Unexpected placenta accreta spectrum after the use of assisted reproductive technology in women with adenomyomectomy

Placenta accreta spectrum (PAS) is a rare complication that can lead to life-threatening postpartum hemorrhage. PAS can sometimes occur unexpectedly, without placenta previa;such cases can lead to higher maternal mortality and morbidity than expected cases. Here, the authors report a case of unexpected PAS caused by assisted reproductive technology (ART) in a woman with adenomyosis. The patient was a 37-year-old Japanese primipara woman who presented to our hospital at 11 weeks gestation, later returning to her parents' house to give birth. The woman had adenomyosis and underwent adenomyomectomy, which was followed by an ART pregnancy. The patient was admitted to our hospital because of a life-threatening preterm birth, with a short cervix and no evidence of placenta previa. Despite strict perinatal management, preterm rupture of the membrane (PROM) occurred. During laparotomy, the small intestine, rectum, and both right and left ovaries were clumped together and severely adhered to the surface of the uterus. After delivery, manual partial removal of the placenta was performed, resulting in heavy bleeding from the implantation site, which was diagnosed as an unexpected PAS. Following several uterine compression efforts, we successfully preserved the uterus

First trimester heterotopic pregnancy with shock treated laparoscopically, followed by uneventful term pregnancy and normal birth

Heterotopic pregnancy (HP), a coexistence of intrauterine and ectopic pregnancies, is extremely rare. Although there have been many reports of maternal outcomes in pregnant women with HP, they have not described fetal neurodevelopmental outcomes and survival. A 30-year-old Japanese woman in early gestation who had undergone two previous cesarean deliveries was transferred to our hospital with vital signs of shock. HP was confirmed by ultrasonography and laparoscopic surgery, and right salpingectomy was performed. At term, a 2,875 g neonate was delivered via cesarean section without any complications

青色光は滑膜肉腫に対して活性酸素種によるミトコンドリア機能障害を起こし、アポトーシスとオートファジーを誘導する

Background: Synovial sarcoma (SS) has limited treatment options and there is an urgent need to develop a novel therapeutic strategy to treat SS. Blue light (BL) has been shown to inhibit the growth of several cancer cells. However, the efficacy of BL in soft tissue sarcomas such as SS has not been demonstrated, and the detailed mechanism underlying the antitumor activity of BL is not fully understood. In this study, we investigated the antitumor effect of BL on SS. Methods: Human SS cell lines were continuously irradiated with BL using light-emitting diodes (LEDs) in an incubator for in vitro analysis. The chicken chorioallantoic membrane (CAM) tumors and xenograft tumors in mice were subjected to daily BL irradiation with LEDs. Results: BL caused growth inhibition of SS cells and histological changes in CAM tumors. BL also suppressed the migration and invasion abilities of SS cells. The type of cell death in SS cells was revealed to be apoptosis. Furthermore, BL induced excessive production of reactive oxygen species (ROS) in mitochondria, resulting in oxidative stress and malfunctioned mitochondria. Reducing the production of ROS using N-acetylcysteine (NAC), a ROS scavenger, attenuated the inhibitory effect of BL on SS cells and mitochondrial dysfunction. In addition, BL induced autophagy, which was suppressed by the administration of NAC. The autophagy inhibitor of 3-methyladenine and small interfering RNA against the autophagy marker light chain 3B facilitated apoptotic cell death. Moreover, BL suppressed tumor growth in a mouse xenograft model. Conclusion: Taken together, our results revealed that BL induced apoptosis via the ROS-mitochondrial signaling pathway, and autophagy was activated in response to the production of ROS, which protected SS cells from apoptosis. Therefore, BL is a promising candidate for the development of an antitumor therapeutic strategy targeting SS

整形外科予定手術患者における鼻腔黄色ブドウ球菌保菌調査 : 保菌者と非保菌者間で手術部位感染発生を比較

Background: Staphylococcus aureus (S. aureus), including MRSA, is considered to be the leading cause of surgical site infection (SSI) after orthopedic surgery. We screened for nasal carriers of S. aureus among patients who were scheduled to undergo orthopedic surgery at our hospital to reveal the effect of nasal S. aureus carriage on SSI. Our study design clearly has the intent of finding S. aureus nasal carriage and eradicating MRSA when found, and this strategy is to verify whether it's effective for preventing orthopedic surgical infections. Methods: Subjects were 4148 patients who underwent preoperative screening for nasal carrier and subsequently underwent orthopedic surgery during a 7-year period between April 2007 and March 2014. The incidence of SSI among patients who were operated in our department was investigated, and the rates were compared between patients with and without nasal carriage to reveal the effect of preoperative nasal carriage on SSI. Results: In total, 1036 patients were nasal carriers of S. aureus (carriage rate, 25.0%), whereas 140 patients carried MRSA (carriage rate, 3.4%). SSI developed in 24 patients [incidence, 0.58% (24/4148)] consisting of 12 non-carriers [0.39% (12/3112)] and 12 carriers [1.16% (12/1036)] with a significant difference in the incidence between the groups. Among 24 cases of SSI, more than half (13 cases) were caused by bacterial species other than S. aureus or those that could not be detected by the tests used. Only 7 patients out of 24 SSI patients, S. aureus was the bacterium detected in preoperative nasal cultures and the causal bacterium for SSI (concordance rate of 29.2%) Conclusions: It was difficult to reduce the incidence rate of SSI in eradication group to the same level as nasal culture negative group. However, nasal carriage of S. aureus or MRSA may be a risk factor for SSI in orthopedic surgery

Respiratory syncytial virus infection activates IL-13–producing group 2 innate lymphoid cells through thymic stromal lymphopoietin

BACKGROUND: Respiratory syncytial virus (RSV) is a major health care burden with a particularly high worldwide morbidity and mortality rate among infants. Data suggest that severe RSV-associated illness is in part caused by immunopathology associated with a robust type 2 response. OBJECTIVE: We sought to determine the capacity of RSV infection to stimulate group 2 innate lymphoid cells (ILC2s) and the associated mechanism in a murine model. METHODS: Wild-type (WT) BALB/c, thymic stromal lymphopoietin receptor (TSLPR) knockout (KO), or WT mice receiving an anti-TSLP neutralizing antibody were infected with the RSV strain 01/2-20. During the first 4 to 6 days of infection, lungs were collected for evaluation of viral load, protein concentration, airway mucus, airway reactivity, or ILC2 numbers. Results were confirmed with 2 additional RSV clinical isolates, 12/11-19 and 12/12-6, with known human pathogenic potential. RESULTS: RSV induced a 3-fold increase in the number of IL-13-producing ILC2s at day 4 after infection, with a concurrent increase in total lung IL-13 levels. Both thymic stromal lymphopoietin (TSLP) and IL-33 levels were increased 12 hours after infection. TSLPR KO mice did not mount an IL-13-producing ILC2 response to RSV infection. Additionally, neutralization of TSLP significantly attenuated the RSV-induced IL-13-producing ILC2 response. TSLPR KO mice displayed reduced lung IL-13 protein levels, decreased airway mucus and reactivity, attenuated weight loss, and similar viral loads as WT mice. Both 12/11-19 and 12/12-6 similarly induced IL-13-producing ILC2s through a TSLP-dependent mechanism. CONCLUSION: These data demonstrate that multiple pathogenic strains of RSV induce IL-13-producing ILC2 proliferation and activation through a TSLP-dependent mechanism in a murine model and suggest the potential therapeutic targeting of TSLP during severe RSV infection

Microbiological Investigation of the Iron-Containing Floculent Mats in Various Deep Sea Environments

Conference abstract (August 14-19, 2011, Goldschmidt 2011 in Prague, Czech Republic)http://www.godac.jamstec.go.jp/darwin/cruise/natsushima/nt10-13_leg2/ehttp://www.godac.jamstec.go.jp/darwin/cruise/yokosuka/yk10-10/

Prostaglandin I2 Signaling Drives Th17 Differentiation and Exacerbates Experimental Autoimmune Encephalomyelitis

BACKGROUND: Prostaglandin I(2) (PGI(2)), a lipid mediator currently used in treatment of human disease, is a critical regulator of adaptive immune responses. Although PGI(2) signaling suppressed Th1 and Th2 immune responses, the role of PGI(2) in Th17 differentiation is not known. METHODOLOGY/PRINCIPAL FINDINGS: In mouse CD4(+)CD62L(+) naïve T cell culture, the PGI(2) analogs iloprost and cicaprost increased IL-17A and IL-22 protein production and Th17 differentiation in vitro. This effect was augmented by IL-23 and was dependent on PGI(2) receptor IP signaling. In mouse bone marrow-derived CD11c(+) dendritic cells (BMDCs), PGI(2) analogs increased the ratio of IL-23/IL-12, which is correlated with increased ability of BMDCs to stimulate naïve T cells for IL-17A production. Moreover, IP knockout mice had delayed onset of a Th17-associated neurological disease, experimental autoimmune encephalomyelitis (EAE), and reduced infiltration of IL-17A-expressing mononuclear cells in the spinal cords compared to wild type mice. These results suggest that PGI(2) promotes in vivo Th17 responses. CONCLUSION: The preferential stimulation of Th17 differentiation by IP signaling may have important clinical implications as PGI(2) and its analogs are commonly used to treat human pulmonary hypertension

各地の深海底に存在する褐色変色域での微生物調査

BE11-P72ポスター要旨 / ブルーアース2011（2011年3月7日～8日, 東京海洋大学品川キャンパス）http://www.godac.jamstec.go.jp/darwin/cruise/natsushima/nt05-18/ehttp://www.godac.jamstec.go.jp/darwin/cruise/natsushima/nt10-06_leg2/ehttp://www.godac.jamstec.go.jp/darwin/cruise/natsushima/nt10-13_leg2/ehttp://www.godac.jamstec.go.jp/darwin/cruise/yokosuka/yk10-10/

VeNAS: Versatile Negotiating Agent Strategy via Deep Reinforcement Learning (Student Abstract)

Existing research in the field of automated negotiation considers a negotiation architecture in which some of the negotiation components are designed separately by reinforcement learning (RL), but comprehensive negotiation strategy design has not been achieved. In this study, we formulated an RL model based on a Markov decision process (MDP) for bilateral multi-issue negotiations. We propose a versatile negotiating agent that can effectively learn various negotiation strategies and domains through comprehensive strategies using deep RL. We show that the proposed method can achieve the same or better utility than existing negotiation agents

Scalable Negotiating Agent Strategy via Multi-Issue Policy Network (Student Abstract)

Previous research on the comprehensive negotiation strategy using deep reinforcement learning (RL) has scalability issues of not performing effectively in the large-sized domains. We improve negotiation strategy via deep RL by considering an issue-based represented deep policy network to deal with multi-issue negotiation. The architecture of the proposed learning agent considers the characteristics of multi-issue negotiation domains and policy-based learning. We demonstrate that proposed method achieve equivalent or higher utility than existing negotiation agents in the large-sized domains