ABSTRACT
Objective To investigate the cognitive characteristics and vascular risk factor between early onset de?pression and late onset depression in late life depression and provide a clue to elucidate the cause of cognitive impairment in late life depression. Method Fifty-six late life depression patients were recruited in our hospital, including 29 early on?set depression patients and 27 late onset depression patients. 25 controls were recruited from Guangzhou community. Cog?nitive evaluation were conducted in all the patients and controls, including MMSE, memory, attention, language, visuospa?tial abilities,executive function and Framingham vascular risk assessment, and analyze the cognitive and vascular risk be?tween the patients. Result There were statistically significant differences in overall cognitive assessment MMSE(24.8 ± 2.9,22.8±3.5,P=0.030), symbol digit modalities test(SDMT)(29.8±10.5, 22.9±11.8, P=0.028), clock drawing test(CDT) (3.6 ± 0.8, 2.9 ± 1.3, P=0.006) and trail making test(TMT) (60.4 ± 20.6, 74.7 ± 28.8, P=0.027) between late onset depression and early onset depression. In addition, the score of vascular risk assessment was significant between late onset depression and early onset depression(14.6±2.7,12.3±2.2,P=0.001). Conclusion Compare with early onset depression, late onset de?pression has much severe cognitive impairments and increased vascular risk factors.
ABSTRACT
Objective To analyze the characteristics and influencing factors of sleep disorders and nocturnal hypoxemia of patients with different degrees of obstructive sleep apnea-hypopnea syndrome (OSAHS). Methods Four hundred and twenty-five patients with snoring were scored by Epworth Sleepiness Scale ( ESS), and monitored by polysomnography (PSG). The possible correlations between sleep structure, hypoxia parameters, ESS and clinical features were analyzed and compared in those patients. Results Four hundred and twenty-five patients were divided into 4 groups according to the apnea-hypopnea index (AHI). There were 65 primary snoring patients (15.3%) and 360 OSAHS patients (84. 7% ) including 187 patients (44. 0% ) in severe OSAHS group. ESS was increased as aggravation of OSAHS. There were significant statistical differences in ESS among each group. Compared with primary snoring group, sleep efficiency, NREM1 + 2, oxygen desaturation index ( ODI), time with pulse oxygen saturation below 90% (T(SpO2 <90% ) ) were significantly higher in the OSAHS groups, and NREM3 +4, lowest pulse oxygen saturation level ( LSpO2 ) were lower. ESS was correlated positively with AHI (r= 0. 474,P <0. 01 ). They were both correlated positively with ODI, T (SpO2 <90% ) and NREM1 + 2( ESSr =0. 392, 0. 356,0. 194;AHI r = 0. 714, O. 682, 0. 365, all P < 0. 01 ), and correlated negatively with LSpO2, NREM3 + 4 ( ESS r = - 0. 414, - 0. 196; AHI r = - 0. 740, - 0. 385, both P < 0. 01 ). LSpO2, ODI and T (SpO2 < 90% ) were the primary influencing factors. Common clinical presentations and subjective symptoms were presented including daytime sleepiness, impaired memory, fatigue, dry mouth, oppressive wake and morning headache, etc. Percentage of individuals with daytime sleepiness in the severe OSAHS group was 73. 3% (137/187). These had serious impact on the patients' quality of life, leading to difficulty concentrating, poor memory and cognitive impairment. Conclusions Sleep disorders are found in the patients with different degrees of OSAHS. The excessive daytime sleepiness interrelated partly with the structure of sleep, and totally with hypoxia parameters. The more severity the patients have, the more nocturnal hypoxia, sleep disorders and higher ESS are found.
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Objective To study the association of LPL gene polymorphism with type 2 diabetes and the lipids spectrum in Uygurs. Methods Based on the case-siblings control design, the lipid spectrum of Uygur were tested by Automatic biochemical analyzer and the polymorphism of LPL gene were analyzed by RLFP with Hind Ⅲ in 62 T2DM patients, 62 IGT patients and 124 normal controls of Uygurs. Results The genotype distribution and allele frequencies of LPL gene in three groups were not statistically significant. The average of TG in H+H+group, H-H-group and H+H-group were 2.26, 1.73 and 1.80 mmol/L; Compared with the three genotypes and lipid indicators, TG content of Mutant H +H + group were higher than that in other groups. Multi-factor Logistic regression analysis showed T2DM was closely related to TG (P=0.034)and waist circumference (P=0.001). Conclusion The relation between LPL gene polymorphism by Hind Ⅲ and the risk for T2DM in Xinjiang Uygur population are no statistical relevance, LPL gene mutations may be one of the factors causing elevated levels of plasma TG.