[A case of Budd-Chiari syndrome associated with anti-phospholipid syndrome].
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Biomedical subjects
Publications and source records attributed to S Kiyono.
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Tetracycline (TC) was administered indirectly to rat pups through maternal milk, giving mothers diluted TC solutions as a single source of drinking water, during 13-16 days of postnatal age (PND) in Experiment 1. In Experiment 2, using rats of a different strain, TC dose and its application period were reduced from 0.5 mg/ml to 0.25 mg/ml and from PND 13-16 to PND 13-15, respectively. In Experiment 3, TC was administered directly to the pups via stomach intubation during PND 13-16. The effects of these short-term treatments were tested in adulthood. Brain weight decreased, although no abnormal changes were found histologically in the cerebral cortex. Immobility time in the forced swimming test was decreased more in the TC group as compared to the controls. These results suggest that even a small amount of TC could affect physiological development and behavior. In Experiment 4, mothers were given TC in their drinking water (0.5 mg/ml) for 1 to 5 days, beginning on PND 12. On each of the treatment days, measurements were made of the weight of brain and body, and of the concentration of TC in the brain and in gastric curd of offspring. The greater the TC intake by dams was, the more remarkable was the decrease in the brain weight of offspring. TC concentration of gastric curd was on the order of 1-3.5 micrograms/g curd.
Behavioral states of rats were automatically classified with a newly developed computer program into three sleep stages (awake, slow-wave sleep and REM sleep) from continuous long-term EEG and EMG recordings for several circadian cycles under entrained circumstances (L:D = 12:12). Histamine was depleted by 100 mg/kg intraperitoneal administration of a specific inhibitor of its synthesis, alpha-fluoromethylhistidine, in the mid-light period. This treatment had no effect on the amount of each sleep stage in the total 24-h period or in the light period, but caused significant increases in slow-wave sleep and REM sleep in the dark period. Equivalent decrease in the awake stage during the dark period was also observed. As a result, histamine depletion decreased the light:dark ratio of slow-wave sleep. These findings suggest that decrease of the histamine content of the brain attenuated the circadian amplitude of sleep-wakefulness by suppressing the surge of wakefulness during the dark period. From these results, histamine is suggested to modulate the circadian amplitude of the sleep-wakefulness cycle.
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We developed a simple and precise program for the on-line judgement of the sleep stages of four rats simultaneously for an unlimited period, using a commercially available general purpose signal processor (NEC-Sanei 7T17; 32-bit, 5 MHz, 4 Mbyte, 1 Mbyte 1 floppy disc drive). EEG and EMG were recorded with an 8-channel polygraph (NEC-Sanei, System 380) through electrodes chronically implanted into the brain. The signals were A/D converted every ms and integrated for 2760 ms after full-wave rectification, and the subsequent 2240 ms was used for calculation and further analysis. All data were handled with this 5000 ms as the minimum unit. Then 3 sleep stages, i.e., waking, slow-wave sleep, and REM sleep, were determined by a template matching method from the relative amplitudes and durations of the integrated EEG, EMG and EMG surge data based on algorithms of standard visual amplitude analysis criteria for the sleep-stage classification. An agreement matrix was constructed between the data scored by the visual and by the automatic analysis, and the agreement value was satisfactory, although slight variability was seen in the REM sleep-stage determination. This result indicated that EEG and EMG data analysis is appropriate for researching the circadian rhythmic mechanism of the sleep-wake cycle.
To determine the onset time, duration of action and recovery time of high-dose vecuronium, 70 patients were assigned to receive either 100, 150, 200 or 300 micrograms.kg-1 of vecuronium for muscle relaxation during elective surgery. Neuromuscular blockade was continuously quantitated by recording the EMG response to stimulation of the ulnar nerve. The onset time from the time of vecuronium administration to maximum blockade decreased from 4.6 +/- 1.1 to 2.4 +/- 0.5 min when the vecuronium doses increased from 100 to 300 micrograms.kg-1. Significant differences were observed in the onset time between the 100 micrograms.kg-1 dose and the other dose groups. Endotracheal intubating conditions were excellent in all patients except 3 in the 100 micrograms.kg-1 dose group. The duration of action from the time of injection to 25% recovery increased from 32 +/- 9 to 138 +/- 48 min in a dose dependent manner. The duration of action after increment doses of 40 or 50 micrograms.kg-1 up to 25% recovery of T1 did not vary significantly within the same dose group. With an initial dose of 150 micrograms.kg-1 and subsequent increment doses of 50 micrograms.kg-1 or less, the duration of action remained constant. The recovery time from 25 to 75% recovery was within 11 minutes when antagonists were administered. High-dose vecuronium may, therefore, be a useful alternative to SCC, when a rapid onset is required and to pancuronium, when a rapid recovery from neuromuscular blockade is requested.
The effects of ONO 3708, a new thromboxane A2 (TXA2) receptor antagonist, on platelet aggregation in human plasma, the survival rate of rats subjected to lethal endotoxin shock, and the pathophysiological consequences of endotoxin shock in anesthetized dogs were investigated. ONO 3708 inhibited dose dependently human platelet aggregation induced by 2.5 microM of STA2, analogue of TXA2. Treatment with ONO 3708, 1 mg/100 g i.v., significantly improved the survival rate of rats in endotoxin shock from 38 to 72% at 24 hr and from 27 to 61% at 48 hr. ONO 3708 significantly attenuated endotoxin-induced thrombocytopenia, but not leukopenia. In anesthetized dogs, endotoxin-induced pulmonary hypertension was completely prevented, and increased airway pressure was significantly attenuated by ONO 3708. These results suggest that ONO 3708, the antagonist of TXA2 receptor, has beneficial effects during endotoxin shock, at least in part by inhibiting platelet aggregation.
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The effects of ONO 3708, a new thromboxane A2 receptor antagonist, on cardiovascular and airway responses, at an early phase during endotoxin shock were investigated in anesthetized dogs. The i.v. infusion (1mg.kg-1) of E.coli endotoxin caused an increase in mean pulmonary artery pressure (MPAP) from 9.9 +/- 1.0 to 19.1 +/- 2.3 mmHg at 5 min, and at 15 min after infusion, elevated MPAP returned toward the control level. Pretreatment with ONO 3708 abolished these effects of endotoxin on pulmonary artery pressure at an early phase. The change in airway pressure reached a maximum of 14.4 +/- 1.7 cmH2O from 10.0 +/- 1.9 at 5 min, followed by a gradual decline toward a baseline value at 30 min in the control group. ONO 3708 significantly attenuated increase in airway pressure induced by E. coli endotoxin. But pretreatment with ONO 3708 could not prevent decrease in systemic arterial pressure and cardiac output induced by endotoxin. These results suggest that role of thromboxane A2 on the cardiovascular response during endotoxin shock is played only on pulmonary vascular changes, and ONO 3708 has a beneficial effect at least during the early phase of endotoxin shock.
C-reactive protein (CRP) is one of the most characteristic acute phase proteins which appear in the serum during certain inflammatory diseases. We report here that human CRP acquired the ability to augment platelet reactivity when treated with an Fe2+ (Cu2+)-ascorbate system. CRP modified by such treatment showed no appreciable activation of platelets in the absence of platelet activators such as platelet-activating factor, thrombin, or ADP. However, in the presence of the modified-CRP, irreversible activation of platelets occurred with sub-optimal doses of platelet-activating factor and other stimulatory agents for platelets. CRP without any treatment did not show any modulating activity. Each component of the Fe2+-ascorbate system was required for modification of CRP, suggesting that CRP was modified through an oxidative process. The modification of the CRP structure was confirmed by the change in the fluorescence spectrum of 8-anilino-1-naphthalene sulfonate complexed with CRP, the increased susceptibility of CRP to proteolytic enzymes and the altered reactivity to anti-CRP mAb. We also found an inactivating system for the modified CRP in plasma. The modified human CRP did not show any modulating activity toward rabbit platelets, suggesting that the activity is species specific.
REM sleep latency observed in 61 mentally retarded infants (4-13 months of age) was studied throughout nocturnal sleep. Mentally retarded infants revealed a J distribution of short (less than 8 min) and long (more than 8 min) REM sleep latencies. This feature of distribution was similar to that obtained by other authors from normal infants under 3 months of age. REM sleep latency did not depend on the duration of prior wakefulness. Long REM sleep latencies were no more often preceded by long episodes of wakefulness than were short REM sleep latencies. No correlation was found between REM sleep latency and age, developmental quotient or daytime clinical EEG abnormalities.
Skin potential responses (SPRs) of 89 mentally retarded children were studied during their nocturnal sleep. Forty-three out of the 89 subjects showed more SPRs (type A) during NREM sleep than in REM sleep. The opposite was observed in 10 cases (type C), and 4 had evenly distributed SPRs during both sleep phases (type B). The remaining 32 subjects had mixed types AB (n = 19), AC (n = 6) or BC (n = 7). Types B and C (including the mixed type) were observed more frequently for subjects with low developmental quotient (DQ) and abnormal clinical EEGs than for those with high DQ and normal clinical EEGs. Since it has been well established that normal subjects of 3 months and over exhibit exclusively type A, SPRs may be used as an additional tool for the diagnostic assessment of mental retardation in early infancy.
The correlation between the delta and spindle components in compressed spectral array in 96 mentally retarded children (from 3 months to 12 years of age) was studied throughout nocturnal sleep. In 57 (59.4%, group A) of 96 subjects, periodic changes of delta and spindle rhythm powers were noted in sleep EEG. In 29 subjects (30.2% group B), delta but not spindle rhythm powers were found, and in the remaining 10 subjects (10.4%, group C) neither delta nor spindle rhythm powers were found throughout nocturnal sleep. A significant increase in abnormal clinical EEG was found in groups B and C as compared with group A. A significant decrease in the developmental quotient (DQ) was found in groups B and C as compared with group A. A significant decrease in DQ was also found in group C as compared with group B.
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The correlations between the delta and spindle components in compressed spectral array in 21 mentally retarded children with cerebral palsy (CP) (from 4 months to 5 years of age) and 32 reference mentally retarded children of no abnormality with the exception of psychomotor retardation (from 4 months to 12 years of age) were studied throughout nocturnal sleep. In 11 (52%) out of 21 CP cases and 27 (84%) out of 32 reference cases, periodic changes of delta and spindle rhythm powers were noted in sleep EEG (group A). In 5 (24%) other cases in CP and 5 (16%) reference cases delta but not spindle rhythm powers were found (group B), and in the remaining 5 (24%) CP cases neither delta nor spindle rhythm powers were found throughout nocturnal sleep (groups C). A significant decrease in the developmental quotient (DQ) was found in group C as compared with group A in both CP and reference cases. Moreover, a significant decrease in DQ was also found in group B as compared with group A of reference cases.
Sleep EEG patterns in 17 infants with cerebral malformations (4 months to 4 years of age) were studied throughout nocturnal sleep and the following results were obtained. Seven cases evidenced normal sleep/wakefulness EEG patterns that could be classified into 6 stages. Ten cases showed abnormal sleep EEG patterns as follows: absence of sleep spindles (n = 7) which included cases of absence of EEG patterns characteristic of wakefulness, NREM sleep and REM sleep (n = 5), no characteristic EEG patterns of stages 1-4 (n = 1) and stages W, 1, 2 and REM (n = 1) and the remaining cases with absence of spindles (n = 1), and spindles with an extremely low incidence (n = 2). Short sleep and long awaking times, and no delta rhythmicity during the night, were noted in 5 out of 17 subjects. A significant decrease of DQ was found in subjects with indistinguishable stages including stages W, 1, 2 and REM, as compared with those patients whose stages were all distinguishable.
The correlation between the delta and spindle components in compressed spectral array in 18 infants with congenital cerebral malformation (from 4 months to 4 years of age) was studied throughout nocturnal sleep. In 7 (39%, Group A) out of 18 subjects, periodic changes of delta and spindle rhythm powers were noted in the sleep EEG. In 5 subjects (28%, Group B), delta but not spindle rhythm powers were found, and in the remaining 6 subjects (33%, Group C) neither delta nor spindle rhythm powers were found throughout nocturnal sleep. A significant decrease in the developmental quotient was found in group C as compared with group A.
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