Search

The phonological abilities of congenitally deaf individuals are inferior to those of people who can hear. However, deaf individuals can acquire spoken languages by utilizing orthography and lip-reading. The present study used functional magnetic resonance imaging (fMRI) to show that deaf individuals utilize phonological representations via a mnemonic process. We compared the brain activation of deaf and hearing participants while they memorized serially visually presented Japanese kana letters (Kana), finger alphabets (Finger), and Arabic letters (Arabic). Hearing participants did not know which finger alphabets corresponded to which language sounds, whereas deaf participants did. All of the participants understood the correspondence between Kana and their language sounds. None of the participants knew the correspondence between Arabic and their language sounds, so this condition was used as a baseline. We found that the left superior temporal gyrus (STG) was activated by phonological representations in the deaf group when memorizing both Kana and Finger. Additionaly, the brain areas associated with phonological representations for Finger in the deaf group were the same as the areas for Kana in the hearing group. Overall, despite the fact that they are superior in visual information processing, deaf individuals utilize phonological rather than visual representations in visually presented verbal memory. [ABSTRACT FROM AUTHOR]

Abstract: The aim of this study was to identify the location associated with primitive sentence processing. Processing related to generation and comprehension of sentences (“sentence processing”) is postulated to be largely divided into syntactic processing (processing related to the formation of sentences and to verb reflection and particles) and verb information (argument structure and thematic role). Numerous lesion studies and functional brain imaging studies on unimpaired individuals have suggested that the left inferior frontal gyrus (IFG) is involved in syntactic processing. In addition, some studies have reported that the area from the left parietal lobe to the posterior superior temporal gyrus is involved in processing information such as argument structure and thematic role. However, studies on sentence processing using functional brain imaging have used complex sentences as tasks, raising the possibility that the results show the demands on not only language processing, but also on working memory. To clarify the brain areas involved in basic sentence processing in human language, there is a need to examine tasks involved in sentence processing that assume more primitive processing with minimal demands on working memory. The present study used sentence-completion tasks in the Japanese language that include basic sentence processing. The results showed activation in the left IFG and left parietal lobe, suggesting that these areas are involved in sentence processing. We then investigated the proportion of patients showing impaired sentence processing from among patients with aphasia and a lesion in the left IFG or from the parietal lobe to the posterior superior temporal gyrus. Four of 5 patients (80%) with lesions mostly in the left IFG showed impaired sentence processing, suggesting that this site plays a critical role in sentence processing. Of the 4 patients with lesions mostly in the area from the left parietal lobe to the posterior superior temporal gyrus, 1 patient (25%) showed impaired sentence processing. Unlike the other 3 subjects, this subject exhibited impaired recalling of verbs. This area is mainly involved in lexical-semantics and the present results suggest that verb information within that field became impaired, in turn causing impaired sentence processing. [Copyright &y& Elsevier]

The short-day plant pharbitis (also called Japanese morning glory), Ipomoea nil (formerly Pharbitis nil ), was induced to flower by poor-nutrition stress. This stress-induced flowering was inhibited by aminooxyacetic acid (AOA), which is a known inhibitor of phenylalanine ammonia-lyase (PAL) and the synthesis of indole-3-acetic acid (IAA) and 1-aminocycropropane-1-carboxylic acid (ACC) and thus regulates endogenous levels of salicylic acid (SA), IAA and polyamine (PA). Stress treatment increased PAL activity in cotyledons, and AOA suppressed this increase. The observed PAL activity and flowering response correlate positively, indicating that AOA functions as a PAL inhibitor. The inhibition of stress-induced flowering by AOA was also overcome by IAA. An antiauxin, 4 -chlorophenoxy isobutyric acid, inhibited stress-induced flowering. Both SA and IAA promoted flowering induced by stress. PA also promoted flowering, and the effective PA was found to be putrescine (Put). These results suggest that all of the pathways leading to the synthesis of SA, IAA and Put are responsive to the flowering inhibition by AOA and that these endogenous factors may be involved in the regulation of stress-induced flowering. However, as none of them induced flowering under non-stress conditions, they may function cooperatively to promote flowering. [ABSTRACT FROM AUTHOR]

Abstract: A genome-wide association study identified that LRP2 rs2544390 in intron 1 was associated with serum uric acid (SUA) levels among Japanese, as well as polymorphisms of SLC22A12, ABCG2, and SLC2A9. This study aimed to confirm the association of rs2544390 C/T with SUA, as well as another LRP2 polymorphism (rs3755166 G/A) in the promoter. Subjects were 5016 health checkup examinees (3409 males and 1607 females) aged 35 to 69years with creatinine<2.0mg/dL. The subjects with SLC22A12 258WW, SLC2A9 rs11722228C allele, ABCG2 126QQ and 141Q allele (2546 males and 1199 females) were selected for analysis. Mean SUA was 6.03mg/dL for CC, 6.18mg/dL for CT, and 6.19mg/dL for TT among males (p=0.012), and 4.49mg/dL, 4.45mg/dL, and 4.42mg/dL among females (not significant), respectively. No association was observed for rs3755166. The association with rs2544390 was stronger among male drinkers. The odds ratio of drinking ≥5/week relative to no drinking for hyperuricemia (SUA≥7mg/dL and/or under medication for hyperuricemia) was 1.11 (95% confidence interval, 0.67–1.84) among CC males, 1.75 (1.22–2.51) among CT males, and 3.13 (1.80–5.43) among TT males. The interaction terms with drinking ≥5/week were 1.56 (p=0.156) for CT and 2.87 (p=0.005) for TT. This was the first report on the interaction between LRP2 genotype and alcohol drinking for SUA. Since the low density lipoprotein-related protein 2 (megalin) encoded by LRP2 is a multi-ligand endocytic receptor expressed in many tissues including the kidney proximal tubules, the association/interaction remained to be confirmed both epidemiologically and biologically. [Copyright &y& Elsevier]

To investigate the association between alcohol intake pattern in amount and frequency and metabolic syndrome (Mets) components, we simulated the change in the prevalence of Mets components by intake reduction. In order to manage Mets, alcohol intake reduction with moderation of intake pattern is required. However, evidence investigating the comparative impact of alcohol intake reduction in amount and frequency for Mets components is limited. We conducted a large-scale cross-sectional study in the general Japanese population. The study subjects included 37,371 non-drinkers and current drinkers recruited in the Japan Multi-Institutional Collaborative Cohort Study. Odds ratios (ORs) for Mets components according to alcohol intake amount and frequency were estimated using a multiple logistic regression model. The prevalence of Mets components was estimated after assumed alcohol intake reduction of a) none, b) 10 g/day (men) or 5 g/day (women), c) 20 g/day (men) or 10 g/day (women), d) less than 20 g/day (men) or 10 g/day (women) for moderate-to-heavy drinkers, e) 1-2 times/week, and f) 3-4 times/week. The ORs with alcohol intake amount and frequency increased with high blood pressure while decreasing with dyslipidemia. A J-shaped association was observed between intake amount and Mets. The estimated prevalence (%) of high blood pressure and dyslipidemia in men were a) 45.2, b) 43.0, c) 41.4, d) 40.4, e) 42.9, and f) 42.0; and a) 50.3, b) 51.8, c) 52.9, d) 50.2, e) 52.7, and f) 53.4 in women. The estimated prevalence of high blood pressure in women did not evidently decrease. Simulated alcohol intake reduction showed decreased prevalence for high blood pressure and increased prevalence for dyslipidemia in men after reduced intake amount and frequency. The largest decreased prevalence for high blood pressure was observed in men when all moderate-to-heavy drinkers reduced their alcohol intake amount to less than 20 g/day. [ABSTRACT FROM AUTHOR]

• Defect of Hexb leads to change in sox2 gene in embryonic cortices. • Defect of Hexb leads to reduced neuronal precursor migration in embryonic cortices. • The production of layer-specific neurons is delayed in cortices of hexb −/− mice. Sandhoff disease (SD) is a genetic disorder caused by a mutation of HEXB , which is the β-subunit gene of β-hexosaminidase A and B (HexA and HexB) in humans. HEXB mutation reduces HexA and HexB enzymatic activities, and results in the massive accumulation of ganglioside GM2 in the nervous system. Severe phenotypes of SD show progressive neurodegeneration in human infants, and lysosomal dysfunction that may affect the early development of the nervous system. In a previous study, neural stem cells (NSCs) and induced pluripotent stem cells derived from SD model mice, which are Hexb -deficient (Hexb −/−), demonstrated impaired neuronal differentiation. This study investigated early neurodevelopment in vivo using Hexb −/− mice. The structure of adult cerebral cortices of Hexb −/− mice was normal. However, the expression of Sox2 , an NSC-related gene, was reduced in the embryonic cerebral cortices of Hexb −/− mice. Moreover, a reduction of early neuronal migration and differentiation was observed in the embryonic cerebral cortices of Hexb −/− mice. In addition, we showed that the production of layer-specific neurons was delayed in somatosensory cerebral cortices of Hexb −/− mice. These findings suggest that the alterations observed in embryonic Hexb −/− mice may contribute to deficits in neurodevelopment of SD. [ABSTRACT FROM AUTHOR]

Erythrocyte count and volume are the commonly used hematological indices for anemia that change in various diseases. To date, however, only one study ever exists that addressed erythrocyte trait-associated single nucleotide polymorphisms (SNPs) in a Japanese population. Because that study was performed in patients with various diseases, we confirmed the reported associations in a general population. Participants in the current study were from the Shizuoka component of the Japan Multi-Institutional Collaborative Cohort Study, which included 4971 men and women aged 35 to 69 years who were recruited between 2006 and 2007. We analyzed the association of seven selected SNPs with the following erythrocyte traits: red blood cell count, hemoglobin (Hb) and hematocrit (Ht) levels, mean corpuscular volume, mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration. The erythrocyte traits were regressed on a number of minor alleles of selected SNPs. Then we compared our findings with those from a genome-wide association study performed in a Japanese population. We replicated the association of ABO rs495828, PDGFRA-KIT rs218237, USP49-MED20-BSYL-CCND3 rs3218097, C6orf182-CD164 rs11966072, TERT rs2736100, and TMPRSS6 rs5756504 with erythrocyte traits in our independent Japanese population. In addition, we found a significant interaction between TERT rs2736100 and smoking habit that affected Hb and Ht levels. [ABSTRACT FROM AUTHOR]

Abstract: Urokinase plasminogen activator (uPA) plays important physiological and pathological roles in fibrinolysis, cancer metastasis, and atherosclerosis. One study suggested that uPA also has a major role in cholesterol biosynthesis in humans via its receptor uPAR. Thus, we investigated the associations of functional uPA polymorphism (plasminogen activator, urokinase; PLAU Pro141Leu, rs2227564) with serum lipid profiles in a Japanese cohort. The study included 5152 participants (1465 male, 3687 female; age range, 35–69years) of the Daiko Study, a part of the Japan Multi-Institutional Collaborative Cohort Study (J-MICC Study). Subjects were enrolled at the Daiko Medical Center from June 2008 to May 2010. Low-density lipoprotein cholesterol (LDL-C) and non-HDL-C (subtraction of high-density lipoprotein cholesterol from total cholesterol) in fasting blood of participants were each classified into two groups, < or ≥140mg/dL, and < or ≥170mg/dL, respectively. Genotype frequencies of PLAU Pro141Leu (rs2227564) were 59.1% for ProPro, 35.6% for ProLeu, and 5.3% for LeuLeu, and were in Hardy–Weinberg equilibrium (p =0.789). The allele frequencies were 0.769 for Pro and 0.231 for Leu. The multivariate-adjusted odd ratios (ORs) and 95% confidence intervals (CIs) for high LDL-C and non-HDL-C were 1.11 (95%CI; 1.00–1.23) and 1.16 (95%CI; 1.03–1.30) for those with Leu allele relative to ProPro. This study suggested that PLAU Pro141Leu (rs2227564) is significantly associated with serum lipid levels in a Japanese population. [Copyright &y& Elsevier]

Abstract: In our previous proteomic study in rat liver damaged by carbon tetrachloride, soluble catechol-O-methyltransferase (COMT) increased as a phosphorylated form and decreased as a dephosphorylated form. This finding raised the possibility that the COMT protein is associated with liver function. Thus, we hypothesized that (1) the COMT gene contributes to liver homeostasis and (2) a COMT polymorphism (rs4680: Val158Met) causing thermolability of enzymatic activity affects liver enzymes (e.g., aspartate aminotransferase (AST), alanine aminotransferase (ALT) and gamma-glutamyl transpeptidase (γ-GT)) in serum. To investigate (2), we statistically analyzed the association between COMT genotypes and serum ALT activity in a cross-sectional study using data from the Japan Multi-Institutional Collaborative Cohort (J-MICC) Study. We conducted a multiple logistic regression analysis for males (n=838) and females (n=970). Those participants having missing values or a past history of liver cirrhosis or liver cancer were excluded. ALT values were divided into two; elevated (30IU/L ≤; males n=239, females n=90) and normal (<30IU/L; males n=599, females n=880). In females, non-adjusted and adjusted odds ratios for ALT values in the rs4680 A/A homozygote (n=126) compared with the wild-type G/G homozygote (n=397) were 0.37 (95% CI 0.14–0.96) and 0.34 (95% CI 0.13–0.93), respectively. In males, an analysis of the population aged 35–69 did not reveal any significant difference, but the population aged 45–54 had a significant difference in the non-adjusted and adjusted odds ratio in the G/A heterozygote (n=89) (0.50 (95% CI 0.27–0.92) and 0.35 (95% CI 0.18–0.71)) and in the A/A homozygote (n=22) (0.34 (95% CI 0.11–0.99) and 0.22 (95% CI 0.07–0.72)), compared with the G/G homozygote (n=88). These data suggest that the COMT polymorphism affects serum ALT activity to maintain liver function. [Copyright &y& Elsevier]

• We conducted two cross-sectional studies of community-dwelling adults. • We examined the association of PPAR-γ polymorphisms with serum lipids. • Two polymorphisms were related to a lower prevalence of dyslipidemia and/or high LDL-C. • Similar reductions in prevalence were found in the second survey. Dyslipidemia is a well-established risk factor for cardiovascular disease. Experimental studies have reported that peroxisome proliferator-activated receptor γ (PPAR-γ) regulates adipocyte differentiation, lipid storage, and glucose metabolism. Therefore, we examined the associations between PPAR-γ polymorphisms (rs1801282, rs3856806, rs12497191, rs1151999, and rs1152003) and serum lipids in two cross-sectional studies. In the Shizuoka area of the Japan Multi-Institutional Collaborative Cohort Study, we examined 4,952 participants (3,356 men and 1,596 women) in a baseline survey and 2,245 participants (1,550 men and 695 women) in a second survey 5 years later. Outcome measures were the prevalence of dyslipidemia (low-density lipoprotein-cholesterol [LDL-C] ≥ 140 mg/dl, high-density lipoprotein-cholesterol < 40 mg/dl, triglycerides ≥ 150 mg/dl, and/or use of cholesterol-lowering drugs) and the prevalence of high LDL-C (LDL-C ≥ 140 mg/dl and/or use of cholesterol-lowering drugs). Multivariate odds ratios (ORs) were estimated by using unconditional logistic regression models. A total of 2,114 and 1,431 individuals (42.7% and 28.9%) had dyslipidemia and high LDL-C in the baseline survey, respectively, as did 933 and 716 (41.6% and 31.9%), respectively, in the second survey. In the baseline study, compared with major allele homozygotes, minor allele homozygotes of rs3856806 and rs12497191 had a 42% (OR, 0.58; 95% confidence interval (CI), 0.39–0.85) and 23% (OR, 0.77; 95% CI, 0.60–0.99) lower risk of dyslipidemia, respectively, after adjustment for potential confounding factors. In addition, minor allele homozygotes of rs3856806 had a 45% (OR, 0.55; 95% CI, 0.35–0.86) lower risk of high LDL-C. Similar risk reductions were found in the second survey. In conclusion, rs3856806 and rs12497191 polymorphisms may be related to a lower risk of dyslipidemia and high LDL-C. [ABSTRACT FROM AUTHOR]