Byung-Hun Kang

Analysis of monocyte subsets and toll-like receptor 4 expression in peripheral blood monocytes of women in preterm labor

Preterm labor is associated with both localized inflammation of the uterus and elevated proinflammatory cytokines. Recently, specific roles have been suggested for distinct monocyte subsets and toll-like receptor 4 (TLR4) expression in inflammation. The aim of this study was to determine whether specific monocyte subsets and increased TLR4 expression in monocyte subsets contribute to preterm labor. The study included 30 preterm labor, 40 full-term labor and 20 pregnant women (not in labor). Four-color flow cytometry was used to examine the distribution of three monocyte subsets (CD14(+)CD16(-), CD14(high)CD16(+), and CD14(low)CD16(+)) and the TLR4 expression in each monocyte subset in each group of women. A larger percentage of CD14(high)CD16(+) cells was found in the preterm labor group than in the other groups (P=0.08, P=0.06). Women in preterm labor also showed significantly higher TLR4 expression in all monocyte subsets and increased fluorescence intensity in the CD14(+)CD16(-) and CD14(high)CD16(+) cells. Expression of TLR4 and mean fluorescence intensity on each monocyte subset were also significantly correlated. We conclude that women with preterm labor have higher CD16 monocytes, with high concomitant expression of CD14 and enhanced TLR4 expression in monocytes, and that monocyte TLR4 levels could be used as a marker to predict preterm delivery.

Trichonomas vaginalis Metalloproteinase Induces Apoptosis of SiHa Cells through Disrupting the Mcl-1/Bim and Bcl-xL/Bim Complexes

To elucidate the roles of metalloproteinases and the Bcl-2 family of proteins in Trichovaginalis. vaginalis-induced apoptosis in human cervical cancer cells (SiHa cells) and vaginal epithelial cells (MS74 cells), SiHa cells and MS74 cells were incubated with live T. vaginalis, T. vaginalis excretory and secretory products (ESP), and T. vaginalis lysates, either with or without the specific metalloproteinase inhibitor 1,10-phenanthroline (1,10-PT), and examined apoptotic events and Bcl-2 signaling. The live T. vaginalis and the T. vaginalis ESP induced the release of cytochrome c into the cytosol, the activation of caspase-3 and caspase-9, and the cleavage of PARP. Additionally, the live T. vaginalis, but not the T. vaginalis lysate, induced the cleavage of the proapoptotic Bim protein. The live T. vaginalis and the T. vaginalis ESP, but not the T. vaginalis lysate, induced the dose-dependent cleavage of the antiapoptotic Bcl-xL and Mcl-1 proteins and decreased the association levels of Bcl-xL/Bim and Mcl-1/Bim complexes. We performed gelatin zymography and casein-hydrolysis assays on the live T. vaginalis and the T. vaginalis ESP to identify the apoptosis-inducing factor. Both the live T. vaginalis and the ESP contained high levels of metalloproteinases, of which activities were significantly inhibited by 1,10-PT treatment. Furthermore, the 1,10-PT blocked the cleavage of Bcl-xL, Mcl-1, PARP, caspase-3, and caspase-9, as well as the release of cytochrome c into the cytosol, and it significantly increased the association levels of the Bcl-xL/Bim and Mcl-1/Bim protein complexes, returning them to normal levels. Our results demonstrate that T. vaginalis induces mitochondria-dependent apoptosis in SiHa cells through the dissociation of Bcl-xL/Bim and Mcl-1/Bim complexes and that the apoptosis is blocked by the metalloproteinase inhibitor 1,10-PT. These results expand our understanding of the role of metalloproteinases in T. vaginalis-induced apoptosis and the signaling pathway in trichomoniasis of the cervicovaginal epithelial cells.

Recovery of net photosynthetic rate after SO2 fumigation in Quercus acutissima, Pinus densiflora, Populus alba×glandulosa, and Acanthopanax sessiliflorus

After SO2 fumigation, Quercus acutissima and Pinus densiflora maintained high net photosynthetic rate (PN) and did not show visible symptoms of damage. In contrast, Populus alba×glandulosa and Acanthopanax sessiliflorus had significantly reduced PN and showed visible necrosis.

Single port access laparoscopic hysterectomy for large uterus of more than 500 g

Results There were no significant difference in patients` age, body mass index, past surgical history, postoperative additional pain control and duration of hospital stay between the two groups. Uterine weight was 706.5±363.2 g (range, 500–2,415 g) for SPA laparoscopic hysterectomy and 634.0±153.3 g (range, 500–1,130 g) for conventional laparoscopic hysterectomy and signifi cantly not different between the two groups. Operation time was signifi cantly longer in SPA laparoscopic hysterectomy than conventional laparoscopic hysterectomy (81.1±18.1 minutes vs. 67.2±16.8 minutes). Postoperative change in hemoglobin and hematocrit was statistically higher in SPA laparoscopic hysterectomy than conventional laparoscopic hysterectomy (1.9±0.9 g/dL, 2.9±4.2% vs. 1.0±1.3 g/dL, 6.2±2.9%, respectively).

Two pregnancy cases of uterine scar dehiscence after laparoscopic myomectomy

Uterine scar dehiscence following laparoscopic myomectomy rarely occurs but can compromise both maternal and fetal well-being in subsequent pregnancy. We here present two cases of pregnancy complicated by preterm birth that resulted from uterine scar dehiscence following laparoscopic myomectomy. First case was a nulligravida who had scar dehiscence at 26 weeks of gestation after having a laparoscopic myomectomy 3 months prior to conception. Two weeks later, we observed her fetal leg protruding through the defect. The other case was a primigravida with a history of prior cesarean delivery, whose sonography revealed myomectomy scar dehiscence at 31 weeks of gestation. Within a few hours after observing, the patient complained of abdominal pain that was aggravating as fetal leg protruded through the defect. In both cases, babies were born by emergency cesarean section. Conservative management can be one of treatment options for myomectomy scar dehiscence in preterm pregnancy. However, clinicians should always be aware of the possibility of obstetric emergencies.

EP16.07: Two cases of twin pregnancy with a hydatidiform mole and a coexisting live fetus, especially with high levels of βhCG: Electronic Poster Abstracts

Introduction Twin pregnancy with a hydatidiform mole and a coexisting live fetus is rare occurrence associated with the increased risk of obstetric complications and poor perinatal outcome. Here we reported two cases of twin molar pregnancy opted for conservative management resulted with unfavorable consequences Second Case A 29-year-old primigravida woman in natural conception. At 11 weeks of gestation, she was diagnosed with molar pregnancy by abnormal ultrasound imaging (Figure2) and high levels of βhCG (above 200,000mIU/mL). At 22 weeks of gestation, she came to the hospital with massive vaginal bleeding and the elevated βhCG level upto 896,503mIU/mL. The pregnancy was to be terminated immediately. The βhCG level showed rapid regression and reached normal in 5 weeks without any treatment.

Prenatal 3D sonography of an isolated lateral facial cleft

Lateral facial cleft is a rare congenital anomaly, but all affected infants require surgery under general anesthesia. Conventional 2‐dimensional coronal view of the face, which is typically used for identification of facial clefts, has limitations with regard to detection of this anomaly. We describe a case of prenatal diagnosis of isolated lateral facial cleft made with 3D sonography and highlight the importance of this tool in the diagnosis of this rare facial deformity.

Safety of umbilical cord milking in very preterm neonates: a randomized controlled study

Objective To investigate the safety of umbilical cord milking on both the mother and neonate among very preterm deliveries of less than 33 weeks of gestation. Methods Pregnant women who were expected to deliver at between 24 0/7 and 32 6/7 weeks of gestation were randomized to either the umbilical cord milking or immediate cord clamping group. Maternal and neonatal data associated with delivery, in addition to neonatal morbidity and mortality data, were collected and analyzed. Results Of the 66 preterm deliveries included in the study, 34 were randomized into the milking and 32 into the clamping group. Differences between maternal pre- and post-partum hemoglobin levels were 1.35 g/dL in the milking and 1.58 g/dL in the clamping group (P=0.451). Neonatal Apgar scores at both 1 and 5 minutes, initial blood gas analysis results, body temperature at admission, need for early intubation, and maximum bilirubin levels were all similar between the 2 groups. However, neonatal hemoglobin levels at birth (15.79 vs. 14.69 g/dL; P<0.05) and at 24 hours of age (14.83 vs. 13.29 g/dL; P<0.05) were significantly higher in the milking group. Neonates in the clamping group required more blood transfusion (1.78 vs. 0.93; P=0.049), and a higher percentage of neonates in the clamping group required inotropic drugs (63% vs. 29%; P=0.007). The mortality rate was significantly lower in the milking group (6% vs. 28%; P=0.015). Conclusion Umbilical cord milking can be a safe and beneficial procedure for both the mother and the neonate in deliveries of less than 33 weeks of gestation.

IL-12 and IL-23 Production in Toxoplasma gondii- or LPS Treated Jurkat T Cells via PI3K and MAPK Signaling Pathways

IL-12 and IL-23 are closely related in structure, and have been shown to play crucial roles in regulation of immune responses. However, little is known about the regulation of these cytokines in T cells. Here, we investigated the roles of PI3K and MAPK pathways in IL-12 and IL-23 production in human Jurkat T cells in response to Toxoplasma gondii and LPS. IL-12 and IL-23 production was significantly increased in T cells after stimulation with T. gondii or LPS. T. gondii and LPS increased the phosphorylation of AKT, ERK1/2, p38 MAPK, and JNK1/2 in T cells from 10 min post-stimulation, and peaked at 30–60 min. Inhibition of the PI3K pathway reduced IL-12 and IL-23 production in T. gondii-infected cells, but increased in LPS-stimulated cells. IL-12 and IL-23 production was significantly reduced by ERK1/2 and p38 MAPK inhibitors in T. gondii- and LPS-stimulated cells, but not in cells treated with a JNK1/2 inhibitor. Collectively, IL-12 and IL-23 production was positively regulated by PI3K and JNK1/2 in T. gondii-infected Jurkat cells, but negatively regulated in LPS-stimulated cells. And ERK1/2 and p38 MAPK positively regulated IL-12 and IL-23 production in Jurkat T cells. These data indicate that T. gondii and LPS induced IL-12 and IL-23 production in Jurkat T cells through the regulation of the PI3K and MAPK pathways; however, the mechanism underlying the stimulation of IL-12 and IL-23 production by T. gondii in Jurkat T cells is different from that of LPS.

Trichomonas vaginalis Induces SiHa Cell Apoptosis by NF-κB Inactivation via Reactive Oxygen Species

Trichomonas vaginalis induces apoptosis in host cells through various mechanisms; however, little is known about the relationship between apoptosis, reactive oxygen species (ROS), and NF-κB signaling pathways in the cervical mucosal epithelium. Here, we evaluated apoptotic events, ROS production, and NF-κB activity in T. vaginalis-treated cervical mucosal epithelial SiHa cells, with or without specific inhibitors, using fluorescence microscopy, DNA fragmentation assays, subcellular fractionation, western blotting, and luciferase reporter assay. SiHa cells treated with live T. vaginalis at a multiplicity of infection of 5 (MOI 5) for 4 h produced intracellular and mitochondrial ROS in a parasite-load-dependent manner. Incubation with T. vaginalis caused DNA fragmentation, cleavage of caspase 3 and PARP, and release of cytochrome c into the cytoplasm. T. vaginalis-treated SiHa cells showed transient early NF-κB p65 nuclear translocation, which dramatically dropped at 4 h after treatment. Suppression of NF-κB activity was dependent on parasite burden. However, treatment with the ROS scavenger, N-acetyl-C-cysteine (NAC), reversed the effect of T. vaginalis on apoptosis and NF-κB inactivation in SiHa cells. Taken together, T. vaginalis induces apoptosis in human cervical mucosal epithelial cells by parasite-dose-dependent ROS production through an NF-κB-regulated, mitochondria-mediated pathway.