Hydatidiform moles are known to pose an extremely high risk of severe early-onset preeclampsia if left untreated. TNF superfamily cytokine, LIGHT has recently been reported to contribute to pathophysiology of preeclampsia. The present study aimed to investigate the involvement of LIGHT in hydatidiform moles. We measured the serum levels of LIGHT and sFlt-1 by ELISA in 17 women with complete hydatidiform mole (HM) and 20 gestational-age-matched normal pregnant women (control). As a result, the serum LIGHT levels were significantly higher in HM as compared with those in control (69.9 ± 9.6 pg/ml vs 25.4 ± 5.3 pg/ml, p = 0.0001) and the serum levels of LIGHT were significantly positively correlated with those of sFlt-1 in HM (r = 0.68, p = 0.0029). Immunohistochemical analysis revealed that the expression levels of LIGHT were increased in HM placentas as compared with controls, and LIGHT and sFlt-1 were co-localized in the trophoblast cells of HM. In vitro studies using primary syncytiotrophoblast cells demonstrated that LIGHT directly induced sFlt-1 expression in trophoblast cells. Our results indicated that elevated LIGHT in the trophoblast cells of hydatidiform mole induces sFlt-1, which might underlie the pathogenic mechanism of early-onset preeclampsia developing secondary to molar pregnancies.

It is widely accepted that enhanced uterine inflammation associated with microbial infection is a main causative factor for preterm birth. However, little is known about the molecular basis by which inflammation is associated with preterm birth. Here, we demonstrate that apoptosis signal-regulating kinase 1 (ASK1), a member of the mitogen-activated protein 3-kinase family, facilitates inflammationinduced preterm birth and that inhibition of ASK1 activity is sufficient to suppress preterm birth. ASK1-deficient pregnant mice exhibited reduced incidence of lipopolysaccharide (LPS)-induced preterm birth. ASK1 was required for the induction of LPS-induced inflammatory responses related to preterm birth, including pro-inflammatory cytokine production in the uterus and peritoneal cavities. In addition, selective suppression of uterine ASK1 activity through a chemical genetic approach reduced the incidence of LPS-induced preterm birth. Moreover, translational studies with human choriodecidua demonstrated that ASK1 was required for LPS-induced activation of JNK and p38 and pro-inflammatory cytokine production. Our findings suggest that ASK1 activation is responsible for the induction of inflammation that leads to preterm birth and that the blockade of ASK1 signaling might be a promising therapeutic target for preventing preterm birth. Preterm birth is a major health issue worldwide, occurring in 5-18% of all pregnancies, and is the leading cause of neonatal morbidity and mortality 1. Excessive inflammation induced by an exaggerated immune response is known to trigger preterm birth and various other complications in pregnancy 2. The key pathological mechanism underlying preterm birth is enhanced uterine inflammation associated with infection 3. Bacterial infection ascending from the vagina to the uterus, and the subsequent progression to intrauterine inflammation are the most substantially confirmed causative factors for preterm birth 4,5. Bacterial infection results in an increased production of pro-inflammatory cytokines, such as TNF-α, and triggers cervical ripening, uterine contraction, and fetal membrane rupture, all of which lead to preterm birth 6. The above is supported not only by a number of clinical findings, but also by multiple pathophysiological findings from animal models in which preterm birth was triggered by administration of lipopolysaccharides (LPS) and other bacteria-derived substances 7. However, despite intense research efforts to date, current strategies for treating preterm labor are limited to targeting bacterial infection and uterine contraction. These treatment options are insufficient with respect to improving perinatal outcomes, since increased myometrial contraction reflects the end stage of uterine inflammatory processes, which adversely affect the fetus 8. Therefore, regarding therapeutics targeting preterm birth, there is an emerging interest in blocking the inflammatory cascade leading to excessive uterine inflammation, as it induces not only uterine contraction and subsequent preterm bir...

Leiomyomas of the Fallopian tube are rare and their correct diagnosis is extremely difficult. A 39-year-old woman presented with lower abdominal pain. Magnetic resonance imaging revealed a solid extrauterine mass 12 cm in diameter with an area of decreased enhancement. Our preoperative diagnosis was torsion of a subserosal uterine leiomyoma.Laparoscopic surgery was performed and the tumor was found to have originated from the isthmus of the left Fallopian tube. A laparoscopic left salpingectomy was performed. Her postoperative course was uneventful. The final pathology report noted a primary tubal leiomyoma with ischemic changes. We report a case of torsion of a tubal leiomyoma, which was successfully managed laparoscopically.

Uterine necrosis is a rare complication in uterine artery embolization (UAE) for postpartum hemorrhage (PPH). Preeclampsia (PE) is a condition characterized with systemic endothelial damage and intravascular volume depletion. Whether a patient with PE is at high risk for uterine necrosis after UAE for PPH has been unknown. A 30-year-old primipara woman was diagnosed with PE based on hypertension and proteinuria during delivery. UAE was performed for PPH after forceps delivery. After UAE, the patient presented with pleural effusion and massive ascites as well as persistent fever unresponsive to antibiotics. Ultrasonography and contrast-enhanced magnetic resonance imaging (MRI) led to the diagnosis of uterine necrosis, for which we performed total laparoscopic hysterectomy. It should be kept in mind that patients with PE associated with massive ascites may be at high risk for uterine necrosis after UAE due to decreased uterine perfusion. Therefore, it is important to pay attention to persistent symptoms such as fever and abdominal pain after UAE to diagnose uterine necrosis.

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