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1.  Primary Care Physicians’ Attitudes and Beliefs towards Chronic Low Back Pain: An Asian Study 
PLoS ONE  2015;10(1):e0117521.
Chronic low back pain is a serious global health problem. There is substantial evidence that physicians’ attitudes towards and beliefs about chronic low back pain can influence their subsequent management of the condition.
(1) to evaluate the attitudes and beliefs towards chronic low back pain among primary care physicians in Asia; (2) to study the cultural differences and other factors that are associated with these attitudes and beliefs.
A cross sectional online survey was sent to primary care physicians who are members of the Hong Kong College of Family Physician (HKCFP). The Pain Attitudes and Beliefs Scale for Physiotherapist (PABS-PT) was used as the questionnaire to determine the biomedical and biopsychosocial orientation of the participants.
The mean Biomedical (BM) score was 34.8+/-6.1; the mean biopsychosocial (BPS) score was 35.6 (+/- 4.8). Both scores were higher than those of European doctors. Family medicine specialists had a lower biomedical score than General practitioners. Physicians working in the public sector tended to have low BM and low BPS scores; whereas physicians working in private practice tended to have high BM and high BPS scores.
The lack of concordance in the pain explanatory models used by private and public sector may have a detrimental effect on patients who are under the care of both parties. The uncertain treatment orientation may have a negative influence on patients’ attitudes and beliefs, thus contributing to the tension and, perhaps, even ailing mental state of a person with chronic LBP.
PMCID: PMC4311983  PMID: 25635919
2.  The Role of Circulating Serotonin in the Development of Chronic Obstructive Pulmonary Disease 
PLoS ONE  2012;7(2):e31617.
Cigarette smoking is a major risk factor in the development of age-related chronic obstructive pulmonary disease (COPD). The serotonin transporter (SERT) gene polymorphism has been reported to be associated with COPD, and the degree of cigarette smoking has been shown to be a significant mediator in this relationship. The interrelation between circulating serotonin (5-hydroxytyptamine, 5-HT), cigarette smoking and COPD is however largely unknown. The current study aimed at investigating the mediation effects of plasma 5-HT on cigarette smoking-induced COPD and the relation between plasma 5-HT levels and age.
The association between plasma 5-HT, age and COPD was analyzed in a total of 62 COPD patients (ever-smokers) and 117 control subjects (healthy non-smokers and ever-smokers). Plasma 5-HT levels were measured by enzyme-linked immuno assay (EIA).
The elevated plasma 5-HT levels were significantly associated with increased odds for COPD (OR = 1.221, 95% CI = 1.123 to 1.319, p<0.0001). The effect remained significant after being adjusted for age and pack-years smoked (OR = 1.271, 95% CI = 1.134 to 1.408, p = 0.0003). Furthermore, plasma 5-HT was found to mediate the relation between pack-years smoked and COPD. A positive correlation (r = 0.303, p = 0.017) was found between plasma 5-HT levels and age in COPD, but not in the control subjects (r = −0.149, p = 0.108).
Our results suggest that cigarette smoke-induced COPD is partially mediated by the plasma levels of 5-HT, and that these become elevated with increased age in COPD. The elevated plasma 5-HT levels in COPD might contribute to the pathogenesis of this disease.
PMCID: PMC3272036  PMID: 22319639
3.  Estimating the Total Number of Susceptibility Variants Underlying Complex Diseases from Genome-Wide Association Studies 
PLoS ONE  2010;5(11):e13898.
Recently genome-wide association studies (GWAS) have identified numerous susceptibility variants for complex diseases. In this study we proposed several approaches to estimate the total number of variants underlying these diseases. We assume that the variance explained by genetic markers (Vg) follow an exponential distribution, which is justified by previous studies on theories of adaptation. Our aim is to fit the observed distribution of Vg from GWAS to its theoretical distribution. The number of variants is obtained by the heritability divided by the estimated mean of the exponential distribution. In practice, due to limited sample sizes, there is insufficient power to detect variants with small effects. Therefore the power was taken into account in fitting. Besides considering the most significant variants, we also tried to relax the significance threshold, allowing more markers to be fitted. The effects of false positive variants were removed by considering the local false discovery rates. In addition, we developed an alternative approach by directly fitting the z-statistics from GWAS to its theoretical distribution. In all cases, the “winner's curse” effect was corrected analytically. Confidence intervals were also derived. Simulations were performed to compare and verify the performance of different estimators (which incorporates various means of winner's curse correction) and the coverage of the proposed analytic confidence intervals. Our methodology only requires summary statistics and is able to handle both binary and continuous traits. Finally we applied the methods to a few real disease examples (lipid traits, type 2 diabetes and Crohn's disease) and estimated that hundreds to nearly a thousand variants underlie these traits.
PMCID: PMC2984437  PMID: 21103334

Results 1-3 (3)