Muscle tone is profoundly suppressed during rapid-eye-movement sleep (REMS). Two indices that quantify this muscle activity suppression were introduced; the tonic inhibition index (TII) and the phasic inhibition index (PII). TII expresses the shortness of phasic chin muscle activity, and PII indicates the weakness of rapid eye movements-related phasic chin muscle activity loss. TII increased significantly with age, while PII decreased significantly. These chronological changes were concluded to indicate that the activity of the human nervous systems involved in both tonic and phasic inhibition in REMS increases with age. TII was found to reach the adult level at 12.3 years of age, while PII decreased to the adult value at 0.4 years. According to this difference in age between their maturation, the human nervous systems involved in muscle activity suppression during REMS are hypothesized to comprise at least 2 independent systems. TII and PII are also hypothesized to be affected by the activity of the brainstem inhibitory/facilitatory centers, which might be implicated in the control of muscle activity during wakefulness as well.

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The management of a postoperative rectovaginal fistula after low anterior resection for rectal cancer is difficult and requires reconstruction of the anastomotic site and fistula. The results of reconstructive operation are often unsatisfactory. Herein, we describe our reconstruction technique using the posterior approach through the vaginal lumen for a high rectovaginal fistula repair. This reconstructive operation is useful for post­operative rectovaginal fistulas accompanied by severe stenosis of the anastomotic site following low anterior resection for rectal cancer.

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To investigate left ventricular wall motion asynchrony in patients with hypertensive heart dis­ ease, we measured regional myocardial velocity in hypertensive patients with left ventricular hyper trophy and in normotensive individuals using tis­ sue Doppler imaging. The endocardial velocity and the myocardial velocity gradient were mea­ sured in the basal and mid segments of the septal and posterior walls. The dilating velocity of the left ventricular cavity were deter.mined for the basal and mid ventricular segments of left ventricle. The peak myocardial velocity gradient was significant­ ly lower in the hypertensive group than in the control group for all regions. The peak endocardial velocity during early dia'stole in the mid ventricular septum was significantly lower in the hypertensive group (Hypertensive vs Controls; 3.8 ± 1.3 vs 5.1 ± 1.6 cm/s, P < 0.05), whereas the peak endocardial velocity at the other three sites were similar in the two groups. The peak dilating velocity was signifi­ cantly lower in the hypertensive group only in the mid portion of the left ventricle _(Hypertensive vs Controls; 7.2 ± 2.4 vs 9.8 ± 1.3 s^-1, P < 0.005). These results suggest that there were regional wall motion abnormalities and nonuniformity during the early diastolic phase in the hypertensive hearts with left ventricular hypertrophy.

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Ca²⁺ liberation from the endoplasmic reticulum activates sarco-endoplasmic reticulum Ca²⁺-ATPase (SERCA) to return Ca²⁺ to storage. We explored the role of SERCA in dynamic changes of intranuclear Ca²⁺ in single HeLa cells. Application of forskolin, as an activator of SERCA, caused the phosphorylation of SERCA2b but not SERCA3 on serine residues, which increased the rate of Ca²⁺ uptake. Forskolin also induced the changes of Ca²⁺ movement pattern in the nucleus when cells were stimulated with the Ca²⁺-releasing agents, histamine or A23187. lmmunofluorescence staining showed that SERCA2b was densely populated on special parts of the nuclear envelope, but SERCA3 only existed in endoplasmic reticulum. Injection of an anti-SERCA2 antibody into the cytoplasm blocked the rise in the nuclear Ca²⁺ concentration ([Ca²⁺]_n). However, injection of an anti-SERCA3 antibody did not affect the initiation of Ca²⁺ oscillations in the nucleus. Our data suggest that the activated-SERCA2b elevates the rate of uptake of free Ca²⁺ into stores along the nuclear envelope, which might support and maintain the nuclear Ca²⁺ homeostasis.

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