Development and Validation of CT-Based Radiomics Signature for Overall Survival Prediction in Multi-organ Cancer.

The malignant tumors in nature share some common morphological characteristics. Radiomics is not only images but also data; we think that a probability exists in a set of radiomics signatures extracted from CT scan images of one cancer tumor in one specific organ also be utilized for overall survival prediction in different types of cancers in different organs. The retrospective study enrolled four data sets of cancer patients in three different organs (420, 157, 137, and 191 patients for lung 1 training, lung 2 testing, and two external validation set: kidney and head and neck, respectively). In the training set, radiomics features were obtained from CT scan images, and essential features were chosen by LASSO algorithm. Univariable and multivariable analyses were then conducted to find a radiomics signature via Cox proportional hazard regression. The Kaplan-Meier curve was performed based on the risk score. The integrated time-dependent area under the ROC curve (iAUC) was calculated for each predictive model. In the training set, Kaplan-Meier curve classified patients as high or low-risk groups (p-value < 0.001; log-rank test). The risk score of radiomics signature was locked and independently evaluated in the testing set, and two external validation sets showed significant differences (p-value < 0.05; log-rank test). A combined model (radiomics + clinical) showed improved iAUC in lung 1, lung 2, head and neck, and kidney data set are 0.621 (95% CI 0.588, 0.654), 0.736 (95% CI 0.654, 0.819), 0.732 (95% CI 0.655, 0.809), and 0.834 (95% CI 0.722, 0.946), respectively. We believe that CT-based radiomics signatures for predicting overall survival in various cancer sites may exist.

Parameterized optical properties of InxAl1-xP alloys.

We report values of parametric-model (PM) parameters that can be used to obtain dielectric functions (refractive indices) from 1.5 to 6.0 eV for ${{\rm In}_x}{{\rm Al}_{1 - x}}{\rm P}$InxAl1-xP alloys of arbitrary compositions $x$x. Using reported pseudo-dielectric data for several In compositions, we extract their dielectric functions by multilayer calculations, then parameterize them with PM lineshapes that well describe the asymmetric nature of their critical point (CP) contributions. We follow the ${E_0}$E0 fundamental bandgap as a function of $x$x, and determine the composition of the indirect-to-direct crossover.

A Parametric Model for Temperature Dependence of Dielectric Function of AlSb Film.

We present analytic representation of dielectric function (ɛ ═ ɛ1 + iɛ2) data from 1.7 to 5.0 eV for the temperature from 300 to 803 K of oxide-free AlSb that are the closest representation to date of the intrinsic bulk dielectric response ɛ of the material. Pseudodielectric functions 'ɛ' were measured on a 1.5 µm thick film grown on (001) GaAs by molecular beam epitaxy. Data were obtained with the film in situ to avoid surface oxidation artifacts. The dielectric function parametric model and multilayer calculation were performed to obtain pure dielectric function and fundamental bandgap (E0) of the AlSb film. The ɛ spectrum was successfully reconstructed by seven polynomials and a pole, which can be used to determine ɛ for arbitrary temperatures. Our results should be useful for device design based on AlSb.

Temperature Dependence of the Dielectric Response and Critical Point Energies of Bi1.85Gd0.15Te3.

The complex dielectric function and band-edge critical point structures of Bi1.85Gd0.15Te3 are reported for temperatures from 28 to 300 K and energies from 0.74 to 6 eV, obtained on bulk Bi1.85Gd0.15Te3 by rotating-compensator spectroscopic ellipsometry. The critical point (CP) energies are determined using numerically calculated second energy derivatives of the data. At low temperature, eight CP structures are identified, while only four CPs are observed at room temperature. As temperature decreases, we also observe blue shifts and significantly enhanced CP structures relative to those obtained at room temperature. The temperature dependence of the CPs are determined by fitting the data to the temperature coefficient and a phenomenological expression that contains the Bose-Einstein statistical factor.

Therapeutic Effects of Engineered Exosomes from RAW264.7 Cells Overexpressing hsa-let-7i-5p against Sepsis in Mice-A Comparative Study with Human Placenta-Derived Mesenchymal Stem Cell Exosomes.

This study compared the therapeutic effects of engineered exosomes derived from RAW264.7 cells overexpressing hsa-let-7i-5p (engineered exosomes) to exosomes from human placenta-derived mesenchymal stem cells (hpMSC exosomes) against sepsis-induced acute lung injury. Adult male C57BL/6 mice were divided into lipopolysaccharide (LPS), LPS plus engineered exosome (LEExo), or LPS plus hpMSC exosome (LMExo) groups, alongside control groups. The results showed that lung injury scores (based on pathohistological characteristics) and the levels of lung function alterations, tissue edema, and leukocyte infiltration in LEExo and LMExo groups were comparable and significantly lower than in the LPS group (all p < 0.05). Furthermore, the levels of inflammation (nuclear factor-κB activation, cytokine upregulation), macrophage activation (hypoxia-inducible factor-1α activation, M1 phase polarization), oxidation, and apoptosis were diminished in LEExo and LMExo groups compared to the LPS group (all p < 0.05). Inhibition of hsa-let-7i-5p attenuated the therapeutic effects of both engineered and hpMSC exosomes. These findings underscore the potent therapeutic capacity of engineered exosomes enriched with hsa-let-7i-5p and their potential as an alternative to hpMSC exosomes for sepsis treatment. Continued research into the mechanisms of action and optimization of engineered exosomes could pave the way for their future clinical application.

Exosomes from Human Placenta Choriodecidual Membrane-Derived Mesenchymal Stem Cells Mitigate Endoplasmic Reticulum Stress, Inflammation, and Lung Injury in Lipopolysaccharide-Treated Obese Mice.

Endoplasmic reticulum (ER) stress mediates the effects of obesity on aggravating sepsis-induced lung injury. We investigated whether exosomes from human placenta choriodecidual membrane-derived mesenchymal stem cells (pcMSCs) can mitigate pulmonary ER stress, lung injury, and the mechanisms of inflammation, oxidation, and apoptosis in lipopolysaccharide-treated obese mice. Diet-induced obese (DIO) mice (adult male C57BL/6J mice fed with a 12-week high-fat diet) received lipopolysaccharide (10 mg/kg, i.p.; DIOLPS group) or lipopolysaccharide plus exosomes (1 × 108 particles/mouse, i.p.; DIOLPSExo group). Our data demonstrated lower levels of ER stress (upregulation of glucose-regulated protein 78, phosphorylated eukaryotic initiation factor 2α, and C/EBP homologous protein; p = 0.038, <0.001, and <0.001, respectively), inflammation (activation of nuclear factor-kB, hypoxia-inducible factor-1α, macrophages, and NLR family pyrin domain containing 3; upregulation of tumor necrosis factor-α, interleukin-1ß, and interleukin-6; p = 0.03, <0.001, <0.001, <0.001, <0.001, <0.001, and <0.001, respectively), lipid peroxidation (p < 0.001), and apoptosis (DNA fragmentation, p = 0.003) in lung tissues, as well as lower lung injury level (decreases in tidal volume, peak inspiratory flow, and end expiratory volume; increases in resistance, injury score, and tissue water content; p < 0.001, <0.001, <0.001, <0.001, <0.001, and =0.002, respectively) in the DIOLPSExo group than in the DIOLPS group. In conclusion, exosomes from human pcMSCs mitigate pulmonary ER stress, inflammation, oxidation, apoptosis, and lung injury in lipopolysaccharide-treated obese mice.

High-Fructose/High-Fat Diet Downregulates the Hepatic Mitochondrial Oxidative Phosphorylation Pathway in Mice Compared with High-Fat Diet Alone.

Both high-fat diet (HFD) alone and high-fructose plus HFD (HFr/HFD) cause diet-induced non-alcoholic fatty liver disease in murine models. However, the mechanisms underlying their impacts on inducing different levels of liver injury are yet to be elucidated. This study employed a proteomic approach to elucidate further on this issue. Adult male C57BL/6J mice were allocated to the HFD or the HFr/HFD group. After feeding for 12 weeks, all mice were euthanized and samples were collected. The proteomic profiles in liver tissues were analyzed using liquid chromatography-tandem mass spectrometry followed by canonical pathway analysis. We demonstrated that the mitochondrial oxidative phosphorylation (OXPHOS) pathway was the most significantly downregulated canonical pathway in the HFr/HFD group when compared with the HFD group. Within the OXPHOS pathway, the HFr/HFD group demonstrated significant downregulation of complexes I and III and significant upregulation of complex IV when compared with the HFD group. Moreover, the HFr/HFD group had lower protein levels of NADH: ubiquinone oxidoreductase subunits S3, S6, A5, and A12 in complex I (p < 0.001, =0.03, <0.001, and <0.001, respectively), lower protein level of cytochrome C in complex III (p < 0.001), and higher protein level of cytochrome C oxidase subunit 2 in complex IV (p = 0.002), when compared with the HFD group. To summarize, we have demonstrated that the hepatic mitochondrial OXPHOS pathway is significantly downregulated in long-term HFr/HFD feeding when compared with long-term HFD feeding. These data support the concept that the hepatic mitochondrial OXPHOS pathway should be involved in mediating the effects of HFr/HFD on inducing more severe liver injury than HFD alone.

Simultaneous Inhibition of Three Major Cytokines and Its Therapeutic Effects: A Peptide-Based Novel Therapy against Endotoxemia in Mice.

Three major cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and IL-6, mediate endotoxemia-induced liver injury. With the similar structures to the binding domains of the three cytokines to their cognate receptors, the novel peptide KCF18 can simultaneously inhibit TNF-α, IL-1ß, and IL-6. We elucidated whether KCF18 can alleviate injury of liver in endotoxemic mice. Adult male mice (BALB/cJ) were intraperitoneally (i.p.) administered lipopolysaccharide (LPS, 15 mg/kg; LPS group) or LPS with KCF18 (LKCF group). Mice in the LKCF group received KCF18 (i.p.) at 2 h (0.6 mg/kg), 4 h (0.3 mg/kg), 6 h (0.3 mg/kg), and 8 h (0.3mg/kg) after LPS administration. Mice were sacrificed after receiving LPS for 24 h. Our results indicated that the binding levels of the three cytokines to their cognate receptors in liver tissues in the LKCF group were significantly lower than those in the LPS group (all p < 0.05). The liver injury level, as measured by performing functional and histological analyses and by determining the tissue water content and vascular permeability (all p < 0.05), was significantly lower in the LKCF group than in the LPS group. Similarly, the levels of inflammation (macrophage activation, cytokine upregulation, and leukocyte infiltration), oxidation, necroptosis, pyroptosis, and apoptosis (all p < 0.05) in liver tissues in the LKCF group were significantly lower than those in the LPS group. In conclusion, the KCF18 peptide-based simultaneous inhibition of TNF-α, IL-1ß, and IL-6 can alleviate liver injury in mice with endotoxemia.

Parameterization of Dielectric Functions and Phase Transitions of SrTiO3 from 26 to 674 K.

We present parameters that allow the dielectric function (ε = ε1 + iε2) of perovskite SrTiO3 (STO) to be calculated for spectral range from 0.74 to 6.42 eV and temperatures from 26 to 674 K. The ε data of STO were reproduced from a previous report. We use the Tauc-Lorentz model to express ε of STO analytically for each temperature. The ε spectra are successfully parameterized with six Tauc-Lorentz components and a pole. To obtain ε data for arbitrary energies and temperatures over the range given above, we interpolated the parameterized results using cubic polynomials. It is well known that STO has phase transitions near 40 and 105 K, which are reflected well in our modeling. Our data allow complex refractive indices to be calculated at any temperature for device design.

Temperature dependence of the dielectric function and critical points of α-SnS from 27 to 350 K.

We report the temperature dependence of the dielectric function ε = ε1 + iε2 and critical point (CP) energies of biaxial α-SnS in the spectral energy region from 0.74 to 6.42 eV and temperatures from 27 to 350 K using spectroscopic ellipsometry. Bulk SnS was grown by temperature gradient method. Dielectric response functions were obtained using multilayer calculations to remove artifacts due to surface roughness. We observe sharpening and blue-shifting of CPs with decreasing temperature. A strong exciton effect is detected only in the armchair direction at low temperature. New CPs are observed at low temperature that cannot be detected at room temperature. The temperature dependences of the CP energies were determined by fitting the data to the phenomenological expression that contains the Bose-Einstein statistical factor and the temperature coefficient for describing the electron-phonon interaction.

Temperature Dependence of the Dielectric Function of Monolayer MoSe2.

The dielectric function [Formula: see text] of monolayer molybdenum diselenide (MoSe2) is obtained and analyzed at temperatures from 31 to 300 K and at energies from 0.74 to 6.42 eV. The sample is a large-area, partially discontinuous monolayer (submonolayer) film of MoSe2 grown on a sapphire substrate by selenization of pulsed laser deposited MoO3 film. Morphological and optical characterizations verified the excellent quality of the film. The MoSe2 data were analyzed using the effective medium approximation, which treats the film and bare substrate regions as a single layer. Second derivatives of ε with respect to energy were numerically calculated and analyzed with standard lineshapes to extract accurate critical-point (CP) energies. We find only 6 CPs for monolayer MoSe2 at room temperature. At cryogenic temperatures 6 additional structures are resolved. The separations in the B- and C-excitonic peaks are also observed. All structures blue-shift and sharpen with decreasing temperature as a result of the reducing lattice constant and electron-phonon interactions. The temperature dependences of the CP energies were determined by fitting the data to the phenomenological expression that contains the Bose-Einstein statistical factor and the temperature coefficient.