Ternary maximal self-orthogonal codes of lengths 21,2221,22 and 2323

We give a classification of ternary maximal self-orthogonal codes of lengths $21,22$ and $23$. This completes a classification of ternary maximal self-orthogonal codes of lengths up to $24$

OCTAD-S: Digital Fast Fourier Transform Spectrometers by FPGA

We have developed a digital fast Fourier transform (FFT) spectrometer made of an analog-to-digital converter (ADC) and a field-programmable gate array (FPGA). The base instrument has independent ADC and FPGA modules, which allow us to implement different spectrometers in a relatively easy manner. Two types of spectrometers have been instrumented, one with 4.096 GS/s sampling speed and 2048 frequency channels and the other with 2.048 GS/s sampling speed and 32768 frequency channels. The signal processing in these spectrometers has no dead time and the accumulated spectra are recorded in external media every 8 ms. A direct sampling spectroscopy up to 8 GHz is achieved by a microwave track-and-hold circuit, which can reduce the analog receiver in front of the spectrometer. Highly stable spectroscopy with a wide dynamic range was demonstrated in a series of laboratory experiments and test observations of solar radio bursts.Comment: 20 pages, 7 figures, accepted for publication in Earth, Planets and Spac

Unmutated Immunoglobulin M Can Protect Mice from Death by Influenza Virus Infection

To elucidate the role of class switch recombination (CSR) and somatic hypermutation (SHM) in virus infection, we have investigated the influence of the primary and secondary infections of influenza virus on mice deficient of activation-induced cytidine deaminase (AID), which is absolutely required for CSR and SHM. In the primary infection, AID deficiency caused no significant difference in mortality but did cause difference in morbidity. In the secondary infection with a lethal dose of influenza virus, both AID−/− and AID+/− mice survived completely. However, AID−/− mice could not completely block replication of the virus and their body weights decreased severely whereas AID+/− mice showed almost complete prevention from the reinfection. Depletion of CD8+ T cells by administration of an anti-CD8 monoclonal antibody caused slightly severer body weight loss but did not alter the survival rate of AID−/− mice in secondary infection. These results indicate that unmutated immunoglobulin (Ig)M alone is capable of protecting mice from death upon primary and secondary infections. Because the titers of virus-neutralizing antibodies were comparable between AID−/− and AID+/− mice at the time of the secondary infection, a defect of AID−/− mice in protection of morbidity might be due to the absence of either other Ig classes such as IgG, high affinity antibodies with SHM, or both

Linalool Odor-Induced Anxiolytic Effects in Mice

In folk medicine, it has long been believed that odorous compounds derived from plant extracts can have anxiolytic effects. Among them, linalool, one of the terpene alcohols in lavender extracts, has been reported to have the anxiolytic effects. However, the anxiolytic nature of the linalool odor itself as well as its potential action through the olfactory system has not been thoroughly examined. In this study, we examined the anxiolytic effects of linalool odor with light/dark box test and with elevated plus maze (EPM), and found that linalool odor has an anxiolytic effect without motor impairment in mice. The effect was not observed in anosmic mice, indicating that it was triggered by olfactory input evoked by linalool odor. Furthermore, the effect was antagonized by flumazenil, indicating that the linalool odor-induced anxiolytic effect was mediated by γ-aminobutyric acid (GABA)ergic transmission via benzodiazepine (BDZ)-responsive GABAA receptors. These results provide information about the potential central neuronal mechanisms underlying the odor-induced anxiolytic effects and the foundation for exploring clinical application of linalool odor in anxiety treatments

Collective fusion activity determines neurotropism of an en bloc transmitted enveloped virus

麻疹（はしか）ウイルスが「協力」して脳炎を引き起こす仕組みを解明 --新規治療薬の開発やウイルス共通の進化メカニズム解明に期待--. 京都大学プレスリリース. 2023-01-30.Measles virus (MeV), which is usually non-neurotropic, sometimes persists in the brain and causes subacute sclerosing panencephalitis (SSPE) several years after acute infection, serving as a model for persistent viral infections. The persisting MeVs have hyperfusogenic mutant fusion (F) proteins that likely enable cell-cell fusion at synapses and "en bloc transmission" between neurons. We here show that during persistence, F protein fusogenicity is generally enhanced by cumulative mutations, yet mutations paradoxically reducing the fusogenicity may be selected alongside the wild-type (non-neurotropic) MeV genome. A mutant F protein having SSPE-derived substitutions exhibits lower fusogenicity than the hyperfusogenic F protein containing some of those substitutions, but by the wild-type F protein coexpression, the fusogenicity of the former F protein is enhanced, while that of the latter is nearly abolished. These findings advance the understanding of the long-term process of MeV neuropathogenicity and provide critical insight into the genotype-phenotype relationships of en bloc transmitted viruses