Prevalence of work environment factors among nonparticipants at baseline, participants at baseline and participants at follow-up.

<p>Prevalence of work environment factors among nonparticipants at baseline, participants at baseline and participants at follow-up.</p

Associations between symptom 3-year incidence and baseline exposure and change of exposure ^b.

<p>Associations between symptom 3-year incidence and baseline exposure and change of exposure <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0164954#t006fn002" target="_blank">^b</a>.</p

Associations between symptom prevalence and baseline exposure (N = 436) ^b.

<p>Associations between symptom prevalence and baseline exposure (N = 436) <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0164954#t005fn002" target="_blank">^b</a>.</p

Prevalence of demographic data, allergies and respiratory illness among nonparticipants at baseline, participants at baseline and participants at follow-up.

<p>Prevalence of demographic data, allergies and respiratory illness among nonparticipants at baseline, participants at baseline and participants at follow-up.</p

Flow chart of the study population.

<p>Flow chart of the study population.</p

Prevalence of current home factors among nonparticipant at baseline, participants at baseline and participants at follow-up.

<p>Prevalence of current home factors among nonparticipant at baseline, participants at baseline and participants at follow-up.</p

Is IMRT Superior or Inferior to 3DCRT in Radiotherapy for NSCLC? A Meta-Analysis

<div><p>Introduction</p><p>There are no adequate data to determine whether intensity-modulated radiotherapy (IMRT) is superior to three-dimensional conformal radiotherapy (3DCRT) in the treatment of non-small cell lung cancer (NSCLC). This meta-analysis was conducted to compare the clinical outcomes of IMRT and 3DCRT in the treatment of NSCLC.</p><p>Methods</p><p>No exclusions were made based on types of study design. We performed a literature search in PubMed, EMBASE and the Cochrane library databases from their inceptions to April 30, 2015. The overall survival (OS) and relative risk (RR) of radiation pneumonitis and radiation oesophagitis were evaluated. Two authors independently assessed the methodological quality and extracted data. Publication bias was evaluated by funnel plot using Egger’s test results.</p><p>Results</p><p>From the literature search, 10 retrospective studies were collected, and of those, 5 (12,896 patients) were selected for OS analysis, 4 (981 patients) were selected for radiation pneumonitis analysis, and 4 (1339 patients) were selected for radiation oesophagitis analysis. Cox multivariate proportional hazards models revealed that 3DCRT and IMRT had similar OS (HR = 0.96, P = 0.477) but that IMRT reduced the incidence of grade 2 radiation pneumonitis (RR = 0.74, P = 0.009) and increased the incidence of grade 3 radiation oesophagitis (RR = 2.47, P = 0.000).</p><p>Conclusions</p><p>OS of IMRT for NSCLC is not inferior to that of 3DCRT, but IMRT significantly reduces the risk of radiation pneumonitis and increases the risk of radiation oesophagitis compared to 3DCRT.</p></div

Effects of Targeted Suppression of Glutaryl-CoA Dehydrogenase by Lentivirus-Mediated shRNA and Excessive Intake of Lysine on Apoptosis in Rat Striatal Neurons

<div><p></p><p>In glutaric aciduria type 1 (GA1), glutaryl-CoA dehydrogenase (GCDH) deficiency has been shown to be responsible for the accumulation of glutaric acid and striatal degeneration. However, the mechanisms by which GA1 induces striatal degeneration remain unclear. In this study, we aimed to establish a novel neuronal model of GA1 and to investigate the effects of GCDH deficiency and lysine-related metabolites on the viability of rat striatal neurons. Thus we constructed a lentiviral vector containing short hairpin RNA targeted against the GCDH gene expression (lentivirus-shRNA) in neurons. A virus containing a scrambled short hairpin RNA construct served as a control. Addition of lysine (5 mmol/L) was used to mimic hypermetabolism. Cell viability was measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide. Apoptosis was assessed using Hoechst33342 staining and Annexin V-PE/7-AAD staining. The mitochondrial membrane potential (MPP) was monitored using tetramethylrhodamine methyl ester. The expression levels of caspases 3, 8, and 9 were determined by Western blotting. We found that lentivirus-shRNA induced apoptosis and decreased MMP levels in neurons, and addition of 5 mmol/L lysine enhanced this effect markedly. Lentivirus-shRNA upregulated the protein levels of caspases 3 and 9 regardless of the presence of 5 mmol/L lysine. The expression level of caspase 8 was higher in neurons co-treated with lentivirus-shRNA and 5 mmol/L lysine than in control. Benzyloxy-carbonyl-Val-Ala-Asp(OMe)-fluoromethylketone, a pan-caspase inhibitor, blocked the apoptosis induced by lentivirus-shRNA and 5 mmol/L lysine to a great extent. These results indicate that the targeted suppression of GCDH by lentivirus-mediated shRNA and excessive intake of lysine may be a useful cell model of GA1. These also suggest that GA1-induced striatal degeneration is partially caspase-dependent.</p></div

Protein expression of caspases 3, 8, and 9.

<p>(A) NC; (B) lentivirus-shRNA#1; (C) NC +5 mmol/L lysine; and (D) lentivirus-shRNA#1+5 mmol/L lysine. *<i>P<</i>0.05. The protein levels of caspases 3 and 9 were significantly upregulated by lentivirus-shRNA#1, and this upregulation was intensified by 5 mmol/L lysine. Neither lentivirus-shRNA#1 nor 5 mmol/L lysine changed the expression of caspase 8 alone. Exposure to both conditions increased the protein level of caspase 8.</p

Meta-analysis results of grade 3–4 AEs.

<p>Meta-analysis results of grade 3–4 AEs.</p