[Relationship between systolic blood pressure load and sleep stability in patients with essential hypertension].

Objective: To explore the relationship between blood pressure load and sleep stability in hypertensive patients by cardiopulmonary coupling monitoring (CPC) and 24-hour ambulatory blood pressure monitoring. Methods: One hundred and fifty-five patients with essential hypertension were divided into high load group and low load group according to whether the blood pressure load was higher than 50%. The relationship between sleep stability and systolic blood pressure load was analyzed by logistic regression. Results: After adjusting for sex, age and body mass index (BMI), logistic regression analysis showed that stable sleep was the protective factor (OR=0.736,P=0.047) for the decrease of nocturnal blood pressure load, and unstable sleep was the risk factor for increasing day time blood pressure load (OR=1.336, P=0.037) in patients with hypertension. Conclusions: The effect of sleep stability on blood pressure load is different between day and night. Stable sleep is the protective factor of nocturnal systolic blood pressure load decrease, and unstable sleep is the harmful factor of daytime systolic blood pressure load increase. Increasing sleep stability helps to reduce systolic blood pressure load.

The CIT3 gene of Saccharomyces cerevisiae encodes a second mitochondrial isoform of citrate synthase.

We have identified a third citrate synthase gene in Saccharomyces cerevisiae which we have called CIT3. Complementation of a citrate synthase-deficient strain of Escherichia coli by lacZ::CIT3 gene fusions demonstrated that the CIT3 gene encodes an active citrate synthase. The CIT3 gene seems to be regulated in the same way as CIT1, which encodes the mitochondrial isoform of citrate synthase. Deletion of the CIT3 gene in a delta cit1 background severely reduced growth on the respiratory substrate glycerol, whilst multiple copies of the CIT3 gene in a delta cit1 background significantly improved growth on acetate. In vitro import experiments showed that cit3p is transported into the mitochondria. Taken together, these data show that the CIT3 gene encodes a second mitochondrial isoform of citrate synthase.