No abstract

Little is known about the nature or extent of everyday variability in voice quality. This paper describes a series of principal component analyses to explore within-and between-talker acoustic variation and the extent to which they conform to expectations derived from current models of voice perception. Based on studies of faces and cognitive models of speaker recognition, we hypothesized that a few measures would be important across speakers, but that much of within-speaker variability would be idiosyncratic. Analyses used multiple sentence productions from fifty female and fifty male speakers of English, recorded over three days. Twenty-six acoustic variables from a psychoacoustic model of voice quality were measured every 5 ms on vowels and approximants. Across speakers the balance between higher harmonic amplitudes and inharmonic energy in the voice accounted for the most variance (fe-males=20%, males=22%). Formant frequencies and their variability accounted for an additional 12% of variance across speakers. Remaining variance appeared largely idiosyncratic, suggesting that the speaker-specific voice space is different for different people. Results further showed that voice spaces for individuals and for the population of talkers have very similar acoustic structures. Implications for prototype models of voice perception and recognition are discussed.

DJ-1 is one of the causative genes for early onset familiar Parkinson’s disease (PD) and is also considered to influence the pathogenesis of sporadic PD. DJ-1 has various physiological functions which converge on controlling intracellular reactive oxygen species (ROS) levels. In RNA-sequencing analyses searching for novel anti-oxidant genes downstream of DJ-1, a gene encoding NADP+-dependent isocitrate dehydrogenase (IDH), which converts isocitrate into α-ketoglutarate, was detected. Loss of IDH induced hyper-sensitivity to oxidative stress accompanying age-dependent mitochondrial defects and dopaminergic (DA) neuron degeneration in Drosophila, indicating its critical roles in maintaining mitochondrial integrity and DA neuron survival. Further genetic analysis suggested that DJ-1 controls IDH gene expression through nuclear factor-E2-related factor2 (Nrf2). Using Drosophila and mammalian DA models, we found that IDH suppresses intracellular and mitochondrial ROS level and subsequent DA neuron loss downstream of DJ-1. Consistently, trimethyl isocitrate (TIC), a cell permeable isocitrate, protected mammalian DJ-1 null DA cells from oxidative stress in an IDH-dependent manner. These results suggest that isocitrate and its derivatives are novel treatments for PD associated with DJ-1 dysfunction.

The effect of secretory group II phospholipase A2 (sPLA2) on the expression of the inducible NO synthase (iNOS) and the production of NO by macrophages was investigated. sPLA2 by itself barely stimulated nitrite production and iNOS expression in Raw264.7 cells. However, in combination with LPS, the effects were synergistic. This potentiation was shown for sPLA2 enzymes from sPLA2-transfected stable cells or for purified sPLA2 from human synovial fluid. The effect of PLA2 on iNOS induction appears to be specific for the secretory type of PLA2. LPS-stimulated activation of iNOS was inhibited by the well-known selective inhibitors of sPLA2 such as 12-epi-scalaradial and ρ-bromophenacyl bromide. In contrast, the cytosolic PLA2-specific inhibitors methyl arachidonyl fluorophosphate and arachidonyltrifluoromethyl ketone did not affect LPS-induced nitrite production and iNOS expression. Moreover, when we transfected cDNA-encoding type II sPLA2, we observed that the sPLA2-transfected cells produced two times more nitrites than the empty vector or cytosolic PLA2-transfected cells. The sPLA2-potentiated iNOS expression was associated with the activation of NF-κB. We found that the NF-κB inhibitor pyrrolidinedithiocarbamate prevented nitrite production, iNOS induction, and mRNA accumulation by sPLA2 plus LPS in Raw264.7 cells. Furthermore, EMSA analysis of the activation of the NF-κB involved in iNOS induction demonstrated that pyrrolidinedithiocarbamate prevented the NF-κB binding by sPLA2 plus LPS. Our findings indicated that sPLA2, in the presence of LPS, is a potent activator of macrophages. It stimulates iNOS expression and nitrite production by a mechanism that requires the activation of NF-κB.

This study investigated the transition between the free and bound forms of functional compounds in germinated black soybean. Black soybean was germinated at 25°C over 6 days and then the free and bound forms of functional compounds were extracted. Total free polyphenol, flavonoid, and phenolic acid contents in raw black soybean increased from 1.03 mg GAE/g, 0.29 mg CE/g, and 315.67 μg/g to 1.44mg GAE/g, 0.64mg CE/g, and 511.01 μg/g, respectively, by 4 days after germination. Changes to phenolic acid compositions can be divided into four groups, and the germination process can convert compounds to phenolic acid via anabolism and catabolism. The highest total free isoflavone content in germinated black soybean (3,724.40 μg/g) was observed at 4 days. Bound polyphenol, flavonoid, phenolic acid, and isoflavone contents decreased as the germination period increased. These results suggest that the germination process increased compound functionality in black soybean.