22 research outputs found
Isoborneol as a natural sporulation quenching agent to control <i>Aspergillus flavus</i>
In an effort to seek natural antisporulating agents used in the control of Aspergillus flavus, 54 essential oil compounds were employed to evaluate their antisporulating activity against A. flavus at the concentration of 100 μg/mL. The results indicated that isoborneol could inhibit spore production at 100 μg/mL. The light microscopy and scanning electron microscopy (SEM) observations revealed that A. flavus did not produce any conidia, vesicles, phialides and conidiophores after treatment with isoborneol at 80 μg/mL, confirming the effectiveness of isoborneol. The in vivo bioassay results demonstrated that isoborneol could prevent the peanuts from A. flavus contamination by inhibiting the sporulation when treated with isoborneol at concentrations higher than 100 μg/mL. RT-qPCR results suggested that isoborneol exerts its antisporulating activity by suppressing the fluG expression. These results proved that isoborneol could be used as a natural and safe antisporulating agent for commercial applications to control spore infections of A. flavus.</p
Additional file 1 of A patient with multiple primary malignant neoplasms with high variant allele frequencies of RB1, TP53, and TERT
Additional file 1: Fig. S1. Squamous cell carcinoma in the middle of the esophagus. The unstained area under endoscopy (A). En bloc resection of the lesion (B). Fig. S2. High-grade dysplasia of squamous epithelium on the left posterior pharyngeal wall. Intrapapillary capillary loop under NBI magnifying observation was classified as type B1 (A). En bloc resection of the lesion (B). Fig. S3. Two 1 cm isoechoic protrusions on the right wall of bladder (yellow arrows). Fig. S4. Ultrasound showed a hypoechoic mass in the posterior wall of the bladder (yellow arrow). Fig. S5. Hematoxylin-eosin staining (HE) and immunohistochemical staining (IHC) of some of the lesions. Vocal cord cancer (HE staining) (A); urothelium carcinomas of urinary bladder (HE staining) (B); urothelium carcinomas of urinary bladder (IHC with GATA antibody) (C); small cell carcinoma of urinary bladder (HE staining) (D); small cell carcinoma of urinary bladder (IHC with CgA antibody) (E); small cell carcinoma of urinary bladder (IHC with Syn antibody) (F). Fig. S6. CT image showed multiple liver metastases of SCCB
Results of overall and stratified analyses for the associations of <i>ERCC1</i> polymorphisms and risk of lung cancer<sup>**</sup>.
<p>CI, confidence interval; OR, odds ratio. The results were in bold, if the 95% CI excluded 1 or <i>P</i><0.05.</p><p><i>P</i><sup>het</sup> value of Q-test for heterogeneity test; random-effects model was used when <i>P</i><0.05 for heterogeneity test; otherwise, fixed-effects model was used. Significant results are listed in bold.</p><p>**Study by Zienolddiny <i>et al</i>. was excluded for rs11615 analysis.</p
Forest plots of lung cancer risk associated with the <i>ERCC1</i> polymorphisms.
<p>A, Forest plot of lung cancer risk associated with the <i>ERCC1</i> rs3212986 polymorphism. The plot of dominant model was shown. B, Forest plot of lung cancer risk associated with the <i>ERCC1</i> rs3212948 polymorphism. The plot of dominant model was shown. C, Forest plot of lung cancer risk associated with the <i>ERCC1</i> rs2298881 polymorphism. The plot of dominant model was shown.</p
Association Studies of <i>ERCC1</i> Polymorphisms with Lung Cancer Susceptibility: A Systematic Review and Meta-Analysis
<div><p>Background</p><p>Excision repair cross-complimentary group 1 (ERCC1) is an essential component of the nucleotide excision repair system that is responsible for repairing damaged DNA. Functional genetic variations in the <i>ERCC1</i> gene may alter DNA repair capacity and modulate cancer risk. The putative roles of <i>ERCC1</i> gene polymorphisms in lung cancer susceptibility have been widely investigated. However, the results remain controversial.</p><p>Objectives</p><p>An updated meta-analysis was conducted to explore whether lung cancer risk could be attributed to the following <i>ERCC1</i> polymorphisms: rs11615 (T>C), rs3212986 (C>A), rs3212961 (A>C), rs3212948 (G>C), rs2298881 (C>A).</p><p>Methods</p><p>Several major databases (MEDLINE, EMBASE and Scopus) and the Chinese Biomedical database were searched for eligible studies. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to measure the strength of associations.</p><p>Results</p><p>Sixteen studies with 10,106 cases and 13,238 controls were included in this meta-analysis. Pooled ORs from 11 eligible studies (8,215 cases vs. 11,402 controls) suggested a significant association of <i>ERCC1</i> rs11615 with increased risk for lung cancer (homozygous: CC versus TT, OR = 1.24, 95% CI: 1.04–1.48, <i>P</i> = 0.02). However, such an association was disproportionately driven by a single study. Removal of that study led to null association. Moreover, initial analyses suggested that <i>ERCC1</i> rs11615 exerts a more profound effect on the susceptibility of non-smokers to lung cancer than that of smokers. Moreover, no statistically significant association was found between remaining <i>ERCC1</i> polymorphisms of interest and lung cancer risk, except for rs3212948 variation (heterozygous: CG vs.GG, OR = 0.78, 95% CI: 0.67–0.90, <i>P</i> = 0.001; dominant: CG/CC vs.GG, OR = 0.79, 95% CI: 0.69–0.91, <i>P = </i>0.001).</p><p>Conclusion</p><p>Overall, this meta-analysis suggests that <i>ERCC1</i> rs3212948 G>C, but not others, is a lung cancer risk-associated polymorphism. Carefully designed studies with large sample size involving different ethnicity, smoking status, and cancer types are needed to validate these findings.</p></div
Forest plots of lung cancer risk associated with the <i>ERCC1</i> polymorphism.
<p>A, Forest plot of risk of lung cancer associated with the <i>ERCC1</i> rs11615 polymorphism by a homozygous model. B,Forest plot of lung cancer risk associated with the <i>ERCC1</i> rs11615 polymorphism in the stratified analyses by smoking status. The plots of heterozygous model were shown. SMK, smoker; NSMK, non-smoker. The estimate of OR and its 95% CI are plotted with a box and a horizontal line for each study; â—Š represents pooled ORs and its 95% CIs.</p
<i>ERCC1</i> mRNA expression by the genotypes of <i>ERCC1</i> rs11615 and rs3212986 polymorphisms.
<p><i>ERCC1</i> mRNA expression by the genotypes of <i>ERCC1</i> rs11615 and rs3212986 polymorphisms.</p
Flow diagram of included studies for the associations between <i>ERCC1</i> polymorphisms and lung cancer risk.
<p>Flow diagram of included studies for the associations between <i>ERCC1</i> polymorphisms and lung cancer risk.</p
Funnel plots of Begg's were used to detect publication bias on <i>ERCC1</i> rs11615 (recessive model) and <i>ERCC1</i> rs3212986 polymorphisms (homozygous model).
<p>No significant publication bias was found. Each point represents a separate study for the indicated association. Size of each point is proportional to its weight.</p
Characteristics of studies that explored the association between <i>ERCC1</i> polymorphisms and lung cancer risk.
<p>AC, adenocarcinoma; HB, Hospital based; NSCLC, non small cell lung cancer; PB, Population based; PCR-RFLP, Polymerase chain reaction-restriction fragment length polymorphism; LDR-PCR, ligase detection reaction coupled with PCR; MAF, Minor allele frequency; HWE, Hardy-Weinberg equilibrium.</p><p>*mixed: small cell lung cancer, non-small cell lung cancer (adenocarcinoma, squamous carcinoma, large-cell carcinoma, etc.)</p