Effects of slow breathing training on hemodynamic changes, cardiac autonomic function and neuroendocrine response in people with high blood pressure: A randomized control trial.

BACKGROUND: High blood pressure (BP) is a non-communicable disease that is a risk factor for cardiovascular disease and is the leading cause of mortality and morbidity worldwide. High BP can be managed by both pharmacological and non-pharmacological interventions. Non-pharmacological treatment, such as slow-breathing training (SBT), has been shown to reduce BP. However, there are few studies on the effect of SBT on both cardiac activation and oxidative stress in people with high BP. OBJECTIVES: To explore the effect of SBT on cardiac autonomic function (i.e., heart rate variability: HRV) and neuroendocrine response (i.e., salivary cortisol). METHODS: One hundred people (including 89 women) with high BP were randomly assigned to either a control (n = 50) or intervention group (n = 50). The intervention program was conducted for 30 min per day, for 5 days per week, for 4 weeks, with a total of 20 sessions of the SBT at the rate of 10 times per minute, whereas the control group was required to continue with their daily routine. HRV, BP, and salivary cortisol were measured before and after the intervention program. A two-way mixed ANOVA was performed for within-group and between-group comparisons over time. RESULTS: Of the 100 participants, 71 individuals completed the study. The participants in the intervention group had a lower BP and salivary cortisol levels compared to those in the control group (p < .05). Further, those participants showed an increase in the standard deviation of normal R-R intervals after the 4-week intervention program (p < .05). CONCLUSION: This study provided evidence demonstrating the effect of SBT on cardiac autonomic and stress reactivity, which has important implications for health promotion in people with high BP. CLINICAL TRIAL REGISTRATION NUMBER: TCTR20180302008.

Distribution and Clinical Significance of Hepatitis B virus A1762T/G1764A Double Mutation in Chronic Hepatitis B Patients: A Cross-Sectional Study.

BACKGROUND: Chronic hepatitis B (CHB) is well-known as a major risk for liver cirrhosis and hepatocellular carcinoma (HCC). The A1762T/G1764A double mutation in the hepatitis B virus genome affects the production of HBe antigen and is established as a predictive marker for progression to HCC. Thus, this study aimed to investigate the prevalence and clinical significance of the mutation in Thai CHB patients. METHODS:  A cross-sectional study was conducted in 78 Thai CHB patients who were assessed for hepatitis B profiles, HBsAg, HBeAg and anti-HBeAg, transaminitis, liver fibrosis defined by FIB-4 (FIB-4) score and AST to platelet ratio index (APRI), alpha-fetoprotein (AFP) and active hepatitis B status. HBV A1762T/G1764A mutation was examined by SYBR Green I Real-time PCR. Chi-square and Mann-Whiney U tests were performed to determine the association between the mutation and variables. RESULTS: The prevalence of patients infected with the A1762T/G1764A mutation was 44.9%. The mutation was associated with HBeAg status (p=0.027) and HBsAg levels (p=0.008), transaminitis (p=0.011), and active hepatitis B (p=0.037), but not liver fibrosis markers, FIB-4 score and APRI, and AFP. Binary logistic regression identified the mutation as a predictive factor of active hepatitis B (OR 3.5, 95%CI, 1.1-11.3, p=0.037). Patients infected with the mutant exhibited significantly higher levels of HBsAg (p=0.011) and HBV viral load (p=0.047), but lower levels of HBeAg (p=0.12) than those infected with the wild-type HBV. CONCLUSION: The data indicate the high prevalence of the A1762T/G1764A mutation and its significant association with the severity of Thai CHB patients and the HBV mutation is proposed as a predictive marker of active hepatitis B status in CHB patients.

Lack of Association between IFN-γ, CXCL10 and TGF-ß1 Gene Polymorphisms and Liver Complication in HIV-infected Thais.

OBJECTIVE: Chronic liver disease has become a leading cause of illness and death in people living with HIV and the production of the cytokines IFN-γ and TGF-ß1, and chemokine CXCL10 during chronic inflammation contributes to liver disease progression in HIV patients under long-term anti-retroviral therapy. This study aimed to examine association of IFN-γ +874T/A, CXCL10 G-201A and C-1596T, and TGF-ß1 -509C/T single nucleotide polymorphisms (SNPs) with liver complications in the HIV-infected Thais. METHODS: A cross-sectional study was conducted in 200 Thai HIV patients who were evaluated for transaminitis and significant liver fibrosis by fibrosis-4 score (FIB-4), and genotypes for IFN-γ +874T/A, CXCL10 G-201A and C-1596T, and TGF-ß1 -509C/T SNPs using PCR-based methods. RESULT: There were high rates of transaminitis (30.1%) and significant liver fibrosis assessed by FIB-4 score > 1.45 (18.8%) in this group of patients, mostly under anti-retroviral therapy (73.0%). The genotypes and alleles of IFN-γ +874T/A, CXCL10 G-201A and C-1596T, and TGF-ß1 -509C/T SNPs were not associated with either transaminitis or FIB-4 score > 1.45 (p > 005). Logistic regression analysis identified age and gender as risk factors, and CD4+ cell count higher than 350 cells/ul as a protective factor of liver fibrosis in this study group. CONCLUSION: The IFN-γ +874T/A, CXCL10 G-201A and C-1596T, and TGF-ß11 -509C/T SNPs were not significantly associated with liver complication in HIV-infected Thais, mostly under ART.

Genotypic and allelic distribution of IFN-γ +874T/A and TGF-ß1 -509C/T single-nucleotide polymorphisms in human immunodeficiency virus-infected Thais.

Advances in antiretroviral therapy (ART) have led to a decrease of acquired immunodeficiency syndrome (AIDS)-related mortality, and an increase of non-AIDS illnesses in people living with HIV (PLWH). Risks for HIV-related chronic inflammation leading to non-AIDS illnesses in PLWH have been increasingly clarified including immunogenetic factors. This study aimed to examine distribution of genotypic and allelic frequencies of the well-characterized interferon-γ (IFN-γ) +874T/A and transforming growth factor-ß1 (TGF-ß1) -509C/T single nucleotide polymorphisms (SNPs) in Thai PLWH. The cross-sectional study was conducted in 191 Thai HIV patients. Most patients were under ART (74.3%) and maintained a relatively high median of CD4+  cell count (364.5 [5-1601] cells/µl). The frequencies of IFN-γ +874T/A  SNP genotypes were 9.0% AA, 38.3% AT, and 52.7% TT and those of the SNP alleles were 28.1% A and 71.9% T. The rates of TGF-ß1-509C/T SNP genotypes were 15.7% CC, 44.0% CT, and 40.3% TT and those of the SNP alleles were 37.7% C and 62.3% T. The more frequent TT genotypes and T allele of the IFN-γ +874T/A SNP, and relatively more prevalent TT and CT genotypes and T allele of TGF-ß1 -509C/T SNP were potentially associated with disease progression to non-AIDS complication in Thai PLWH and required further investigation. This study provides the immunogenetic data potentially supporting mechanisms for chronic immune activation in PLWH under long-term suppressive ART.

Evaluation of quantitative biosensor for glucose-6-phosphate dehydrogenase activity detection.

Neonatal jaundice is a common and severe disease in premature infants with Glucose-6-Phosphate Dehydrogenase (G-6-PD) deficiency. The World Health Organization (WHO) has recommended screening for G-6-PD deficiency in newborns for early recognition as well as to prevent unwanted outcomes in a timely manner. The present study aimed to assess a point-of-care, careSTARTTM G6PD biosensor as a quantitative method for the diagnosis of G-6-PD deficiency. Factors influencing the evaluation of G-6-PD enzyme activity were examined in 40 adults, including ethylenediaminetetraacetic acid (EDTA) anticoagulant, hematocrit concentration, storage temperature and time. Analytic performance of the careSTARTTM G6PD biosensor was evaluated in 216 newborns and compared with fluorescent spot test (FST) and standard quantitative G-6-PD enzyme activity (SGT) assay. The results of factors affecting the G-6-PD enzyme activity showed that the activity determined from finger-prick was not statistically different from venous blood (p = 0.152). The G-6-PD value was highly dependent on the hematocrit and rose with increasing hematocrit concentration. Its activity was stable at 4°C for 3 days. Reliability analysis between the careSTARTTM G6PD biosensor and SGT assay showed a strong correlation with a Pearson's correlation coefficient of 0.82 and perfect agreement by intraclass correlation coefficient (ICC) of 0.90. Analysis of the area under the Receiver Operating Curve (AUC) illustrated that the careSTARTTM G6PD biosensor had 100% sensitivity, 96% specificity, 73% positive predictive value (PPV), 100% negative predictive value (NPV) and 97% accuracy at 30% of residual activity. While the diagnostic ability for identifying G-6-PD deficiency had 78% sensitivity, 89% specificity, 56% positive predictive value (PPV), 96% negative predictive value (NPV) and 88% accuracy when stratified by gender. The careSTARTTM G6PD biosensor is an attractive option as a point-of-care quantitative method for G-6-PD activity detection. Quantification of G-6-PD enzyme activity in newborns is the most effective approach for the management of G-6-PD deficiency to prevent severe jaundice and acute hemolysis.

CXCL12 G801A polymorphism is associated with significant liver fibrosis in HIV-infected Thais: a cross-sectional study.

BACKGROUND: Previous studies indicate high prevalence of liver diseases in HIV-infected patients, and their genetic risk factors are still unclear. The chemokine CXCL12 plays important roles in development of chronic liver injury and a single nucleotide polymorphism (SNP) G to A change at position 801 in CXCL12 gene has been demonstrated to affect CXCL12 production levels. OBJECTIVE: This study aimed to analyze the association of CXCL12 G801A SNP with liver complication in HIV-infected Thais. METHODS: A cross-sectional study was conducted in 164 patients who were evaluated for transaminitis and significant liver fibrosis, defined by fibrosis-4 (FIB-4) score and AST to platelet ratio index (APRI), and genotyped for the SNP using tetra-primer PCR-SSP. RESULTS: There were high rates of patients with transaminits (28.0%), and significant liver fibrosis by FIB-4 score (18.9%) and by APRI (14.0%). The CXCL12 G801A AA/GA genotypes were significantly associated with transaminitis (p = 0.014) and significant fibrosis by APRI (p = 0.020). Univariate and multivariate analyses identified the AA/GA genotypes as predictive factors for significant fibrosis (OR 6.8, 95%CI 1.7-28.2, p = 0.008), together with age older than 40 years, CD4+ cell count < 350 cells/µl and hepatitis B and/or C virus coinfection. The significantly higher medians of APRI and FIB-4 score, in patients with AA/GA than those with GG genotypes (p < 0.05) were observed in the ART-naïve, but not ART-experienced groups. CONCLUSION: The CXCL12 G801A AA/GA genotypes are significant predictive factors for hepatic fibrosis potentially in the ART-naïve HIV-infected Thais.

Brown rice and retrograded brown rice alleviate inflammatory response in dextran sulfate sodium (DSS)-induced colitis mice.

The present study was aimed to investigate the impacts of brown rice (BR) and retrograded brown rice (R-BR) consumption on colonic health and gut microbiota in dextran sulfate sodium (DSS) induced colitis mice. Thirty two female C57Bl/6Mlac mice were fed with modified AIN 93G diets by replacing cornstarch in the original composition with white rice (WR), BR and R-BR powder. The mice were divided into 4 groups and fed with the following experimental diets for 4 weeks: (1) negative control (WR: diet with WR), (2) positive control (DSS_WR: DSS and diet with WR), (3) DSS_BR: DSS and diet with BR, and (4) DSS_R-BR: DSS and diet with R-BR. BR and R-BR had a greater content of fat, dietary fiber, GABA, γ-oryzanol, γ-tocotrienol, ferulic acid and p-coumaric acid than WR (p < 0.05). No significant difference in the level of these bioactive compounds was noted between BR and R-BR. Nevertheless, R-BR had a 1.8 fold resistant starch (RS) content of BR (p < 0.05). The DSS_BR and DSS_R-BR groups showed a lower ratio of colonic weight to length, and a lower content of iNOS, COX-2, MPO, IL-6 and INF-γ in colonic homogenates than the DSS_WR group. However, the DSS treated mice fed with the R-BR diet had significantly milder histopathological inflammatory injury and lower colonic iNOS expression than the DSS_BR and DSS_WR groups. The percentage of mesenteric regulatory T cells significantly increased in the DSS_R-BR group compared to that in the DSS_WR group. The DSS treated mice fed with the R-BR diet showed a significant increase in cecal bacterial diversity and abundance of genera Prevotella, Ruminococcus, Dorea, Coprococcus and Dehalobacterium but a significant decrease in pathogenic bacteria including Bacteroides and Enterococcus compared to the DSS_WR group. Thus, the present data indicate that BR and R-BR ameliorate colonic inflammation in experimental colitis induced by DSS in mice by suppressing inflammatory mediators and modulating regulatory T cell responses as well as bacterial diversity in the cecum.

Human neutrophil alloantigen genotype frequencies in Thai blood donors.

BACKGROUND: Antibodies to human neutrophil antigens (HNA) can cause transfusion reactions, as well as autoimmune and neonatal neutropenia. This study is the first to report the frequencies of human neutrophil antigen genotypes in the Thai population. MATERIALS AND METHODS: Three hundred unrelated, healthy Thai blood donors at the National Blood Centre, Thai Red Cross Society, Bangkok, Thailand were typed for HNA-1a, -1b, -1c, -3a, -3b and -4a using polymerase chain reaction with sequence-specific primers. Moreover, HNA-5a genotyping was performed using polymerase chain reaction-restriction fragment length polymorphism. RESULTS: The gene frequencies of HNA-1a, -1b and -1c were 0.470, 0.530 and 0.005, respectively. The frequencies of HNA-3a and -3b were 0.490 and 0.510, respectively. Additionally, the HNA-4a+/+ and HNA-4a+/- genotype frequencies were 0.947 and 0.053, respectively. The frequencies of HNA-5a+/+, HNA-5a+/- and HNA-5a-/- genotypes were 0.641, 0.297 and 0.062, respectively. Compared with other Asian populations, Thais have higher frequencies of HNA-1b (P<0.001). On the other hand, the frequency of HNA-5a observed in Thais is lower than that reported among Koreans (P<0.001). DISCUSSION: These findings suggest that Thais would be more susceptible to HNA-1b alloimmunisation. Furthermore, our results could establish a useful human neutrophil antigen donor file to provide more effective transfusion of blood and blood components.

Molecular mechanism of high hemoglobin F production in Southeast Asian-type hereditary persistence of fetal hemoglobin.

Hereditary persistence of fetal hemoglobin (HPFH) is associated with a high level of hemoglobin F (HbF) synthesis in adult heterozygotes. In this study, 2 of 6 unrelated HPFH Thai families were found to be Southeast Asian-type HPFH (SEA-HPFH) by analyses of the hematologic data and Southern blot hybridization with polymerase chain reaction-amplified DNA probes. DNA mapping with a probe for a delta-globin fragment showed a 27-kb deletion of DNA that included the beta-globin gene and the 3' deoxyribonuclease I hypersensitive site 1 (3'HS1) sequence downstream. Deletion of the insulator, 3'HS1, and the juxta-position of the HPFH-3 core enhancer downstream to the 3' breakpoint have been postulated to be the cause of high HbF production in these individuals. To test this hypothesis, we transfected K562 cells with 4 different bacterial artificial chromosome constructs containing the enhanced green fluorescent protein (EGFP) gene at the position of the Agamma-globin gene (pEBAC/148beta:EGFP). Flow cytometry was used to compare EGFP expression from the pEBAC/148beta:EGFP construct with the HPFH-3 core enhancer immediately 5' to the SEA-HPFH breakpoint (pEnH), from the pEBAC/148beta:EGFP construct with 8 kb of the breakpoint sequence and the HPFH-3 core enhancer (pSEA-HPFH), and from the construct with 3'HS1 followed by the pSEA-HPFH sequence (pSEA-HPFH_3pHS1). The results show that high HbF production in SEA-HPFH occurs from a deletion of the 3'HS1 sequence and the juxtaposition of the HPFH-3 enhancer downstream to the delta-globin gene.