may consider the rotary deformity as a cause of symptomatic degenerative spondylolisthesis in case that any other cause is not detected.
Congenital Abnormalities* ; Spondylolisthesis*

Supplementation of antihypertensive action of sodium nitroprusside (SNP) is almost standard practice and should obviate the need for potentially toxic doses to control blood pressure. Clonidine, an antihypertensive agent known to reduce sympathetic outfiow via alpha2-adrenergic receptor stimulation, has been shown to decrease MAC of halogenated agent, and to reduce the amount of SNP required to reduce the desired hypotension. To determine the effects of clonidine on the hemodynamics and intrapulmonary shunting during SNP infusion, clonidine and/or SNP were administered to 22 patients anesthetized with halothane-N2, O-O2 (FIO2:0.5) In one group of 11 patients, clonidine 1.5ug/kg was injected intravenously. In another group of 11 patients, clonidine 1.5 ug/kg was injected intravenously 30 minutes after starting the SNP infusion (3 ug/kg/min). The results were as follows. 1) Clonidine alone produced a small decrease in MAP (10%) and CI (8%) but other hemodynamic values remained unaltered. 2) Arterial oxygen tension and intrapulmonary shunting was not changed by clonidine. 3) Heart rate (15%) was increased , but MAP (29%), MPAP (24%), PCWP (25%), CVP (32% ), SVR (29%)and PVR(24%) were decreased significantly, and CI, SVI remained unchanged during SNP hypotension. 4) SNP caused a significant increase in intrapulmonary shunt fraction from 8.62% to 10.58% and a decrease in PaO2. 5) In group of clonidine under SNP infusion, conidine did not significantly affect the hemodynamic response to SNP except for 15% decrease in BP. 6) Clonidine caused no significant change on gas exchange effect of SNP. These results indicate that clonidine did not significantly affect the hemodynamics and intrapul-monary shunting during SNP hypotension. Therefore, clonidine could be used as a valuable adjuvant for reducing the amount of SNP and decreasing MAC of halothane.
Anesthesia* ; Blood Pressure ; Clonidine* ; Halothane ; Heart Rate ; Hemodynamics* ; Humans ; Hypotension* ; Nitroprusside* ; Oxygen ; Sodium*