Evaluation of the feasibility and preference of Nox-A1 type 2 ambulatory device for unattended home sleep test: a randomized crossover study

Sleep and Biological Rhythms - There is an increasing need for portable sleep monitoring in clinical practice, but there is no comparative study that used the same device for home and in-laboratory...     

Efficacy of Intrauterine Bakri Balloon Tamponade in Cesarean Section for Placenta Previa Patients

Purpose

The aims of this study were to analyze the predictive factors for the use of intrauterine balloon insertion and to evaluate the efficacy and factors affecting failure of uterine tamponade with a Bakri balloon during cesarean section for abnormal placentation.

Methods

We reviewed the medical records of 137 patients who underwent elective cesarean section for placenta previa between July 2009 and March 2014. Cesarean section and Bakri balloon insertion were performed by a single qualified surgeon. The Bakri balloon was applied when blood loss during cesarean delivery exceeded 1,000 mL.

Results

Sixty-four patients (46.7%) required uterine balloon tamponade during cesarean section due to postpartum bleeding from the lower uterine segment, of whom 50 (78.1%) had placenta previa totalis. The overall success rate was 75% (48/64) for placenta previa patients. Previous cesarean section history, anterior placenta, peripartum platelet count, and disseminated intravascular coagulopathy all significantly differed according to balloon success or failure (all p<0.05). The drainage amount over 1 hour was 500 mL (20–1200 mL) in the balloon failure group and 60 mL (5–500 mL) in the balloon success group (p<0.01).

Conclusion

Intrauterine tamponade with a Bakri balloon is an adequate adjunct management for postpartum hemorrhage following cesarean section for placenta previa to preserve the uterus. This method is simple to apply, non-invasive, and inexpensive. However, possible factors related to failure of Bakri balloon tamponade for placenta previa patients such as prior cesarean section history, anterior placentation, thrombocytopenia, presence of DIC at the time of catheter insertion, and catheter drainage volume more than 500 mL within 1 hour of catheter placement should be recognized, and the next-line management should be prepared in advance.     

Recording of elapsed time and temporal information about biological events using Cas9

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Drug scheduling of cancer chemotherapy based on natural actor-critic approach

Recently, reinforcement learning methods have drawn significant interests in the area of artificial intelligence, and have been successfully applied to various decision-making problems. In this paper, we study the applicability of the NAC (natural actor-critic) approach, a state-of-the-art reinforcement learning method, to the drug scheduling of cancer chemotherapy for an ODE (ordinary differential equation)-based tumor growth model. ODE-based cancer dynamics modeling is an active research area, and many different mathematical models have been proposed. Among these, we use the model proposed by de Pillis and Radunskaya (2003), which considers the growth of tumor cells and their interaction with normal cells and immune cells. The NAC approach is applied to this ODE model with the goal of minimizing the tumor cell population and the drug amount while maintaining the adequate population levels of normal cells and immune cells. In the framework of the NAC approach, the drug dose is regarded as the control input, and the reward signal is defined as a function of the control input and the cell populations of tumor cells, normal cells, and immune cells. According to the control policy found by the NAC approach, effective drug scheduling in cancer chemotherapy for the considered scenarios has turned out to be close to the strategy of continuing drug injection from the beginning until an appropriate time. Also, simulation results showed that the NAC approach can yield better performance than conventional pulsed chemotherapy.     

Expression of Versican V3 by Arterial Smooth Muscle Cells Alters Tumor Growth Factor β (TGFβ)-, Epidermal Growth Factor (EGF)-, and Nuclear Factor κB (NFκB)-dependent Signaling Pathways,Creating a Microenvironment That Resists Monocyte Adhesion

Monocyte/macrophage accumulation plays a critical role during progression of cardiovascular diseases, such as atherosclerosis. Our previous studies demonstrated that retrovirally mediated expression of the versican V3 splice variant (V3) by arterial smooth muscle cells (ASMCs) decreases monocyte adhesion in vitro and macrophage accumulation in a model of lipid-induced neointimal formation in vivo. We now demonstrate that V3-expressing ASMCs resist monocyte adhesion by altering the composition of the microenvironment surrounding the cells by affecting multiple signaling pathways. Reduction of monocyte adhesion to V3-expressing ASMCs is due to the generation of an extracellular matrix enriched in elastic fibers and depleted in hyaluronan, and reduction of the proinflammatory cell surface vascular cell adhesion molecule 1 (VCAM1). Blocking these changes reverses the protective effect of V3 on monocyte adhesion. The enhanced elastogenesis induced by V3 expression is mediated by TGFβ signaling, whereas the reduction in hyaluronan cable formation induced by V3 expression is mediated by the blockade of epidermal growth factor receptor and NFκB activation pathways. In addition, expression of V3 by ASMCs induced a marked decrease in NFκB-responsive proinflammatory cell surface molecules that mediate monocyte adhesion, such as VCAM1. Overall, these results indicate that V3 expression by ASMCs creates a microenvironment resistant to monocyte adhesion via differentially regulating multiple signaling pathways.     

Transient Receptor Potential Cation Channel V1 (TRPV1) Is Degraded by Starvation- and Glucocorticoid-Mediated Autophagy

A mammalian cell renovates itself by autophagy, a process through which cellular components are recycled to produce energy and maintain homeostasis. Recently, the abundance of gap junction proteins was shown to be regulated by autophagy during starvation conditions, suggesting that transmembrane proteins are also regulated by autophagy. Transient receptor potential vanilloid type 1 (TRPV1), an ion channel localized to the plasma membrane and endoplasmic reticulum (ER), is a sensory transducer that is activated by a wide variety of exogenous and endogenous physical and chemical stimuli. Intriguingly, the abundance of cellular TRPV1 can change dynamically under pathological conditions. However, the mechanisms by which the protein levels of TRPV1 are regulated have not yet been explored. Therefore, we investigated the mechanisms of TRPV1 recycling using HeLa cells constitutively expressing TRPV1. Endogenous TRPV1 was degraded in starvation conditions; this degradation was blocked by chloroquine (CLQ), 3MA, or downregulation of Atg7. Interestingly, a glucocorticoid (cortisol) was capable of inducing autophagy in HeLa cells. Cortisol increased cellular conversion of LC3-I to LC-3II, leading autophagy and resulting in TRPV1 degradation, which was similarly inhibited by treatment with CLQ, 3MA, or downregulation of Atg7. Furthermore, cortisol treatment induced the colocalization of GFP-LC3 with endogenous TRPV1. Cumulatively, these observations provide evidence that degradation of TRPV1 is mediated by autophagy, and that this pathway can be enhanced by cortisol.     

LinkNMF: Identification of histone modification modules in the human genome using nonnegative matrix factorization

Histone modifications are ubiquitous processes involved in various cellular mechanisms. Systemic analysis of multiple chromatin modifications has been used to characterize various chromatin states associated with functional DNA elements, gene expression, and specific biological functions. However, identification of modular modification patterns is still required to understand the functional associations between histone modification patterns and specific chromatin/DNA binding factors. To recognize modular modification patterns, we developed a novel algorithm that combines nonnegative matrix factorization (NMF) and a clique-detection algorithm. We applied it, called LinkNMF, to generate a comprehensive modification map in human CD4 + T cell promoter regions. Initially, we identified 11 modules not recognized by conventional approaches. The modules were grouped into two major classes: gene activation and repression. We found that genes targeted by each module were enriched with distinguishable biological functions, suggesting that each modular pattern plays a unique functional role. To explain the formation of modular patterns, we investigated the module-specific binding patterns of chromatin regulators. Application of LinkNMF to histone modification maps of diverse cells and developmental stages will be helpful for understanding how histone modifications regulate gene expression. The algorithm is available on our website at biodb.kaist.ac.kr/LinkNMF.