LncRNA LINC00342 regulated cell growth and metastasis in non-small cell lung cancer via targeting miR-203a-3p.

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.

Dose dependency PM2.5 aggravated airway inflammation in asthmatic mice via down-regulating expression of ITGB4.

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 ß4 (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 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.

[Clinical characteristics and prognostic analysis of sudden sensorineural hearing loss with metabolic syndrome].

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.

IL-9 exacerbates the development of chronic obstructive pulmonary disease through oxidative stress.

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.

Role of microRNA-218-5p in the pathogenesis of chronic obstructive pulmonary disease.

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-ß1 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.

IL-33 induced inflammation exacerbated the development of chronic obstructive pulmonary disease through oxidative stress.

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.

Characteristics and source apportionment of PM1 emissions at a roadside station.

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.

Characterization of ambient volatile organic compounds at a landfill site in Guangzhou, South China.

Ambient air monitoring was conducted at Datianshan landfill, Guangzhou, South China in 1998 to investigate the seasonal and horizontal variations of trace volatile organic compounds (VOCs). Twelve sampling points over the Datianshan landfill were selected and samples were collected simultaneously using Carbontrap(TM) adsorption tubes. Thirty eight VOCs were detected in the winter, whereas 60 were detected in the summer. The VOC levels measured in summer were alkanes, 0.5-6.5 microg/m(3); aromatics, 2.3-1667 microg/m(3); chlorinated species, 0.2-31 microg/m(3); terpines, 0.1-34 microg/m(3); carbonyl species, 0.3-5.6 microg/m(3) and naphthalene and its derivatives, 0.4-27 microg/m(3). Compared to the summer samples the VOC levels in winter were much lower (mostly 1-2 orders of magnitude lower). The aromatics are dominant VOCs in landfill air both in winter and summer. High levels of alkylbenzene and terpines such as methyl-isopropylbenzene (max 1667 microg/m(3)) and limonene (max 162 microg/m(3)) cause undesirable odor. The similar correlation coefficients of BTEX in summer and winter suggest VOCs emissions were from landfill site sources. The variation of BTEX ratio at landfill site is different from that in the urban area of Guangzhou. It shows that the ambient VOCs at landfill site were different from the urban areas.

Volatile organic compounds (VOCs) in urban atmosphere of Hong Kong.

The assessment of volatile organic compounds (VOCs) has become a major issue of air quality network monitoring in Hong Kong. This study is aimed to identify, quantify and characterize volatile organic compounds (VOCs) in different urban areas in Hong Kong. The spatial distribution, temporal variation as well as correlations of VOCs at five roadside sampling sites were discussed. Twelve VOCs were routinely detected in urban areas (Mong Kok, Kwai Chung, Yuen Long and Causeway Bay). The concentrations of VOCs ranged from undetectable to 1396 microg/m3. Among all of the VOC species, toluene has the highest concentration. Benzene, toluene, ethylbenzene and xylenes (BTEX) were the major constituents (more than 60% in composition of total VOC detected), mainly contributed from mobile sources. Similar to other Asian cities, the VOC levels measured in urban areas in Hong Kong were affected both by automobile exhaust and industrial emissions. High toluene to benzene ratios (average T/B ratio = 5) was also found in Hong Kong as in other Asian cities. In general, VOC concentrations in the winter were higher than those measured in the summer (winter to summer ratio > 1). As toluene and benzene were the major pollutants from vehicle exhausts, there is a necessity to tighten automobile emission standards in Hong Kong.

Carbonaceous characteristics of atmospheric particulate matter in Hong Kong.

To determine the characteristic of carbonaceous species in atmospheric particles in Hong Kong, PM10 and PM2.5 samples were collected using high volume (hi-vol.) air samplers from November 2000 to February 2001. The organic carbon (OC) and elemental carbon (EC) were analyzed by the selective thermal manganese dioxide oxidation (TMO) method. The ratios of PM2.5/PM10 mass ratios were 0.61, 0.78 and 0.53 for particulate matter collected at PolyU station (PolyU, near a major traffic corridor), Kwun Tong station (KT, mixed residential/commercial/industrial) and the Hok Tsui background station (HT), respectively. These results indicate that the PM2.5 concentrations constitute the majority of the PM10) concentrations, especially in urban and industrial areas of Hong Kong. The average concentrations at the three sites ranged from 73.11 to 83.52 microg/m3 for PM10 and from 42.37 to 57.38 microg/m3 for PM2.5. The highest daily mass concentrations of PM10 and PM2.5 were 125.89 microg/m3 and 116.89 microg/m3 at KT, respectively. The correlation between PM10 and PM2.5 was high at KT and HT (r > 0.9, P < 0.01). This means that the sources of PM10 and PM2.5 may be the same at both sites. The highest mean concentration of OC (12.02 microg/m3) and EC (6.86 microg/m3) in PM10 was found at the PolyU among the three sites. For PM2.5, the highest mean concentration of OC (10.16 microg/m3) was at KT while the highest mean concentration of EC (7.95 microg/m3) was at PolyU. However, the background concentrations at HT were higher than another background area, Kosan, Korea. Transportation of pollutants from the Asian continent may be responsible for the elevations of EC+ OC at the remote site. More than 74% of the EC and more than 79% of the OC were found in the PM2.5 fraction at the three sampling locations. At PolyU station, PM2.5 consisted of 18.18% OC and 11.16% EC while 17.70% OC and 8.81% EC were found in KT station. Thus OC and EC are major constituents of aerosols in Hong Kong. OC/EC ratios for PM10 and PM2.5 were less than 2 at PolyU and KT stations while the ratio exceeded 3 at HT background station. This indicates that OC measured in the urban area may be emitted directly as a primary aerosol.

Direct ultrasonic agitation for rapid extraction of organic matter from airborne particulate.

Direct ultrasonic extraction (DUE) is proposed as simple and rapid sample pretreatment method. This new approach is applied to the extraction of particulate organic matter (POM) from airborne particulate by using dichloromethane (DCM) or DCM/methanol (90/10, v/v) as extractant. The analytical determination was carried out by weighing the extractable POM on an electrobalance. Total recovery for POM could be obtained when the sample was extracted three times with 25-50 mL extractant each for about 5 min at 50 W ultrasonic power. In comparison with conventional Soxhlet extraction, less extraction time (total 15 min only) and solvent consumption (100 mL) were required by DUE. The efficiency of the DUE was similar or even higher than the routine Soxhlet method. Additionally, the new extractor is very simple and easy to use and can accelerate the extraction procedures of organic components from various solid samples.