ABSTRACT
Objective To understand the association between peripheral leukocytes telomere length (TL) and sleep in middle-aged and old adults.Methods A total of 176 middle-aged and old adults were investigated by using the Pittsburgh Sleep Quality Index and questionnaire.TL was measured by fluorescence quantitative PCR.The correlation and regression analysis between sleep and telomere length was performed.Results TL had a mean T/S ratio of 0.995 ± 0.23.There was a negative correlation between TL and age (r=-0.241,P=0.003).With increasing age,sleep quality became worse (r=-0.230,P＜0.01),the time to fall asleep became longer (r=0.227,P＜0.01),sleep duration was shorter (r=-0.486,P＜0.01),sleep efficiency became worse (r=-0.226,P＜0.01).After controlling for the effects of gender,age,marital status,income level,residence,smoking,drinking,physical exercise and disease status,multiple linear regression analysis indicated that sleep quality (β3=0.057,P＜0.01),time to fall asleep (β =-0.046,P＜0.01),sleep duration (β3=0.086,P＜0.01) were independent influencing factors of telomere length,suggesting that the people who had better sleep quality,the shorter time to fall asleep,the longer sleep time would have longer telomere length.Conclusions Sleep is a relevant factor affecting TL in middle-aged and elderly population.Good sleep may delay aging by slowing TL.We encourage to conduct health education about the importance of sleep quality in community.
ABSTRACT
Objective To understand the association between peripheral leukocytes telomere length (TL) and sleep in middle-aged and old adults.Methods A total of 176 middle-aged and old adults were investigated by using the Pittsburgh Sleep Quality Index and questionnaire.TL was measured by fluorescence quantitative PCR.The correlation and regression analysis between sleep and telomere length was performed.Results TL had a mean T/S ratio of 0.995 ± 0.23.There was a negative correlation between TL and age (r=-0.241,P=0.003).With increasing age,sleep quality became worse (r=-0.230,P＜0.01),the time to fall asleep became longer (r=0.227,P＜0.01),sleep duration was shorter (r=-0.486,P＜0.01),sleep efficiency became worse (r=-0.226,P＜0.01).After controlling for the effects of gender,age,marital status,income level,residence,smoking,drinking,physical exercise and disease status,multiple linear regression analysis indicated that sleep quality (β3=0.057,P＜0.01),time to fall asleep (β =-0.046,P＜0.01),sleep duration (β3=0.086,P＜0.01) were independent influencing factors of telomere length,suggesting that the people who had better sleep quality,the shorter time to fall asleep,the longer sleep time would have longer telomere length.Conclusions Sleep is a relevant factor affecting TL in middle-aged and elderly population.Good sleep may delay aging by slowing TL.We encourage to conduct health education about the importance of sleep quality in community.
ABSTRACT
Objective To study the FMS-like tyrosine kinase-3 (FLT3) gene, NPM1 gene and c-kit gene mutations in acute myeloid leukemia (AML) by extracting DNA from the storage of bone marrow slides, and to investigate the relationship between the three gene mutations and clinical features in AML. Methods The bone marrow slides of 55 patients diagnosed with AML were enrolled in this study. The PCR, DNA sequencing and molecular cloning were used to detect and analyse the FLT3-ITD, NPM1 and c-kit gene mutations. Patients' remission, progression and survival time were also recorded. Results The DNA was successfully extracted from the bone marrow slides with -20 ℃ frozen storage without Wright stained, chemically fixed, and room temperature storage Wright stained discoloured by phenol ∶ chloroform ∶ isoamyl alcohol method, which can be used in PCR, direct sequencing and molecular cloning sequencing analysis. 10 of the 55 cases (18.2 %) were FLT3-ITD positive, including 9 cases with heterozygous mutations and 1 case with homozygous mutation. FLT3-ITD positive group had lower complete remission (CR) rate, shorter event-free survival (EFS) time and overall survival (OS) time than the negative group (P< 0.05). 9 of the 55 cases (16.4 %) had NPM1 heterozygous gene mutations, all belonging to type A. The EFS rate of the patients with NPM1 mutation was higher in 10 months and the OS rate was higher in 19 months (P< 0.05). 3 of 9 NPM1 mutations patients were FLT3-ITD positive. The CR rates of the four groups after initial remission induction therapy in order were NPM1+FLT3-ITD-, NPM1-FLT3-ITD-, NPM1-FLT3-ITD+, NPM1+FLT3-ITD+(P<0.05). Besides, NPM1-FLT3-ITD+was a risk factor affecting the OS (RR=1.250, P=0.005). 2 of the 55 cases (3.6 %) had c-kit gene mutations, namely mutant D816H and mutant D816V. The c-kit gene mutations were not found in patients with FLT3-ITD and NPM1 mutations. Conclusions The FLT3-ITD mutation is a poor prognosis molecular marker in AML, and NPM1 mutation is a good factor for the prognosis. NPM1-FLT3-ITD+is a risk factor affecting OS. The rate of c-kit gene mutation is low in AML, without the overlap of FLT3 and NPM1 mutations.