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Growth impairment was previously described in milk-allergic children but was not examined in adults on reaching final height.

Aims To evaluate the role of pretreatment CA 15-3 levels as a predictor of disease-free survival in patients with advanced epithelial ovarian cancer.Methods A cohort of 65 patients with FIGO stage III or IV epithelial ovarian cancer was evaluated. Patients were treated either with primary cytoreductive surgery followed by adjuvant platinum-based chemotherapy or with neoadjuvant chemotherapy with interval debulking surgery. All patients had pretreatment CA 15-3 and CA 125 tumor marker determinations. The patients were divided into a group with elevated CA 15–3 and a group with normal levels. The two groups were compared with regard to clinical and survival measures.Results The patients' median age was 65 years (range, 37–90); 34 (52%) were at stage III and 31 (48%) at stage IV. CA 15–3 was elevated (>30 units/mL) in 44 (68%) patients, with a median level of 39 units (range, 4-2282). CA 125 was elevated (>35 units/mL) in 61 (94%) patients, with a median level of 947 units (range, 4-30,642). CA 125 and CA 15-3 levels were not correlated (r = 0.015, P = 0.332). The median follow-up was 22 months (range, 3–120 months). Fifty-three (81%) patients had disease recurrence and 43 (66%) died. Survival analysis showed that patients with elevated and normal CA 15-3 levels had similar recurrence-free survival (P= 0.78) and overall survival (P= 0.55).Conclusions Although elevated in the majority of patients with advanced epithelial ovarian cancer, CA 15-3 levels are not predictive of survival.

Objectives Ripening of the cervix with a Foley catheter commonly results in cervical dilatation without contractions. We examined the outcome of labour in women who underwent induction of labour using a Foley catheter, followed by either 1. early amniotomy, or 2. augmentation of labour by oxytocin and late amniotomy

Prostanoids influence differentiation in diverse cell types. Altered expression of cyclooxygenase and prostaglandins has been implicated in the pathophysiology of placental dysfunction, which results in preeclampsia and fetal growth restriction. We hypothesized that prostanoids modulate differentiation and apoptosis in cultured human trophoblasts. Villous cytotrophoblasts were isolated from term human placentas and cultured in serum-free medium. The level of human chorionic gonadotropin was used as a marker of biochemical differentiation of primary trophoblasts, and syncytia formation was used as a marker of morphologic differentiation. Of the prostanoids tested, we found exposure to thromboxane A2hindered both biochemical and morphologic differentiation of cultured trophoblasts. As expected, human chorionic gonadotropin levels in the media were elevated in a concentration-dependent manner in the presence of the thromboxane synthase inhibitor, sodium furegrelate, or the thromboxane A2receptor blocker SQ 29,548. Furthermore, thromboxane A2enhanced trophoblast apoptosis, determined using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining, cell morphology, and a concentration-dependent increase in p53 expression. We conclude that thromboxane A2hinders differentiation and enhances apoptosis in cultured trophoblasts from term human placenta. We speculate that thromboxane may contribute to placental dysfunction by restricting differentiation and enhancing apoptosis in human trophoblasts.

Prostanoids influence differentiation in diverse cell types. Altered expression of cyclooxygenase and prostaglandins has been implicated in the pathophysiology of placental dysfunction, which results in preeclampsia and fetal growth restriction. We hypothesized that prostanoids modulate differentiation and apoptosis in cultured human trophoblasts. Villous cytotrophoblasts were isolated from term human placentas and cultured in serum-free medium. The level of human chorionic gonadotropin was used as a marker of biochemical differentiation of primary trophoblasts, and syncytia formation was used as a marker of morphologic differentiation. Of the prostanoids tested, we found exposure to thromboxane A2hindered both biochemical and morphologic differentiation of cultured trophoblasts. As expected, human chorionic gonadotropin levels in the media were elevated in a concentration-dependent manner in the presence of the thromboxane synthase inhibitor, sodium furegrelate, or the thromboxane A2receptor blocker SQ 29,548. Furthermore, thromboxane A2enhanced trophoblast apoptosis, determined using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining, cell morphology, and a concentration-dependent increase in p53 expression. We conclude that thromboxane A2hinders differentiation and enhances apoptosis in cultured trophoblasts from term human placenta. We speculate that thromboxane may contribute to placental dysfunction by restricting differentiation and enhancing apoptosis in human trophoblasts.

Fetal infection by Parvovirus B 19 is a common cause of fetal anemia and nonimmune hydrops fetalis and may result in fetal death. Recent improvements in diagnosing parvovirus infections by sensitive molecular biology techniques now allow for a new insight into its pathogenic rule, immunology, and the varied clinical manifestations. The estimated overall risk of fetal loss after maternal exposure is about 6.5 percent, which is much less than previously thought. Inasmuch as complete spontaneous reversal of fetal hydrops has been commonly described, controversy exists regarding the management of the fetus with clinical signs of infection by Parvovirus B 19. According to the experience that has accumulated, it seems that only cases with severe fetal anemia or signs of fetal compromise should be managed by intrauterine transfusion. This procedure, however, is not without risk. Although an association between fetal viral infection and structural abnormalities has been described, it has not been proved yet. However, infection by Parvovirus B 19 has been recently proposed as a causative factor for congenital red blood cell aplasia.

Fetal infection by Parvovirus B 19 is a common cause of fetal anemia and nonimmune hydrops fetalis and may result in fetal death. Recent improvements in diagnosing parvovirus infections by sensitive molecular biology techniques not allow for a new insight into its pathogenic rule, immunology, and the varied clinical manifestations. The estimated overall risk of fetal loss after maternal exposure is about 6.5 percent, which is much less than previously thought. Inasmuch as complete spontaneous reversal of fetal hydrops has been commonly described, controversy exists regarding the management of the fetus with clinical signs of infection by Parvovirus B 19. According to the experience that has accumulated, it seems that only cases with severe fetal anemia or signs of fetal compromise should be managed by intrauterine transfusion. This procedure, however, is not without risk. Although an association between fetal viral infection and structural abnormalities has been described, it has not been proved yet. However, infection by Parvovirus B 19 has been recently proposed as a causative factor for congenital red blood cell aplasia.