Hemorrhagic morbidity in nulliparous patients with placenta previa without placenta accrete spectrum disorders.

Background: Placental adhesion spectrum (PAS) is a disease in which the trophoblast invades the myometrium, and is a well-known high-risk condition associated with placental previa. Aim: The morbidity of nulliparous women with placenta previa without PAS disorders is unknown. Patients and Methods: The data from nulliparous women who underwent cesarean delivery were collected retrospectively. The women were dichotomized into malpresentation (MP) and placenta previa groups. The placenta previa group was categorized into previa (PS) and low-lying (LL) groups. When the placenta covers the internal cervical os, it is called placenta previa, when the placenta is near the cervical os, it is called the low-lying placenta. Their maternal hemorrhagic morbidity and neonatal outcomes were analyzed and adjusted using multivariate analysis based on univariate analysis. Results: A total of 1269 women were enrolled: 781 women in the MP group and 488 women in the PP-LL group. Regarding packed red blood cell transfusion, PP and LL had adjusted odds ratio (aOR) of 14.7 (95% confidence interval (CI): 6.6 - 32.5), and 11.3 (95% CI: 4.9 - 26) during admission, and 51.2 (95% CI: 22.1 - 122.7) and 10.3 (95% CI: 3.9 - 26.6) during operation, respectively. For intensive care unit admission, PS and LL had aOR of 15.9 (95% CI: 6.5 - 39.1) and 3.5 (95% CI: 1.1 - 10.9), respectively. No women had cesarean hysterectomy, major surgical complications, or maternal death. Conclusion: Despite placenta previa without PAS disorders, maternal hemorrhagic morbidity was significantly increased. Thus, our results highlight the need for resources for those women with evidence of placenta previa including a low-lying placenta, even if those women do not meet PAS disorder criteria. In addition, placenta previa without PAS disorder was not associated with critical maternal complications.

Nanoconfinement effects of chemically reduced graphene oxide nanoribbons on poly(vinyl chloride).

Polymeric nanocomposites with graphene-based nanocarbons (GNCs) have been extensively studied with emphasis on the percolation of nanofillers toward electrical, rheological, and mechanical reinforcement. In this study, we report an unusual indirect reinforcing phenomenon of highly defective GNCs dispersed in the poly(vinyl chloride) (PVC) matrix via densification of the polymer packing originating from nanoscale confinement. Herein, chemically reduced graphene oxide nanoribbons (C-rGONRs) are employed as a nanofiller. The inclusion of defective and oxygen-functionalized C-rGONRs resulted in a dramatic densification of the PVC host with extremely low C-rGONR loading, largely exceeding the theoretical calculation from a rule of mixture. Along with the densification, the glass transition temperature of PVC also increased by 28.6 °C at 0.1 wt% filler loading. Remarkably, the oxygen barrier property and mechanical toughness under tension for the PVC/C-rGONR nanocomposite were the maximum when the greatest densification occurred. The structure-property relationship of the nanocomposites has been discussed with an emphasis on the nanoscale confinement phenomenon.

Preferential binding of Chlamydia trachomatis to subsets of human lymphocytes and induction of interleukin-6 and interferon-gamma.

The interactions between Chlamydia trachomatis and human blood mononuclear leukocytes were studied using flow cytometry, immunofluorescence, electron microscopy and cytokine assays. Under serum-free conditions, elementary bodies (EB) of C. trachomatis were found to bind to human T lymphocytes as well as to B cells and monocytes/macrophages (M phi). For all cell types the binding was saturable, rapid, temperature-independent and independent of the chlamydia-specific serological status of the donor. Similar proportions of T and B cells bound EB at similar levels. In the T cell population, proportionally less CD8+ cells bound EB. Whereas M phi phagocytosed and destroyed the bound micro-organisms for lymphocytes, the Chlamydia remained at the surface, adherent to morphologically featureless membrane areas and showed no evidence of uptake even after long periods at 37 degrees C. Host molecules modulated these basic binding patterns: a heat-stable serum factor inhibited EB binding to T cells and a heat-labile serum factor enhanced binding to B cells. Stimulation with C. trachomatis EB rapidly elicited cytokine production by lymphocytes including interleukin-6 from B cells and interferon-gamma (IFN-gamma) from T and/or nonT/nonB cells. The responses were irrespective of the serological status of the donor. The findings suggest that C. trachomatis-leucocyte interactions may differ from the interactions of other bacteria and human leucocytes. The possible relationship between leucocyte-binding, cytokine induction, and the pathognomonic development of lymphoid follicles during mucosal C. trachomatis infections is discussed.