How to Best Convey Information About Intensive/Comfort Care to the Family Members of Premature Infants to Enable Unbiased Perinatal Decisions

Background: As the infant's best interests are determined through the perinatal decisions of family members and physicians, it is important to understand the factors that affect such decisions. This paper investigated the separate and combined effects of various factors related to perinatal decision making and sought to determine the best way to convey information in an unbiased manner to family members.Methods: In total, 613 participants were consecutively recruited. Each participant completed a series of surveys. All responses to four items were examined via a latent class analysis (LCA) to identify subgroups of participants with similar preferences for intensive care (IC) and comfort care (CC) regarding their potentially premature infant. Multiple logistic regression analyses were applied to identify the sociodemographic predictors for the classification of participants into different subgroups.Results: χ2-tests indicated that perinatal decision making for Item 2 was influenced by framing information, whereas decision making wasn't affected by presentation modes. Furthermore, the endorsement rates of IC significantly decreased with the information increased from brief to detailed, regardless of framing or presentation mode. The LCA indicated that a 3-subgroup model, which included the IC, CC, and variation subgroups, was optimal. Logistic regression analyses demonstrated that, compared with the IC subgroup, negative framing, higher education, parenthood, and poor numeracy predicted participants' preferences for CC. Meanwhile, worrying about physical or mental disabilities predicted preferences for CC and sensitivity to the amount of information provided regarding treatment options (variation subgroup).Conclusions: Perinatal decision making is affected by many factors, suggesting that more detailed information, improved understandability of numerical data, and a neutral tone of voice regarding therapeutic outcomes would be helpful for the families of premature infants to make unbiased decisions. Our findings should be replicated in future research

Laser-assisted collision effect on nonsequential double ionization of helium in a few-cycle laser pulse

Nonsequential double ionization (NSDI) of helium in an intense few-cycle laser pulse is investigated by applying the three-dimensional semi-classical re-scattering method. It is found that the momentum distribution of He$^{2+}$ shows a single-double-single peak structure as the pulse intensity increases. According to the different mechanisms dominating the NSDI process, the laser intensity can be classified into three regimes where the momentum distribution of He$^{2+}$ exhibits different characteristics. In the relatively high intensity regime, an NSDI mechanism named the "laser-assisted collision ionization" is found to be dominating the NSDI process and causing the single peak structure. This result can shed light on the study of non-sequential ionization of a highly charged ion in a relatively intense laser pulse

Somatic SF3B1 hotspot mutation in prolactinomas.

The genetic basis and corresponding clinical relevance of prolactinomas remain poorly understood. Here, we perform whole genome sequencing (WGS) on 21 patients with prolactinomas to detect somatic mutations and then validate the mutations with digital polymerase chain reaction (PCR) analysis of tissue samples from 227 prolactinomas. We identify the same hotspot somatic mutation in splicing factor 3 subunit B1 (SF3B1R625H) in 19.8% of prolactinomas. These patients with mutant prolactinomas display higher prolactin (PRL) levels (p = 0.02) and shorter progression-free survival (PFS) (p = 0.02) compared to patients without the mutation. Moreover, we identify that the SF3B1R625H mutation causes aberrant splicing of estrogen related receptor gamma (ESRRG), which results in stronger binding of pituitary-specific positive transcription factor 1 (Pit-1), leading to excessive PRL secretion. Thus our study validates an important mutation and elucidates a potential mechanism underlying the pathogenesis of prolactinomas that may lead to the development of targeted therapeutics

A Common SMAD7 Variant Is Associated with Risk of Colorectal Cancer: Evidence from a Case-Control Study and a Meta-Analysis

<div><h3>Background</h3><p>A common genetic variant, rs4939827, located in <em>SMAD7</em>, was identified by two recent genome-wide association (GWA) studies to be strongly associated with the risk of colorectal cancer (CRC). However, the following replication studies yielded conflicting results.</p> <h3>Method and Findings</h3><p>We conducted a case-control study of 641 cases and 1037 controls in a Chinese population and then performed a meta-analysis, integrating our and published data of 34313 cases and 33251 controls, to clarify the relationship between rs4939827 and CRC risk. In our case-control study, the dominant model was significant associated with increased CRC risk [Odds Ratio (OR) = 1.46; 95% confidence interval (95% CI), 1.19–1.80]. The following meta-analysis further confirmed this significant association for all genetic models but with significant between-study heterogeneity (all <em>P</em> for heterogeneity <0.1). By stratified analysis, we revealed that ethnicity, sample size, and tumor sites might constitute the source of heterogeneity. The cumulative analysis suggested that evident tendency to significant association was seen with adding study samples over time; whilst, sensitive analysis showed results before and after removal of each study were similar, indicating the highly stability of the current results.</p> <h3>Conclusion</h3><p>Results from our case-control study and the meta-analysis collectively confirmed the significant association of the variant rs4939827 with increased risk of colorectal cancer. Nevertheless, fine-mapping of the susceptibility loci defined by rs4939287 should be imposed to reveal causal variant.</p> </div

The scavenging of superoxide radicals promotes apoptosis induced by a novel cell-permeable fusion protein, sTRAIL:FeSOD, in tumor necrosis factor-related apoptosis-inducing ligand-resistant leukemia cells

<p>Abstract</p> <p>Background</p> <p>Many cancer cells develop resistance to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis, necessitating combination with chemotherapy, and normal cells manifest side effects due to the combined treatment regimen of TRAIL and chemotherapeutic drugs. A novel cancer therapy utilizing TRAIL is thus urgently needed.</p> <p>Results</p> <p>In this study, we exploited TRAIL receptor-mediated endocytosis for the first time to produce a cell-permeable molecule, soluble forms of recombinant TRAIL:iron superoxide dismutase (sTRAIL:FeSOD), which possesses sTRAIL-induced apoptotic ability and FeSOD antioxidant activity. The FeSOD component was rapidly introduced into the cell by sTRAIL and intracellular superoxide radical (O₂^-), which have been implicated as potential modulators of apoptosis in cancer cells, was eliminated, resulting in a highly reduced cellular environment. The decrease in cellular O₂^-, which was accompanied by a brief accumulation of H₂O₂and downregulation of phosphorylated Akt (p-Akt) and cellular FLICE-inhibitory protein, sensitized K562 leukemia cells and human promyelocytic leukemia (HL-60) cells to TRAIL-induced apoptosis. The low H₂O₂levels protected human LO2 hepatocytes from sTRAIL:FeSOD-induced apoptosis despite downregulation of p-Akt. We also obtained evidence that the lack of response to sTRAIL:FeSOD in normal T cells occurred because sTRAIL:FeSOD shows much stronger shifts of redox state in erythroleukemia (K562) and HL-60 cells compared to that in normal T cells. K562 and HL-60 cells underwent sTRAIL:FeSOD-induced apoptosis without the dysfunction of mitochondria.</p> <p>Conclusions</p> <p>The fusion protein overcomes the inability of FeSOD to permeate the cell membrane, exhibits synergistic apoptotic effects on K562 and HL-60 cells and demonstrates minimal toxicity to normal T cells and the normal liver cell line LO2, indicating its potential value for the treatment of leukemia.</p

Spatial-Temporal Attentive LSTM for Vehicle-Trajectory Prediction

Vehicle-trajectory prediction is essential for intelligent traffic systems (ITS), as it can help autonomous vehicles to plan a safe and efficient path. However, it is still a challenging task because existing studies have mainly focused on the spatial interactions of adjacent vehicles regardless of the temporal dependencies. In this paper, we propose a spatial-temporal attentive LSTM encoder&ndash;decoder model (STAM-LSTM) to predict vehicle trajectories. Specifically, the spatial attention mechanism is used to capture the spatial relationships among neighboring vehicles and then obtain the global spatial feature. Meanwhile, the temporal attention mechanism is designed to distinguish the effects of different historical time steps on future trajectory prediction. In addition, the motion feature of vehicles is extracted to reveal the influence of dynamic information on vehicle-trajectory prediction, and is combined with the local and global spatial features to represent the integrated features of the target vehicle at each historical moment. The experiments were conducted on public highway trajectory datasets&mdash;US-101 and I-80 in NGSIM&mdash;and the results demonstrate that our model achieves state-of-the-art prediction performance