Objectives: To identify any craniofacial morphological changes induced by a mandibular-repositioning oral appliance (MRA) and to explore the possibility of predicting the treatment response to MRA by cephalometric analysis in patients with obstructive sleep apnea (OSA). Methods: Seventy OSA patients [male/female: 63/7; age: (50.5±11.6) years; BMI: (27.6±4.6) kg/m2; AI: (34.9±21.3) episodes/hour; and oxygen saturation nadir: (66.3±16.5) %] were enrolled. MRA was fabricated individually for each patient after the consultation by a dentist. Polysomnographic (PSG) examination was repeated with MRA in place 3 months after the initiation of the MRA therapy. For cephalometric analysis, a pair of cephalograms of each patient was obtained, one with and another without MRA. Results and Conclusions: After 3 months' treatment, AI was (156±19.2) episodes/hour, significantly reduced compared with the pre-treatment average AI (34.9±21.3 episodes/hour,P<0.000 1). Oxygen saturation nadir improved from (66.3±16.5)% (pre-treatment) to (74.1±15.5)% (with MRA) (P<0.001). A reduction of AI≥50% was achieved in 42 patients. Insertion of MRA led to anterior shift of the mandible, increase in upper airway width and area and decrease in upper airway length. Those with evident retrognathia and longer anterior upper facial height were more likely to benefit from the MRA management.

Objective To analyze the prevalence and risk factors of the hyperuricemia ( HUA) in the adult population (aged≥20)in Shandong Province.Methods A cross-sectional survey was conducted among 11 234 subjects(8399 males and 2835 females)selected in a randomized, stratified study between January and December of 2012.The serum samples were collected and some biochemical indicators were assayed including serum uric acid (SUA), glucose, blood lipids, liver function and renal function .The body height , body mass and blood pressure were also measured , and the body mass index (BMI)was calculated.Multiple linear regression was used to clarify the contributions of different variables to SUA .The risk factors of HUA were analyzed using univariate and multivariate logistic regression analysis .Results The overall incidence of HUA was 15.71%,and was 18.89% in men and 6.31% in women, respectively.After age 35,the level of SUA declined with age in males.However,the opposite was true in women .Our results also indicated that drinking , obesity, hyper-triglyceridemia , hypertension , serum creatinine ( SCr ) , blood urea nitrogen ( BUN ) , alanine aminotransferase ( ALT ) , serum gamma-glutamyltransferase ( GGT ) were associated with HUA in men while hypertension , low-density lipoprotein, hyper-triglyceridemia,ALT,SCr and BUN were related to HUA in women .Conclusion HUA is prevalent in Shandong Province .Drinking,obesity,hypertension,abnormal liver and renal functions might increase the risk of HUA while changing lifestyle by decreasing alcohol consumption , adopting a proper diet and controlling hypertension and obesity might decrease the risk of HUA .

Objective:To analyze the distribution of clopidogrel metabolism-related gene variability in Kawasaki disease (KD) children with coronary artery lesions (CAL) across different age groups and the impact of genetic variability on the efficacy of clopidogrel antiplatelet therapy.Methods:A retrospective cohort study was conducted. Clinical data were collected from 46 KD children with CAL who were hospitalized in the Cardiovascular Center of Children′s Hospital of Fudan University between January 2021 and August 2022 and were treated with clopidogrel, including gender, age, body mass index, course of KD, CAL severity grade, and baseline platelet count. According to their age, the children were divided into ≥2-year-old group and <2-year-old group. Their platelet responsiveness was assessed by adenosine diphosphate-induced platelet inhibition rate (ADPi) calculated via thromboelastography, and children were categorized into high on-treatment platelet reactivity (HTPR) and normal on-treatment platelet reactivity (NTPR) groups. Genotypes of CYP2C19, PON1 and ABCB1 were detected. The t test, one-way analysis of variance and Chi-square test were used for intergroup comparison. Results:Among the 46 KD children with CAL, 34 were male and 12 were female; 37 were ≥2-year-old and 9 were <2-year-old; 25 cases were in the HTPR group and 21 cases were in the NTPR group, with 19 HTPR and 18 NTPR in the ≥2-year-old group, and 6 HTPR and 3 NTPR in the <2-year-old group. Genetic analysis showed that 92 alleles among the 46 children, with frequencies of CYP2C19*1, CYP2C19*2, CYP2C19*3, CYP2C19*17, PON1 192Q, PON1 192R, ABCB1 3435C, ABCB1 3435T at 59% (54/92), 32% (29/92), 9% (8/92), 1% (1/92), 36% (36/92), 64% (59/92), 63% (58/92) and 37% (34/92), respectively. Analysis of the impact of genotype on ADPi revealed that in children aged ≥2 years, those with CYP2C19*1/*3 genotype had significantly lower ADPi than those with CYP2C19*1/*1 genotype ((34±15)% vs. (61±29)%, t=2.18, P=0.036). There were also no significant difference in ADPi among children with PON1 192Q homozygous, PON1 192R heterozygote and PON1 192R homozygous genotypes ((40±22)% vs. (52±33)% vs. (65±27)%, F=2.17, P=0.130), or among those with ABCB1 3435C homozygous, ABCB1 3435T heterozygote and ABCB1 3435T homozygous genotypes ((55±34)% vs. (60±27)% vs. (49±24)%, F=0.33, P=0.719). In <2-year-old group, there were no significant differences in ADPi across CYP2C19*1/*1, CYP2C19*1/*2 and CYP2C19*2*2 genotypes ((40±20)% vs. (53±37)% vs. (34±16)%, F=0.37, P>0.05). There were no significant differences in ADPi across CYP2C19*1/*1 and CYP2C19*1/*3 genotypes ((44±27)% vs. (42±20)%, t=0.08, P>0.05). There were no significant differences in ADPi across PON1 192Q homozygous, PON1 192R heterozygote and PON1 192R homozygous genotypes (45% vs. (55±27)% vs. (24±5)%, F=1.83, P>0.05). There were no significant differences in ADPi across ABCB1 3435C homozygous, ABCB1 3435T heterozygote and ABCB1 3435T homozygous genotypes ((36±16)% vs. (50±35)% vs. 45%, F=0.29, P>0.05). The risk analysis of HTPR in different genotypes revealed that in children aged ≥2 years, carrying at least 1 or 2 loss-of-function alleles of CYP2C19 was a risk factor for HTPR ( OR=4.69, 10.00, 95% CI 1.11-19.83, 0.84-119.32, P=0.033, 0.046, respectively), and PON1 192R homozygosity and carrying at least one PON1 192R allele were protective factors against HTPR ( OR=0.08, 0.13, 95% CI 0.01-0.86, 0.01-1.19, P=0.019, 0.043, respectively). Conclusion:KD children aged ≥2 years carrying CYP2C19 loss-of-function alleles and PON1 192Q are more likely to develop HTPR.

BACKGROUND: Both aldehyde dehydrogenase 2 (ALDH2) rs671 polymorphism and lifestyle behaviors are involved in coronary artery disease (CAD), while the interaction between them is currently unknown. METHODS: A nested case-control study was conducted in 161 patients with CAD and 495 controls in dyslipidemia population in Yinzhou District, Ningbo, Zhejiang Province, China, in August 2013. Anthropometric data and blood samples were collected, demographic characteristics and lifestyle behaviors information were obtained by a face-to-face interview, dietary intake was assessed by a food frequency questionnaire, and genomic DNA was genotyped. RESULTS: Carriers with increasing number of A alleles had an elevated CAD risk compared with G allele carriers (adjusted OR = 1.483, 95% CI = 1.114-1.974). Carriers of rs671 A/G and A/A genotypes had a higher CAD risk than carriers of G/G genotype (adjusted OR = 1.492, 95% CI = 1.036-2.148). Similarly, individuals with rs671 A/A genotype had a higher CAD risk than individuals with A/G and G/G genotypes (adjusted OR = 2.161, 95% CI = 1.139-4.101). We found a borderline additive interaction between regular fried food intake and A/A and A/G genotypes, and a significantly additive interaction between sedentary/light physical activity and A/A and A/G genotypes. CONCLUSIONS Individuals with A/A or A/G genotypes of rs671 have a higher CAD risk, if they lack physical activity and take fried food regularly, than individuals with G/G genotypes. These findings can help to provide a guide to targeted heart health management.
Adult ; Aged ; Aged, 80 and over ; Aldehyde Dehydrogenase, Mitochondrial ; genetics ; Alleles ; Case-Control Studies ; China ; Coronary Artery Disease ; blood ; genetics ; Dyslipidemias ; blood ; genetics ; Female ; Genetic Association Studies ; Genetic Predisposition to Disease ; Genotype ; Humans ; Life Style ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Risk Factors