Theoretical and Three-Dimensional Molecular Dynamics Study of Droplet Wettability and Mobility on Lubricant-Infused Porous Surfaces.

Profiting from their slippery nature, lubricant-infused porous surfaces endow with droplets excellent mobility and consequently promise remarkable heat transfer improvement for dropwise condensation. To be a four-phase wetting system, the droplet wettability configurations and the corresponding dynamic characteristics on lubricant-infused porous surfaces are closely related to many factors, such as multiple interfacial interactions, surface features, and lubricant thickness, which keeps a long-standing challenge to promulgate the underlying physics. In this work, thermodynamically theoretical analysis and three-dimensional molecular dynamics simulations with the coarse-grained water and hexane models are carried out to explore droplet wettability and mobility on lubricant-infused porous surfaces. Combined with accessible theoretical criteria, phase diagrams of droplet configurations are constructed with a comprehensive consideration of interfacial interactions, surface structures, and lubricant thickness. Subsequently, droplet sliding and coalescence dynamics are quantitatively defined under different configurations. Finally, in terms of the promotion of dropwise condensation, a non-cloaking configuration with the encapsulated state underneath the droplet is recommended to achieve high droplet mobility owing to the low viscous drag of the lubricant and the eliminated pinning effect of the contact line. On the basis of the low oil-water and water-solid interactions, a stable lubricant layer with a relatively low thickness is suggested to construct slippery surfaces.

Asymmetric Condensation Characteristics during Dropwise Condensation in the Presence of Non-condensable Gas: A Lattice Boltzmann Study.

In this work, the condensation characteristics of droplets considering the non-condensable gas with different interaction effects are numerically studied utilizing a multicomponent multiphase thermal lattice Boltzmann (LB) model, with a special focus on the asymmetric nature induced by the interaction effect. The results demonstrate that for isolated-like growth with negligible interactions, the condensation characteristics, that is, the concentration profile, the temperature distribution, and the flow pattern, are typically symmetric in nature. For the growth regime in a pattern, the droplet has to compete with its neighbors for catching vapor, which leads to an overlapping concentration profile (namely the interaction effect). The distribution of the condensation flux on the droplet surface is consequently modified, which contributes to the asymmetric flow pattern and temperature profile. The condensation characteristics for droplet growth in a pattern present an asymmetric nature. Significantly, the asymmetric condensation flux resulting from the interaction effect can induce droplet motion. The results further demonstrate that the interaction strongly depends on the droplet's spatial and size distribution, including two crucial parameters, namely the inter-distance and relative size of droplets. The asymmetric condensation characteristics are consequently dependent on the difference in the interaction intensities on both sides of the droplet. Finally, we demonstrate numerically and theoretically that the evolution of the droplet radius versus time can be suitably described by a power law; the corresponding exponent is kept at a constant of 0.50 for isolated-like growth and is strongly sensitive to the interaction effect for the growth in a pattern.

Serum Metabolomic Analysis of Radiation-Induced Lung Injury in Rats.

Radiation-induced lung injury is a common complication of radiotherapy for lung cancer, breast cancer, esophageal cancer, and thymoma. This study aims to illustrate biomarkers of radiation-induced lung injury and its potential mechanism through the study of metabolomic alterations in serum of Sprague-Dawley rats with different radiation doses. Serum from 0, 10, or 20 Gy irradiated rats were collected and subjected to gas chromatography-mass spectrometry. The result showed that there were 23 dysregulated metabolites between the 10 Gy irradiation group and the 0 Gy control group, whereas 36 preferential metabolites were found between the 20 Gy irradiated rat serum and the control groups. Among them, there were 19 common differential metabolites in the 2 irradiation groups, including 3 downregulated (benzyl thiocyanate, carbazole, and N-formyl-L-methionine) and 16 upregulated metabolites. We further analyzed the metabolic pathways of different metabolites; the results showed that there were 3 significant enrichment pathways in the 10 Gy vs 0 Gy group and 7 significant enrichment pathways in the 20 Gy vs 0 Gy group. Among them, taurine and hypotaurine metabolism, riboflavin metabolism, and glyoxylate and dicarboxylate metabolism were the common metabolic enrichment pathways of the 10 Gy vs 0 Gy group and the 20 Gy vs 0 Gy group.

The PPARγ Agonist Rosiglitazone Enhances the Radiosensitivity of Human Pancreatic Cancer Cells.

PURPOSE: As radiation therapy is widely used for the management of pancreatic cancer, identifying novel targets to improve the radiosensitivity of cancer cells is beneficial. Rosiglitazone, a specific peroxisome proliferator-activated receptor γ (PPARγ) agonist, has an inhibitory effect on various types of cancer cells. The purpose of this paper is to investigate the effect of rosiglitazone on the radiosensitivity of pancreatic cancer cells and the potential mechanism. MATERIALS AND METHODS: PPARγ expression in pancreatic cancer and adjacent tissues was evaluated using immunohistochemistry analysis. The viability, migration and invasion ability of PANC1 and PaTu8988 cells were detected using MTT assay, scratch-wound assay and transwell invasion assay. The effect of rosiglitazone on radiosensitivity of the cells was determined using the clonogenic assay. PANC1 cells were inoculated into BALB/c mice to establish tumors. Microarray was used to investigate changes of genes involved. RESULTS: Higher PPARγ expression was demonstrated in pancreatic cancer tissues compared with para-carcinoma tissues. Rosiglitazone inhibited the cell viability and enhanced the radiation-induced anti-migration and anti-invasion effect. Rosiglitazone potentiated the radiosensitivity of pancreatic cancer cells and PANC1 xenografts. Microarray analysis revealed that rosiglitazone plus radiation altered the expression of multiple genes and affected multiple pathways. CONCLUSION: Rosiglitazone enhances the radiosensitivity of human pancreatic cancer cells in vitro and in vivo via complex mechanisms.

Alteration of Metal Elements in Radiation Injury: Radiation-Induced Copper Accumulation Aggravates Intestinal Damage.

Ionizing radiation causes damage to a variety of tissues, especially radiation-sensitive tissues, such as the small intestine. Radiation-induced damage is caused primarily by increased oxidative stress in the body. Studies have shown that trace metal elements play an irreplaceable role in oxidative stress in humans, which may be associated with radiation-induced tissue damage. However, the alteration and functional significance of trace metal elements in radiation-induced injury is not clear. In this study, we explored the association between radiation-induced damage and 7 trace metal elements in mouse models. We found that the concentration of zinc and copper in mice serum was decreased significantly after irradiation, whereas that of nickel, manganese, vanadium, cobalt, and stannum was not changed by inductively coupled plasma mass spectrometry. The role of copper in radiation-induced intestines was characterized in detail. The concentration of copper was increased in irradiated intestine but reduced in irradiated heart. Immunohistochemistry staining showed that copper transporter protein copper transport 1 expression was upregulated in irradiated mouse intestine, suggesting its potential involvement in radiation-induced copper accumulation. At the cellular level, the addition of CuCl2 potentiated radiation-induced reactive oxygen species in intestine-derived human intestinal epithelial cell and IEC-6 cells. Moreover, the level of copper in damaged cells may be related to the severity of radiation-induced damage as evidenced by a cell viability assay. These results indicate that copper may be involved in the progression of radiation-induced tissue damage and may be a potential therapeutic target.

Genome-Wide Analysis Reveals Zinc Transporter ZIP9 Regulated by DNA Methylation Promotes Radiation-Induced Skin Fibrosis via the TGF-ß Signaling Pathway.

Radiation-induced skin fibrosis is a detrimental and chronic disorder that occurs after radiation exposure. DNA methylation has been characterized as an important regulatory mechanism of multiple pathological processes. In this study, we compared the genome-wide DNA methylation status in radiation-induced fibrotic skin and adjacent normal tissues of rats by methylated DNA immunoprecipitation sequencing. Radiation-induced fibrotic skin showed differentially methylated regions associated with 3,650 protein-coding genes, 72 microRNAs, 5,836 long noncoding RNAs and 3 piwi-interacting RNAs. By integrating the mRNA and methylation profiles, the zinc transporter SLC39A9/ZIP9 was investigated in greater detail. The protein level of ZIP9 was increased in irradiated skin tissues of humans, monkeys, and rats, especially in radiogenic fibrotic skin tissues. Radiation induced the demethylation of a CpG dinucleotide in exon 1 of ZIP9 that resulted in recruitment of the transcriptional factor Sp1 and increased ZIP9 expression. Overexpression of ZIP9 resulted in activation of the profibrotic transforming growth factor-ß signaling pathway through protein kinase B in human fibroblasts. In addition, radiation-induced skin fibrosis was associated with increased zinc accumulation. The zinc chelator N,N,N',N'-tetrakis(2-pyridylmethyl)-1,2-ethylenediamine abrogated ZIP9-induced activation of the transforming growth factor-ß signaling pathway and attenuated radiation-induced skin fibrosis in a rat model. In summary, our findings illustrate epigenetic regulation of ZIP9 and its critical role in promoting radiation-induced skin fibrosis.

Metabolomic Analysis of Radiation-Induced Lung Injury in Rats: The Potential Radioprotective Role of Taurine.

Radiation-induced lung injury is a major dose-limiting toxicity that occurs due to thoracic radiotherapy. Metabolomics is a powerful quantitative measurement of low-molecular-weight metabolites in response to environmental disturbances. However, the metabolomic profiles of radiation-induced lung injury have not been reported yet. In this study, male Sprague-Dawley rats were subjected to a single dose of 10 or 20 Gy irradiation to the right lung. One week after radiation, the obvious morphological alteration of lung tissues after radiation was observed by hematoxylin and eosin staining through a transmission electron microscope. We then analyzed the metabolites and related pathways of radiation-induced lung injury by gas chromatography-mass spectrometry, and a total of 453 metabolites were identified. Compared to the nonirradiated left lung, 19 metabolites (8 upregulated and 11 downregulated) showed a significant difference in 10 Gy irradiated lung tissues, including mucic acid, methyl-ß-d-galactopyranoside, quinoline-4-carboxylic acid, and pyridoxine. There were 31 differential metabolites (16 upregulated and 15 downregulated) between 20 Gy irradiated and nonirradiated lung tissues, including taurine, piperine, 1,2,4-benzenetriol, and lactamide. The Kyoto Encyclopedia of Genes and Genomes-based pathway analysis enriched 32 metabolic pathways between the irradiated and nonirradiated lung tissues, including pyrimidine metabolism, ATP-binding cassette transporters, aminoacyl-tRNA biosynthesis, and ß-alanine metabolism. Among the dysregulated metabolites, we found that taurine promoted clonogenic survival and reduced radiation-induced necrosis in human embryonic lung fibroblast (HELF) cells. This study provides evidence indicating that radiation induces metabolic alterations of the lung. These findings significantly advance our understanding of the pathophysiology of radiation-induced lung injury from the perspective of metabolism.

mRNA and lncRNA Expression Profiling of Radiation-Induced Gastric Injury Reveals Potential Radiation-Responsive Transcription Factors.

Radiation-induced gastric injury is a serious concern that may limit the duration and the delivered dose of radiation. However, the genome-wide molecular changes in stomach upon ionizing radiation have not been reported. In this study, mouse stomach was irradiated with 6 or 12 Gy X-ray irradiation and we found that radiation resulted in the atrophy of gastric mucosa and abnormal morphology of chief and parietal cells. Radiation-induced gastric injury was accompanied by an increase in the serum levels of pepsinogen A and pepsinogen C but not gastrin-17. The expression profiles of messenger RNA (mRNA) and long noncoding RNA (lncRNA) in normal and irradiated gastric tissues were measured by microarray analysis. Results revealed 17 upregulated and 10 downregulated mRNAs were consistent in 6 and 12 Gy irradiated gastric tissues, including D site-binding protein (Dbp) and fibrinogen-like protein 1 (Fgl1). Thirteen upregulated and 96 downregulated lncRNAs were commonly changed in 6 and 12 Gy irradiated gastric tissues. The dysregulated mRNAs were implicated in multiple pathways and showed coexpression with lncRNAs. To identify motifs for transcription factors and coactivators in the proximal promoter regions of the dysregulated RNAs, the bioinformatic tool Biopython was used. A variety of common motifs that are associated with transcription factors were identified, including ZNF263, LMX1B, and Dlx1. Our findings illustrate the molecular changes during radiation-induced gastric injury and the potential transcription factors driving this alteration.

Mixed-Surfactant-Assisted Synthesis of Dual-Phase Li4 Ti5 O12 -TiO2 Hierarchical Microspheres as High-Performance Anode Materials for Li-Ion Batteries.

A mixed-surfactant-assisted method was developed to synthesize dual-phase Li4 Ti5 O12 -TiO2 hierarchical microspheres. The ratio of anionic/cationic surfactant could regulate the primary structure morphology and the dual-phase ratio of the final product, in which the primary structure morphology could be stacked nanosheets, small nanoparticles, or large nanoparticles. The sample with a primary structure morphology of small nanoparticles had the highest specific surface area of 79.38 m2 g-1 and the best electrochemical performance because of its high Li+ migration rate, low polarization, and appropriate TiO2 content. Its capacity reached 153.5 mA h g-1 at a current rate of 40 C, and it retained nearly 100 % of its capacity after 100 cycles. A self-assembly mechanism of the mixed surfactant was highlighted to explain the formation of hierarchical microspheres. The physical and electrochemical properties of obtained material were correlated effectively.

The Involvement of SDF-1α/CXCR4 Axis in Radiation-Induced Acute Injury and Fibrosis of Skin.

Radiation-induced acute skin injury and consequent fibrosis are common complications of cancer radiotherapy and radiation accidents. Stromal cell-derived factor-1α (SDF-1α) and its receptor, CXC chemokine receptor 4 (CXCR4) have been shown to be involved in multiple cellular events. However, the role of SDF-1α/CXCR4 axis in radiation-induced acute injury and fibrosis of skin has not been reported. In this study, we found that the expression of SDF-1α and CXCR4 was significantly increased in irradiated skin tissues of humans, monkeys and rats, compared to their nonirradiated counterparts. Mice with keratinocyte-specific ablation of CXCR4 showed less severe skin damage than wild-type mice after receiving a 35 Gy dose of radiation. Consistently, subcutaneous injection of AMD3100, an FDA approved SDF-1α/CXCR4 inhibitor, attenuated skin injury and fibrosis induced by exposure to radiation in a rat model. Mechanically, the SDF-1α/CXCR4 axis promotes pro-fibrotic TGF-b/Smad signaling through the PI3K-MAPK signaling cascade in human keratinocyte HaCaT cells and skin fibroblast WS1 cells. AMD3100 inhibited Smad2 nuclear translocation and transcriptional activity of Smad2/3 induced by radiation, which suppressed the pro-fibrotic TGF-b/Smad signaling pathway activated by exposure. Taken together, these findings demonstrate the involvement of SDF-1α/CXCR4 axis in radiation-induced acute injury and fibrosis of skin, and indicate that AMD3100 would be an effective countermeasure against these diseases.

Response of Fingernail Growth to Out-of-Field Low-Dose X ray in Cancer Patients Receiving Radiotherapy.

The entire body of a patient with cancer is exposed to low-dose levels of radiation (mGy) during radiation therapy. The safety and biological impact of such exposure to low-dose radiation on the human body are largely unknown. The fingernail is a highly proliferative tissue, and its growth can be monitored during radiation treatment to analyze early effects of low-dose radiation. The fingernails of 30 patients who received external beam radiotherapy (EBRT) were used in this study to investigate the change in nail growth during fractionated radiotherapy. Lead shields were applied to some fingers to create dose variance within individual patients. The absorbed dose was measured, and the relationship between the dose and change in nail growth rate was analyzed. Other factors, including serum albumin, hemoglobin level, body weight index, age, gender and chemotherapy, were also subjected to multivariate analysis. Fingernails from patients received an average of 0.96 mGy per treatment fraction. We observed a surprising decline in fingernail growth rate during radiotherapy, which was more prominent in the nonshielded fingernails with a relatively high-absorbed dose. Such growth delay could be observed as early as one week postirradiation and lasted the entire treatment course. Using fingernail growth as a novel marker for radioresponse, the current study showed that exposure to very low-dose ionizing radiation has previously unrecognized early effects on human tissue.