The effect of hyperthyroidism on the contractile properties and Ca²⁺ sequestering abilities by the sarcoplasmic reticulum (SR) in the soleus muscles was examined in rats treated with thyroid hormone (3, 5, 3'-triiodo-L-thyronine, T₃) (300μg/kg body weight) for 3, 7 and 21 days. At the end of a given treatment period, the right or left soleus muscle was mounted isometrically at 30°C, and stimulated directly using supramaximal current intensity. A twitch contraction was elicited by a 1 msec square-wave pulse and a tetanic contraction by 20 Hz stimulation for 600 msec. To evaluate fatigue resistance, muscles were stimulated at 40 Hz for 350 msec with tetani repeated at an interval of 2 sec during a 4-min period. Another soleus muscle was used, for analysis of SR Ca²⁺ -uptake rate and SR Ca²⁺ -ATPase activity. Pronounced increases in SR Ca²⁺ -uptake rate and ATPase activity were observed after T₃ treatment periods longer than 6 days. These alterations were accompanied by decreases in twitch and tetanic tension, half-relaxation time, and fatigue resistance. The T₃-treated muscles stimulated at 20 Hz relaxed during the interval between successive stimuli, indicating that the mechanical fusion of tetanic contractions was incomplete. SR Ca²⁺ uptake rate was significantly correlated both to tetanic tension and to fatigue resistance. These data suggest that there may be a causal relationship between changes in SR Ca²⁺ uptake and the loss of muscular strength in the hyperthyroid soleus.

Repeated contractions of skeletal muscle cause fatigue, as manifested by a reduced ability to produce force and slowed contraction. During studies of muscle fatigue, a phenomenon known as low-frequency fatigue (LFF) was observed in human skeletal muscles. It is characterized by a greater loss of force in response to low- versus high-frequency muscle stimulation and a long period of time for full recovery. This force deficit is most likely to be owing to disturbances in sarcoplasmic reticulum (SR) Ca²⁺ release and/or reductions in myofibrillar Ca²⁺ sensitivity. Studies on metabolites have implied that inorganic phosphate and Mg²⁺ might have some role in reduced SR Ca²⁺ release that occurs immediately after fatiguing contraction. In addition, recent experiments have shown that impaired myofibril function may relate to increased nitric oxide and hydroxyl radical production, whereas deterioration of SR function may be attributable to increased superoxide production, elevation of cytoplasmic Ca²⁺ concentration and/or decreased muscle glycogen. Finally, we will discuss possible proteins which are affected and contribute to the development of LFF.

A 57-year old woman with a left renal aneurysm in a solitary kidney was successfully treated by in situ aneurysmectomy under careful renal preservation (intermittent perfusion combined with topical cooling). In our knowledge, 219 cases of renal aneurysms have been reported in the Japanese literatures by 1987. Among those cases, only 9 cases including our case were noted to have a solitary kidney. Surgical repair was recommended for renal aneurysm, especially, in a solitary kidney because of the high incidence of nephrectomy when ruptured.

The purpose of this study was to investigate changes in sarcoplasmic reticulum (SR) Ca²⁺-sequestering capacity in rat fast-twitch plantaris (PL) and slow-twitch soleus (SOL) muscles during recovery after high-intensity exercise. The rats were subjected to treadmill runs to exhaustion at the intensity (10% incline at 50 m/min) estimated to require 100% of maximal O₂ consumption. The muscles were excised immediately after exercise, and 15, 30 and 60 min after exercise. Acute high-intensity exercise evoked a 27 % and 38 % depression (P<0.05) in SR Ca²⁺-uptake rate in the PL and SOL, respectively. In the PL, uptake rate remained lower (P<0.05) at 30 min of recovery but recovered 60 min after exercise. These alterations were paralleled by those of SR Ca²⁺-ATPase activity. On the other hand, SR Ca²⁺-uptake rate in the SOL recovered 15 min after exercise. Unlike the PL, discordant time-course changes between SR Ca²⁺-ATPase activity and uptake occurred in the SOL during recovery. SR Ca²⁺-ATPase activities were unaltered with exercise and elevated (P<0.05) by 25, 30 and 30% at 15, 30 and 60 min of recovery, respectively. These results demonstrate that SR Ca²⁺-sequestering ability is restored faster in slow-twitch than in fast-twitch muscle during recovery periods following a single bout of high-intensity exercise and suggest that the rapid restoration of SR Ca²⁺-sequestering ability in slow-twitch muscle could contribute to inhibition of disturbances in contractile and structural properties that are known to occur with raised myoplasmic Ca²⁺ concentrations.

To investigate the influences of high-intensity training and/or a single bout of exercise on in vitro Ca²⁺-sequestering function of the sarcoplasmic reticulum (SR), the rats were subjected to 8 weeks of an interval running program (final training : 2.5-min running×4 sets per day, 50 m/min at 10% incline). Following training, both trained and untrained rats were run at a 10% incline, 50 m/min for 2.5 min or to exhaustion. SR Ca²⁺-ATPase activity, SR Ca²⁺-uptake rate and carbonyl group contents comprised in SR Ca²⁺-ATPase activity were examined in the superficial portions of the gastrocnemius and vastus lateralis muscles. For rested muscles, a 12.7% elevation in the SR Ca²⁺-uptake rate was induced by training. Training led to improved running performance (avg time to exhaustion : untrained-191.1 vs trained-270.9 sec ; P<0.01). Regardless of training status, a single bout of exercise caused progressive reductions in SR Ca²⁺-ATPase activity and SR Ca²⁺-uptake rate. Increases in carbonyl content only occurred after exhaustive exercise (P<0.05). At both point of 2.5-min and exhaustion, no differences existed in SR Ca²⁺-sequestering capacity and carbonyl content between untrained and trained muscles. These findings confirm the previous findings that oxidative modifications may account, at least partly, for exercise-induced deterioration in SR Ca²⁺-sequestering function ; and raise the possibility that in the final phase of acute exercise, high-intensity training could delay the progression of protein oxidation of SR Ca²⁺-ATPase.

Using various types of monoclonal antibodies and flow cytometer, whole blood analysis were conducted on subsets of lymphocytes taken from peripheral blood samples of healthy persons and umbilical cord blood samples of mature babies.
The findings were as follows:
(1) Normal values of healthy persons (Mean ± SD) were: T-cell phenotypes-OKT3⁺: 66.2 ± 9.4%, OKT4⁺: 40.9±8.3%, OKT8⁺: 28.2±6.6%, OKT11⁺: 80.1±4.8%, OKT4/OKT8 ratio: 1.57±0.60; B-cell phenotype-SmIg (polyvalent) ⁺: 15.9±6.5%; others-OKTal⁺: 12.9±3.2%, Leu7⁺: 16.2±8.9%.
(2) Of the healthy persons, 17% showed 1.0 or below and 6.5% showed 2.5 or above, in the OKT4/OKT8 ratio.
(3) The OKT4+ OKT8/OKT3 ratio was significantly high (P<0.001) in the babies and persons of 40 years and over.
(4) Physiologic variations were noted in some degree in children and the aged, and between men and women. The individual values of the lymphocyte subsets were almost constant, but the difference between individuals was large. It is suggested that the difference of the immune response of each individual or each family partly depends on the different values of the lymphocyte subsets.

We tested the hypothesis that a force reduction in soleus muscles from hyperthyroid rats would be associated with oxidative modification of myofibrillar proteins. Daily injection of thyroid hormone [3, 5, 3’-triiodo-_L-thyronine (T₃)] for 21 days depressed isometric forces in whole soleus muscle across a range of stimulus frequencies (1, 10, 20, 40, 75 and 100 Hz) (P<0.05). In fiber bundles, hyperthyroidism also led to pronounced reductions (P<0.05) in both K⁺- and 4-chloro-m-cresol-induced contracture forces. The degrees of the reductions were similar between these two contractures. These reductions in force production were accompanied by a remarkable increment (103% ; P<0.05) in carbonyl groups comprised in myofibrillar proteins. In additional experiments, we have also tested the efficacy of carvedilol, a non-selective β₁-β₂-blocker that possesses anti-oxidative properties. Treatment with carvedilol prevented T₃-induced oxidation of myofibrillar proteins. However, carvedilol did not improve the hyperthyroid-induced reductions in force production. These data suggest that oxidative modification of myofibrillar proteins may not account for the reductions in force production of hyperthyroid rat soleus muscle.

Objective: Because patients with diabetes mellitus (DM) were forced to stay indoors during the state of emergency, resulting in stress and a lack of physical activity, concerns about their glycemic control were raised.Patients and Methods: The 165 patients’ glycated hemoglobin (HbA1c) levels were compared during the following periods: the 4 months that were selected as a representative condition 1 year before the COVID-19 pandemic (May 2018, March 2019, June 2019, and July 2019) and the latter 3 months as a 1-year follow-up during the COVID-19 pandemic (May 2019, March 2020, June 2020, and July 2020).Results: The patients’ HbA1c levels were 7.32 ± 1.23, 7.44 ± 1.20, 7.16 ± 1.06, 7.01 ± 1.05, 7.23 ± 1.06, 7.45 ± 1.18, 7.15 ± 10.7, and 7.11 ± 1.17 in May 2018, March 2019, June 2019, July 2019, May 2019, March 2020, June 2020, and July 2020, respectively (expressed as mean ± standard deviation).Conclusion: The analysis showed that HbA1c levels did not worsen during the self-restraint period.