Analysis of complete hydatidiform mole in one twin using traditional and molecular techniques.

A pregnant woman with hydatidiform mole in one twin was misdiagnosed as one of the twins with embryonic arrest. She chose to terminate the pregnancy and developed distant lung metastasis. After chemotherapy, she eventually recovered. This article systematically analyzes the diagnosis and treatment of hydatidiform mole in one twin to increase the awareness and reduce misdiagnosis of the disease.

Angiopoietin-Like 8 in Gestational Diabetes Mellitus: Reduced Levels in Third Trimester Maternal Serum and Placenta, Increased Levels in Cord Blood Serum.

Gestational diabetes mellitus (GDM) poses a significant health risk to pregnant women, and thus exploring the potential underlying mechanism is highly desirable. The aim of the study was to compare maternal serum, cord blood serum, and placental angiopoietin-like 8 (ANGPTL8) levels in the third trimester of pregnancy in women with and without gestational diabetes and explore the potential underlying mechanism. A total of 42 pregnant women (23 with GDM and 19 with normal glucose tolerance (NGT)) along with 29 age-matched non-pregnant healthy females were enrolled. All pregnant subjects were in the late third trimester. Maternal serum and cord blood serum ANGPTL8 levels were measured with an enzyme-linked immunosorbent assay and the protein levels of ANGPTL8 in placentas were assessed with western blotting. The associations between maternal serum and cord blood serum ANGPTL8 levels and metabolic parameters were investigated with the Spearman correlation analysis. Significantly lower levels of maternal serum and placental ANGPTL8 levels were observed in GDM patients compared to NGT pregnant women, while remarkably higher ANGPTL8 levels were present in the cord blood serum samples. The maternal serum ANGPTL8 level was positively correlated with BMI, total cholesterol, triglycerides, and AUC for OGTT and birthweight. Additionally, the cord blood serum ANGPTL8 level was positively correlated with insulin and the homeostatic model assessment for insulin resistance. Both maternal serum and cord blood serum ANGPTL8 levels seemed to correlate with GDM and has the potential to be used as a biomarker for GDM and birthweight prediction.

Peptoniphilus indolicus infection in a pregnant woman: a case report.

BACKGROUND: Peptoniphilus indolicus belongs is a gram-positive anaerobic coccus (GPAC), which can cause bacterial vaginitis. However, only a few studies have reported severe infection of P. indolicus. This study presented the first case of severe infection of P. indolicus during pregnancy. It aimed to help to fill the gap in the literature, find out the factors that accelerate infection and discuss the significance of the GPAC test. CASE PRESENTATION: A 35-year-old woman was admitted due to unbearable abdominal pain with dilation of the cervical opening at 22+ weeks of gestation. A blood test revealed electrolyte disturbance and hypoproteinemia. A day before admission, the patient developed pain in the lower abdomen accompanied by yellow-green vaginal discharge. Two hours after admission, the patient suddenly presented with hyperpyrexia and chills. Timely and adequate antibiotic and cooling treatments were administered. After 14 h, the patient again developed chills that lasted for approximately 20 min, accompanied by uterine contractions and membrane rupture. After 3 h, she had a miscarriage and rapidly developed septic shock. She was transferred to the intensive care unit for further infection control, shock correction, and circulatory stabilization. The cultures of blood, secretion specimen, and amniotic fluid indicated P. indolicus infection using a matrix-assisted laser desorption/ionization time-of-flight mass spectrometry, an advanced tool for bacterial species identification. CONCLUSIONS: P. indolicus is an opportunistic pathogen in pregnant women. Poor physical conditions and pregnancy may accelerate disease progression and lead to severe inflammation.

Recombinant betatrophin (Angptl­8/lipasin) ameliorates streptozotocin­induced hyperglycemia and ß­cell destruction in neonatal rats.

Betatrophin [also known as lipasin, angiopoietin­like 8 (ANGPTL8), refeeding induced in fat and liver (RIFL), or hepatocellular carcinoma­associated gene TD26], a 22­kDa protein in the angiopoietin­like family, is a liver­derived hormone that promotes pancreatic ß­cell proliferation and lipid metabolism. The aim of the present study was to investigate the effect of recombinant betatrophin on ß­cell regeneration in a neonatal streptozotocin (STZ)­induced diabetic rat model. One­day­old Wistar rats were injected with STZ (100 mg/kg), followed by intraperitoneal administration of betatrophin to the STZ­injected rats for 6 days. Plasma glucose and body weight were monitored. On days 4 and 7, expression levels of pancreatic duodenal homeobox gene­1 (PDX­1), the Bax/B­cell lymphoma­2 (Bcl­2) ratio and plasma insulin were assessed, and the ß­cell proliferation rate was determined. Pancreatic islet area and number were determined at 10 weeks. It was found that betatrophin treatment alleviated STZ­induced hyperglycemia, elevated pancreatic expression levels of Bcl­2, PDX­1, plasma insulin levels and the ß­cell proliferation rate on days 4 and 7. Long­term betatrophin treatment improved glucose tolerance, associated with improved plasma insulin levels and ß­cell mass. These results suggest that early administration of betatrophin promotes ß­cell proliferation in STZ­induced diabetic neonates and prevents the development of diabetes in adults.

Reduced ELABELA expression attenuates trophoblast invasion through the PI3K/AKT/mTOR pathway in early onset preeclampsia.

INTRODUCTION: Early onset preeclampsia is linked to abnormal trophoblast invasion, leading to insufficient recasting of uterine spiral arteries and shallow placental implantation. This study investigated ELABELA (ELA) expression and its involvement in the pathogenesis of early onset preeclampsia. METHODS: We used immunohistochemistry, quantitative PCR and Western blot to calculate ELA levels in the placentas. Transwell assays were utilize to assess the invasion and migration of trophoblastic Cells. Western blot was used to identify the concentrations of vital kinases in PI3K/AKT/mTOR pathways and invasion-related proteins in trophoblast cells. RESULTS: ELA was expressed in villous cytotrophoblasts and syncytiotrophoblasts in placental tissue. Compared with the normal pregnancies, ELA mRNA and protein expression was significantly reduced in early onset preeclampsia placentas. In the HTR-8/SVneo cells, when ELA was knocked down, the invasion and migration capability of cells decreased significantly, with MMP2 and MMP9 expression downregulated and the expression of important kinases in the PI3K/AKT/mTOR pathways being significantly decreased compared to the control group. Overexpression of ELA was on the contrary. Besides, while PI3K was blocked, the invasion and migration capability of HTR-8/SVneo cells and the expression of key kinases in PI3K/AKT/mTOR pathways were decreased significantly. DISCUSSION: ELA stimulates the invasion and migration of trophoblastic cells through activation of downstream PI3K/AKT/mTOR pathway and is complicit in early onset preeclampsia pathogenesis. Our research offers a potential novel treatment for PE.

[Expression of glucose regulated protein 78 and the pathogenesis of gestational diabetes mellitus].

OBJECTIVE: To investigate the relationship between the expression of glucose regulated protein 78 (GRP78) in the placental trophoblast cells and the pathogenesis of gestational diabetes mellitus (GDM). METHODS: All the patients were recruited from Qingdao Municipal Hospital from May 2013 to May 2014. Among them, fifty women with GDM were assigned to the GDM group, and fifty healthy women were defined as the control group. All of them received cesarean section because of breech presentation, contracted pelvis, scarred uterus or on mother's demand. Real-time PCR was conducted to analyze the expression of GRP78 mRNA in the trophoblasts. Immunohistochemistry was performed to detect the localization of GRP78 protein in the placentasl trophoblast cells. RESULTS: (1) GRP78 mRNA expressed in the cytoplasm of trophoblasts of both the GDM group and the control group. The GRP78 mRNA levels in the GDM group and the control group were 15.6±0.4 and 6.0±0.7, respectively. The relative expression level of GRP78 mRNA in the GDM group was 2.6 times of that in the control group, with statistically significant difference (P<0.01). (2) The expression of GRP78 protein was found in the cytoplasm of the trophoblasts of the GDM group. It showed in deep, light brown or yellow after staining, according to the expression degree. The expression of GRP78 protein was also found in the cytoplasm of the trophoblasts of the control group, but it mainly showed yellow color (38/50). The strong positive rate of GRP78 protein in the GDM group (96%, 48/50) was higher than that in the control group (22%, 11/50; P<0.01). CONCLUSION: The expression of GRP78 increased in the placental trophoblast cells of GDM patients. It might suggest that GRP78 had some effect on the pathogenesis of GDM.

Effects of lead exposure on placental cellular apoptosis and endoplasmic reticulum stress in rats.

BACKGROUND: Lead exposure during pregnancy contributes to fetal abortion and/or teratogenesis. Endoplasmic reticulum (ER) apoptosis can be induced by various pathological conditions when ER function is disturbed. However, it is unclear whether ER stress and apoptosis play a role in the etiology of lead-exposed disease status. We aimed to investigate whether lead induced placental apoptosis and subsequent toxicity is initiated by ER apoptosis via caspase-12. METHODS: Sixty-three female Wistar rats were exposed to lead in drinking water during various gestational periods. Blood lead level was determined by atomic absorption spectrophotometry. Placental cytoplasmic organelles were examined by electronic microscopy. Placental caspase-12 mRNA expression was evaluated by qRT-PCR. TUNEL assay was used to determine the placental apoptosis. RESULTS: Lead exposure significant induced ER apoptosis compared to that of the controls (P < 0.05), accompanied with increased caspase-12 mRNA expression. Significant differences of caspase-12 mRNA expression levels were observed among the four groups (F = 13.78, P < 0.05). Apoptotic index (AI) was significantly increased in experimental groups compared to that of the controls (F = 96.15, P < 0.05). In lead-exposed groups, trophoblast cells underwent degeneration and fibrin deposition; Mitochondria were swollen and decreased in number; ER swelling, expansion, and vacuolization were observed. CONCLUSION: Lead exposure contributes to placental apoptosis, as well as increased caspase-12 mRNA expression, which in turn promoted ER stress.

[Effects of lead exposure to rat placenta and pups during different gestation periods].

OBJECTIVE: To investigate the effects of lead exposure to rat placenta and pups during different gestation periods. METHODS: All 108 Wistar rats (72 females, 36 males) were randomly divided into four groups. All rats were orally fed with 0.025% lead acetate during different gestation periods. Blood was obtained from the abdominal vena cava and the lead level in maternal blood was measured by means of atomic absorption spectrometry at the end of the pregnancy. The number of pups, their body weight, body length and tail length were measured. The effects of lead to rat placenta were observed by level of microscopy, optical microscopy and electronic microscopy. RESULTS: Experimental groups the blood lead level at the end of gestation were above 0.483 micromol/L. There were significant differences among, of pups, during different groups (P < 0.01). Among them the drinking lead group of whole distant was the lowest in placenta weight [(0.31 +/- 0.13) g] body weight of pups [(2.08 +/- 0.88) g] length and tail length of pups [(2.37 +/- 0.32) cm, (0.98 +/- 0.09) cm]. There were significantly differences between the experimental groups and controls. Maternal blood lead level was negatively related to placenta weight (r = 0.652, P < 0.01), and had no relation with the body weight of pups (r = -0.107, P = 0.46). In the experimental groups of lead poisoned rats, the placenta showed focus necrosis in the deciduas, and increased the trophoblastic giant cells and light staining cells in the trophospongium. Trophoblast in the labyrinth and trophospongium showed degeneration; fibrin deposition around the villi was increased. Microvilli around the trophoblast were shorter and less, mitochondrion was swollen and decreased in number, rough endoplasmic reticulum was distended and ribosomal number on membrane decreased. CONCLUSION: Lead exposure during different gestation periods should have a traumatic effect on the trophoblast, leading to interference of nutrition and oxygen exchange. Furthermore, the blood supply to the placenta and nutrition and oxygen exchange between mother and pups were also interfered, leading to reduction of placenta weight and retardation of development of pups.

[Expression and significance of metallothionein in the placenta of women with low level lead exposure during pregnancy].

OBJECTIVE: To investigate the significance of metallothionein (MT) expression in the placenta of women exposed to low level lead during pregnancy. METHODS: Sixty-seven pregnant women with blood lead level ranging from 1.5 micromol/L to 4.8 micromol/L were randomly selected from the Department of Obstetrics of Qingdao Municipal Hospital between Mar 2005 and Mar 2006. Among them, 35 were with blood lead level less than 2.9 micromol/L (group A) and 32 more than 2.9 micromol/L (group B). Immunohistochemical streptavidin-peroxidase-biotin methods were used to observe the expression of MT in the placental tissue. RESULTS: (1) Among the 67 pregnant women, the highest level of blood lead was 4.7 micromol/L, and the lowest level was 1.6 micromol/L. The blood lead level of groups A and B was (1.7 +/- 0.3) micromol/L, and (3.1 +/- 0.4) micromol/L, with a significant difference between them (P < 0.05). (2) The positive expression of MT was mainly cytoplastic in the cytotrophoblast, decidual cell and small vascular endothelial cells. The positive cell staining was diffuse or scattered. (3) The positive staining of MT was 91% (29/32) and 74% (26/35) in the placental tissue of groups A and B, respectively, with a significant difference between them (P < 0.05). (4) The blood lead level of pregnant women was correlated with the expression of MT of placenta. CONCLUSIONS: Lead can induce the expression of MT in the placental tissue in a dose-dependent manner. MT is mainly located in the cytotrophoblast, decidual cell and small vascular endothelial cells of the placenta. MT expression in the placenta is important to the structural integrity and function of the placenta.

[Effects of intervening measures on postpartum depression].

OBJECTIVE: To study the related factors of postpartum depression (PPD) and the effects of intervening measures to PPD incidence. METHODS: 1 597 pregnant women selected from our antenatal care clinic were investigated by using the hospital anxiety and depression questionnaire (HAD) during pregnancy and the Edinburgh postpartum depression scale (EPDS) after childbirth. All the enrolled women were randomly divided into control group and intervening group by the proportion of 1 to 2. Six intervening measures were used in the latter group. RESULTS: (1) There were 49 women whose HAD >or= 11 score (anxiety-depression mood) with 28 cases (57.1%) had got postpartum depression in the control group. In the intervening group, however, there were 94 women whose HAD >or= 11 score with 24 cases (25.5%) had got postpartum depression. There is a significant difference between the two groups (P < 0.01). (2) There were 71 (13.0%) women whose EPDS >or= 13 score (postpartum depression) in the control group. In the intervening group, however, there were 63 (6.0%) women whose EPDS >or= 13 score. There had a significant difference between the two groups (P < 0.01). (3) PPD women had higher N and P scores than those of non-PPD women (P < 0.01). CONCLUSION: (1) Prenatal anxiety, depression, negative personality and postpartum psychological and physiological changes were high risk factors to PPD. (2) Psychological personality play an important role in PPD. (3) Incidence of PPD was significantly reduced by social support.