PMID: 

Exp Ther Med. 2019 Oct ;18(4):2503-2511. Epub 2019 Aug 1. PMID: 31572502

Abstract Title: 

The influence of PMon lung injury and cytokines in mice.

Abstract: 

Exposure to particulate matter≤2.5 µm in diameter (PM) profoundly affects human health. However, the role of PMon lung injury and cytokine levels in mice is currently unknown. The aim was to examine the effect of PMpollution on lung injury in mice fed at an underground parking lot. A total of 20 female Kunming mice were randomly divided into control and polluted groups, with 10 rats in each group. The control group was kept in the laboratory, while the pollution group was fed in an underground parking lot. The concentrations of pollutants were measured using ambient air quality monitoring instruments. After 3 months of treatment, the lungs were collected and examined using electron microscopy, and the morphological structures were assessed using hematoxylin and eosin staining. The polarization of macrophages was evaluated by immunofluorescence. The concentration of interleukin (IL)-4, tumor necrosis factor (TNF)-α and transforming growth factor (TGF)-β1 in peripheral sera were assessed by ELISA. The mRNA and protein levels of IL-4, TNF-α, and TGF-β1 in lung tissues were assessed by reverse transcription-quantitative polymerase chain reaction and western blot analyses, respectively. In the polluted group, the levels of CO, NOand PMwere significantly higher compared with the control group. Compared with the controls, intracellular edema, an increased number of microvilli and lamellar bodies, smaller lamellar bodies in type II alveolar epithelial cells, and abundant particles induced by PMin macrophages were observed in the polluted group. The lung ultrastructure changed in the polluted group, revealing exhaust-induced lung injury: The tissues were damaged, and the number of inflammatory cells, neutrophils, polylymphocytes and eosinophils increased in the polluted group compared with the control group. The authors also observed that the number of M1 and M2 macrophages markedly increased after the exhaust treatment. The levels of IL-4, TNF-α and TGF-β1 in the sera and tissues were significantly increased in the polluted group. PMpollutants in underground garages can lead to lung injury and have a significant impact on the level of inflammatory cytokines in mice. Therefore, the authors suggest that PMcan activate the inflammatory reaction and induce immune dysfunction, leading to ultrastructural damage.

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PMID: 

Pediatr Infect Dis J. 2016 Jan ;35(1):94-6. PMID: 26379162

Abstract Title: 

Severe Upper Extremity Dysfunction After 4CMenB Vaccination in a Young Infant.

Abstract: 

The 4-component meningococcal serogroup B vaccine 4CMenB (Bexsero) is the first vaccine against this serogroup and has been approved by licensing authorities in Europe, Canada and Australia. Therefore, the vaccine may enter soon nationwide vaccine recommendation schemes. We report on a case of a 5-month-old infant who developed prolonged upper extremity dysfunction after the second injection of the 4CMenB vaccine in the left deltoid muscle and was concomitantly applied with 2 routine vaccinations. Myositis, periostitis, (peri-) vasculitis and axillary inflammation were confirmed by magnetic resonance imaging. Two months after initial initiation of an anti-inflammatory and an antibiotic treatment, symptoms completely resolved. Administration of 3 vaccines requires clear recommendations for the preferred injection site in infants because increased reactogenicity of 4CMenB may lead to local severe adverse events.

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PMID: 

Environ Monit Assess. 2019 Oct 24 ;191(11):668. Epub 2019 Oct 24. PMID: 31650348

Abstract Title: 

Airborne microplastics: a review study on method for analysis, occurrence, movement and risks.

Abstract: 

Microplastics (of size

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PMID: 

Ecotoxicol Environ Saf. 2020 Jan 30 ;188:109867. Epub 2019 Nov 2. PMID: 31689658

Abstract Title: 

Prenatal Oexposure increases the severity of OVA-induced asthma in offspring.

Abstract: 

BACKGROUND: Accumulating epidemiological studies showed that prenatal and early life exposure to ambient air pollution was important contributor to the development of childhood asthma. However, the effects and mechanisms of prenatal exposure to ozone (O), a type of ambient air pollution, on the progression of asthma in offspring remain unclear.OBJECTIVE: This study aimed to determine the effects and mechanism of asthma in offspring after prenatal Oexposure.METHODS: Pregnant BALB/c mice were exposed to Oor air on gestational days (GDs) 13-18. Their offspring were sensitized and challenged to ovalbumin (OVA) to establish asthma model, and the asthma features were evaluated. The splenic natural killer (NK) cells in the offspring were measured to explore the mechanism on the effects of asthma in the offspring. The responses of the pregnant mice and dams after Oexposure were evaluated.RESULTS: Airway inflammation, mucus secretion, OVA-specific immunoglobulin (Ig) E, T helper (Th) 2-skewed response, the frequency of CD3εCD49bsplenic NK cells, the expression of tumor necrosis factor (TNF)-α, and IL (interleukin)-17 were significantly exacerbated in the OVA-induced asthma offspring after prenatal Oexposure. In addition, airway inflammation, a lower number of CD3εCD49bsplenic NK cells, and systemic oxidative stress were caused at the end of pregnancy after Oexposure, which did not recover at the end of lactation for the first two responses.CONCLUSIONS: Prenatal Oexposure increased the severity of OVA-induced asthma in the offspring, which might be directly induced by CD3εCD49bsplenic NK cells in the offspring and indirectly related to the damaged maternal immune system.

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PMID: 

Biochem Pharmacol. 2002 Feb 1 ;63(3):437-53. PMID: 11853695

Abstract Title: 

In vitro induction of apoptosis vs. necrosis by widely used preservatives: 2-phenoxyethanol, a mixture of isothiazolinones, imidazolidinyl urea and 1,2-pentanediol.

Abstract: 

Preservatives are added to many final products, such as detergents, cosmetics, pharmaceuticals and vaccines. We conducted an in vitro investigation of the apoptosis- and necrosis-inducing potential of brief applications (10 min) of four common preservatives: ethylene glycol monophenyl ether, 2-phenoxyethanol (EGPE), imidazolidinyl urea (IMU), a mixture of 5-chloro-2-methyl-4-isothiazolin-3-one and 2-methyl-4-isothiazolin-3-one (CMI/MI), and 1,2-pentanediol, a"preservative-non-preservative"best known as pentylene glycol. Using HL60 cells, we monitored the kinetics of cell toxicity with the MTT test and analysed extranuclear end points of apoptosis, i.e. phosphatidylserine exposure and nuclear fragmentation. Preservative treatment resulted in a dose-dependent decrease of cell viability. The mode of cell death was dose-dependent: necrosis occurred at high concentrations while apoptosis, shown by DNA laddering, DNA sub-diploid peak and caspase-3 activation, occurred at lower concentrations 0-24hr after exposure to a single dose: CMI/MI induced apoptosis at low concentrations (0.001-0.01%) and necrosis at high concentrations (0.5-0.1%); IMU and EGPE required higher concentrations to induce apoptosis (IMU 0.01-0.1% and EGPE 0.01-0.5%) or necrosis (IMU 0.5-1% and EGPE only at 1%). PG induced apoptosis only at 5%. Externalization of PS, a hallmark of apoptosis, occurred early in HL60 treated with low concentrations of CMI/MI and EGPE and was concomitant with the subdiploid peak in HL60 treated with PG. However, it did not occur in HL60 treated with IMU. In conclusion, at appropriate concentrations, each of the four preservatives modulates the apoptotic machinery by a caspase-dependent mechanism. Thus, apoptosis could be a good parameter to evaluate the cytoxicity of these chemical compounds.

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PMID: 

Respir Res. 2015 Mar 14 ;16:37. Epub 2015 Mar 14. PMID: 25849069

Abstract Title: 

Cigarette smoke inhibits BAFF expression and mucosal immunoglobulin A responses in the lung during influenza virus infection.

Abstract: 

BACKGROUND: It is incompletely understood how cigarette smoke (CS) exposure affects lung mucosal immune responses during viral respiratory infections. B cell activating factor belonging to the tumor necrosis factor family (BAFF) plays an important role in the induction of secretory immunoglobulin A (S-IgA) which is the main effector of the mucosal immune system. We therefore investigated the effects of CS exposure on BAFF expression and S-IgA responses in the lung during influenza virus infection.METHODS: Mice were exposed to CS and/or infected with influenza virus. Bronchoalveolar lavage fluid and lung compartments were analyzed for BAFF expression, influenza-specific S-IgA level and histological changes. Lung B cells were isolated and the activation-induced cytidine deaminase (Aicda) expression was determined. BEAS-2B cells were treated with CS extract (CSE), influenza virus, interferon beta or N-acetylcysteine and BAFF expression was measured.RESULTS: CS inhibited BAFF expression in the lung, particularly after long-term exposure. BAFF and S-IgA levels were increased during influenza virus infection. Three-month CS exposure prior to influenza virus infection resulted in reduced BAFF and S-IgA levels in the lung as well as augmented pulmonary inflammation on day 7 after infection. Prior CS exposure also caused decreased Aicda expression in lung B cells during infection. Neutralization of BAFF in the lung resulted in reduced S-IgA levels during influenza virus infection. CSE inhibited virus-mediated BAFF induction in a dose-dependent manner in BEAS-2B cells, while this inhibition of BAFF by CSE was prevented by pretreatment with the antioxidant N-acetylcysteine.CONCLUSIONS: Our findings indicate that CS may hinder early mucosal IgA responses in the lung during influenza virus infection through oxidative inhibition of BAFF, which might contribute to the increased incidence and severity of viral infections in smokers.

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PMID: 

Contact Dermatitis. 1998 Jan ;38(1):50-1. PMID: 9504254

Abstract Title: 

Generalized eczema in an 18-month-old boy due to phenoxyethanol in DPT vaccine.

Abstract: 

[n/a]

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PMID: 

Respir Med. 2001 Jun ;95(6):448-56. PMID: 11421501

Abstract Title: 

Long-term administration of N-acetylcysteine decreases hydrogen peroxide exhalation in subjects with chronic obstructive pulmonary disease.

Abstract: 

Patients with chronic obstructive pulmonary disease (COPD) exhale more hydrogen peroxide (H2O2) and lipid peroxidation products than healthy subjects. This may reflect oxidative stress in the airways that plays important role in the development and progression of COPD. N-acetylcysteine (NAC), a mucolytic drug, possesses antioxidant properties as it is a precursor of reduced glutathione that together with glutathione peroxidase may decompose H2O2 and lipid peroxides. We aimed to determine the effect of NAC, 600 mg effervescent tablets (Fluimucil), once a day for 12 months, and placebo on the concentration of H2O2 and thiobarbituric acid reactive substances (TBARs) in expired breath condensate and serum levels of two lipid peroxidation products (TBARs, lipid peroxides) in patients with COPD. The study was performed as a double-blind, double-dummy comparison between active drug and placebo in two parallel groups. Forty-four outpatients with stable COPD (22 in the NAC group and 22 in the placebo group) completed the study. Specimens of expired breath condensate and serum were collected at the randomization visit and then every 3 months over 1 year. The concentration of TBARs and H2O2 in expired breath condensate was measured spectrofluorimetrically by the thiobarbituric acid and homovanillic acid methods, respectively. Serum levels of lipid peroxides were determined spectrophotometrically after extraction with butanol and pyridine. Initially, H2O2 exhalation did not differ between the placebo and NAC groups up to 6 months of treatment. After this the significant differences were observed. After 9 and 12 months of treatment NAC group exhaled 2.3-fold (0.17+/-0.33 microM vs. 041+/-0.26 microM, P

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PMID: 

. PMID: 28921942

Abstract Title: 

Biomarkers of Neuroinflammation: Proceedings of a Workshop

Abstract: 

[n/a]

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PMID: 

Arch Pharm Res. 2017 Nov ;40(11):1314-1327. Epub 2017 Oct 12. PMID: 29027136

Abstract Title: 

Oligonol promotes glucose uptake by modulating the insulin signaling pathway in insulin-resistant HepG2 cells via inhibiting protein tyrosine phosphatase 1B.

Abstract: 

Insulin resistance and protein tyrosine phosphatase 1B (PTP1B) overexpression are strongly associated with type 2 diabetes mellitus (T2DM), which is characterized by defects in insulin signaling and glucose intolerance. In a previous study, we demonstrated oligonol inhibits PTP1B andα-glucosidase related to T2DM. In this study, we examined the molecular mechanisms underlying the anti-diabetic effects of oligonol in insulin-resistant HepG2 cells. Glucose uptake was assessed using a fluorescent glucose tracer, 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxyglucose, and the signaling pathway was investigated by western blotting. Oligonol significantly increased insulin-provoked glucose uptake and decreased PTP1B expression, followed by modulation of ERK phosphorylation. In addition, oligonol activated insulin receptor substrate 1 by reducing phosphorylation at serine307 and increasing that at tyrosine 895, and enhanced the phosphorylations of Akt and phosphatidylinositol 3-kinase. Interestingly, it also reduced the expression of two key enzymes of gluconeogenesis (glucose 6-phosphatase and phosphoenolpyruvate carboxykinase), attenuated oxidative stress by scavenging/inhibiting peroxynitrite, and reactive oxygen species (ROS) generation, and augmented the expression of nuclear factor kappa B. These findings suggest oligonol improved the insulin sensitivity of insulin-resistant HepG2 cells by attenuating the insulin signaling blockade and modulating glucose uptake and production. Furthermore, oligonol attenuated ROS-related inflammation and prevented oxidative damage in our in vitro model of type 2 diabetes. These result indicate oligonol has promising potential as a treatment for T2DM.

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