The use of Zhukovsky vaginal and intrauterine balloons to improve the outcome of postpartum hysterectomies in patients with severe bleeding.

Aim: To assess the efficacy of a Zhukovsky obstetric double balloon for improving outcomes in women undergoing hysterectomy for postpartum hemorrhage.Materials and methods: This was a randomized controlled study. Participants were divided into two groups to undergo insertion of a Zhukovsky obstetric double balloon prior to hysterectomy (n = 16) or conventional hysterectomy (n = 25).Results: The main reasons for major obstetric hemorrhage were placenta accreta (53.6%), uterine atony (26.8%), uteroplacental apoplexy (14.6%), and amniotic fluid embolism (4.8%). The use of a Zhukovsky obstetric double balloon during postpartum hysterectomy was associated with a 1.7-fold reduction in blood loss and a 2.3-fold reduction in blood loss > 2000 ml compared with conventional hysterectomy.Conclusion: The use of a Zhukovsky obstetric double balloon represents a potent tool for improvement of immediate outcomes of hysterectomy in women with severe postpartum bleeding.

Bone marrow laminins influence hematopoietic stem and progenitor cell cycling and homing to the bone marrow.

Hematopoietic stem and progenitor cell (HSPC) functions are regulated by a specialized microenvironment in the bone marrow - the hematopoietic stem cell niche - of which the extracellular matrix (ECM) is an integral component. We describe here the localization of ECM molecules, in particular the laminin α4, α3 and α5 containing isoforms in the bone marrow. Laminin 421 (composed of laminin α4, ß2, γ1 chains) is identified as a major component of the bone marrow ECM, occurring abundantly surrounding venous sinuses and in a specialized reticular fiber network of the intersinusoidal spaces of murine bone marrow (BM) in close association with HSPC. Bone marrow from Lama4-/- mice is significantly less efficient in reconstituting the hematopoietic system of irradiated wildtype (WT) recipients in competitive bone marrow transplantation assays and shows reduced colony formation in vitro. This is partially due to retention of Lin-c-kit+Sca-1+CD48- long-term and short-term hematopoietic stem cells (LT-HSC/ST-HSC) in the G0 phase of the cell cycle in Lama4-/- bone marrow and hence a more quiescent phenotype. In addition, the extravasation of WT BM cells into Lama4-/- bone marrow is impaired, influencing the recirculation of HSPC. Our data suggest that these effects are mediated by a compensatory expression of laminin α5 containing isoforms (laminin 521/522) in Lama4-/- bone marrow. Collectively, these intrinsic and extrinsic effects lead to reduced HSPC numbers in Lama4-/- bone marrow and reduced hematopoietic potential.

p53-Responsive micrornas 192 and 215 are capable of inducing cell cycle arrest.

microRNAs provide a novel layer of regulation for gene expression by interfering with the stability and/or translation of specific target mRNAs. Overall levels of microRNAs are frequently down-regulated in cancer cells, and reducing general microRNA processing increases cancerogenesis in transgenic models, suggesting that at least some microRNAs might act as effectors in tumor suppression. Accordingly, the tumor suppressor p53 up-regulates miR-34a, a microRNA that contributes to apoptosis and acute senescence. Here, we used array hybridization to find that p53 induces two additional, mutually related clusters of microRNAs, leading to the up-regulation of miR-192, miR-194, and miR-215. The same microRNAs were detected at high levels in normal colon tissue but were severely reduced in many colon cancer samples. On the other hand, miR-192 and its cousin miR-215 can each contribute to enhanced CDKN1A/p21 levels, colony suppression, cell cycle arrest, and cell detachment from a solid support. These effects were partially dependent on the presence of wild-type p53. Antagonizing endogenous miR-192 attenuated 5-fluorouracil-induced accumulation of p21. Hence, miR-192 and miR-215 can act as effectors as well as regulators of p53; they seem to suppress cancerogenesis through p21 accumulation and cell cycle arrest.