Open Multi-Access Network Platform with Dynamic Task Offloading and Intelligent Resource Monitoring

We constructed an open multi-access network platform using open-source hardware and software. The open multi-access network platform is characterized by the flexible utilization of network functions, integral management and control of wired and wireless access networks, zero-touch provisioning, intelligent resource monitoring, and dynamic task offloading. We also propose an application-driven dynamic task offloading that utilizes intelligent resource monitoring to ensure effective task processing in edge and cloud servers. For this purpose, we developed a mobile application and server applications for the open multi-access network platform. To investigate the feasibility and availability of our developed platform, we experimentally and analytically evaluated the effectiveness of application-driven dynamic task offloading and intelligent resource monitoring. The experimental results demonstrated that application-driven dynamic task offloading could reduce real-time task response time and traffic over metro and core networks

Cross-Speaker Emotion Transfer for Low-Resource Text-to-Speech Using Non-Parallel Voice Conversion with Pitch-Shift Data Augmentation

Data augmentation via voice conversion (VC) has been successfully applied to low-resource expressive text-to-speech (TTS) when only neutral data for the target speaker are available. Although the quality of VC is crucial for this approach, it is challenging to learn a stable VC model because the amount of data is limited in low-resource scenarios, and highly expressive speech has large acoustic variety. To address this issue, we propose a novel data augmentation method that combines pitch-shifting and VC techniques. Because pitch-shift data augmentation enables the coverage of a variety of pitch dynamics, it greatly stabilizes training for both VC and TTS models, even when only 1,000 utterances of the target speaker's neutral data are available. Subjective test results showed that a FastSpeech 2-based emotional TTS system with the proposed method improved naturalness and emotional similarity compared with conventional methods.Comment: Submitted to Interspeech 202

H3K9 Demethylases JMJD1A and JMJD1B Control Prospermatogonia to Spermatogonia Transition in Mouse Germline

Histone H3 lysine 9 (H3K9) methylation is dynamically regulated by methyltransferases and demethylases. In spermatogenesis, prospermatogonia differentiate into differentiating or undifferentiated spermatogonia after birth. However, the epigenetic regulation of prospermatogonia to spermatogonia transition is largely unknown. We found that perinatal prospermatogonia have extremely low levels of di-methylated H3K9 (H3K9me2) and that H3K9 demethylases, JMJD1A and JMJD1B, catalyze H3K9me2 demethylation in perinatal prospermatogonia. Depletion of JMJD1A and JMJD1B in the embryonic germline resulted in complete loss of male germ cells after puberty, indicating that H3K9me2 demethylation is essential for male germline maintenance. JMJD1A/JMJD1B-depleted germ cells were unable to differentiate into functional spermatogonia. JMJD1 isozymes contributed to activation of several spermatogonial stem cell maintenance genes through H3K9 demethylation during the prospermatogonia to spermatogonia transition, which we propose is key for spermatogonia development. In summary, JMJD1A/JMJD1B-mediated H3K9me2 demethylation promotes prospermatogonia to differentiate into functional spermatogonia by establishing proper gene expression profiles

Selective Gene Transfer to the Retina Using Intravitreal Ultrasound Irradiation

This paper aims to evaluate the efficacy of intravitreal ultrasound (US) irradiation for green fluorescent protein (GFP) plasmid transfer into the rabbit retina using a miniature US transducer. Intravitreal US irradiation was performed by a slight modification of the transconjunctival sutureless vitrectomy system utilizing a small probe. After vitrectomy, the US probe was inserted through a scleral incision. A mixture of GFP plasmid (50 μL) and bubble liposomes (BLs; 50 μL) was injected into the vitreous cavity, and US was generated to the retina using a SonoPore 4000. The control group was not exposed to US. After 72 h, the gene-transfer efficiency was quantified by counting the number of GFP-positive cells. The retinas that received plasmid, BL, and US showed a significant increase in the number (average ± SEM) of GFP-positive cells (32 ± 4.9; n = 7; P < 0.01 ). No GFP-positive cells were observed in the control eyes (n = 7). Intravitreal retinal US irradiation can transfer the GFP plasmid into the retina without causing any apparent damage. This procedure could be used to transfer genes and drugs directly to the retina and therefore has potential therapeutic value

正常ラット口蓋粘膜におけるメルケル細胞の脱落とアポトーシスの有無について

The life span of Merkel cells (MCs) in normal epitheha is not known During the course of a previous study we found that the numerical density of MCs in the postrugal field (PRF) of the rat hard palate is very low in adults compared to juveniles We also noticed that PRFs of premature rats contain many ectopic MCs in epithelial surface layers It is of interest to know whether the reduction of MC density in PRFs is related to expansion of the area of PRFs or to the disappearance of MCs from the epithelium, and also whether the ectopic MCs mean cell turnover accompanied by apoptosis Therefore, we examined changes of numbers and numerical densities of MCs in PRFs of rats of various days of age Apoptosis of ectopic MCs was examined by a fluorescence nick end labeling combined with mmunohistochemistry for anti-cytokeratm 18 It was found that MCs in PRFs are reduced not only in numerical density but also in number during prematuration stages of rats There were no MCs that had a nucleus with nick end label, not only in surface layers but also in basal layers of PRF epithelium It was concluded that a large number of MCs are lost from epitheha of growing rat PRFs by desquamation and apoptosis is probably irrelevant to this phenomenon

Tuning of Sry expression by H3K9 methylation and demethylation

Histone H3 lysine 9 (H3K9) methylation is a hallmark of heterochromatin. H3K9 demethylation is crucial in mouse sex determination; The H3K9 demethylase Jmjd1a deficiency leads to increased H3K9 methylation at the Sry locus in embryonic gonads, thereby compromising Sry expression and causing male-to-female sex reversal. We hypothesized that the H3K9 methylation level at the Sry locus is finely tuned by the balance in activities between the H3K9 demethylase Jmjd1a and an unidentified H3K9 methyltransferase to ensure correct Sry expression. Here we identified the GLP/G9a H3K9 methyltransferase complex as the enzyme catalyzing H3K9 methylation at the Sry locus. Based on this finding, we tried to rescue the sex-reversal phenotype of Jmjd1a-deficient mice by modulating GLP/G9a complex activity. A heterozygous GLP mutation rescued the sex-reversal phenotype of Jmjd1a-deficient mice by restoring Sry expression. The administration of a chemical inhibitor of GLP/G9a enzyme into Jmjd1a-deficient embryos also successfully rescued sex reversal. Our study not only reveals the molecular mechanism underlying the tuning of Sry expression but also provides proof on the principle of therapeutic strategies based on the pharmacological modulation of epigenetic balance

Combined Loss of JMJD1A and JMJD1B Reveals Critical Roles for H3K9 Demethylation in the Maintenance of Embryonic Stem Cells and Early Embryogenesis

Histone H3 lysine 9 (H3K9) methylation is unevenly distributed in mammalian chromosomes. However, the molecular mechanism controlling the uneven distribution and its biological significance remain to be elucidated. Here, we show that JMJD1A and JMJD1B preferentially target H3K9 demethylation of gene-dense regions of chromosomes, thereby establishing an H3K9 hypomethylation state in euchromatin. JMJD1A/JMJD1B-deficient embryos died soon after implantation accompanying epiblast cell death. Furthermore, combined loss of JMJD1A and JMJD1B caused perturbed expression of metabolic genes and rapid cell death in embryonic stem cells (ESCs). These results indicate that JMJD1A/JMJD1B-meditated H3K9 demethylation has critical roles for early embryogenesis and ESC maintenance. Finally, genetic rescue experiments clarified that H3K9 overmethylation by G9A was the cause of the cell death and perturbed gene expression of JMJD1A/JMJD1B-depleted ESCs. We summarized that JMJD1A and JMJD1B, in combination, ensure early embryogenesis and ESC viability by establishing the correct H3K9 methylated epigenome