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Background Gout stems from both modifiable and genetic sources. We evaluated the risk of gout among Taiwanese adults with aldehyde dehydrogenase-2 (ALDH2) rs671 single nucleotide polymorphism (SNP) according to body mass index (BMI) and alcohol drinking. Methods We obtained information of 9253 individuals having no personal history of cancer from the Taiwan Biobank (2008–2016) and estimated the association between gout and independent variables (e.g., rs671, BMI, and alcohol drinking) using multiple logistic regression. Results Alcohol drinking and abnormal BMI were associated with a higher risk of gout whereas the rs671 GA+AA genotype was associated with a lower risk. The odds ratios (ORs) and 95% confidence intervals (CIs) were 1.297 and 1.098–1.532 for alcohol drinking, 1.550 and 1.368–1.755 for abnormal BMI, and 0.887 and 0.800–0.984 for GA+AA. The interaction between BMI and alcohol on gout was significant for GG (p-value = 0.0102) and GA+AA (p-value = 0.0175). When we stratified genotypes by BMI, alcohol drinking was significantly associated with gout only among individuals with a normal BMI (OR; 95% CI = 1.533; 1.036–2.269 for GG and 2.109; 1.202–3.699 for GA+AA). Concerning the combination of BMI and alcohol drinking among participants stratified by genotypes (reference, GG genotype, normal BMI, and no alcohol drinking), the risk of gout was significantly higher in the following categories: GG, normal BMI, and alcohol drinking (OR, 95% CI = 1.929, 1.385–2.688); GG, abnormal BMI, and no alcohol drinking (OR, 95% CI, = 1.721, 1.442–2.052); GG, abnormal BMI, and alcohol drinking (OR, 95% CI = 1.941, 1.501–2.511); GA+AA, normal BMI, and alcohol drinking (OR, 95% CI = 1.971, 1.167–3.327); GA+AA, abnormal BMI, and no alcohol drinking (OR, 95% CI = 1.498, 1.256–1.586); and GA+AA, abnormal BMI, and alcohol drinking (OR, 95% CI = 1.545, 1.088–2.194). Conclusions Alcohol and abnormal BMI were associated with a higher risk of gout, whereas the rs671 GA+AA genotype was associated with a lower risk. Noteworthy, BMI and alcohol had a significant interaction on gout risk. Stratified analyses revealed that alcohol drinking especially among normal-weight individuals might elevate the risk of gout irrespective of the genotype.

Background Hypertension increases the likelihood of cardiovascular diseases (CVDs). Cytochrome P450 1A2 (CYP1A2) single nucleotide polymorphism (SNP) is related to caffeine metabolism and the risk of CVD among coffee drinkers. CYP1A2 rs762551 influenced the risk of stroke among hypertensive patients. We examined the relationship between hypertension and coffee drinking based on CYP1A2 rs762551 SNP in Taiwanese adults. Methods We used data contained in the Taiwan Biobank database (2011–2018) and included 19,133 participants having complete information on hypertension, rs762551 polymorphism, coffee intake, etc. The risk of hypertension was determined using multiple logistic regression. Results Coffee intake was significantly associated with a lower risk of hypertension. The odds ratio (OR), 95% confidence interval (CI), and p-value were 0.877, 0.807–0.954, and 0.0032, respectively. CYP1A2 rs762551 was not significantly associated with the risk of hypertension, but it had a significant interactive association with coffee drinking (p value = 0.0303). After stratification by rs762551 genotypes, the inverse coffee drinking-hypertension association was retained, but significant results were observed only in those with the AC + CC genotype (OR 0.678, 95% CI 0.722–900, p value = 0.0001). According to the combination of coffee drinking and rs762551 genotypes (reference group: no coffee drinking and rs762551 AA), the coffee drinking-AC + CC group had a lower risk of hypertension (OR 0.888, 95% CI 0.789–0.999, p value = 0.0483). Conclusion Coffee drinking, particularly among individuals with the CYP1A2 rs762551 AC + CC genotype was associated with lower odds of hypertension.

The phenol nerve block has been widely used in clinical practice for spasticity reduction, but the correlation between the dosage of phenol and its effectiveness has seldom been discussed. The objective was to determine the optimal duration of phenol in contact with the nervous tissue and to investigate the dose-response relationship of 5% aqueous phenol solution by percutaneous nerve block in rats. Group I (n = 8) received sciatic nerve block by bathing the nerves in phenol solution, and group II (n = 40) by injecting phenol percutaneously. Group IIa to IId received different volumes (0.80, 0.16, 0.08 and 0.04 ml) and group IIe received normal saline. Compound muscle action potential (CMAP) was measured pre-injection and at 90 and 270 sec after injection and after surgical exposure of the nerves. The duration of CMAP reduced by 10%, 25%, 50%, 75% and 100% after phenol injection was also recorded. The mean latency for the evoked response to subside in direct phenol application (group I) and percutaneous nerve block (group IIa) were 73.5 ± 5.9 and 62.4 ± 7.6 sec, respectively. There was no statistical difference for the time periods in the blocking effect elicited by phenol solution between these two methods. Ninety sec was set as the optimal duration for phenol to produce complete conduction blockage. Higher volume of phenol produced more significant blocking effect at 90 and 270 sec after injection. Percutaneous injection with 0.16 ml of phenol solution had the same blocking effect as 0.8 ml. The continuous injection model for percutaneous phenol block indeed used significantly more phenol than actually needed. Clinically, the progressive injection model can be used to minimize injection volume.

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Isorhamnetin (IRh), which has a wide range of pharmacological effects, is one of the most significant active components in the fruits of Hippophae rhamnoides L. and the leaves of Ginkgo biloba L. It protects the heart and brain, in addition to possessing anti-tumor, anti-inflammatory, antioxidant, organ protection, and anti-obesity properties. We sought to assess IRh’s anti-psoriatic activity, explore its immunomodulatory properties in reducing the severity of psoriatic symptoms, and evaluate its potential immunotherapeutic effects. We used IRh to treat imiquimod (IMQ)-induced psoriasis in BALB/C mice and examined the underlying mechanisms. The outcomes demonstrated that IRh reduced epidermal hyperplasia, lowered PASI scores, and improved histopathological psoriasiform lesions in IMQ-induced mice. IRh attenuated the accumulation of malondialdehyde (MDA), and also reversed the reduction caused by IMQ of superoxide dismutase (SOD) and catalase (CAT) in skin tissues. Additionally, IRh effectively inhibited IMQ’s ability to increase proinflammatory cytokines such as TNF-α, IL-6, IL-17A, and transcription factor NF-κB. Furthermore, IRh significantly reduced the percentage of Th1 and Th17 in the spleens of mice treated with IMQ and suppressed the maturation of splenic dendritic cells. Overall, our research suggests that IRh protects against oxidative stress and inflammation in the pathogenesis of psoriasis, with potential for the development of new and potent medication for the treatment of psoriasis.

We investigated the association between high-density lipoprotein cholesterol (HDL-C) and rs2014355 variant in the gene, short-chain acyl-coenzyme A dehydrogenase (ACADS) based on exercise habits. Data collected between 2008 and 2015 for individuals aged 30 to 70 years were available in the Taiwan Biobank (TWB) database. Backward stepwise linear regression was used to evaluate the associations of rs2014355 and exercise with HDL-C levels. We analyzed data of 5515 physically active and 4169 inactive biobank participants. The HDL-C concentrations were higher in the exercise compared to no exercise group (beta value, β = 1.79856; P < .0001). We observed that the test for interaction was significant for the ACADS rs2014355 variant and exercise (P for interaction =.0412). Multivariate analyses showed significant association between TC+CC genotype and HDL-C in the exercise (β = 1.09785; P value = .0146) compared to the no-exercise group (β = −0.03754, P = .9154). In summary, the association between HDL-C and exercise differed significantly with respect to ACADS rs2014355 genotypes. Compared to the TT genotype, the TC+CC genotype together with exercise was associated with higher levels of HDL-C.