Fetal brain imaging: a comparison between magnetic resonance imaging and dedicated neurosonography.

OBJECTIVES: To evaluate whether fetal brain magnetic resonance imaging (MRI) adds useful clinical information to that obtained by dedicated fetal neurosonography using a combined transabdominal and transvaginal approach in fetuses with suspected brain anomalies. METHODS: In the 2-year period between January 2000 and January 2002, 42 fetuses underwent neurosonographic and MRI examinations of the brain. The referral indications were: asymmetric ventriculomegaly (13), ventriculomegaly (7), periventricular cysts (2), suspected midline findings (7), agenesis of the corpus callosum (3), infratentorial pathology (3), cytomegalovirus (CMV) infection (2) and miscellaneous indications (5). RESULTS: Neurosonography and MRI produced similar diagnoses in 29 fetuses: normal examination (10), isolated asymmetric ventriculomegaly (11), isolated ventriculomegaly (3), periventricular cysts (2), agenesis of the corpus callosum (1), pericallosal lipoma (1) and cerebellar hemorrhage (1). The neurosonographic diagnoses were more accurate in seven patients: hemimegalencephaly, pericallosal lipoma, signs of CMV infection, brain anomalies associated with agenesis of the corpus callosum and three fetuses with a normal ultrasound scan in which MRI suggested a parenchymal abnormality. MRI provided a more accurate diagnosis in three patients: a third ventricular dilatation was ruled out, normal ventricles in a fetus with an ultrasonographic finding of asymmetric ventricles, and diagnosis of progression of asymmetric ventriculomegaly. In three patients the identified pathologies were differently interpreted, each examination provided another aspect of the anomaly or a definitive diagnosis was not possible. CONCLUSIONS: Our study demonstrated that dedicated neurosonography is equal to MRI in the diagnosis of fetal brain anomalies. In most of the cases MRI confirmed the ultrasonographic diagnosis; in a minority of cases each modality provided additional/different information. The major role of MRI was in reassurance of the parents regarding the presence or absence of brain anomalies.

Ripening of the uterine cervix in a post-cesarean parturient: prostaglandin E2 versus Foley catheter.

OBJECTIVE: To compare the success and complication rates of prostaglandin E2 tablets (PGE2) and a Foley catheter for the ripening of the uterine cervix in post-Cesarean section parturients. STUDY DESIGN: The study population in this retrospective cohort study consisted of parturients in their second pregnancy who had undergone Cesarean section in their previous delivery and who underwent ripening of the uterine cervix by using PGE2 (n = 55) or Foley catheter (n = 161) in the current pregnancy. The control group consisted of 1432 post-Cesarean section parturients without induction of labor. We compared the rates of placental abruption, non-reassuring fetal heart rate patterns, intrapartum fetal deaths (IPFD), uterine rupture, Apgar scores, labor dystocia, severe birth canal lacerations, vacuum deliveries and repeated Cesarean section rates in the three groups by using ANOVA, chi2 analysis and Fisher's exact test when appropriate. RESULTS: A significant increase in the rates of labor dystocia during the first stage (30.4% vs. 11.6%, p < 0.01) and repeated Cesarean deliveries (49.1% vs. 35.2%, p < 0.01) were observed in women in whom the Foley catheter was used as compared to controls, respectively. No such changes were demonstrated in the PGE2 group as compared to the controls. No significant differences were found between the PGE2 group and Foley catheter group as compared to the controls in rates of placental abruption, IPFD, uterine rupture, fetal distress, birth canal lacerations, vacuum deliveries and Apgar scores. CONCLUSIONS: PGE2 was found to be superior to the Foley catheter for ripening of the uterine cervix in a post-Cesarean parturient, as demonstrated by a lower repeated Cesarean delivery rate.

Activation of HTLV-I long terminal repeat by stress-inducing agents and protection of HTLV-I-infected T-cells from apoptosis by the viral tax protein.

HTLV-I is etiologically implicated with tropical spastic paraparesis/HTLV-I associated myelopathy, adult T-cell leukemia and certain other diseases. However, after infection the virus enters into a dormant state, whereas the characteristics of the HTLV-I related diseases indicate that their genesis requires activation of the dormant virus by a Tax-independent mechanism. In the present study we demonstrate that a variety of stress-inducing agents (TPA, cisplatin, etoposide, taxol, and 3-methylcholanthrene) are capable of Tax-independent activation of HTLV-I LTR and that this activation is detected mainly in cells that are undergoing through the apoptotic process. Furthermore, it is demonstrated that both apoptosis induction and HTLV-I LTR activation are inhibited by Bcl-2 and by PKC, indicating that these two processes are mechanistically cross-linked. In addition, using an HTLV-I producing human T-cell line which permanently express the negatively transdominant tax mutant, Delta58tax, under the Tet-Off control system, we prove that the virally encoded Tax protein protects the host cells from apoptosis. Together, these data suggest that activation of the dormant virus in the carriers' infected T-cells by certain stress-inducing conditions and protecting these cells from the consequent apoptotic death by the viral Tax protein emerging after this activation, might be the basis for switching the virus from latency to a pathogenic phase.

Sp1-p53 heterocomplex mediates activation of HTLV-I long terminal repeat by 12-O-tetradecanoylphorbol-13-acetate that is antagonized by protein kinase C.

We have previously demonstrated that 12-O-tetradecanoylphorbol-13-acetate (TPA) activates human T-cell leukemia virus type-I long terminal repeat (LTR) in Jurkat cells by a protein kinase C (PKC)-independent mechanism involving a posttranslational activation of Sp1 binding to an Sp1 site located within the Ets responsive region-1 (ERR-1). By employing the PKC inhibitor, bisindolylmaleimide I and cotransfecting the reporter LTR construct with a vector expressing PKC-alpha, we demonstrated, in the present study, that this effect of TPA was not only independent of, but actually antagonized by, PKC. Electrophoretic mobility shift assays together with antibody-mediated supershift and immuno-coprecipitation analyses, revealed that the posttranslational activation of Sp1 was exerted by inducing the formation of Sp1-p53 heterocomplex capable of binding to the Sp1 site in ERR-1. Furthermore, we demonstrated that Jurkat cells contain both wild-type (w.t.) and mutant forms of p53 and we detected both of them in this complex at variable combinations; some molecules of the complex contained either the w.t. or the mutant p53 separately, whereas others contained the two of them together. Finally, we showed that the Sp1-p53 complexes could bind also to an Sp1 site present in the promoter of another gene such as the cyclin-dependent kinase inhibitor p21(WAF-1), but not to consensus recognition sequences of the w.t. p53. Therefore, we speculate that there might be several other PKC-independent biological effects of TPA which result from interaction of such Sp1-p53 complexes with Sp1 recognition sites residing in the promoters of a wide variety of cellular and viral genes.