The present work was undertaken to study in hairdressers exposed to several irritants and allergens (prevalently hairdyeing) and affected by hand contact dermatitis the possible correlation between exposure and direct...The present work was undertaken to study in hairdressers exposed to several irritants and allergens (prevalently hairdyeing) and affected by hand contact dermatitis the possible correlation between exposure and direct- oxidative DNA damage, production of tumour necrosis factor alpha (TNFα ) and allergic inflammatory disease. We evaluated in 19 hairdressers with hand contact dermatitis, 14 allergic contact dermatitis (ACD) and 5 irritant contact dermatitis (ICD) and in a selected control group TNFα serum levels by ELISA and direct- oxidative DNA damage by Fpg (formamido- pyrimidine glycosylase) modified Comet test on blood. Hairdressers were divided on the basis of number of hair- dyeing carried out weekly into 2 groups: low- exposure (<60 hair- dyeing/week) and highexposure hairdressers (≥ 60 hair- dyeing/week) that reflect also the exposure to other allergens and irritants and 2 different tasks (hairdressers and apprentice hairdressers, respectively). Serum levels of TNFα in hairdressers with ACD were significantly higher than controls with a correlation to exposure level. Significant DNA damage in ICD hairdressers with higher exposure as compared to controls was found. These findings suggest that occupational exposure can induce in hairdressers, particularly ICD, DNA damage, increase the TNFa levels particularly in ACD and induce allergic sensitization, suggesting a relationship between direct- oxidativeDNA damage, TNFα production and allergic inflammatory disease.展开更多
AIM：To investigate the association of variations in the cyclooxygenase-2 （COX2） and uridine diphosphate glucuronosyltransferase 1A6 （UGTIA6） genes and non-steroidal anti-inflammatory drugs （NSAIDs） use with ris...AIM：To investigate the association of variations in the cyclooxygenase-2 （COX2） and uridine diphosphate glucuronosyltransferase 1A6 （UGTIA6） genes and non-steroidal anti-inflammatory drugs （NSAIDs） use with risk of colon cancer.METHODS： NSAIDs, which are known to reduce the risk of colon cancer, act directly on COX2 and reduce its activity. Epidemiological studies have associated variations in the COX2 gene with colon cancer risk, but others were unable to replicate this finding. Similarly,enzymes in the UGT1A6 gene have been demonstrated to modify the therapeutic effect of NSAIDs on colon adenomas. Polymorphisms in the UGTIA6 gene have been statistically shown to interact with NSAID intake to influence risk of developing colon adenomas, but not colon cancer. Here we examined the association of tagging single nucleotide polymorphisms （SNPs） in the COX2 and UGTIA6 genes, and their interaction with NSAID consumption, on risk of colon cancer in a population of 422 colon cancer cases and 481 population controls.RESULTS： No SNP in either gene was individually statistically significantly associated with colon cancer, nor did they statistically significantly change the protective effect of NSAID consumption in our sample. Like others, we were unable to replicate the association of variants in the COX2 gene with colon cancer risk （P 〉 0.05）,and we did not observe that these variants modify the protective effect of NSAIDs （P 〉 0.05）. We were able to confirm the lack of association of variants in UGT1A6 with colon cancer risk, although further studies will have to be conducted to confirm the association of these variants with colon adenomas.CONCLUSION： Our study does not support a role of COX2 and UGTIA6 genetic variations in the development of colon cancer.展开更多
The mechanisms for fine-tuning ABA level related to grape berry ripening remain elusive. Here, transcription analysis showed that the mRNA expression level of 9-cis-epoxycarotenoid dioxygenase gene （VvNCED1） increas...The mechanisms for fine-tuning ABA level related to grape berry ripening remain elusive. Here, transcription analysis showed that the mRNA expression level of 9-cis-epoxycarotenoid dioxygenase gene （VvNCED1） increases first, rapidly in mesocarp before the onset of grape berry ripening. After VvNCED1 peaks its expression level, ABA content increases rapidly in mesocarp coupled with an increase in both soluble sugar content and pH value. On the onset of berry ripening, VvNCED1 transcripts decline rapidly to its lowest point, then increases slightly. Whereas, the mRNA expression level of B-glucosidase gene VvBGI, on the whole, increases constantly during grape berry ripening. During berry de-greening, ABA glucosyltransferase （VvGT） and ABA 8＇-hydroxylase （VvCYPI） equilibrate ABA level; during berry coloring-up, VvGT predominantly equilibrates ABA level, namely, the up-regulation of ABA level mainly leads from VvNCED1 and VvBG1 gene high expression; the down-regulation of ABA level leads mainly from VvCYP! transcript level both in ABA content- and developmental phase-dependence manner. In conclusion, our main results show that VvNCED1 and VvBG1 genes are closely related to grape berry ripening.展开更多
Cdgler-Najjar syndrome type Ⅰ （CN-I） is the most severe type of hereditary unconjugated hyperbilirubinemia. It is caused by homozygous or compound heterozygous mutations of the UDP-glycuronosyltransferase gene （UG...Cdgler-Najjar syndrome type Ⅰ （CN-I） is the most severe type of hereditary unconjugated hyperbilirubinemia. It is caused by homozygous or compound heterozygous mutations of the UDP-glycuronosyltransferase gene （UGT1A1） on chromosome 2q37. Two patients clinically diagnosed with CN-I were examined in this paper. We sequenced five exons and their flanking sequences, specifically the promoter region of UGT1A 1, of the two patients and their parents. Quantitative real-time polymerase chain reaction （qRT-PCR） was used to determine the UGT1A1 gene copy number of one patient. In patient A, two mutations, c.239_245delCTGTGCC （p.Pro80HisfsX6; had not been reported previously） and c.1156G〉T （p.Va1386Phe）, were identified. In patient B, we found that this patient had lost heterozygosity of the UGTIA1 gene by inheriting a deletion of one allele, and had a novel mutation c.1253delT （p.Met418ArgfsX5） in the other allele. In summary, we detected three UGTIA 1 mutations in two CN-I patients： c.239_ 245delCTGTGCC （p.Pro80HisfsX6）, c.1253delT （p.MeH18ArgfsX5）, and c.1156G〉T （p.Va1386Phe）. The former two mutations are pathogenic; however, the pathogenic mechanism of c.1156G〉T （p.Va1386Phe） is unknown.展开更多
文摘The present work was undertaken to study in hairdressers exposed to several irritants and allergens (prevalently hairdyeing) and affected by hand contact dermatitis the possible correlation between exposure and direct- oxidative DNA damage, production of tumour necrosis factor alpha (TNFα ) and allergic inflammatory disease. We evaluated in 19 hairdressers with hand contact dermatitis, 14 allergic contact dermatitis (ACD) and 5 irritant contact dermatitis (ICD) and in a selected control group TNFα serum levels by ELISA and direct- oxidative DNA damage by Fpg (formamido- pyrimidine glycosylase) modified Comet test on blood. Hairdressers were divided on the basis of number of hair- dyeing carried out weekly into 2 groups: low- exposure (<60 hair- dyeing/week) and highexposure hairdressers (≥ 60 hair- dyeing/week) that reflect also the exposure to other allergens and irritants and 2 different tasks (hairdressers and apprentice hairdressers, respectively). Serum levels of TNFα in hairdressers with ACD were significantly higher than controls with a correlation to exposure level. Significant DNA damage in ICD hairdressers with higher exposure as compared to controls was found. These findings suggest that occupational exposure can induce in hairdressers, particularly ICD, DNA damage, increase the TNFa levels particularly in ACD and induce allergic sensitization, suggesting a relationship between direct- oxidativeDNA damage, TNFα production and allergic inflammatory disease.
基金Supported by A Damon Runyon Cancer Research Foundation Clinical Investigator Award,CI-8An R25 training grant from the National Cancer Institute,R25T CA094186+1 种基金The Case Center for Transdisciplinary Research on Energetics and Cancer,1U54 CA-116867-01A National Cancer Institute K22 Award,1K22 CA120545-01
文摘AIM：To investigate the association of variations in the cyclooxygenase-2 （COX2） and uridine diphosphate glucuronosyltransferase 1A6 （UGTIA6） genes and non-steroidal anti-inflammatory drugs （NSAIDs） use with risk of colon cancer.METHODS： NSAIDs, which are known to reduce the risk of colon cancer, act directly on COX2 and reduce its activity. Epidemiological studies have associated variations in the COX2 gene with colon cancer risk, but others were unable to replicate this finding. Similarly,enzymes in the UGT1A6 gene have been demonstrated to modify the therapeutic effect of NSAIDs on colon adenomas. Polymorphisms in the UGTIA6 gene have been statistically shown to interact with NSAID intake to influence risk of developing colon adenomas, but not colon cancer. Here we examined the association of tagging single nucleotide polymorphisms （SNPs） in the COX2 and UGTIA6 genes, and their interaction with NSAID consumption, on risk of colon cancer in a population of 422 colon cancer cases and 481 population controls.RESULTS： No SNP in either gene was individually statistically significantly associated with colon cancer, nor did they statistically significantly change the protective effect of NSAID consumption in our sample. Like others, we were unable to replicate the association of variants in the COX2 gene with colon cancer risk （P 〉 0.05）,and we did not observe that these variants modify the protective effect of NSAIDs （P 〉 0.05）. We were able to confirm the lack of association of variants in UGT1A6 with colon cancer risk, although further studies will have to be conducted to confirm the association of these variants with colon adenomas.CONCLUSION： Our study does not support a role of COX2 and UGTIA6 genetic variations in the development of colon cancer.
基金This study is supported by China National Nattu-al Science Foundation （Project 31040006） and Beijing Natural Science Foundation and Scientific Research Key Program of Beijing Commission of Education （NO. KZ200910020001）.
文摘The mechanisms for fine-tuning ABA level related to grape berry ripening remain elusive. Here, transcription analysis showed that the mRNA expression level of 9-cis-epoxycarotenoid dioxygenase gene （VvNCED1） increases first, rapidly in mesocarp before the onset of grape berry ripening. After VvNCED1 peaks its expression level, ABA content increases rapidly in mesocarp coupled with an increase in both soluble sugar content and pH value. On the onset of berry ripening, VvNCED1 transcripts decline rapidly to its lowest point, then increases slightly. Whereas, the mRNA expression level of B-glucosidase gene VvBGI, on the whole, increases constantly during grape berry ripening. During berry de-greening, ABA glucosyltransferase （VvGT） and ABA 8＇-hydroxylase （VvCYPI） equilibrate ABA level; during berry coloring-up, VvGT predominantly equilibrates ABA level, namely, the up-regulation of ABA level mainly leads from VvNCED1 and VvBG1 gene high expression; the down-regulation of ABA level leads mainly from VvCYP! transcript level both in ABA content- and developmental phase-dependence manner. In conclusion, our main results show that VvNCED1 and VvBG1 genes are closely related to grape berry ripening.
文摘Cdgler-Najjar syndrome type Ⅰ （CN-I） is the most severe type of hereditary unconjugated hyperbilirubinemia. It is caused by homozygous or compound heterozygous mutations of the UDP-glycuronosyltransferase gene （UGT1A1） on chromosome 2q37. Two patients clinically diagnosed with CN-I were examined in this paper. We sequenced five exons and their flanking sequences, specifically the promoter region of UGT1A 1, of the two patients and their parents. Quantitative real-time polymerase chain reaction （qRT-PCR） was used to determine the UGT1A1 gene copy number of one patient. In patient A, two mutations, c.239_245delCTGTGCC （p.Pro80HisfsX6; had not been reported previously） and c.1156G〉T （p.Va1386Phe）, were identified. In patient B, we found that this patient had lost heterozygosity of the UGTIA1 gene by inheriting a deletion of one allele, and had a novel mutation c.1253delT （p.Met418ArgfsX5） in the other allele. In summary, we detected three UGTIA 1 mutations in two CN-I patients： c.239_ 245delCTGTGCC （p.Pro80HisfsX6）, c.1253delT （p.MeH18ArgfsX5）, and c.1156G〉T （p.Va1386Phe）. The former two mutations are pathogenic; however, the pathogenic mechanism of c.1156G〉T （p.Va1386Phe） is unknown.
