Intragastric pressure at gastric empty state was measured by radio capsule method during various exercises in three human subjects. The E. I. L. Type. 70. pressure sensitive radio capsule of England make was used in this experiment.
1) The empty intragastric pressure at rest was 30.0-33.0 cmH₂O and the gastric peristalsis was 2-3 sec. in frequency and less than 3 cmH₂O in amplitude.
2) The resting gastric peristalsis was disappeared immediately after the onset of deep respiration or exercise. The pressure raised to maximum 76.0 cmH₂O at the end of deep abdominal inspiration.
3) The intragastric temperature raised during various exercises and increasing grade was showed in Table of the text.

Heart rate and R-R intervals of ECG during sleep were examined in healthy young men. Heart rate per minute were gradually decreased when the subject fell asleep. Whole through one night sleep data there were two typical heart rate variation patterns, namely stable stage and fluctuating stage. Sleep stages determined by EEG, EOG and EMG of chin corresponded with these two patterns; slow wave stage (Stage III/IV) showed the stable pattern, REM Stage and Stage I showed the fluctuating pattern, Stage II both patterns. The fluctuating pattern showed higher heart rate level.
Further studies computed R-R intervals and its variations of ECG revealed 4 typical patterns on the variations, and well corresponded with sleep patterns determined by the above methods. R-R interval varied from 1.39 to 0.67 sec during sleep. R-R interval variation befor onset of sleep showed lightly rythmical periodicity (20-40 sec) and small fluctuation (0.1 sec) (awaking pattern) . R-R intervals after onset of sleep extended gradually, fluctuating midly (0.1 sec) and did not show any periodicity (transient pattern) . R-R interval reached its maximum level then. At slow wave stage (S-III/IV) R-R interval showed mild fluctuation as the transient strage, and did not show any periodicity (stable pattern) . At REM stage and S-I it showed large fluctuation (more than 0.2 sec) and significant periodicity (10-30 sec) . At S-2 if the stage was in the course of deepening the sleep, it showed stable pattern and if it was in the course of lightening the sleep it showed fluctuating pattern.

We present the case of a patient with primary ciliary dyskinesia who later developed clinically probable multiple system atrophy. Multiple system atrophy is a sporadic neurodegenerative disorder clinically characterised by various combinations of parkinsonism, cerebellar ataxia, autonomic failure, and pyramidal sign. Primary ciliary dyskinesia is a genetically heterogeneous disorder of motile cilia and results in chronic bronchitis, bronchiectasis, chronic rhinosinusitis, chronic otitis media, situs inversus, and male infertility. Most of the causative genes for primary ciliary dyskinesia encode proteins that are part of the heavy or intermediate chain of axonemal dynein in ciliary outer dynein arms. We hypothesised that axonemal dynein dysfunction in primary ciliary dyskinesia results in reduced autophagy, accompanied by impaired cytoplasmic dynein function, which in turn accelerates -synucleinopathy in multiple system atrophy. Furthermore, we contemplated a potential association between primary cilia and neuronal function. Although it is not yet clear if a causal link between multiple system atrophy and primary ciliary dyskinesia exists, further investigation into the relationship between axonemal dynein dysfunction in primary ciliary dyskinesia and α-synucleinopathy should be conducted.

Objective: To clarify the profile of cognitive dysfunction and the effects of intensive exercise in spinocerebellar degeneration (SCD). Methods: We enrolled 60 healthy controls and 16 patients with purely cerebellar type SCD without gait disturbance or organic changes other than cerebellar changes. To assess cognitive function, we evaluated the participants using the Mini-Mental State Examination (MMSE), Frontal Assessment Battery (FAB), and Montreal Cognitive Assessment-Japanese (MoCA-J) at admission and after intensive exercise. Results: Compared to the controls, SCD patients showed significant cognitive decline. As a result of intensive exercise, significant improvements in motor and cognitive functions were observed: the MMSE score improved from 27.7±1.9 to 29.0±1.3 points (p<0.001); the FAB score improved from 14.8±2.2 to 15.8±2.0 points (p=0.002); and the MoCA-J score improved from 24.6±2.2 to 26.7±1.9 points (p<0.001). For sub-scores, significant improvements were noted in serial 7, lexical fluency, motor series, and delayed recall. Conclusion Our study indicates that intensive exercise can be effective not only for motor dysfunction but also for cognitive dysfunction (Clinical Trial Registration No. UMIN-CTR: UMIN000040079).

OBJECTIVESThe present study investigated the involvement of oxidative stress in the degeneration of the cerebellum during methylmercury (MeHg) intoxication and the protective effect of α-tocopherol (Vit E) against MeHg toxicity.

METHODSAfter 5 mg/kg of MeHg was administered to Wistar rats for 12 consecutive days, the cerebellum were examined histopathologically. In addition, the same amount of MeHg was administered to 3 different groups of Wistar rats: rats with a Vit E-deficient diet, rats fed 150 mg/kg of Vit E for 20 consecutive days after initial MeHg administration, and rats with an ordinary diet.

RESULTSPositive immunoreactivity against anti-hydroxynonenal (HNE), a marker of lipid peroxidation, was observed in the cerebellum after MeHg administration. Levels of thiobarbituric acid reactive substance (TBARS), another marker of lipid peroxidation, and those of protein carbonyl, a biomarker for protein oxidation, increased after MeHg administration. In the rats with MeHg and a Vit E-deficient diet, mortality and prevalence of piloerection significantly increased, and in the rats with MeHg and Vit E, mortality, piloerection, retracted and crossed hind leg, and ataxic gait significantly decreased, compared with the rats with MeHg alone. The levels of NO(2) (-) and NO(3) (-) in the serum significantly increased in the rats with MeHg alone 14 days after the initial MeHg administration, but were significantly suppressed by Vit E administration.

CONCLUSIONSOxidative stress, especially lipid peroxidation, may play an important role in the cerebellar degeneration process during MeHg intoxication and Vit E may play a protective role against MeHg toxicity as an effective antioxidant.