Displaying publications 41 - 42 of 42 in total

Abstract:
Sort:
  1. Li Q, Zhang K, Li R, Yang L, Yi Y, Liu Z, et al.
    Sci Total Environ, 2023 May 10;872:162071.
    PMID: 36775179 DOI: 10.1016/j.scitotenv.2023.162071
    Biomass burning (BB) has significant impacts on air quality and climate change, especially during harvest seasons. In previous studies, levoglucosan was frequently used for the calculation of BB contribution to PM2.5, however, the degradation of levoglucosan (Lev) could lead to large uncertainties. To quantify the influence of the degradation of Lev on the contribution of BB to PM2.5, PM2.5-bound biomass burning-derived markers were measured in Changzhou from November 2020 to March 2021 using the thermal desorption aerosol gas chromatography-mass spectrometry (TAG-GC/MS) system. Temporal variations of three anhydro-sugar BB tracers (e.g., levoglucosan, mannosan (Man), and galactosan (Gal)) were obtained. During the sampling period, the degradation level of air mass (x) was 0.13, indicating that ~87 % of levoglucosan had degraded before sampling in Changzhou. Without considering the degradation of levoglucosan in the atmosphere, the contribution of BB to OC were 7.8 %, 10.2 %, and 9.3 % in the clean period, BB period, and whole period, respectively, which were 2.4-2.6 times lower than those (20.8 %-25.9 %) considered levoglucosan degradation. This illustrated that the relative contribution of BB to OC could be underestimated (~14.9 %) without considering degradation of levoglucosan. Compared to the traditional method (i.e., only using K+ as BB tracer), organic tracers (Lev, Man, Gal) were put into the Positive Matrix Factorization (PMF) model in this study. With the addition of BB organic tracers and replaced K+ with K+BB (the water-soluble potassium produced by biomass burning), the overall contribution of BB to PM2.5 was enhanced by 3.2 % after accounting for levoglucosan degradation based on the PMF analysis. This study provides useful information to better understand the effect of biomass burning on the air quality in the Yangtze River Delta region.
  2. Ariffin H, Azanan MS, Abd Ghafar SS, Oh L, Lau KH, Thirunavakarasu T, et al.
    Cancer, 2017 Nov 01;123(21):4207-4214.
    PMID: 28654149 DOI: 10.1002/cncr.30857
    BACKGROUND: Large epidemiologic studies have reported the premature onset of age-related conditions, such as ischemic heart disease and diabetes mellitus, in childhood cancer survivors, decades earlier than in their peers. The authors investigated whether young adult survivors of childhood acute lymphoblastic leukemia (ALL) have a biologic phenotype of cellular ageing and chronic inflammation.

    METHODS: Plasma inflammatory cytokines were measured using a cytometric bead array in 87 asymptomatic young adult survivors of childhood ALL (median age, 25 years; age range, 18-35 years) who attended annual follow-up clinic and compared with healthy, age-matched and sex-matched controls. Leukocyte telomere length (LTL) was measured using Southern blot analysis.

    RESULTS: Survivors had significant elevation of plasma interleukin-2 (IL-2), IL-10, IL-17a, and high-sensitivity C-reactive protein levels (all P 0.8 mg/dL) was related to increased odds of having metabolic syndrome (odds ratio, 7.256; 95% confidence interval, 1.501-35.074). Survivors also had significantly shorter LTL compared with controls (median, 9866 vs 10,392 base pairs; P = .021). Compared with published data, LTL in survivors was similar to that in healthy individuals aged 20 years older. Survivors who received cranial irradiation had shorter LTL compared with those who had not (P = .013).

    CONCLUSIONS: Asymptomatic young adult survivors of childhood ALL demonstrate a biologic profile of chronic inflammation and telomere attrition, consistent with an early onset of cellular processes that drive accelerated aging. These processes may explain the premature development of age-related chronic conditions in childhood cancer survivors. Understanding their molecular basis may facilitate targeted interventions to disrupt the accelerated aging process and its long-term impact on overall health. Cancer 2017;123:4207-4214. © 2017 American Cancer Society.

Related Terms
Filters
Contact Us

Please provide feedback to Administrator (afdal@afpm.org.my)

External Links