Inflammation plays a significant role in the etiology of type 2 diabetes mellitus(T2DM).The rise in the pro-inflammatory cytokines is the essential step in glucotoxicity and lipotoxicity induced mitochondrial injury,o...Inflammation plays a significant role in the etiology of type 2 diabetes mellitus(T2DM).The rise in the pro-inflammatory cytokines is the essential step in glucotoxicity and lipotoxicity induced mitochondrial injury,oxidative stress and beta cell apoptosis in T2 DM.Among the recognized markers are interleukin(IL)-6,IL-1,IL-10,IL-18,tissue necrosis factor-alpha(TNF-α),C-reactive protein,resistin,adiponectin,tissue plasminogen activator,fibrinogen and heptoglobins.Diabetes mellitus has firm genetic and very strong environmental influence; exhibiting a polygenic mode of inheritance.Many single nucleotide polymorphisms(SNPs) in various genes including those of pro and antiinflammatory cytokines have been reported as a risk for T2 DM.Not all the SNPs have been confirmed by unifying results in different studies and wide variations have been reported in various ethnic groups.The inter-ethnic variations can be explained by the fact that gene expression may be regulated by gene-gene,gene-environment and gene-nutrient interactions.This review highlights the impact of these interactions on determining the role of single nucleotide polymorphism of IL-6,TNF-α,resistin and adiponectin in pathogenesis of T2 DM.展开更多
As genetic factors can hardly explain the changes taking place during short time spans, environmental and lifestyle-related factors have been suggested as the causes of time-related deterioration of male reproductive ...As genetic factors can hardly explain the changes taking place during short time spans, environmental and lifestyle-related factors have been suggested as the causes of time-related deterioration of male reproductive function. However, considering the strong heterogeneity of male fecundity between and within populations, genetic variants might be important determinants of the individual susceptibility to the adverse effects of environment or lifestyle. Although the possible mechanisms of such interplay in relation to the reproductive system are largely unknown, some recent studies have indicated that specific genotypes may confer a larger risk of male reproductive disorders following certain exposures. This paper presents a critical review of animal and human evidence on how genes may modify environmental effects on male reproductive function. Some examples have been found that support this mechanism, but the number of studies is still limited. This type of interaction studies may improve our understanding of normal physiology and help us to identify the risk factors to male reproductive malfunction. We also shortly discuss other aspects of gene-environment interaction specifically associated with the issue of reproduction, namely environmental and lifestyle factors as the cause of sperm DNA damage. It remains to be investigated to what extent such genetic changes, by natural conception or through the use of assisted reproductive techniques, are transmitted to the next generation, thereby causing increased morbidity in the offspring.展开更多
Styrene and ethylbenzene(S/EB)are identified as hazardous air contaminants that raise significant concerns.The association between S/EB exposure and the incidence of type 2 diabetes mellitus(T2DM),and the interaction ...Styrene and ethylbenzene(S/EB)are identified as hazardous air contaminants that raise significant concerns.The association between S/EB exposure and the incidence of type 2 diabetes mellitus(T2DM),and the interaction between genes and environment,remains poorly understood.Our study consisted of 2219 Chinese adults who were part of the Wuhan-Zhuhai cohort.A follow-up assessment was conducted after six years.Exposure to S/EB was quantified by determining the concentrations of urinary biomarkers of exposure to S/EB(UBE-S/EB;urinary phenylglyoxylic acid level plus urinary mandelic acid level).Logistic regression models were constructed to investigate the relations of UBE-S/EB and genetic risk score(GRS)with T2DM prevalence and incidence.The interaction effects of UBE-S/EB and GRS on T2DM were investigated on multiplicative and additive scales.UBE-S/EB was dose-dependently and positively related to T2DM prevalence and incidence.Participants with high levels of UBE-S/EB[relative risk(RR)=1.930,95%confidence interval(CI):1.157-3.309]or GRS(1.943,1.110-3.462)demonstrated the highest risk of incident T2DM,in comparison to those with low levels of UBE-S/EB or GRS.Significant additive interaction between UBE-S/EB and GRS on T2DM incidence was discovered with relative excess risk due to interaction(95%CI)of 0.178(0.065-0.292).The RR(95%CI)of T2DM incidence was 2.602(1.238-6.140)for individuals with high UBE-S/EB and high GRS,compared to those with low UBE-S/EB and low GRS.This study presented the initial evidence that S/EB exposure was significantly related to increased risk of T2DM incidence,and the relationship was interactively aggravated by genetic predisposition.展开更多
Attention-deficit/hyperactivity disorder(ADHD)is increasingly conceptualized as a dynamic neurodevelopmental condition,marked by fluctuating symptom trajectories across development rather than the traditional static p...Attention-deficit/hyperactivity disorder(ADHD)is increasingly conceptualized as a dynamic neurodevelopmental condition,marked by fluctuating symptom trajectories across development rather than the traditional static patterns of persistence or remission.This review synthesizes empirical evidence on the varied trajectories of ADHD symptoms-including late-onset,partial remission,and recurrent fluctuation patterns-and underscores their clinical significance in longterm functioning.We adopt a multifactorial framework to explore how genetic,environmental,and gene–environment interactions contribute to the emergence and evolution of ADHD symptoms over time.In addition,we consider how medication-related variables-particularly tolerance and adherence-may influence symptom fluctuation.Characterizing these developmental dynamics offers critical guidance for designing flexible,personalized interventions that align with individual trajectories and transitional vulnerabilities.展开更多
目的了解西安市非小细胞肺癌(non-smal cel lung cancer,NSCLC)患者驱动基因突变情况,分析其与环境暴露因素的关联性。方法纳入2019年1月至2023年12月空军军医大学第一附属医院收治的305例NSCLC患者,观察其驱动基因突变情况,分析其与环...目的了解西安市非小细胞肺癌(non-smal cel lung cancer,NSCLC)患者驱动基因突变情况,分析其与环境暴露因素的关联性。方法纳入2019年1月至2023年12月空军军医大学第一附属医院收治的305例NSCLC患者,观察其驱动基因突变情况,分析其与环境暴露因素的关系。结果305例患者驱动基因突变率为46.89%,以EGFR基因突变占比最高,同时检出4例基因共突变;不同单驱动基因突变患者在性别上存在差异(P<0.05),EGFR以女性占比明显较高(P<0.05);单因素分析显示:驱动基因突变与非驱动基因突变患者在家族史、吸烟史、长期烹饪史、煎炸烟熏食物摄取间比较差异有统计学意义(P<0.05);logistic回归分析显示:长期烹饪史(OR=2.392)、煎炸烟熏食物摄取(OR=2.849)是影响EGFR基因突变环境暴露因素(P<0.05),有吸烟史(OR=1.377)是KRAS基因突变环境暴露因素(P<0.05)。结论西安市NSCLC患者以EGFR基因突变占比最高,且以女性为主,长期烹饪史、煎炸烟熏食物摄取与EGFR基因突变有关,有吸烟史与KRAS基因突变有一定的关联性。展开更多
文摘Inflammation plays a significant role in the etiology of type 2 diabetes mellitus(T2DM).The rise in the pro-inflammatory cytokines is the essential step in glucotoxicity and lipotoxicity induced mitochondrial injury,oxidative stress and beta cell apoptosis in T2 DM.Among the recognized markers are interleukin(IL)-6,IL-1,IL-10,IL-18,tissue necrosis factor-alpha(TNF-α),C-reactive protein,resistin,adiponectin,tissue plasminogen activator,fibrinogen and heptoglobins.Diabetes mellitus has firm genetic and very strong environmental influence; exhibiting a polygenic mode of inheritance.Many single nucleotide polymorphisms(SNPs) in various genes including those of pro and antiinflammatory cytokines have been reported as a risk for T2 DM.Not all the SNPs have been confirmed by unifying results in different studies and wide variations have been reported in various ethnic groups.The inter-ethnic variations can be explained by the fact that gene expression may be regulated by gene-gene,gene-environment and gene-nutrient interactions.This review highlights the impact of these interactions on determining the role of single nucleotide polymorphism of IL-6,TNF-α,resistin and adiponectin in pathogenesis of T2 DM.
文摘As genetic factors can hardly explain the changes taking place during short time spans, environmental and lifestyle-related factors have been suggested as the causes of time-related deterioration of male reproductive function. However, considering the strong heterogeneity of male fecundity between and within populations, genetic variants might be important determinants of the individual susceptibility to the adverse effects of environment or lifestyle. Although the possible mechanisms of such interplay in relation to the reproductive system are largely unknown, some recent studies have indicated that specific genotypes may confer a larger risk of male reproductive disorders following certain exposures. This paper presents a critical review of animal and human evidence on how genes may modify environmental effects on male reproductive function. Some examples have been found that support this mechanism, but the number of studies is still limited. This type of interaction studies may improve our understanding of normal physiology and help us to identify the risk factors to male reproductive malfunction. We also shortly discuss other aspects of gene-environment interaction specifically associated with the issue of reproduction, namely environmental and lifestyle factors as the cause of sperm DNA damage. It remains to be investigated to what extent such genetic changes, by natural conception or through the use of assisted reproductive techniques, are transmitted to the next generation, thereby causing increased morbidity in the offspring.
基金supported by National Natural Science Foundation of China (82241088,82203996).
文摘Styrene and ethylbenzene(S/EB)are identified as hazardous air contaminants that raise significant concerns.The association between S/EB exposure and the incidence of type 2 diabetes mellitus(T2DM),and the interaction between genes and environment,remains poorly understood.Our study consisted of 2219 Chinese adults who were part of the Wuhan-Zhuhai cohort.A follow-up assessment was conducted after six years.Exposure to S/EB was quantified by determining the concentrations of urinary biomarkers of exposure to S/EB(UBE-S/EB;urinary phenylglyoxylic acid level plus urinary mandelic acid level).Logistic regression models were constructed to investigate the relations of UBE-S/EB and genetic risk score(GRS)with T2DM prevalence and incidence.The interaction effects of UBE-S/EB and GRS on T2DM were investigated on multiplicative and additive scales.UBE-S/EB was dose-dependently and positively related to T2DM prevalence and incidence.Participants with high levels of UBE-S/EB[relative risk(RR)=1.930,95%confidence interval(CI):1.157-3.309]or GRS(1.943,1.110-3.462)demonstrated the highest risk of incident T2DM,in comparison to those with low levels of UBE-S/EB or GRS.Significant additive interaction between UBE-S/EB and GRS on T2DM incidence was discovered with relative excess risk due to interaction(95%CI)of 0.178(0.065-0.292).The RR(95%CI)of T2DM incidence was 2.602(1.238-6.140)for individuals with high UBE-S/EB and high GRS,compared to those with low UBE-S/EB and low GRS.This study presented the initial evidence that S/EB exposure was significantly related to increased risk of T2DM incidence,and the relationship was interactively aggravated by genetic predisposition.
基金Supported by the Shenzhen Science and Technology Program,No.RCYX20221008092849069The Guangdong High-Level Hospital Construction Fund.
文摘Attention-deficit/hyperactivity disorder(ADHD)is increasingly conceptualized as a dynamic neurodevelopmental condition,marked by fluctuating symptom trajectories across development rather than the traditional static patterns of persistence or remission.This review synthesizes empirical evidence on the varied trajectories of ADHD symptoms-including late-onset,partial remission,and recurrent fluctuation patterns-and underscores their clinical significance in longterm functioning.We adopt a multifactorial framework to explore how genetic,environmental,and gene–environment interactions contribute to the emergence and evolution of ADHD symptoms over time.In addition,we consider how medication-related variables-particularly tolerance and adherence-may influence symptom fluctuation.Characterizing these developmental dynamics offers critical guidance for designing flexible,personalized interventions that align with individual trajectories and transitional vulnerabilities.
文摘目的了解西安市非小细胞肺癌(non-smal cel lung cancer,NSCLC)患者驱动基因突变情况,分析其与环境暴露因素的关联性。方法纳入2019年1月至2023年12月空军军医大学第一附属医院收治的305例NSCLC患者,观察其驱动基因突变情况,分析其与环境暴露因素的关系。结果305例患者驱动基因突变率为46.89%,以EGFR基因突变占比最高,同时检出4例基因共突变;不同单驱动基因突变患者在性别上存在差异(P<0.05),EGFR以女性占比明显较高(P<0.05);单因素分析显示:驱动基因突变与非驱动基因突变患者在家族史、吸烟史、长期烹饪史、煎炸烟熏食物摄取间比较差异有统计学意义(P<0.05);logistic回归分析显示:长期烹饪史(OR=2.392)、煎炸烟熏食物摄取(OR=2.849)是影响EGFR基因突变环境暴露因素(P<0.05),有吸烟史(OR=1.377)是KRAS基因突变环境暴露因素(P<0.05)。结论西安市NSCLC患者以EGFR基因突变占比最高,且以女性为主,长期烹饪史、煎炸烟熏食物摄取与EGFR基因突变有关,有吸烟史与KRAS基因突变有一定的关联性。
