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1.
Medicina (Kaunas) ; 57(1)2021 Jan 02.
Article in English | MEDLINE | ID: mdl-33401676

ABSTRACT

Background and objectives: Faced with the serious problem of an aging population, exercise is one of the most effective ways to maintain the health of the elderly. In recent years, with the popularization of smartphones, the elderly have increasingly accepted technological products that incorporate artificial intelligence (AI). However, there is not much research on using artificial intelligence bracelets to enhance elders' motivation and participation in exercise. Therefore, the purpose of this study is to evaluate the effectiveness of the combination of sports smart bracelets and multi-sport training programs on the motivation of the elderly in Macau. Materials and Methods: The study was conducted with a randomized trial design in a 12 week multi-sport exercise training intervention. According to the evaluation, a total of sixty elders' pre- and post-test data were included in this study. Results: After 12 weeks of multi-sport exercise training, the evaluation scores on the exercise motivation scale (EMS) increased significantly in the group wearing exercise bracelets and those taking part in the multi-component exercise program, and the degree of progress reached a statistically significant level, but the control group did not show any statistically significant difference. The influence of the combination of sports smart bracelets and multi-sport training programs on elders' motivation is clearer. Conclusions: The use of sports smart bracelets by elderly people in conjunction with diverse exercise training can effectively enhance elders' motivation and increase their participation in regular exercise. The combination of sports smart bracelets and multi-sport training programs is worth promoting in the elderly population.


Subject(s)
Artificial Intelligence , Motivation , Aged , Exercise , Exercise Therapy , Humans , Macau
2.
Sex Transm Dis ; 39(1): 21-4, 2012 Jan.
Article in English | MEDLINE | ID: mdl-22183840

ABSTRACT

In a randomized trial among African women with recurrent genital herpes, episodic acyclovir therapy resulted in modestly greater likelihood of lesion healing (hazard ratio [HR] = 1.48, P = 0.098; mean, 5.1 vs. 6.0 days) and cessation of herpes simplex virus shedding (HR = 1.88, P = 0.008; mean, 3.0 vs. 5.0 days) compared with placebo, similar to results of studies in high-income countries (ClinicalTrials.gov registration NCT00808405).


Subject(s)
Acyclovir/therapeutic use , Antiviral Agents/therapeutic use , Herpes Genitalis/drug therapy , Herpesvirus 2, Human/immunology , Ulcer/drug therapy , Adult , DNA, Viral/genetics , Double-Blind Method , Female , HIV Seronegativity , HIV-1/immunology , HIV-1/isolation & purification , Herpes Genitalis/genetics , Herpes Genitalis/virology , Herpesvirus 2, Human/drug effects , Herpesvirus 2, Human/isolation & purification , Humans , Kaplan-Meier Estimate , Middle Aged , Recurrence , Seroepidemiologic Studies , South Africa/epidemiology , Ulcer/genetics , Ulcer/virology , Virus Shedding/drug effects , Zambia/epidemiology
3.
Article in English | MEDLINE | ID: mdl-35564833

ABSTRACT

This study explored whether atrial fibrillation (AF)'s influence on short sleep duration (SD) increases the subsequent risk of fatness in management executives. This study included 25,953 healthy individuals working as management executives with ages ranging from 35 to 65 years (19,100 men and 6853 women) who participated in a qualifying physical filter program from 2006 to 2017 in Taiwan. Men and women who slept < 4 h had a 4.35-fold and 5.26-fold higher risk of developing AF than those who slept 7−8 h normally. Men and women who slept < 4 h had a 6.44-fold and 9.62-fold higher risk of fatness than those who slept 7−8 h. Men and women with AF had a 4.52-fold and 6.25-fold higher risk of fatness than those without AF. It showed that AF induced by short SD increases the risk of fatness. A short SD can predict an increased risk of fatness among management executives in Taiwan.


Subject(s)
Atrial Fibrillation , Sleep Wake Disorders , Adipose Tissue , Adult , Aged , Atrial Fibrillation/epidemiology , Female , Humans , Male , Middle Aged , Risk Factors , Sleep , Time Factors
4.
Lancet ; 375(9717): 824-33, 2010 Mar 06.
Article in English | MEDLINE | ID: mdl-20153888

ABSTRACT

BACKGROUND: Most people infected with HIV-1 are dually infected with herpes simplex virus type 2. Daily suppression of this herpes virus reduces plasma HIV-1 concentrations, but whether it delays HIV-1 disease progression is unknown. We investigated the effect of acyclovir on HIV-1 progression. METHODS: In a trial with 14 sites in southern Africa and east Africa, 3381 heterosexual people who were dually infected with herpes simplex virus type 2 and HIV-1 were randomly assigned in a 1:1 ratio to acyclovir 400 mg orally twice daily or placebo, and were followed up for up to 24 months. Eligible participants had CD4 cell counts of 250 cells per mL or higher and were not taking antiretroviral therapy. We used block randomisation, and patients and investigators were masked to treatment allocation. Effect of acyclovir on HIV-1 disease progression was defined by a primary composite endpoint of first occurrence of CD4 cell counts of fewer than 200 cells per microL, antiretroviral therapy initiation, or non-trauma related death. As an exploratory analysis, we assessed the endpoint of CD4 falling to <350 cells per microL. Analysis was by intention to treat. The trial is registered with ClinicalTrials.gov, number NCT00194519. FINDINGS: At enrollment, the median CD4 cell count was 462 cells per microL and median HIV-1 plasma RNA was 4.1 log(10) copies per microL. Acyclovir reduced risk of HIV-1 disease progression by 16%; 284 participants assigned acyclovir versus 324 assigned placebo reached the primary endpoint (hazard ratio [HR] 0.84, 95% CI 0.71-0.98, p=0.03). In those with CD4 counts >or=350 cells per microL, aciclovir delayed risk of CD4 cell counts falling to <350 cells per microL by 19% (0.81, 0.71-0.93, p=0.002) INTERPRETATION: The role of suppression of herpes simplex virus type 2 in reduction of HIV-1 disease progression before initiation of antiretroviral therapy warrants consideration. FUNDING: Bill & Melinda Gates Foundation.


Subject(s)
Acyclovir/therapeutic use , Antiviral Agents/therapeutic use , HIV Infections/drug therapy , HIV-1 , Herpes Genitalis/drug therapy , Herpesvirus 2, Human , Adult , CD4 Lymphocyte Count , Disease Progression , Double-Blind Method , Female , HIV Infections/complications , HIV Infections/immunology , HIV Infections/virology , HIV-1/isolation & purification , Herpes Genitalis/complications , Herpes Genitalis/virology , Herpesvirus 2, Human/isolation & purification , Humans , Male , Viral Load
5.
Neuropsychiatr Dis Treat ; 17: 587-604, 2021.
Article in English | MEDLINE | ID: mdl-33654401

ABSTRACT

BACKGROUND: Multiple sclerosis (MS) is a demyelinating disease that can damage neurons in the brain and spinal cord and is associated with several psychiatric disorders. However, few studies have evaluated the risk of psychiatric disorders in patients with MS by using a nationwide database. This study investigated the association between MS and the risk of psychiatric disorders. METHODS: Using data from the Taiwan National Health Insurance Research Database from 2000 to 2015, we identified 1066 patients with MS. After adjustment for confounding factors, Fine and Gray's competing risk model was used to compare the risk of psychiatric disorders during 15 years of follow-up. RESULTS: Of the patients with MS, 531 (4622.86 per 105 person years) developed psychiatric disorders; by contrast, 891 of the 3198 controls (2485.31 per 105 person years) developed psychiatric disorders. Fine and Gray's competing risk model revealed an adjusted hazard ratio (HR) of 5.044 (95% confidence interval = 4.448-5.870, p < 0.001) after adjustment for all the covariates. MS was associated with depression, anxiety, bipolar disorder, sleep disorders, schizophrenia, schizophreniform disorder, and other psychotic disorders (adjusted HR: 12.464, 4.650, 6.987, 9.103, 2.552, 2.600, 2.441, and 2.574, respectively; all p < 0.001). Some disease-modifying drugs were associated with a lower risk of anxiety or depression. CONCLUSION: Patients with MS were determined to have a higher risk of developing a wide range of psychiatric disorders.

6.
Am J Physiol Gastrointest Liver Physiol ; 298(1): G57-62, 2010 Jan.
Article in English | MEDLINE | ID: mdl-19892936

ABSTRACT

To test the hypothesis that differences in duodenal iron absorption may explain the variable phenotypic expression among HFE C282Y homozygotes, we have compared relative gene expression of duodenal iron transporters among C282Y homozygotes [hereditary hemochromatosis (HH)] with and without iron overload. Duodenal biopsy samples were analyzed using real-time PCR for expression of DMT1, FPN1, DCYTB, and HEPH relative to GAPDH from 23 C282Y homozygotes, including 5 "nonexpressors" (serum ferritin < upper limit of normal and absence of phenotypic features of hemochromatosis) and 18 "expressors." Four subjects of wild type for HFE mutations without iron overload or liver disease served as controls. There was a significant difference in expression of DMT1 (P = 0.03) and DMT1(IRE) (P = 0.0013) but not FPN1, DCYTB, or HEPH between groups. Expression of DMT1(IRE) was increased among HH subjects after phlebotomy compared with untreated (P = 0.006) and nonexpressor groups (P = 0.026). A positive relationship was observed among all HH subjects regardless of phenotype or treatment status between relative expression of FPN1 and DMT1 (r = 0.5854, P = 0.0021), FPN1, and DCYTB (r = 0.5554, P = 0.0040), FPN1 and HEPH (r = 0.5100, P = 0.0092), and DCYTB and HEPH (r = 0.5400, P = 0.0053). In summary, phlebotomy is associated with upregulation of DMT1(IRE) expression in HH subjects. HFE C282Y homozygotes without phenotypic expression do not have significantly decreased duodenal gene expression of iron transport genes compared with HH subjects with iron overload. There is coordinated regulation between duodenal expression of FPN1 and DMT1, FPN1 and DCYTB, and FPN1 and HEPH and also DCYTB and HEPH in HH subjects regardless of phenotype.


Subject(s)
Cation Transport Proteins/genetics , Hemochromatosis/physiopathology , Histocompatibility Antigens Class I/genetics , Iron/metabolism , Membrane Proteins/genetics , Adult , Biopsy , Cation Transport Proteins/metabolism , Duodenum/physiology , Female , Gene Expression Regulation/physiology , Hemochromatosis/metabolism , Hemochromatosis/pathology , Hemochromatosis Protein , Histocompatibility Antigens Class I/metabolism , Homeostasis/physiology , Humans , Iron-Regulatory Proteins/genetics , Iron-Regulatory Proteins/metabolism , Male , Membrane Proteins/metabolism , Middle Aged , Phenotype , RNA, Messenger/metabolism
7.
Diabetes ; 55(9): 2588-94, 2006 Sep.
Article in English | MEDLINE | ID: mdl-16936208

ABSTRACT

Type 1 diabetes is a chronic autoimmune disease mediated by autoreactive T-cells. Several experimental therapies targeting T-cells are in clinical trials. To understand how these therapies affect T-cell responses in vivo, assays that directly measure human T-cell function are needed. In a blinded, multicenter, case-controlled study conducted by the Immune Tolerance Network, we tested responses in an immunoblot and T-cell proliferative assay to distinguish type 1 diabetic patients from healthy control subjects. Peripheral blood cells from 39 healthy control subjects selected for DR4 and 23 subjects with recently diagnosed type 1 diabetes were studied. Autoantibody responses were measured in serum samples. Positive responses in both assays were more common in peripheral blood mononuclear cells from new-onset type 1 diabetic patients compared with control subjects. The proliferative, immunoblot, and autoantibody assays had sensitivities of 58, 91, and 78% with specificities of 94, 83, and 85%, respectively. When cellular assays were combined with autoantibody measurements, the sensitivity of the measurements was 75% with 100% specificity. We conclude that cellular assays performed on peripheral blood have a high degree of accuracy in discriminating responses in subjects with type 1 diabetes from healthy control subjects. They may be useful for assessment of cellular autoimmune responses involved in type 1 diabetes.


Subject(s)
Autoimmunity/immunology , Diabetes Mellitus, Type 1/immunology , T-Lymphocytes/immunology , Adolescent , Adult , Autoantibodies/analysis , Cell Proliferation , Child , Female , Glutamate Decarboxylase/analysis , Humans , Immunoblotting , Isoenzymes/analysis , Male , Sensitivity and Specificity
8.
Drug Alcohol Depend ; 90(2-3): 159-65, 2007 Oct 08.
Article in English | MEDLINE | ID: mdl-17416470

ABSTRACT

OPRM1, which codes for the mu-opioid receptor, is the most frequently studied candidate gene for opioid dependence. Despite numerous allelic association studies, no definitive conclusion has been reached regarding the role of OPRM1 polymorphisms in determining risk for opioid dependence. We attempted to resolve this by conducting a family-based association study and meta-analysis which may be more robust and powerful, respectively, than traditional case-control analyses. First, we genotyped three single nucleotide polymorphisms (SNPs) of OPRM1 in 1208 individuals from 473 Han Chinese families ascertained on the basis of having two or more siblings with DSM-IV-defined opioid dependence. The Val6Ala and Arg111His SNPs were detected, but with low minor allele frequencies (0.002 and 0.001, respectively). The Asn40Asp SNP was more informative (minor allele frequency: 0.419), but no significant evidence was observed for either a dominant (p=0.810) or additive (p=0.406) effect of this polymorphism on risk for opioid dependence. In addition, a meta-analysis of case-control studies of opioid dependence was performed, and found a similar lack of evidence for an association with the Asn40Asp SNP (p=0.859). Although a role of OPRM1 polymorphisms in determining risk for opioid dependence cannot be entirely discounted, a major contribution of the Asn40Asp polymorphism seems unlikely. Further analysis is warranted in samples from specific ancestral groups. In addition, it is critical that other OPRM1 variants, including all haplotype-tagging and amino-acid-coding SNPs, be tested for an influence on risk for opioid dependence, since the Asn40Asp polymorphism is only one of several hundred known mutations in the gene.


Subject(s)
Heroin Dependence/genetics , Receptors, Opioid, mu/genetics , Alleles , DNA/analysis , Diagnostic and Statistical Manual of Mental Disorders , Genotype , Humans , Polymorphism, Genetic
9.
Schizophr Res ; 73(2-3): 281-90, 2005 Mar 01.
Article in English | MEDLINE | ID: mdl-15653273

ABSTRACT

NOTCH4 initially received consideration as a risk gene for schizophrenia based on its location within a region on chromosome 6p that had previously shown strong evidence for genetic linkage with the illness. The initial published test for allelic association found strong evidence for involvement of this gene in schizophrenia, but subsequent studies failed to confirm this finding. Presently, we have used meta-analysis to derive a best estimate of the nature and magnitude of the associations between schizophrenia and five polymorphisms in and around the NOTCH4 gene. No significant association was detected between schizophrenia and repeat length of alleles at the (TAA)n, (CTG)n, or (TTAT)n polymorphisms, or between the disease and specific risk alleles at these polymorphisms or at the SNP1 or SNP2 polymorphisms. Heterogeneity and stronger evidence of association with the putative risk alleles of the (TAA)n, (CTG)n, SNP1, and SNP2 polymorphisms was observed in family-based studies than in case-control studies, suggesting that these polymorphisms may reliably influence risk for schizophrenia under certain circumstances. Since more consistent and robust associations with schizophrenia risk have been observed for haplotypes of these polymorphisms [especially those containing SNP2 and (CTG)n], additional large family-based or genomic-controlled studies would be helpful for definitively specifying the role of NOTCH4 haplotypes in risk for schizophrenia.


Subject(s)
Polymorphism, Genetic/genetics , Proto-Oncogene Proteins/genetics , Receptors, Cell Surface/genetics , Schizophrenia/genetics , Alleles , Humans , Minisatellite Repeats/genetics , Receptor, Notch4 , Receptors, Notch , Trinucleotide Repeats/genetics
10.
Diabetes Care ; 34(4): 988-93, 2011 Apr.
Article in English | MEDLINE | ID: mdl-21330643

ABSTRACT

OBJECTIVE: GAD antibodies (GADA) are more common in type 1 diabetic subjects diagnosed at an older age, whereas insulinoma-antigen 2 antibodies (IA-2A) are more common in subjects with younger onset. The prevalence of both antibodies decreases with longer duration of type 1 diabetes. We evaluated the interaction between age of diagnosis (onset) and duration of diabetes on the percentage of GADA- and IA-2A-positive subjects. RESEARCH DESIGN AND METHODS: Data were used from 5,020 individuals with type 1 diabetes obtained from the Type 1 Diabetes Genetics Consortium dataset. The percentages of GADA- and IA-2A-positive subjects were modeled with duration as the continuous independent variable using a modified spline. RESULTS: Within the first 5 years from diagnosis, 19.4% of individuals (median age 13 years) had neither GADA nor IA-2A, and by 6 to 13 years after diagnosis (median age 18 years), 31.7% were antibody-negative. There was no significant interaction between onset of disease and duration of diabetes for IA-2A (P = 0.30). The interaction was significant for GADA (P = 0.0002), resulting from differences in subjects diagnosed at or older than age 14. For these individuals, there was no apparent effect of duration of disease on the percentage of GADA-positive subjects within the first 5 years of diagnosis. CONCLUSIONS: Onset and duration of diabetes both have an important effect on antibody status. The interaction of onset and duration on GADA positivity, but not on IA-2A, suggests differences in biology. These data provide a context for clinicians to interpret results of autoantibody testing in clinical practice.


Subject(s)
Autoantibodies/metabolism , Diabetes Mellitus, Type 1/immunology , Glutamate Decarboxylase/immunology , Adolescent , Adult , Autoantibodies/biosynthesis , Child , Child, Preschool , Cross-Sectional Studies , Diabetes Mellitus, Type 1/enzymology , Female , Humans , Male , Middle Aged , Time Factors , Young Adult
11.
PLoS One ; 5(9): e12598, 2010 Sep 13.
Article in English | MEDLINE | ID: mdl-20856886

ABSTRACT

BACKGROUND: The risk of sexual transmission of HIV-1 is strongly associated with the level of HIV-1 RNA in plasma making reduction in HIV-1 plasma levels an important target for HIV-1 prevention interventions. A quantitative understanding of the relationship of plasma HIV-1 RNA and HIV-1 transmission risk could help predict the impact of candidate HIV-1 prevention interventions that operate by reducing plasma HIV-1 levels, such as antiretroviral therapy (ART), therapeutic vaccines, and other non-ART interventions. METHODOLOGY/PRINCIPAL FINDINGS: We use prospective data collected from 2004 to 2008 in East and Southern African HIV-1 serodiscordant couples to model the relationship of plasma HIV-1 RNA levels and heterosexual transmission risk with confirmation of HIV-1 transmission events by HIV-1 sequencing. The model is based on follow-up of 3381 HIV-1 serodiscordant couples over 5017 person-years encompassing 108 genetically-linked HIV-1 transmission events. HIV-1 transmission risk was 2.27 per 100 person-years with a log-linear relationship to log(10) plasma HIV-1 RNA. The model predicts that a decrease in average plasma HIV-1 RNA of 0.74 log(10) copies/mL (95% CI 0.60 to 0.97) reduces heterosexual transmission risk by 50%, regardless of the average starting plasma HIV-1 level in the population and independent of other HIV-1-related population characteristics. In a simulated population with a similar plasma HIV-1 RNA distribution the model estimates that 90% of overall HIV-1 infections averted by a 0.74 copies/mL reduction in plasma HIV-1 RNA could be achieved by targeting this reduction to the 58% of the cohort with plasma HIV-1 levels ≥4 log(10) copies/mL. CONCLUSIONS/SIGNIFICANCE: This log-linear model of plasma HIV-1 levels and risk of sexual HIV-1 transmission may help estimate the impact on HIV-1 transmission and infections averted from candidate interventions that reduce plasma HIV-1 RNA levels.


Subject(s)
HIV Infections/prevention & control , HIV Infections/transmission , HIV-1/isolation & purification , Heterosexuality , RNA, Viral/blood , Africa, Eastern , Africa, Southern , Anti-HIV Agents/therapeutic use , Cohort Studies , Female , Follow-Up Studies , HIV Infections/drug therapy , HIV Infections/virology , HIV-1/genetics , HIV-1/physiology , Humans , Male , RNA, Viral/genetics , Risk Factors , Sexual Partners , Viral Load
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