Molecular phylogeny and historical biogeography of the genus Platycerus (Coleoptera,Lucanidae) in East Asia

The genus Platycerus is a cool temperature zone taxon widely distributed in the Northern Hemisphere. In East Asia, 10, one and 28 species are known in Japan, Korea and China, respectively. Recent studies of Platycerus have revealed the divergence pattern in Japan and South Korea, but that of Chinese Platycerus is unknown. We conducted a phylogenetic and biogeographical study of Platycerus in East Asia, including China, using 68, 87 and 296 sequence data of the nuclear wingless gene, internal transcribed spacer (ITS) region and mitochondrial COI gene, respectively. Although the introgression of mitochondrial genes had been known in Japanese Platycerus, the essential contradiction was not recognized between the phylogenetic trees of nuclear genes and COI in Chinese Platycerus. In the COI tree, the Japanese clade and Asian continental clade diverged around 10.84 million years ago, and four major clades were recognized in the latter. For the shape of the posterolateral corner of the Platycerus pronotum, sharp (S)-type species are distributed in higher latitudinal and lower altitudinal areas than round (R)-type species in the Asian continent. S-type species have evolved from R-type species at least three times in more northerly areas, where the annual amplitude of temperature change is large. The genus Platycerus has been differentiated and speciated by a process unique to South Korea, Japan and China, according to regional topography. Thus, genetic differentiation and speciation in Platycerus are related to latitudinal and altitudinal gradients, as well as the site topographical profile and niche differentiation.     

Neuroticism Delays Detection of Facial Expressions

The rapid detection of emotional signals from facial expressions is fundamental for human social interaction. The personality factor of neuroticism modulates the processing of various types of emotional facial expressions; however, its effect on the detection of emotional facial expressions remains unclear. In this study, participants with high- and low-neuroticism scores performed a visual search task to detect normal expressions of anger and happiness, and their anti-expressions within a crowd of neutral expressions. Anti-expressions contained an amount of visual changes equivalent to those found in normal expressions compared to neutral expressions, but they were usually recognized as neutral expressions. Subjective emotional ratings in response to each facial expression stimulus were also obtained. Participants with high-neuroticism showed an overall delay in the detection of target facial expressions compared to participants with low-neuroticism. Additionally, the high-neuroticism group showed higher levels of arousal to facial expressions compared to the low-neuroticism group. These data suggest that neuroticism modulates the detection of emotional facial expressions in healthy participants; high levels of neuroticism delay overall detection of facial expressions and enhance emotional arousal in response to facial expressions.     

Limited Phenotypic Effects of Selectively Augmenting the SMN Protein in the Neurons of a Mouse Model of Severe Spinal Muscular Atrophy

The selective vulnerability of motor neurons to paucity of Survival Motor Neuron (SMN) protein is a defining feature of human spinal muscular atrophy (SMA) and indicative of a unique requirement for adequate levels of the protein in these cells. However, the relative contribution of SMN-depleted motor neurons to the disease process is uncertain and it is possible that their characteristic loss and the overall SMA phenotype is a consequence of low protein in multiple cell types including neighboring spinal neurons and non-neuronal tissue. To explore the tissue-specific requirements for SMN and, especially, the salutary effects of restoring normal levels of the protein to neuronal tissue of affected individuals, we have selectively expressed the protein in neurons of mice that model severe SMA. Expressing SMN pan-neuronally in mutant mice mitigated specific aspects of the disease phenotype. Motor performance of the mice improved and the loss of spinal motor neurons that characterizes the disease was arrested. Proprioceptive synapses on the motor neurons were restored and defects of the neuromuscular junctions mitigated. The improvements at the cellular level were reflected in a four-fold increase in survival. Nevertheless, mutants expressing neuronal SMN did not live beyond three weeks of birth, a relatively poor outcome compared to the effects of ubiquitously restoring SMN. This suggests that although neurons and, in particular, spinal motor neurons constitute critical cellular sites of action of the SMN protein, a truly effective treatment of severe SMA will require restoring the protein to multiple cell types including non-neuronal tissue.     

Oxidation of Thionocarbamates into Sulfur-free Carbamates by an Iodine-DMSO System

The proliferating activity of Ehrlich ascites tumor cells decreased with the increase of the concentration of DEPC per 3 × 10⁷ cells and disappeared at more than 200 μg. Sixty per cent of the mice immunized with 200 μg DEPC-treated Ehrlich cells twice survived the challenge inoculation. And employment of Freund’s complete adjuvant on the immunization increased the survival ratio up to 90 ~ 100%.

Respiratory activity, trypan blue stainability and agglutination by concanavalin A were investigated. These results and the electronmicroscopical observation suggest that the specific structure of the cell surface must be maintained in the DEPC-treatment in order to display immunogenicity.     

Synergistic Proinflammatory Responses by IL-17A and Toll-Like Receptor 3 in Human Airway Epithelial Cells

Viral respiratory infections activate the innate immune response in the airway epithelium through Toll-like receptors (TLRs) and induce airway inflammation, which causes acute exacerbation of asthma. Although increases in IL-17A expression were observed in the airway of severe asthma patients, the interaction between IL-17A and TLR activation in airway epithelium remains poorly understood. In this study, we demonstrated that IL-17A and polyI:C, the ligand of TLR3, synergistically induced the expression of proinflammatory cytokines and chemokines (G-CSF, IL-8, CXCL1, CXCL5, IL-1F9), but not type I interferon (IFN-α1, -β) in primary culture of normal human bronchial epithelial cells. Synergistic induction after co-stimulation with IL-17A and polyI:C was observed from 2 to 24 hours after stimulation. Treatment with cycloheximide or actinomycin D had no effect, suggesting that the synergistic induction occurred without de novo protein synthesis or mRNA stabilization. Inhibition of the TLR3, TLR/TIR-domain-containing adaptor-inducing interferon β (TRIF), NF-κB, and IRF3 pathways decreased the polyI:C- and IL-17A/polyI:C-induced G-CSF and IL-8 mRNA expression. Comparing the levels of mRNA induction between co-treatment with IL-17A/polyI:C and treatment with polyI:C alone, blocking the of NF-κB pathway significantly attenuated the observed synergism. In western blotting analysis, activation of both NF-κB and IRF3 was observed in treatment with polyI:C and co-treatment with IL-17A/polyI:C; moreover, co-treatment with IL-17A/polyI:C augmented IκB-α phosphorylation as compared to polyI:C treatment alone. Collectively, these findings indicate that IL-17A and TLR3 activation cooperate to induce proinflammatory responses in the airway epithelium via TLR3/TRIF-mediated NF-κB/IRF3 activation, and that enhanced activation of the NF-κB pathway plays an essential role in synergistic induction after co-treatment with IL-17A and polyI:C in vitro.