Yayoi Kajiwara

Inactivation of interleukin-8 by aminopeptidase N (CD13).

Aminopeptidase (APN) was found to degrade interleukin‐8 (IL‐8) and inactivate its chemotactic activity. The chemotactic activity of IL‐8 was decreased by APN or neutrophil plasma membranes dose‐ and time‐dependently. The chemotactic activity was not inactivated in the presence of bestatin or WM15 monoclonal antibody. The expression of IL‐8 was measured by flow cytometry. On lipopolysaccharide (LPS) stimulation, IL‐8 expression increased for 60 min and then decreased markedly. In contrast, on treatment with LPS and bestatin, the expression of IL‐8 increased continuously for at least 120 min. These results suggest that the expression and release of IL‐8 from phagocytic cells are regulated by the proteolytic effect of APN on IL‐8. J. Leukoc. Biol. 57: 129–134; 1995.

Magnetic Resonance Imaging Angiography in a Case of Eclampsia

We experienced a typical case of eclampsia. After the onset of eclampsia, we performed magnetic resonance imaging angiography (MRI angiography) to estimate the function of the cerebral artery. MRI angiography showed that spasm occurred in many cerebral arteries. The spasm was still observed in some arteries 13 day after the onset of eclampsia. Vasospasm of eclampsia was clearly, easily and noninvasively confirmed in this case by MRI angiography. This observation suggests that MRI angiography is very useful and informative for diagnosis and in treatment of eclampsia.

Urinary trypsin inhibitor prevents uterine muscle contraction by inhibition of Ca++ influx.

OBJECTIVE The aim of this research was to elucidate the mechanism of action of urinary trypsin inhibitor, a Kunitz-type protease inhibitor, in suppressing uterine muscle contraction. STUDY DESIGN An isometric uterine contraction test was used to study this inhibitory effect of urinary trypsin inhibitor on the myometrium. Oxytocin, prostaglandin F2 alpha, and lipopolysaccharide were used to stimulate myometrial contraction. Prostaglandins F2 alpha and E2 were measured in the buffer solution. Influx of calcium into uterine smooth muscle cells was assessed by digital imaging microscopy. RESULTS After incubation with urinary trypsin inhibitor or fetal urine, myometrial contractions stimulated by oxytocin, prostaglandin F2 alpha or lipopolysaccharide were suppressed completely. The concentrations of prostaglandins F2 alpha and E2 in the buffer solution during the isometric contraction test were significantly increased by lipopolysaccharide stimulation, but when urinary trypsin inhibitor was present in the buffer solution the concentrations of prostaglandins F2 alpha or E2 did not change significantly. Preincubation with urinary trypsin inhibitor also inhibited calcium influx, resulting in no detectable change in the intracellular free calcium concentration of smooth muscle cells. CONCLUSION We proposed that urinary trypsin inhibitor from fetal urine inhibits uterine muscle contraction by regulation of intracellular Ca++.

Urinary trypsin inhibitor suppresses premature cervical ripening

UNLABELLED Unknown signals from the fetus are thought to be involved in the onset of parturition. We recently discovered that urinary trypsin inhibitor (UTI) from fetal urine inhibits uterine muscle contraction. OBJECTIVES The aim of this research was to elucidate the mechanism of action of UTI in suppressing cervical maturation. STUDY DESIGN Non-pregnant and pregnant rabbits pretreated with and without UTI suppositories containing 1000 U (400 micrograms) for 3 days were treated for 2 days with vaginal suppositories containing 100 ng of interleukin-8 (IL-8). RESULTS IL-8 induced softening and dilatation of the rabbit cervices. In contrast UTI inhibited IL-8 induced cervical softening and dilatation. Water content, collagen content, neutrophil counts, elastase activity and collagenase activity of the cervix were increased by IL-8, but they did not increase by IL-8 with UTI. CONCLUSION These results suggest that UTI inhibits cervical maturation induced by IL-8.

Antithrombin improves fetal condition in women with severe pre-eclampsia before 32 weeks of gestation; a randomized, double-blind, placebo-controlled trial.

Aim:  To see if antithrombin (AT) supplementation improved fetal outcomes in early onset (<32 weeks) severe pre‐eclampsia.

Hypolumbarlordosis: a predisposing factor for preeclampsia

OBJECTIVE The aim of this research was to study the relationship between lumbar lordosis and preeclampsia. STUDY DESIGN We studied lumbar lordosis of 52 primipara patients with pregnancy-induced hypertension and 59 normal primipara pregnant women. We determined the lumbar lordotic deviation (LLD) from lumbar lordosis measurement device in the lateral recumbent position and standing position. Roll-over test was performed for both groups. Resistance index (RI) of internal iliac artery was also measured by color Doppler sonography. RESULTS The LLD was 33 +/- 6.1 degrees week 20-29 and 34 +/- 6.9 degrees week 30-40, respectively. In patients with preeclampsia, the LLD was 19.8 +/- 6.3 degrees week 20-29, 21.3 +/- 7.9 degrees week 30-40. The LLD in patients with preeclampsia was significantly lower than in the normal pregnant women. The LLD correlated to the increase diastolic pressure after roll-over test significantly. Hypolumbarlordosis was frequently associated with high resistance of peripheral vessel. CONCLUSIONS We conclude that hypolumbarlordosis is frequently associated with preeclampsia. It is also closely related to the mechanism for positive roll-over test and increase of resistance of vessels. As lumbar lordosis does not change greatly in individuals before pregnancy, hypolumbarlordosis may be a predisposing factor for preeclampsia.

Antithrombin III administration in premature infant with intracranial hemorrhage

Intracranial hemorrhage (ICH) is a significant cause of mortality and morbidity in the neonatal intensive care unit. Abnormalities of coagulation have been implicated as one of the important causes of intracranial hemorrhage in premature infants. Recent advances in the technique of ultrasound diagnosis of ICH in premature infants have made it possible for us to determine the presence of ICH even in the early stages of the disease. This study was conducted to ascertain whether antithrombin III (AT III) inhibits the progress of ICH in prematurely born infants.