Pilot Study of Intra-Aortic Balloon Occlusion to Limit Morbidity in Patients with Adherent Placentation Undergoing Cesarean Hysterectomy.

 We study whether using an intra-aortic balloon (IAB) during cesarean hysterectomy decreases delivery morbidity in patients with suspected morbidly adherent placentation.  This is a retrospective cohort study of deliveries complicated by suspected abnormal placentation between 2009 and 2016 comparing maternal and neonatal outcomes with an IAB placed prior to cesarean hysterectomy versus no IAB. The primary outcome included quantified blood loss (QBL).

Placental implantation over prior cesarean scar causes activation of fetal regulatory T cells.

Introduction: Maternal-fetal chimerism is miniscule, a testament to the integrity of the uteroplacental interface. The soundness of this border region is potentially altered through cesarean delivery of prior babies with uncertain consequences for the following pregnancies.

Methods: Using multicolor flow cytometry and quantitative PCR of non-inherited maternal antigens we performed a retrospective case control pilot study and formulated the null hypothesis that placental implantation over a prior uterine scar does not result in the presence of memory Treg (CD45RO+) in the fetus.

Maternal-Fetal rejection reactions are unconstrained in preeclamptic women.

The risk factors for preeclampsia, extremes of maternal age, changing paternity, concomitant maternal autoimmunity, and/or birth intervals greater than 5 years, suggest an underlying immunopathology. We used peripheral blood and lymphocytes from the UteroPlacental Interface (UPI) of 3rd trimester healthy pregnant women in multicolor flow cytometry-and in vitro suppression assays. The major end-point was the characterization of activation markers, and potential effector functions of different CD4-and CD8 subsets as well as T regulatory cells (Treg).

Preeclampsia is Characterized by Fetal NK Cell Activation and a Reduction in Regulatory T Cells.

Problem: Preeclampsia affects 3-17% of pregnancies worldwide and has serious consequences for both the mother and the fetus. As maternal-fetal immune tolerance is bidirectional, fetal immunopathology may play a significant role in the pathogenesis of pregnancy disorders. Nevertheless, the impact of preeclampsia on the fetal immune system is unclear.

Normal human pregnancy results in maternal immune activation in the periphery and at the uteroplacental interface.

Pregnancy poses a unique challenge to the human immune system: the semi-allogeneic fetus must be protected from maternal immune attack while immunity towards pathogens is maintained. Breakdown in maternal-fetal tolerance can lead to pregnancy-specific diseases with potentially high degrees of morbidity and mortality for both the mother and her fetus. Various immune cell-types could mediate these functions, but a comprehensive evaluation of the peripheral and local maternal T cell and regulatory T cell compartments in normal human pregnancy is lacking.

Maternal and fetal factors that contribute to the localization of T regulatory cells during pregnancy.

Problem: To determine the interplay between fetal antigenicity and local maternal factors in determining reproductive tract T regulatory (Treg) cell accumulation during pregnancy.

Method Of Study: Examination of maternal Treg composition in the uterus, cervix, and uteroplacental interface (UPI) of murine syngeneic and allogeneic pregnancies and non-pregnant controls by flow cytometry. The impact of fetal antigenicity was defined by either fetal gender in syngeneic pregnancies or by allogeneic paternity.

Pregnancy induces a fetal antigen-specific maternal T regulatory cell response that contributes to tolerance.

A fetus is inherently antigenic to its mother and yet is not rejected. The T regulatory (Treg) subset of CD4(+) T cells can limit immune responses and has been implicated in maternal tolerance of the fetus. Using virgin inbred mice undergoing a first syngenic pregnancy, in which only the male fetuses are antigenic, we demonstrate a maternal splenocyte proliferative response to the CD4(+) T cell restricted epitope of the male antigen (H-Y) in proportion to the fetal antigen load.

Does transforming growth factor-beta1 predict for radiation-induced pneumonitis in patients treated for lung cancer?

The purpose of the study was to reassess the utility of transforming growth factor-beta-1 (TGF-beta1) together with dosimetric and tumor parameters as a predictor for radiation pneumonitis (RP). Of the 121 patients studied, 32 (26.4%) developed grade > or =1 RP, and 27 (22.

Regulation of cytokine expression by ligands of peroxisome proliferator activated receptors.

Peroxisome proliferator activated receptors (PPARs) are ligand-activated transcription factors with diverse actions including adipocyte differentiation and lipid metabolism. Recent studies have revealed anti-inflammatory activities, but the majority of these studies have been performed in monocyte/macrophages. In these studies, we investigate the effects of PPAR ligands in murine mitogen-activated splenocytes.