PMID: 

Gerontology. 2019 Sep 25:1-9. Epub 2019 Sep 25. PMID: 31553969

Abstract Title: 

Inflammation and the Alteration of B-Cell Physiology in Aging.

Abstract: 

Aging results for the immune system in a departure from the optimal homeostatic state seen in young organisms. This divergence regrettably contributes to a higher frequency of compromised responses to infections and inefficient classical vaccination in aged populations. In B cells, the cornerstone of humoral immunity, the development and distribution of the various mature B cell subsets are impacted by aging in both humans and mice. In addition, aged mature B cells demonstrate limited capacity to mount efficient antibody responses. An expected culprit for the decline in effective immunity is the rise of the systemic levels of pro-inflammatory molecules during aging, establishing a chronic low-grade inflammation. Indeed, numerous alterations affecting directly or indirectly B cells in old people and mice are reminiscent of various effects of acute inflammation on this cell type in young adults. The present mini-review will highlight the possible adverse contributions of the persistent low-level inflammation observed in susceptible older organisms to the inadequate B-cell physiology.

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PMID: 

J Biomed Nanotechnol. 2018 Dec 1 ;14(12):2172-2184. PMID: 30305224

Abstract Title: 

Fine Particulate Matter (PM) Promoted the Invasion of Lung Cancer Cells via an ARNT2/PP2A/STAT3/MMP2 Pathway.

Abstract: 

Accumulating evidence indicates that fine particulate matter (PM2.5) exposure is associated with many cardiopulmonary diseases, particularly lung carcinoma. Nevertheless, the underlying biological mechanisms by which PMexposure initiates and aggravates lung carcinoma remain elusive. In the present study, we collected PMin Nanjing and explored the mechanisms underlying the oncogenic roles of PMin the murine lung carcinoma cell line LLCand. PMwas closely attached to and internalized by lung cancer cells. Moreover, PMincreased the production of ARNT2 and the inactivation of the tumor suppressor B56-PP2A, which was followed by the activation ofSTAT3 and the enhancement of invasive ability by MMP-2. Furthermore, we took advantage of an orthotopic lung carcinoma metastasis mouse model to illustrate the prometastatic effect of PM; our results suggested that the ARNT2/PP2A/STAT3/MMP-2 cascade played a key role in PM-related oncogenicity. Finally, we observed that PMwas deposited in human lung carcinoma tissues, indicating that this potential pathway may also be involved in human lung carcinoma. These findings demonstrated that fine particulate matter, or PM, promoted the invasion of lung cancer cells via an ARNT2/PP2A/STAT3/MMP2 pathway, which may be targeted to alleviate the tumorigenic effect of PMin lung cancer.

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PMID: 

Prev Med. 2019 05 ;122:91-99. PMID: 31078178

Abstract Title: 

Estimates of the current and future burden of lung cancer attributable to PMin Canada.

Abstract: 

The International Agency for Research on Cancer has classified PM(fine particulate matter, PM) as a lung cancer carcinogen in humans. We estimated the proportion of lung cancer cases attributable to PMexposure in Canada in 2015, and future avoidable cancers over the period 2016-2042 under different future exposure scenarios. A meta-analysis was conducted to estimate the relative risk of lung cancer associated with PMthat was generalizable to Canada. A population-weighted Canadian distribution of residential PMexposure was estimated annually using ecological-level, satellite-derived PMdata for the period 1990 to 2009. Population attributable risks (PAR) were estimated for PMand applied to lung cancer incidence from the Canadian Cancer Registry. Potential impact fractions based on counterfactual scenarios for the year 2042 were estimated, along with cumulative preventable cases from 2016 to 2042. The relative risk of lung cancer associated with PMwas 1.09 (95% CI: 1.06-1.12) per an increase of 10 μg/m. The average population-weighted exposure to PMcorresponding to a 20-year exposure window from 1990 to 2009 was 8.3 μg/m. The PAR for PMwas estimated at 6.9%, accounting for 1739 attributable lung cancer cases in 2015. If patterns of decline in PMcontinue, over 3000 lung cancer cases could be prevented between 2016 and 2042. Exposure to PMcontributes to a considerable burden of lung cancer in Canada and policies aimed at sustaining outdoor PMdeclines are important for lung cancer prevention in Canada.

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PMID: 

Environ Int. 2020 Jan 8 ;136:105440. Epub 2020 Jan 8. PMID: 31926436

Abstract Title: 

Long-term exposure to ambient air pollution, APOE-ε4 status, and cognitive decline in a cohort of older adults in northern Manhattan.

Abstract: 

BACKGROUND: There is mounting evidence that long-term exposure to air pollution is related to accelerated cognitive decline in aging populations. Factors that influence individual susceptibility remain largely unknown, but may involve the apolipoprotein E genotype E4 (APOE-ε4) allele.OBJECTIVES: We assessed whether the association between long-term exposure to ambient air pollution and cognitive decline differed by APOE-ε4 status and cognitive risk factors.METHODS: The Washington Heights Inwood Community Aging Project (WHICAP) is a prospective study of aging and dementia. Neuropsychological testing and medical examinations occur every 18-24 months. We used mixed-effects models to evaluate whether the association between markers of ambient air pollution (nitrogen dioxide [NO]), fine [PM], and coarse [PM] particulate matter) and the rate of decline in global and domain-specific cognition differed across strata defined by APOE-ε4 genotypes and cognitive risk factors, adjusting for sociodemographic factors and temporal trends.RESULTS: Among 4821 participants with an average of 6 years follow-up, higher concentrations of ambient air pollution were associated with more rapid cognitive decline. This association was more pronounced among APOE-ε4 carriers (p 

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PMID: 

Photodiagnosis Photodyn Ther. 2020 Jan 7:101653. Epub 2020 Jan 7. PMID: 31923632

Abstract Title: 

Evaluation of the effect of photodynamic therapy on chemotherapy induced oral mucositis Photodynamic therapy on oral mucositis.

Abstract: 

BACKGROUND: In this study the effect of photodynamic therapy on chemotherapy induced mucositis was evaluated.METHODS: This randomized single blind clinical pilot evaluation evaluated the effect of PDT with methylene blue on 15 patients with chemotherapy induced bilateral oral mucositis. They were divided into 2 groups (control side and intervention side). Methylene blue was applied on the lesions of both sides, after 10 minutes the lesion of intervention side was irradiated by a 660 nm diode laser InGaAlP(Azor-2 K) for 10 minutes (power: 25 mW, dose:19.23 J/CM2, probe diameter: 0.78 cm2) for three sessions (day1,[3,5] and followed on day 12. In control side only sham laser was used. Data were analyzedby Wilcoxon and Mann-Whitney test using SPSS version 22.RESULTS: Comparing the WCCNR and NCI difference in different sessions between intervention and control group, represented significant improvement in oral mucositis in photodynamic therapy group for sessions 1-0, 2-0, 3-0 (P.value

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PMID: 

Lasers Med Sci. 2020 Jan 10. Epub 2020 Jan 10. PMID: 31925594

Abstract Title: 

Low-level laser therapy prevents muscle oxidative stress in rats subjected to high-intensity resistance exercise in a dose-dependent manner.

Abstract: 

High-intensity resistance exercise (RE) increases oxidative stress leading to deleterious effects on muscle performance and recovery. The aim of this study was to assess the effect of applying low-level laser therapy (LLLT) prior to a RE session on muscle oxidative stress and to determine the possible influence of the dosimetric parameters. Female Wistar rats were assigned to non-LLLT (Ctr: non-exercised control; RNI: RE) or LLLT groups subjected to RE (radiant energy: 4 J, 8 J, and 12 J, respectively). RE consisted of four maximum load climbs. An 830-nm DMC Lase Photon III was used to irradiate three points in gastrocnemius muscles (two limbs) before exercise. Animals were euthanized after 60 min after the end of the exercise, and muscle tissue was removed foranalysis of oxidative stress markers. All doses resulted in the prevention of increased lipoperoxidation; however, LLLT prevented protein oxidation only in rats that were pretreated with 8 J and 12 J of energy by LLLT. RE and LLLT did not change catalase activity. However, RE resulted in lower superoxide dismutase activity, and the opposite was observed in the LLLT group. These data indicate that LLLT prior to RE can prevent muscle oxidative stress. This study is the first to evaluate the impact of dosimetric LLLT parameters on the oxidative stress induced by RE, wherein both 8 J and 12 Jof energy afforded significant protection.

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PMID: 

Photodiagnosis Photodyn Ther. 2019 Dec 10:101621. Epub 2019 Dec 10. PMID: 31841687

Abstract Title: 

Photobiomodulation and photodynamic therapy for the treatment of oral mucositis in patients with cancer.

Abstract: 

BACKGROUND: Photobiomodulation therapy (PBM-T) can penetrate soft tissues and exert analgesic and healing effects, and is thus a promising alternative for prevention and treatment of oral mucositis (OM). The aim of this study was to evaluate the efficacy of PBM-T, alone or combined with photodynamic therapy (PDT), for treatment of OM in cancer patients.METHODS: Fifty-six patients were recruited from the Oncology Department of a teaching hospital. Patients underwent grading of OM and were divided into two groups (n = 28 each): PBM-T and PBM-T + PDT. In the PBM-T group, low-level laser was applied to 61 points in the oral cavity, once weekly for 4 weeks (wavelength 660 nm, power 100 mW, energy density 142 J/cm², spot energy 4 J, irradiation time 40 seconds). In the PBM-T + PDT group, in addition to PBM-T as described above, patients rinsed with 20 mL of photosensitizing mouthwash (curcumin 1.5 g/L) and the oral cavity was irradiated with a blue (468 nm) LED for 5 min.RESULTS: Significant reductions in OM grade were observed after application of PBM-T or PBM-T + PDT (p 

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PMID: 

Int J Hyg Environ Health. 2018 04 ;221(3):510-518. Epub 2018 Jan 31. PMID: 29428699

Abstract Title: 

C-reactive protein (CRP) and long-term air pollution with a focus on ultrafine particles.

Abstract: 

BACKGROUND: Long-term exposure to ambient air pollution contributes to the global burden of disease by particularly affecting cardiovascular (CV) causes of death. We investigated the association between particle number concentration (PNC), a marker for ultrafine particles, and other air pollutants and high sensitivity C-reactive protein (hs-CRP) as a potential link between air pollution and CV disease.METHODS: We cross-sectionally analysed data from the second follow up (2013 and 2014) of the German KORA baseline survey which was conducted in 1999-2001. Residential long-term exposure to PNC and various other size fractions of particulate matter (PMwith size of

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PMID: 

Environ Int. 2018 10 ;119:264-273. Epub 2018 Jul 5. PMID: 29982129

Abstract Title: 

Short- and long-term exposure to ambient air pollution and circulating biomarkers of inflammation in non-smokers: A hospital-based cohort study in South Korea.

Abstract: 

Despite increasing epidemiological evidence of an association between air pollution and adverse health outcomes, the detailed mechanisms underlying the adverse effects of air pollution on medical conditions remain unclear. We evaluated the effects of short- and long-term exposure to ambient air pollution on key inflammatory markers in non-smoking subjects. Serum fibrinogen, C-reactive protein, ferritin, and white blood cell counts were repeatedly measured 3 times in 6589 subjects at the Samsung Medical Center (Seoul, South Korea) between 2010 and 2016. Both short- (≤8-day averages) and long-term (annual averages) exposure measures of 6 air pollutants (particles 

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PMID: 

Arterioscler Thromb Vasc Biol. 2019 03 ;39(3):513-522. PMID: 30700134

Abstract Title: 

Ambient Air Pollution Is Associated With HDL (High-Density Lipoprotein) Dysfunction in Healthy Adults.

Abstract: 

Objective- We aimed to assess whether exposure to higher levels of ambient air pollution impairs HDL (high-density lipoprotein) function and to elucidate the underlying biological mechanisms potentially involved. Approach and Results- In the Beijing AIRCHD study (Air Pollution and Cardiovascular Dysfunction in Healthy Adults), 73 healthy adults (23.3±5.4 years) were followed-up with 4 repeated study visits in 2014 to 2016. During each visit, ambient air pollution concentrations, HDL function metrics, and parameters of inflammation and oxidative stress were measured. Average daily concentrations of ambient particulate matter in diameter

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