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A resonant capacitor, one of the railway signalling equipment, is attached to the impedance bond of the track circuit. If this resonant capacitor fails, the track circuit voltage will have an impermissible drop, resulting in operational trouble. On the other hand, the failure factors of this resonant capacitor such as aged deterioration or lightning strike can’t be identified, so the effective countermeasures have not been taken. We have been studying methods for estimating the probability of occurrence of lightning strikes in the signalling equipment based on the lightning conditions such as lightning current and lightning strike position. Utilizing this study result, we investigated the failure factors of the resonant capacitors, including the effect of lightning surge.

Thalamic Vim is a relay nucleus from the cerebellum and one of the targets for relieving symptoms of upper limb dystonia as well as tremor-dominant Parkinson’s disease (PD) and essential tremor (ET). Beta oscillation is reported to be predominant from the single unit analysis in this nucleus in PD, ET and chronic pain (Basha D et al., 2014). We analyzed the Vim oscillation at rest in five cases with upper limb dystonia (four females, mean age of 31.2 yo) to elucidate whether beta oscillation is predominant also in dystonia. Single unit activities were recorded with microelectrodes during stereotactic surgery while the patients were awake. Each single unit was identified(?) with template matching method at sites where ablation or deep brain stimulation were effective. In results, the spike frequency in the beta range was not predominant (beta: 14–30 Hz 29 ± 7% (SD), below theta: 3–7 Hz 31 ± 13%, alpha: 8–13 Hz 20 ± 10%, gamma: above 31 Hz 20 ± 18%, n = 33). In dystonia, oscillation pattern at rest in Vim is abnormal in Vim but beta oscillation is not predominant, demonstrating a distinctive pattern from those in PD, ET, and chronic pain.

Total synthesis of marine diterpenoid kalihinene X was achieved. This total synthesis involves regioselective coupling reaction of carbanion of alkyl sulfone with epoxyalcohol and construction of cis-decalin ring by intramolecular Diels–Alder reaction. The absolute configuration of kalihinene X could be determined by this total synthesis.

We investigated comparison according to reflux esophagitis and non-erosive reflux disease about “daily” symptom improvement for proton pump inhibitor treatment. We enrolled 57 reflux esophagitis and 90 non-erosive reflux disease patients. They took rabeprazole 10 mg/day for 28 days and completed “daily” in the Frequency Scale for the Symptoms of GERD from baseline until day 14, and after 28 days of treatment. The efficacy endpoint was the improvement rates in Frequency Scale for the Symptoms of GERD, based on baseline. Frequency Scale for the Symptoms of GERD was decreased in reflux esophagitis and non-erosive reflux disease (p

Total synthesis of marine diterpenoid kalihinene X was achieved. This total synthesis involves regioselective coupling reaction of carbanion of alkyl sulfone with epoxyalcohol and construction of cis-decalin ring by intramolecular Diels–Alder reaction. The absolute configuration of kalihinene X could be determined by this total synthesis.

This paper describes the implementation of the Symbolic ROM Monitor for GMICRO F32 series (hereinafter called SRM32) which interfaces to the architecture of the GMICRO F32 series CPU.

Plasma lipids, blood glucose, plasma insulin (IRI) and serum dopamine-beta-hydroxylase (DBH) were measured in 30 subjects undergoing surface-induced deep hypothermia with circulatory arrest for open-heart surgery. Non-esterified fatty acid (NEFA) in the plasma rapidly increased at the lowest temperature (23 degrees C) reached and other lipids in the plasma decreased during the cooling period. An increase of NEFA and a decrease of triglyceride have been attributed to the action of lipoprotein lipase activity stimulated by heparin. It is also likely that the decrease of other lipids and beta-lipoprotein in the plasma results from the transient hypofunction of the liver due to hypothermia. Blood glucose increased during the cooling period, while plasma insulin showed no significant change. Serum DBH reflecting catecholamine also showed no significant change during the cooling or rewarming periods. Therefore, hyperglycemia in hypothermic open-heart surgery may result from the decrease of peripheral utilization of glucose and from the inhibition of insulin secretion due to the transient pancreatic hypofunction.

The present studies were performed to investigate the metabolic role of the lungs in the renin-angiotensin system under hypothermia by measuring plasma renin activity, plasma angiotensin I (A I), plasma angiotensin II (A II), plasma aldosterone and plasma angiotensin converting enzyme activity on 14 patients who underwent open-heart surgery with surface-induced simple hypothermia. In addition, dog experiments were performed, in which changes of renal blood flow and angiotensin metabolism in lungs and kidneys under hypothermia were studied in vivo. The following results were obtained: 1) During and after open-heart surgery with surface-induced simple hypothermia, the homeostasis in the renin-angiotensin system is still maintained. 2) An increase of A II may play an important role in maintaining blood pressure under hypothermia. 3) Under hypothermia, the conversion of A I to A II in the kidneys may contribute to an increase of plasma A II.

Metabolic acidosis observed in open heart surgery under surface induced deep hypothermia is due to lactacidemia, but is reversible, returning to precooling level 24 hours after the operation, and it can be considered more or less as a pathognomonic finding. Although the correction of acidosis present did not influence the level of lactic acid in blood, it was found to be clinically advantageous during the heartresuscitation. Therefore, it is advisable to maintain acid-base balance within-10 mEq per 1 of base excess.

Surface induced deep hypothermia combined with cardiopulmonary bypass (combined method) is excellent in open heart surgery of infants which combines each advantage of cardiopulmonary bypass and hypothermia. The present study was performed to investigate pathophysiological changes, especially metabolic changes, in combined method induced by two stressors such as cardiopulmonary bypass and hypothermia. In general, metabolic changes during hypothermia are temporarily enhanced immediately after the start of cardiopulmonary bypass. Lactacidemia and metabolic acidosis are rapidly improved after the start of perfusion rewarming, but abnormality of ceruloplasmin and cholesterol metabolism in the liver and hypopotassemia are not rapidly improved. Therefore, the treatment for these metabolic abnormalities seems to be necessary during and after the procedure.

In order to clarify the inhibitory mechanism of insulin secretion associated with open-heart surgery, the influence of insulin antagonistic hormones on insulin secretion was studied in 20 patients with congenital heart diseases undergoing open-heart surgery, under simple deep hypothermia. Despite a hyperglycemia, plasma immunoreactive insulin and C-peptide showed no change during the cooling period, while with the exception of plasma human growth hormone, dopamine-beta-hydroxylase, immunoreactive glucagon, cortisol and cyclic AMP in plasma, either showed no change, or a decrease during the cooling period. It is assumed that catecholamine, glucocorticoid and glucagon do not play an important role in the inhibitory mechanism of insulin secretion during hypothermic open-heart surgery, and a transient hypofunction of the pancreas as well as the liver and the adrenal gland is probably involved.

The role of the liver in the changes of acid-base balance and plasma lipids in surface-induced deep hypothermia for open-heart surgery was investigated clinically and experimentally. The metabolic acidosis generally observed in open-heart surgery under surface-induced deep hypothermia is derived from lactacidemia. Although the accelerated anaerobic glycolysis is partly responsible, the depressed acidic metabolite-disposing ability of the liver also plays an important role. The evidence which is presented to show the decrease of plasma lipids other than NEFA under hypothermia is probably due to the hepatic accumulation of lipids and the decreased lipids release from the liver.

The effects of large doses of angiotensin II on the rabbit kidney and heart and or the ability of perfused canine kidney to inactivate angiotensin II were examined to clarify the role of angiotensin II in the low cardiac output syndrome after open-heart surgery. Intravenous infusion of angiotensin II at a rate of 1.1 to 1.4 microgram/Kg/min for 48 hours caused multifocal myocardial necrosis and renal mononuclear cell infiltration and necrosis. Isolated canine kidney preparations inactivated 76% of angiotensin I and 79% of angiotensin II. The results indicates that the kidney can inactivate angiotensin and that high doses of angiotensin II can produce myocardial and renal lesions. It is suggested that an increased concentration of angiotensin II may result in the low cardiac output syndrome through myocardial damage, and that decreased inactivation of angiotensin II by the kidney accelerates the myocardial damage.

One hundred and seven patients with ventricular septal defect who survived one and a half to thirteen years after hypothermic open-heart surgery were reviewed with respect to somatic, intellectual, and psychomotor development. There were no negative effects associated with deep hypothermic arrest in any of these areas. Abnormal electroencephalograms were seen in one-half the number of patients examined, but there was no close relation between the circulatory arrest period and electroencephalographic findings. CT scanning of the brain indicated that the abnormality decreased with the lapse of the time after hypothermic open-heart surgery. It would appear that hypothermic open-heart surgery with limited circulatory arrest is a useful method, providing that the circulatory arrest is not allowed to exceed a limited period. However electroencephalographic assessment suggests that postoperative cerebral abnormalities may occur more frequently than previously suspected, despite the lack of preoperative abnormalities on the electroencephalograms.

Compared to 3′,5′,3,5-tetraiodothyropropionic acid, 3′,5′-dimethyl-3,5-diiodothyropropionic acid was 15 to 36% more active as measured by tissue metabolism or basal metabolic rate, respectively, of injected thyroidectomized rats. Similarly, 3′,5′-dimethyl-3,5-diiodo-DL-thyronine approached 44% of the activity of l-thyroxine and 3′-methyl-3,5-diiodo-l-thyronine was 44% as active as 3′,3,5-l-triiodothyronine on an equimolar basis. In contrast 3′,5′,3,5-tetramethyl-dl-thyronine displayed no detectable metabolic activity.

Plasma kallikrein activity and plasma serotonin were studied during and after open-heart surgery in 15 patients with extracorporeal circulation and in 15 patients with surface-induced deep hypothermia. Following results were obtained: 1) Plasma kallikrein activity which reflects the activation of the kinin system, showed no significant change during extracorporeal circulation, and significantly increased three hours after the termination of perfusion. However, there was no significant difference in plasma kallikrein activity between the patients with and without low cardiac output syndrome (LOS). In surface-induced deep hypothermia, plasma kallikrein activity showed no significant change during and after operation. 2) Plasma serotonin significantly decreased during both extracorporeal circulation and hypothermia. Moreover, there was no significant difference in plasma serotonin between the patients with and without postoperative LOS or pulmonary hypertension. It is assumed that plasma serotonin may not play an important role in regulating blood pressure during or after open-heart surgery with either extracorporeal circulation or surface-induced deep hypothermia.

The effect of hypothermic ischemic arrest on myocardial contractility was investigated with use of isolated blood-perfused canine heart preparation in the hypertrophied left ventricle created by supravascular aortic stenosis and the non-hypertrophied ventricle. The following results were obtained: The percent recovery rate of net developed tension during reperfusion after an ischemic period of 150 minutes at the myocardial temperature of 17 degrees C was 90 +/- 9% in the non-hypertrophied muscle, that is, hypertrophied left ventricle was considered to be more vulnerable to ischemia as compared to nonhypertrophied left ventricle, suggesting the necessity of more intense myocardial protection in addition to cardiac hypothermia against ischemia in the hypertrophied heart.

Myocardial protection by dilazep HCl, an antianginal drug and a potent calcium antagonist, against myocardial damage following acute ischemia and reperfusion was studied with respect to myocardial contractility in isolated blood-perfused canine left ventricular muscle. Myocardial function was expressed by percent recovery rate of maximal net developed tension. 1) The coronary infusion of dilazep revealed significant myocardial protection during normothermic ischemic arrest of 45 min and reperfusion. 2) The intravenous administration of dilazep to the support dog and Young's infusion also showed significant myocardial protection during normothermic ischemic arrest of 45 min and reperfusion. Dilazep showed no persistent depression of myocardial contractility due to its calcium antagonistic effect during reperfusion. 3) The combination of intravenous administration of dilazep to the support dog, Young's infusion, and hypothermia showed significant myocardial protection during prolonged ischemia and reperfusion even in hypertrophied ventricle. These results demonstrate that dilazep provides effective myocardial protection during ischemic arrest and reperfusion by preventing abnormal calcium accumulation in myocardial cells during reperfusion. No persistent depression of myocardial contractility during reperfusion may support dilazep's clinical application as a myocardial protective agent in open-heart surgery.

We treated two patients with rare variants of Hodgkin's disease of the thymus. One was a 17-year-old girl with a thymoma-like shadow on the chest X-rays, an increased erythrocyte sedimentation rate and an elevated eosinophil count. Pathologically, a mixed cellularity variant of thymus Hodgkin's disease was evident. The other patient was 22-year-old girl with evidence of mediastinal tumor on the chest X-rays. Pathological examination revealed Hodgkin's disease of the lymphocyte predominance variety. She also had Von der Haeve syndrome. In both cases, Hodgkin's disease was suspected by scintiscanning, using three kinds of radioisotope, 201Thallium-chloride, 67Garium-citrate and 75Selenomethionine. Radical excision of the lesion plus preoperative and postoperative irradiations were carried out. Both are well 6 and 5 years after the treatment, respectively. We propose a new diagnostic procedure and a method of treatment for such patients.

The present studies were performed to evaluate the protective effect of topical hypothermia on anoxic heart. The myocardial protection was assessed by myocardial contractility in the isolated blood-perfused electrically driven canine left ventricular muscle. The isometric tension and the rate of rise of tension development (dT/dt) were measured before and after hypothermic anoxic arrest and percent recovery of these values was used as a parameter of myocardial contractility. The percent recovery rates of 100, 95, 90, and 65 were obtained after acute anoxia of 90, 120, 150, and 180 min, respectively at the myocardial temperature of 17 degrees C. These data suggest that the safe limit of acute anoxia at the myocardial temperature of 17 degrees C is defined as 90 min in this experimental model and it can be extended to 120 min at the myocardial temperature below 17 degrees C.