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Shunsuke Kiuchi,1 Shinji Hisatake,1 Muneyasu Kawasaki,2 Osamu Hirashima,2 Takayuki Kabuki,1 Junichi Yamazaki,1 Takanori Ikeda1 1Department of Cardiovascular Medicine, Toho University Faculty of Medicine, Tokyo, 2Division of Cardiology and Cardiovascular Surgery, Misato Central General Hospital, Saitama, JapanBackground: The aim of controlling hypertension is to protect against arteriosclerosis. Calcium channel blockers (CCBs) and renin-angiotensin-aldosterone system (RAAS) inhibitors have been reported to have antihypertensive effects, but their effect on the progression of arteriosclerosis is not fully understood. The cardio-ankle vascular index (CAVI) was developed to estimate arterial stiffness, which reflects arteriosclerosis. In this study, we investigated the longer term effects of CCBs and RAAS inhibitors on the progression of arteriosclerosis by monitoring the CAVI.Methods: Our subjects were 115 consecutive, non-smoking hypertensive patients on oral treatment with a CCB and/or RAAS inhibitor for at least 3 years in whom the CAVI was measured on two occasions approximately 1 year apart during the period from January 2009 to December 2011. Changes in CAVI were evaluated in patients administered a CCB alone (group C), an RAAS inhibitor (group R) alone, or both drugs together (group B). Changes in laboratory findings, blood pressure, and ankle-brachial index were similarly evaluated.Results: No significant change in laboratory findings, blood pressure, or ankle-brachial index was noted in any of the groups. The CAVI decreased slightly in group R (first recording 8.80±1.03, second recording 8.57±0.97, P=0.517) and increased significantly in group C (first 8.45±0.92, second 8.95±1.04, P=0.038), but showed no significant change in group B (first 9.01±1.26, second 9.05±1.35, P=0.851).Conclusion: Long-term administration of a CCB alone increased the CAVI, but this effect was offset by the concomitant use of a RAAS inhibitor, indicating that a RAAS inhibitor might protect against arteriosclerosis. Keywords: cardio-ankle vascular index, renin-angiotensin-aldosterone system inhibitor, calcium channel blocker

Evidence suggests a longitudinal association between tooth loss and cognitive function. However, the temporality of this association is not well understood. We investigated the effect of several emulated tooth loss prevention scenarios on cognitive function. We used data from 3 waves (baseline: 2009, second wave: 2011–2012, and third wave: 2015) of the Panel on Health and Ageing of Singaporean Elderly (PHASE). PHASE targeted older adults, aged ≥60 y, in Singapore. Number of teeth was used as a time-varying exposure (baseline, second wave). Cognitive function (Short Portable Mental Status Questionnaire score) in the third wave was assessed as the outcome. Multiple time-invariant (baseline) and time-varying (baseline and second wave) covariates were included. The "longitudinal modified treatment policy approach" combined with targeted minimum loss–based estimation was used to define and estimate additive effects of emulated tooth loss prevention scenarios. Emulated scenarios were the following: what if edentate people retained 1 to 4 teeth (scenario 1), what if those with <5 teeth retained 5 to 9 teeth (scenario 2), what if those with <10 teeth retained 10 to 19 teeth (scenario 3), and what if everyone retained ≥20 teeth (scenario 4)? A total of 1,516 participants, excluding those with severe cognitive impairment, were included (male: 41.6%). The mean age at baseline was 70.6 y (SD = 7.1). The mean SPMSQ score at baseline was 2.06 (SD = 0.02) for edentulous, 1.55 (SD = 0.04) for 1 to 4 teeth, 1.61 (SD = 0.03) for 5 to 9 teeth, 1.73 (SD = 0.02) for 10 to 19 teeth, and 1.71 (SD = 0.02) for ≥20 teeth. Additive effect of hypothetical intervention gradually increased with intensity of prevention from scenario 1 to scenario 4 (scenario 1: −0.02 [95% CI, −0.08 to 0.04], scenario 2: −0.05 [95% CI, −0.11 to −0.00], scenario 3: −0.07 [95% CI, −0.14 to −0.00], scenario 4: −0.15 [95% CI, −0.23 to −0.06]). Emulated tooth loss prevention interventions were associated with better cognitive function score. Therefore, preventing tooth loss could potentially benefit maintenance of cognitive function among older adults. [ABSTRACT FROM AUTHOR]

Tooth loss is a risk factor for increased mortality; however, the underlying mechanism remains unclear. This study aimed to evaluate the mediating effect of weight change on the relationship between tooth loss and mortality risk. This was a 10-y follow-up prospective cohort study using the data from the Japan Gerontological Evaluation Study (JAGES). The participants were independent older adults aged ≥65 y at baseline and were followed up from 2010 to 2020. The incidence of death in 2013 and 2020, incidence of >5% weight loss/gain in 2010 and 2013, and the number of remaining teeth in 2010 were used as the outcome, mediator, and explanatory variables, respectively. We conducted causal mediation analysis by fitting the Cox proportional hazard model, including possible confounders. Hazard ratios (HRs) and 95% confidence intervals (95% CIs) of the total effect (TE), natural indirect effect (NIE), and proportion mediated (PM) were estimated. Among the 34,510 participants, the mean age was 72.6 (SD = 5.4) y, and 47.6% were men. From 2013 to 2020, 14.0% of the participants (n = 4,825) died, 60.5% (n = 20,871) had 0 to 19 remaining teeth, and 17.2% (n = 5,927) and 8.4% (n = 2,907) experienced >5% weight loss and gain, respectively. The mortality rate was 0.016 per person-year among those with ≥20 remaining teeth and 0.027 per person-year among those with 0 to 19 remaining teeth. Weight loss of >5% significantly mediated the association between tooth loss and higher mortality risk (TE: HR, 1.28 [95% CI, 1.16 to 1.40]; NIE: HR, 1.03 [95% CI, 1.02 to 1.04]; PM, 13.1%); however, we observed a slight mediating effect for >5% weight gain (NIE: HR, 1.003 [95%CI, 1.0001 to 1.01]; PM, 1.3%). The present study suggests that a clinically meaningful level of weight loss mediated the association between tooth loss and increased risk of mortality among independent older adults. [ABSTRACT FROM AUTHOR]

Some modifiable risk factors for dementia are closely related to oral health. Although eating and speaking abilities are fundamental oral functions, limited studies have focused on the effect of malnutrition and lack of social interaction between oral health and dementia. We investigated the mediating effects of nutritional and social factors on the association between the number of teeth and the incidence of dementia. This 6-y cohort study used data from the Japan Gerontological Evaluation Study targeting older adults aged 65 y and above. The number of teeth (exposure) and covariates in 2010 (baseline survey), mediators (weight loss, vegetable and fruit intake, homeboundness, social network) in 2013, and the onset of dementia (outcome) between 2013 and 2016 were obtained. The Karlson–Holm–Breen mediation method was applied. A total of 35,744 participants were included (54.0% women). The mean age at baseline was 73.1 ± 5.5 y for men and 73.2 ± 5.5 y for women. A total of 1,776 participants (5.0%) had dementia during the follow-up period. There was a significant total effect of the number of teeth on the onset of dementia (hazard ratio, 1.14; 95% CI, 1.01–1.28). Controlling for nutritional and social mediators, the effect of the number of teeth was reduced to 1.10 (95% CI, 0.98–1.25), leaving an indirect effect of 1.03 (95% CI, 1.02–1.04). In the sex-stratified analysis, the proportion mediated by weight loss was 6.35% for men and 4.07% for women. The proportions mediated by vegetable and fruit intake and homeboundness were 4.44% and 4.83% for men and 8.45% and 0.93% for women, respectively. Furthermore, the proportion mediated by social networks was 13.79% for men and 4.00% for women. Tooth loss was associated with the onset of dementia. Nutritional and social factors partially mediated this association. [ABSTRACT FROM AUTHOR]

Economically important traits such as growth and backfat in pigs have been shown to be influenced by genes in swine chromosome (SSC) 10q12→qter corresponding to human chromosome (HSA) 10p. However, since gene information in the swine chromosomal region was limited, we attempted to generate a dense comparative map between SSC10 and HSA10 by mapping the 115 genes of HSA10 to a swine RH map (IMpRH map). In the mapping ten genes were assigned to SSC10, 88 to SSC14, and one to SSC3. One gene was suggested to link to SSC3, and another to SSC9. The correspondences between HSA10 and SSC10 and between HSA10 and SSC14 were essentially consistent with the observations obtained from bi/uni-directional chromosome painting or other results. This study further indicated that a large number of intrachromosomal rearrangements occurred in the synteny-conserved regions following species separation. Copyright © 2006 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Bi- and uni-directional chromosome painting (ZOO-FISH) and gene mapping have revealed correspondences between human chromosome (HSA) 17 and porcine chromosome (SSC) 12 harboring economically important quantitative trait loci. In the present study, we have assigned 204 genes localized on HSA17 to SSC12 to generate a comprehensive comparative map between HSA17 and SSC12. Two hundred fifty-five primer pairs were designed using porcine sequences orthologous with human genes. Of the 255 primer pairs, 208 (81.6%) were used to assign the corresponding genes to porcine chromosomes using the INRA-Minnesota 7000-rad porcine × Chinese hamster whole genome radiation hybrid (IMpRH) panel. Two hundred three genes were integrated into the SSC12 IMpRH linkage maps; and one gene, PPARBP, was found to link to THRA1 located in SSC12 but not incorporated into the linkage maps. Three genes (GIT1, SLC25A11, and HT008) were suggested to link to SSC12 markers, and the remaining gene (RPL26) did not link to any genes/expressed sequence tags/markers registered, including those in the present study. A comparison of the gene orders among SSC12, HSA17, and mouse chromosome 11 indicates that intra-chromosomal rearrangements occurred frequently in this ancestral mammalian chromosome during speciation. Copyright © 2006 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The human chromosome (HSA)19q region has been shown to correspond to swine chromosome (SSC) 6q11→q21 by bi-directional chromosomal painting and gene mapping. However, since the precise correspondence has not been determined, 26 genes localized in HSA19q13.3→q13.4 were assigned to the SSC6 region mainly by radiation hybrid (RH) mapping, and additionally, by somatic cell hybrid panel (SCHP) mapping, and fluorescent in situ hybridization (FISH). Out of the 26 genes, 24 were assigned to a swine RH map with LOD scores greater than 6 (threshold of significance). The most likely order of the 24 genes along SSC6 was calculated by CarthaGene, revealing that the order is essentially the same as that in HSA19q13.3→q13.4. For AURKC and RPS5 giving LOD scores not greater than 6, SCHP mapping and FISH were additionally performed; SCHP mapping assigned AURKC and RPS5 to SSC6q22→q23 and SSC6q21, respectively, which is consistent with the observation of FISH. Consequently, all the genes (26 genes) examined in the present study were shown to localize in SSC6q12→q23, and the order of the genes along the chromosomes was shown to be essentially the same in swine and human, though several intrachromosomal rearrangements were observed between the species. Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]