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We introduce tetrahedral amorphous-carbon thin films, formed by reactive filtered arc deposition method, as a dielectric material for a silicon-on-insulator substrate in high-power integrated circuits. The sp³/sp² components in the thin films were measured by spectroscopic ellipsometry, which is well known for its nondestructive and in sim characterization application. The dielectric functions of the composite materials were calculated using the Bruggeman effective medium approximation. The surface roughness was studied through atomic force microscopy. Also, the film content and thickness was studied by Rutherford backscattering. [ABSTRACT FROM AUTHOR]

Investigates the infrared optical properties of direct current sputtered silicon carbide (SiC) films on silicon. Analysis of the composition of the films using non-Rutherford backscattering and Auger electron spectroscopy; Formation mechanism of the microcrystalline and amorphous SiC; Optical behavior of the SiC film.

OBJECTIVE: Non-small cell lung cancer (NSCLC) is the main form of lung cancer, leading to major causes of cancer mortality. It is well known that lncRNAs may be involved in the pathogenesis of cancer, including NSCLC. The aim of this study was to provide a novel therapeutic target of LINC00342 for the therapy of NSCLC. PATIENTS AND METHODS: The expression of LINC00342 and miR-203a-3p was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell proliferation was measured using the MTT assay. Colony formation analysis was performed to count the number of colonies. Cell migration and invasion were measured by transwell. Online software DIANA tools were used to predict binding sites of LINC00342 and miR-203a-3p. Luciferase reporter assay was conducted to confirm the interaction between LINC00342 and miR-203a-3p. RESULTS: The expression of LINC00342 was increased in NSCLC tissues and cells compared with normal tissues and cells. Knockdown of LINC00342 suppressed cell proliferation, colony formation, migration, and invasion. LINC00342 regulated the expression of miR-203a-3p by targeting it directly. MiR-203a-3p was down-regulated in NSCLC tissues and cells compared with normal tissues and cells. Furthermore, LINC00342 promoted NSCLC cells proliferation, colony formation, migration, and invasion by depleting the expression of miR-203a-3p. CONCLUSIONS: This work implied that LINC00342 functions in NSCLC acting as an oncogene. Briefly, LINC00342 contributes to NSCLC cells growth and metastasis via targeting miR-203a-3p competitively. [ABSTRACT FROM AUTHOR]

Presents a study that investigated the evolution of surface morphologies of films prepared by ion-based deposition techniques via atomic force microscopy. Comparative studies on the effect of energetic ions on the development of topography between the low-ion-energy and high-ion-energy regime; Relationship between topography and mechanical properties of thin films; Analysis of results on hardness test and optical parameter measurement.

OBJECTIVE: We aimed to investigate whether PM2.5 has the potential to exacerbate neutrophil airway inflammation and to analyze the underlying mechanisms. MATERIALS AND METHODS: The high-volume air sampler (Laoying 2033B, Qingdao, China) was used to collect PM2.5 from January 01, 2016 to December 21, 2016 in Yantai, Shandong Province, China. BALB/c mice were divided into the following four groups: control group, ovalbumin (OVA) group, low-dose PM2.5 group and high-dose PM2.5 group. Mice except for control group were sensitized and challenged by OVA, and those in low-dose PM2.5 group and high-dose PM2.5 group were intranasally administered by PM2.5 suspension. Airway responsiveness of mice was measured. Enzyme- linked immunosorbent assay (ELISA) kit was used to evaluate the expressions of interleukin 17 (IL-17) and tumor necrosis factor-α (TNF-α) in bronchoalveolar lavage fluid (BALF) and serum samples. Cell counting in BALF and histological examination were measured to explore PM2.5-induced airway inflammation. Protein expression of Integrin β4 (ITGB4) was assessed by Western blot. RESULTS: Airway hyperresponsiveness (AHR) exacerbated in PM2.5 exposed asthmatic mice in progressively increased doses of acetylcholine chloride (ACH). Levels of IL-17 and TNF-αin BALF and serum increased significantly in PM2.5 groups compared with other groups with significant differences between two PM2.5 groups. PM2.5 exposure exacerbated inflammatory cell infiltration and mucus secretion in airways of asthmatic mice. Percentage of neutrophils in PM2.5 groups was significantly higher in a dose-dependent manner. OVA and PM2.5 co-exposure inhibited the expression of ITGB4. In particular, ITGB4 expression in mice of high-dose PM2.5 group was significantly lowered than the low-dose PM2.5 group. CONCLUSIONS: We showed that PM2.5 exposure exacerbates neutrophil airway inflammation in asthmatic mice though up-regulating expressions of IL-17 and TNF-α but down-regulating the expression of ITGB4. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the role of IL-9 in chronic obstructive pulmonary disease (COPD), and to explore its potential mechanism. MATERIALS AND METHODS: A mouse COPD model was established by exposure to cigarette smoke. COPD mice were then randomly assigned into two groups, including: the PBS group and the IL-9 antibody group. The above two groups were treated with phosphate-buffered saline (PBS) or IL-9 injection, respectively. The histopathological changes in lung tissues of mice were observed by hematoxylin-eosin (H&E) staining. Immunohistochemistry was performed to detect IL-9-positive (IL-9+) cells in lung tissues. Expression levels of IL-9, sIL-9R, STAT3, and p-STAT3 in peripheral blood of mice were determined by quantitative Real time-polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent assay (ELISA), and Western blot, respectively. In addition, the expression levels of superoxide dismutase (SOD), malondialdehyde (MDA), and reactive oxygen species (ROS) were detected. RESULTS: H&E staining results showed that the airway wall structure of COPD mice in the PBS group was irregular. Ciliated columnar epithelium exhibited marked degeneration, necrosis and shedding. Besides, numerous inflammatory cell infiltration, narrowing and rupture of the alveolar septa, and larger cysts fused by adjacent alveoli were observed. H&E staining also indicated that the structure of alveolar epithelium was severely impaired in COPD mice. However, the pathological changes in lung tissues of mice in the IL-9 antibody group were much milder than those of the PBS group. Immunohistochemistry results showed a significant deposition of IL-9+ cells in the lung tissues of the PBS group. Meanwhile, the mRNA and protein levels of IL-9, sIL-9R, and p-STAT3 in the PBS group were also remarkably higher than those of the IL-9 antibody group. In addition, SOD content in the PBS group was significantly decreased, whereas the levels of MDA and ROS were significantly increased than those of the IL-9 antibody group. CONCLUSIONS: IL-9 activated STAT3 and aggravated lung injury in COPD mice by increasing inflammatory and oxidative stress. [ABSTRACT FROM AUTHOR]

OBJECTIVE: We aimed at exploring the role of IL-33 in mouse chronic obstructive pulmonary disease and its potential molecular mechanism. MATERIALS AND METHODS: The chronic obstructive pulmonary disease (COPD) mice model was established by cigarette smoking (CS). COPD mice were randomly assigned into PBS group and IL-33 antibody group. The peripheral blood and lung tissues of mice from two groups were collected for the following experiments. Pathological changes of the lung tissues in both groups were analyzed by hematoxylin and eosin (HE) staining. IL-33 positive cells in lung tissues were detected by immunohistochemistry. Then, the mRNA and protein levels of IL-33, sST2, ERK and TNF-α in the mice peripheral blood of the two groups were accessed by Real-time polymerase chain reaction (RT-PCR) and Western blot. Finally, the indicators related to oxidative stress, including superoxide dismutase (SOD), malondialdehyde (MDA) and reactive oxygen species (ROS) in the mice serum of two groups were measured. RESULTS: After successful construction of COPD mouse model by CS, HE staining illustrated that the structure of airway wall of lung tissue in mice from PBS group was irregular. The ciliated columnar epithelium presented significant degeneration, necrosis and shedding. A large amount of inflammation cell infiltration was observed in vascular tissues. The alveolar epithelial structure was severely damaged and alveolar septum was narrowed and ruptured. Adjacent alveoli were found to be fused into larger cysts. The above pathological changes were relatively better in mice from IL-33 antibody group. Immunohistochemical results demonstrated that IL- 33 was remarkably deposited in the lung tissue of PBS group. The mRNA and protein levels of IL-33, sST2, ERK and TNF-α in peripheral blood of PBS group were much higher than those of IL- 33 antibody group. At the same time, SOD level in PBS group decreased, while MDA level and ROS production increased. CONCLUSIONS: IL-33 aggravates lung injury in COPD mice by increasing inflammation response and oxidative stress, which may serve as a target for predicting and treating COPD. [ABSTRACT FROM AUTHOR]

Determines the ambient levels of carbonyls at the roadside urban station of the Hong Kong Polytechnic University campus in China. Basis of the identification and quantification of carbonyl compounds; Characterization of carbonyl compounds; Concentration ratios of carbonyl compounds.

Objective: To analyze the clinical characteristics and prognosis of sudden sensorineural hearing loss (SSNHL) with metabolic syndrome (MetS). Method: Records of 212 patients with SSNHL treated in our department were retrospectively reviewed, including gender, age,course of the disease, concomitant time of tinnitus and vertigo, concomitant rate of hypertension and diabetes mellitus, BMI, systolic pressure, diastolic pressure, HDL-C, TG, fasting plasma glucose level, severity of hearing loss and audiograms. All patients were divided into two groups, the MetS group and the Non-MetS group, and the clinical characteristics and prognosis between two groups were compared. Result: In the MetS group, the BMI, systolic pressure, TG, fasting plasma glucose level were higher than that in the Non-MetS group, while the HDL-C level was lower than that in Non-MetS group ( P <0.01), and the rates of profound hearing loss, flat audiogram and total deafness audiogram were higher than that in the Non-MetS group ( P <0.05). In the MetS group, the overall recovery rate, complete recovery rate and marked recovery rate were 57.8%,6.0% and 14.5%, respectively, which was lower than that in the Non-MetS group (79.8%,19.4% and 27.9%, P <0.05 ). Conclusion: SSNHL patients with MetS suffered a severer hearing loss, the most audiograms were flat and total deafness, and the prognosis of SSNHL patients with MetS was poorer., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Editorial Department of Journal of Clinical Otorhinolaryngology Head and Neck Surgery.)

Objective: Chronic obstructive pulmonary disease (COPD) is an inflammatory lung disease characterized by inflammatory cell activation and the release of inflammatory mediators. By measuring microRNA expression in the plasma of COPD subjects, we aimed to identify the clinical relevance of plasma miRNA levels in these patients., Patients and Methods: A total of 40 COPD patients and 40 healthy controls were enrolled in the study. The COPD model of C57BL/6 mice was also developed by exposing them to cigarette smoke (CS). The expression of microRNA-218-5p was detected by qRT-PCR in all the subjects and mice. The serum level of IL-18 and TGF-β1 was also detected via ELISA kit. To investigate the effects of miR-218-5p, 10 mg/kg of miR-218-5p inhibitor (miR-218-5p antagonist), a scrambled control or PBS (solvent) was intranasally administered on the first and the fourth exposure day, before the start of CS exposure., Results: The results showed that miR-218-5p was significantly down-regulated in patients with COPD, compared to normal subjects. There was a negative correlation between the plasma miR-218-5p level and the duration of disease since diagnosis in COPD ex-smokers. CS-induced COPD mice experiments with a miR-218-5p inhibitor demonstrated a protective role of miR-218-5p in cigarette smoke-induced inflammation and COPD., Conclusions: These findings supported that miR-218-5p may, therefore, play an important role in the pathogenesis of COPD.

The mass concentrations of PM(1) (particles less than 1.0 μm in aerodynamic diameter), organic carbon (OC), elemental carbon (EC), water-soluble ions, and up to 25 elements were reported for 24h aerosol samples collected every sixth day at a roadside sampling station in Hong Kong from October 2004 to September 2005. Annual average PM(1) mass concentration was 44.5 ± 19.5 μg m(-3). EC, OM (organic matter, OC × 1.2), and SO(4)(=) were the dominant components, accounting for ∼ 36%, ∼ 26%, and ∼ 24% of PM(1), respectively. Other components, i.e., NO(3)(-), NH(4)(+), geological material, trace elements and unidentified material, comprised the remaining ∼ 14%. Annual average OC/EC ratio (0.6 ± 0.3) was low, indicating that primary vehicle exhaust was the major source of carbonaceous aerosols. The seasonal variations of pollutants were due to gas-particle partitioning processes or a change in air mass rather than secondary aerosol produced locally. Vehicle exhaust, secondary aerosols, and waste incinerator/biomass burning were dominant air pollution sources, accounting for ∼ 38%, ∼ 22% and ∼ 16% of PM(1), respectively. Pollution episodes during summer (May-August) which were frequently accompanied by tropical storms or typhoons were dominated by vehicle emissions. During winter (November-February) pollution episodes coincided with northeasterly monsoons were characterized by secondary aerosols and incinerator/biomass burning emissions., (Copyright © 2011 Elsevier B.V. All rights reserved.)