PurposeAlthough exercise and sleep duration habits are associated with cognitive function, their beneficial effects on cognitive function remain unclear. We aimed to examine the effect of sleep duration and daily physical activity on cognitive function, elucidating the neural mechanisms using near-infrared spectroscopy (NIRS).MethodsA total of 23 healthy young adults (age 22.0 ± 2.2 years) participated in this study. Exercise amount was assessed using a uniaxial accelerometer. We evaluated total sleep time (TST) and sleep efficiency by actigraphy. Cognitive function was tested using the N-back task, the Wisconsin Card Sorting Test (WCST), and the Continuous Performance Test–Identical Pairs (CPT-IP), and the cortical oxygenated hemoglobin levels during a word fluency task were measured with NIRS.ResultsExercise amount was significantly correlated with reaction time on 0- and 1-back tasks (r = −0.602, p = 0.002; r = −0.446, p = 0.033, respectively), whereas TST was significantly correlated with % corrects on the 2-back task (r = 0.486, p = 0.019). Multiple regression analysis, including exercise amount, TST, and sleep efficiency, revealed that exercise amount was the most significant factor for reaction time on 0- and 1-back tasks (β = −0.634, p = 0.002; β = −0.454, p = 0.031, respectively), and TST was the most significant factor for % corrects on the 2-back task (β = 0.542, p = 0.014). The parameter measured by WCST and CPT-IP was not significantly correlated with TST or exercise amount. Exercise amount, but not TST, was significantly correlated with the mean area under the NIRS curve in the prefrontal area (r = 0.492, p = 0.017).ConclusionExercise amount and TST had differential effects on working memory and cortical activation in the prefrontal area. Daily physical activity and appropriate sleep duration may play an important role in working memory.

One adverse effect of nifedipine, a long‐acting vasodilator, is gingival overgrowth. Preexisting gingival inflammation and/or dental plaque has been suggested to be responsible for the progression of this side effect, but the precise mechanism is uncertain because of a lack of suitable animal models. A study was therefore done to establish an experimental model of gingival overgrowth in rats and to investigate the possible involvement of gingival inflammation and/or dental plaque in its development. Specific pathogen‐free Fischer rats (male, 14 days old) were used . Gingival inflammation and dental plaque accumulation were induced by infection with Streptococccus mutans MT8148R. The nifedipine‐treated rats (experimental group) were fed a caries‐inducing diet contai ning nifedipine either with or without infection, while the nifedipine‐untreated rats (control group) were fed the same diet, similarly with or with out the infection. Marked gingival overgrowth was induced in the mandibular molar region of nifedipine‐treated rats regardless of S. mutans infection, although the infection resulted in a further increase in the degree of gingival overgrowth. Histological examination of the gingival overgrowth revealed the presence of redundant subepithelial connective tissue in the treated rats, and inflammatory cell infiltration was apparent only in the tissue of the S. mutans‐infected rats regardless of the nifedipine administration. These findings suggest that nifedipine induces gingival overgrowth in rats either in the presence or absence of gingival inflammatio n and/or dental plaque, although these factors can augment the effect of the drug. Our experimental system seems to be a useful model for studying the mechanism of this side effect.

The present study revealed that plasma concentration of PAX, 5-HTTLPR genotype, -1019C/G 5-HT(1A) genotype, PAS score at baseline, and adverse effects may influence the therapeutic response to PAX in patients with PD.

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ObjectiveFamily and twin studies have suggested genetic liability for panic disorder (PD) and therefore we sought to determine the role of noradrenergic and serotonergic candidate genes for susceptibility for PD in a Japanese population.MethodsIn this age- and gender-matched case-control study involving 119 PD patients and 119 healthy controls, we examined the genotype distributions and allele frequencies of the serotonin transporter gene linked polymorphic region (5-HTTLPR), −1019C/G (rs6295) promoter polymorphism of the serotonin receptor 1A (5-HT1A), and catechol-O-methyltransferase (COMT) gene polymorphism (rs4680) and their association with PD.ResultsNo significant differences were evident in the allele frequencies or genotype distributions of the COMT (rs4680), 5-HTTLPR polymorphisms or the −1019C/G (rs6295) promoter polymorphism of 5-HT1A between PD patients and controls. Although there were no significant associations of these polymorphisms with in subgroups of PD patients differentiated by gender or in subgroup comorbid with agoraphobia (AP), significant difference was observed in genotype distributions of the −1019C/G (rs6295) promoter polymorphism of 5-HT1A between PD patients without AP and controls (p=0.047).ConclusionIn this association study, the 1019C/G (rs6295) promoter polymorphism of the 5-HT1A receptor G/G genotype was associated with PD without AP in a Japanese population.