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In road traffic crashes, although rollover crashes account for a relatively low proportion, those result in a high fatality rate. The present study performed random parameters ordered logit models to examine risk factors as well as their heterogeneous effects on driver injury severity in single-vehicle passenger car and SUV rollover crashes. Crash data for the empirical analysis were extracted from Texas Crash Record Information System (CRIS) database during the year 2016. Model estimation results show that six variables (male drivers, drivers' age, airbag deployment, failure to drive in single lane, speed limit, and rural area) were found to produce normally distributed parameters in passenger car model, while nine parameters (male drivers, safety belt use, airbag deployment, drug or alcohol use, failure to drive in single lane, improper evasive action, vehicle model year, friday, and rural area) in SUV model were found to be normally distributed. Several other factors with fixed parameters were found to be associated with driver injury severity in single-vehicle passenger car or SUV rollover crashes, most notably: ejection or partial ejection, turning left, intersection, August, adverse weather conditions, and night with light. These variables were significant in both models; most variables have stronger effects on nonincapacitating injury and serious injury outcomes in SUV than in passenger car rollover crashes. These findings provide a deep insight into causality nature and factor involved in driver injury severity in single-vehicle passenger car and SUV rollover crashes and are also helpful for transport agencies to determine appropriate countermeasures aimed at mitigating injuries sustained by drivers in single-vehicle rollover crashes., 1. Introduction Road traffic accidents are the major cause of fatalities and injuries globally. In a worldwide scale, the World Health Organization released that nearly 1.25 million citizens died of [...]

Ga2O3/Ag/Ga2O3-laminated films with high electrical conductivity and ultraviolet (UV) transparency were achieved by radio frequency magnetron sputtering at room temperature (RT) on quartz glass. The influence of annealing temperature and ambient on the structural, electrical and optical properties of Ga2O3/Ag/Ga2O3-laminated films were investigated in detail. As the annealing temperature increases, the optical bandgap of the Ga2O3-laminated films widens. The Ga2O3/Ag/Ga2O3-laminated films exhibited good photoelectric performance with a figure-of-merit (FOM) value of 5.83 × 10−3 Ω−1, a sheet resistance of 12.55 Ω/sq, a transmittance of 95.15% at 325 nm, and an average transmittance of 77.56% (250~300 nm). All these results suggest that RT-fabricated Ga2O3/Ag/Ga2O3-laminated films show great potential in UV transparent conductive electrodes for UV optoelectronic devices and in flexible electronics. [ABSTRACT FROM AUTHOR]

Abstract Background Cancer stem-like cells are proposed to sustain solid tumors by virtue of their capacity for self-renewal and differentiation to cells that comprise the bulk of the tumor, and have been identified for a variety of cancers based on characteristic clonal morphologies and patterns of marker gene expression. Methods Single cell cloning and spheroid culture studies were used to identify a population of cancer stem-like cells in the androgen-independent human prostate cancer cell line PC3. Results We demonstrate that, under standard culture conditions, ~10% of PC3 cells form holoclones with cancer stem cell characteristics. These holoclones display high self-renewal capability in spheroid formation assays under low attachment and serum-free culture conditions, retain their holoclone morphology when passaged at high cell density, exhibit moderate drug resistance, and show high tumorigenicity in scid immunodeficient mice. PC3 holoclones readily form spheres, and PC3-derived spheres yield a high percentage of holoclones, further supporting their cancer stem cell-like nature. We identified one gene, FAM65B, whose expression is consistently up regulated in PC3 holoclones compared to paraclones, the major cell morphology in the parental PC3 cell population, and two genes, MFI2 and LEF1, that are consistently down regulated. This molecular profile, FAM65Bhigh/MFI2low/LEF1low, also characterizes spheres generated from parental PC3 cells. The PC3 holoclones did not show significant enriched expression of the putative prostate cancer stem cell markers CD44 and integrin α2β1. PC3 tumors seeded with holoclones showed dramatic down regulation of FAM65B and dramatic up regulation of MFI2 and LEF1, and unexpectedly, a marked increase in tumor vascularity compared to parental PC3 tumors, suggesting a role of cancer stem cells in tumor angiogenesis. Conclusions These findings support the proposal that PC3 tumors are sustained by a small number of tumor-initiating cells with stem-like characteristics, including strong self-renewal and pro-angiogenic capability and marked by the expression pattern FAM65Bhigh/MFI2low/LEF1low. These markers may serve as targets for therapies designed to eliminate cancer stem cell populations associated with aggressive, androgen-independent prostate tumors such as PC3.

Pulmonary senescence and fibrosis occur with deoxyribonucleic acid (DNA) damage response in the lungs deficient of telomerase. The molecular mechanism mediating pulmonary alveolar cell fates remains to be investigated. The present study shows that pulmonary alveolar epithelial type 2 cells (AEC2) (alveolar stem cells) undergo not only replicative senescence, but also apoptosis and differentiation in association with increased innate immune natural killer (NK) cells in telomerase knockout (KO) mice. Telomerase ribonucleic acid (RNA) component (TERC) deficiency results in increased senescence‐associated heterochromatin foci marker HP1γ, p21, p16 and apoptosis‐associated cleaved caspase‐3 in AEC2. However, p53 deficiency in the Trp53−/− allele of the late generation of TERC KO mice attenuates the increased senescent and apoptotic markers significantly. Moreover, p53 deficiency has no significant effect on the increased gene expression of T1α (a marker of terminal differentiated alveolar epithelial type 1 cells [AEC1]) in AEC2 of the late generation of TERC KO mice. Collectively, our findings suggest that pulmonary senescence takes place in deficiency of telomerase RNA component with the alveolar stem cells undergoing p53‐dependent senescence and apoptosis as well as p53‐independent differentiation. [ABSTRACT FROM AUTHOR]

Elastic scattering spectroscopy (ESS), in the form of wavelength-dependent backscattering measurements, can be used to monitor apoptosis in cell cultures. Early changes in backscattering upon apoptosis induction are characterized by an overall decrease in spectral slope and begin as early as 10 to 15 min post-treatment, progressing over the next 6 to 8 h. The timescale of early scattering changes is consistent with reports of the onset of apoptotic volume decrease (AVD). Modeling cellular scattering with a fixed distribution of sizes and a decreasing index ratio, as well as an increased contribution of the whole cell to cellular scattering, resulting from increased cytoplasmic density, is also consistent with observed spectral changes. Changes in ESS signal from cells undergoing osmotically-induced volume decrease in the absence of apoptosis were similar, but smaller in magnitude, to those of apoptotic cells. Further, blockage of Cl(-) channels, which blocks AVD and delays apoptosis, blocked the early scattering changes, indicating that the early scattering changes during apoptosis result, at least partially, from AVD. Work continues to identify the additional sources of early spectral scattering changes that result from apoptosis induction.

The role of pleiotrophin in fetal lung development was investigated. We found that pleiotrophin and its receptor, protein-tyrosine phosphatase receptor beta/zeta, were highly expressed in mesenchymal and epithelial cells of the fetal lungs, respectively. Using isolated fetal alveolar epithelial type II cells, we demonstrated that pleiotrophin promoted fetal type II cell proliferation and arrested type II cell trans-differentiation into alveolar epithelial type I cells. Pleiotrophin also increased wound healing of injured type II cell monolayer. Knockdown of pleiotrophin influenced lung branching morphogenesis in a fetal lung organ culture model. Pleiotrophin increased the tyrosine phosphorylation of beta-catenin, promoted beta-catenin translocation into the nucleus, and activated T cell factor/lymphoid enhancer factor transcription factors. Dlk1, a membrane ligand that initiates the Notch signaling pathway, was identified as a downstream target of the pleiotrophin/beta-catenin pathway by endogenous dlk1 expression, promoter assay, and chromatin immunoprecipitation. These results provide evidence that pleiotrophin regulates fetal type II cell proliferation and differentiation via integration of multiple signaling pathways including pleiotrophin, beta-catenin, and Notch pathways.