Although it is well established that steroid is effective for treatment of neonatal respiratory distress syndrome (NRDS), the action mechanism of steroid on NRDS is not well known. Several authors have insisted that steroid increases secretion of pulmonary surfactant from type II pneumocyte, but others have insisted that steroid does not affect the secretory function of the type II pneumocyte. And some authors have suggested that steroid may cause compositional change of pulmonary surfactant phospholipid. From these aspects, it is desirable to confirm the effect of steroid on the secretory function of the type II pneumocyte. In order to know the effect of steroid on pulmonary surfactant activity, phospholipid phosphorus of lung lavage was measured and composition of pulmonary surfactant phospholipid of lung lavage was analyzed by thin layer chromatography (TLC) in control (c), pneumonectomized (PN), and pneumonectomized with betamethasone treated (PNS) rabbits. And lung weight and lung weight-body weight ratio were measured in each experimental group also. In PN group, right lung pneumonectomy was performed as PN group, and one day after the surgery, betamethasone was injected for four days intramusculary (4 mg/day) and rabbits were sacrificed. The experiment yielded following results. PNS group's lung weight was significantly (p<0.01) heavier than C group's, but in comparison with PN group's it showed no significant change. PNS group's L/B ratio was significantly (p<0.05) higher than C group's, but compared with PN group's it showed no significant change. The value of phospholipid phosphorus content of PNS group was significantly (p<0.01) higher than that of C group. Even if the value of phospholipid phosphorus content in PNS group was not significantly higher than that of PN group, it showed increasing tendency compared with that of PN group. And in an analysis of the thin layer chromatogram, quantity (µmol/gm of wet weight lung) of phosphatidylcholine in PNS group decreased significantly (p<0.05) compared with C and PN group. From these results, it may be suggested that though steroid inhibits cellular hyperplasia in the compensatory growing lung, it auguments the secretory function of type II pneumocyte and causes compositional change of pulmonary surfactant phospholipid.
Betamethasone* ; Bronchoalveolar Lavage ; Chromatography, Thin Layer ; Hyperplasia ; Lung ; Phosphatidylcholines ; Phosphorus ; Pneumocytes ; Pneumonectomy ; Pulmonary Surfactants* ; Rabbits* ; Respiratory Distress Syndrome, Newborn

No abstract available.
Insulin Resistance* ; Insulin*

The purpose of this study was to know the effect of short termed fasting on the usage of metabolic energy sources and the metabolic differences between non-athletic and athletic subjects. Subjects were divided into non-athletic and athletic group and exercise was loaded on both groups after feeding and fasting. Exercise was loaded by a treadmill running at the speed of 8 km/hour for 30 minutes in both groups. The experiment yielded following results. In the fed state, the level of plasma FFA increased markedly after 15 and 30 minutes of exercise compared with it's level of pre-exercise period in both groups. In the fated state, the level of plasma FFA in non-athletic group increased steadily according to the duration of exercise, while it's level in athletic group showed no changes. At pre-exercise period, the level of plasma FFA was higher in fasted state than fed state. Immediately before the exercise and 15 and 30 minutes after the exercise, blood for the determination of plasma free fatty acid (FFA), glucose, triglyceride (TG) and cholesterol was sampled from antecubital vein, and simultaneously heart rate was measured. In the fed state, the level of plasma glucose was increased mildly according to exercise, and in the fasted state it's level increased according to exercise in both groups also. In the fasted state, the level of plasma TG was lower than that in the fed state. The level of plasma TG and cholesterol in the fed state was no changed by the exercise from the pre-exercise period. The level of plasma cholesterol in athletic group had tendency to lower than that in non-athletic group. Heart rate increased markedly according to exercise in both groups, but the athletic group's increasing rate of heart rate was lower than the non-athletic group's heart rate increased according to exercise and athletic groups heart rate increased early period of exercise, but did not change during latest post-period of exercise.
Blood Glucose ; Cholesterol ; Fasting* ; Glucose ; Heart Rate ; Plasma ; Running ; Sports ; Triglycerides ; Veins

This investigation was undertaken to clarify the in vitro effect of the various stimulations, such as exercise (E), insulin (I) direct electrical stimulation (EST) and the combinations of the above, on the glucose incorporation intro glycogen molecules (glycogen synthesis) of the normal slow (soleus) and fast twitch (plantaris) muscles, and the different responses of slow and fast twitch muscles to persistent overloads causing compensatory muscle hypertrophy. In resting state, slow twitch muscle has greater capacity for glycogen synthesis than fast twitch muscle, and responses of different muscle to various stimuli were differ as follows: In slow twitch muscle, the glycogen synthesis was increased by insulin, and electrical stimulation but not increased by exercise; exercise increased insulin sensitivity and the effect of electrical stimulation. Whereas the glycogen synthesis in fast twitch muscle was increased only by the stimuli combined with E and EST, and E, I, and EST. As the result of removal of synergistic muscle, both muscles were hypertrophied, and the degree of hypertrophy in response to persistent overload was higher in fast twitch muscle (182%) than slow twitch muscle (151%). In hypertrophied muscles, glycogen synthesis of soleus in any groups was lower than that of the control, but similar in plantaris. In conclusions, there were marked heterogeneity in different muscle fiber in the effects of exercise and insulin addition and electrical stimulation on muscle glycogen synthesis, and fast twitch muscle may be adapted more easily to that kind of persistent overload than slow twitch muscle.
Electric Stimulation ; Glucose* ; Glycogen* ; Hypertrophy ; In Vitro Techniques* ; Insulin ; Insulin Resistance ; Muscles* ; Population Characteristics

No abstract available.
Animals ; Insulin Resistance ; Insulin ; Rats

Holt-Oram Syndrome, well described by Holt and Oram in 1960, is an autosomal dominant disorder consisting of upper extremity and cardiovascular anomalies with variable expression. A typical case of this syndrome was experienced by authors recently and is to be presented with review of literatures.
Upper Extremity

No abstract available.

The effect of exercise on plasma insulin, free fatty acid, and glucose uptake and glycogen concentration in soleus, and intravenous glucose tolerance of streptozotocin treated, diabetic Sprague-Dawley rats were studied. Diabetic-trained animals were subjected to a regular program of treadmill running for 4 weeks. Seventy-two hours after the last training session, basal and insulin-stimulated glucose uptake was studied in incubated strips (about 20 mg) of soleus muscle in vitro. Glucose tolerance was measured with intravenous infusion of 0.5 g glucose/kg body weight. In diabetic rats, training was associated with increase glucose uptake in basal and maximal insulin concentrations, decreased fasting glucose concentrations, and increased muscle glycogen levels, but there were no changes in glucose tolerance curve and plasma insulin concentrations. These results suggest that regular running program for 4 weeks improve responsiveness of insulin on soleus muscle, but fails to cause improvement of impaired intravenous glucose tolerance in mild degree streptozotocin induced diabetic rats.
Animals ; Body Weight ; Exercise* ; Fasting ; Glucose Tolerance Test* ; Glucose* ; Glycogen ; In Vitro Techniques ; Infusions, Intravenous ; Insulin ; Muscle, Skeletal ; Plasma ; Rats* ; Rats, Sprague-Dawley ; Running ; Streptozocin*

No abstract available.
Adult* ; Humans ; Lung* ; Pneumocytes* ; Pneumonectomy* ; Rabbits*

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*