Molecular docking and kinetic study of transglycosylation reaction for naringenin using amylosucrase from Deinococcus wulumuqiensis

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Electronic structures of hexagonal RMnO3 (R = Gd, Tb, Dy, and Ho) thin films

We investigated the electronic structure of multiferroic hexagonal RMnO3 (R = Gd, Tb, Dy, and Ho) thin films using both optical spectroscopy and first-principles calculations. Using artificially stabilized hexagonal RMnO3, we extended the optical spectroscopic studies on the hexagonal multiferroic manganite system. We observed two optical transitions located near 1.7 eV and 2.3 eV, in addition to the predominant absorption above 5 eV. With the help of first-principles calculations, we attribute the low-lying optical absorption peaks to inter-site transitions from the oxygen states hybridized strongly with different Mn orbital symmetries to the Mn 3d3z2-r2 state. As the ionic radius of the rare earth ion increased, the lowest peak showed a systematic increase in its peak position. We explained this systematic change in terms of a flattening of the MnO5 triangular bipyramid

Mechanism of Cyclophosphamide-Induced Ovarian Follicle Loss in the Prepubertal Mouse

Background: Cancer therapies cause serious side effects, affecting the quality of life for young cancer survivors. The ovary is affected by cancer therapies, causing premature ovarian insufficiency, leading to endocrine dysfunction, infertility, and ovarian aging. Thus, maintaining ovarian function against cancer treatment is an unmet need for female cancer patients. Cyclophosphamide (CPA), a common chemotherapeutic agent, forms DNA crosslinks to induce apoptosis in rapidly proliferating tumor cells. However, the underlying mechanism of the CPA-induced oocyte death in ovarian reserve remains unclear. Experimental design: This study aims to investigate the mechanism of oocyte death in primordial follicles by generating oocyte-specific Abl1 and p63 knockout and Pik3ca* knockin mouse models using Gdf9-iCre+. Prepubertal day 7 female mice were utilized for further analysis. Results: The quantification of surviving follicles validated that 90% of the primordial follicles from oocyte-specific Abl1 knockout mice were lost following CPA treatment in vivo and in vitro. Concurrently, high expression of CHK2 was detected in the oocytes of the ovary cultured with CPA metabolite in vitro. Most importantly, p63 knockout oocytes were rescued after CPA treatment and maintained functional fertility in the mating trials. To better understand the CPA-induced primordial follicle loss, Pik3ca* mice were examined with or without CPA administration. As expected, ovarian primordial follicles with constitutive PI3K expression inside of oocytes in the Pik3ca* mice survived against CPA. Accordingly, the apoptosis markers, BAX and cleaved PARP were highly induced with CPA injection in a time-dependent manner in the ovaries of wild-type female mice but not from the p63 knockout. The double-strand break also occurred in the nucleus of oocytes post CPA administration as γH2AX was detected. Interestingly, OPA1, a protein required for mitochondrial fusion, was highly induced inside the oocyte cytoplasm of the p63 knockout, while oocytes in wild-type mice time-dependently lost the OPA1 expression by CPA treatment. This indicates that oocytes without p63 in the nucleus survive and induce mitochondrial fusion to escape apoptosis by mitochondrial damage. Conclusion: cAbl is dispensable for primordial follicle depletion caused by CPA. However, TAp63 is the key regulator in CPA-induced apoptosis in oocytes. Furthermore, CHK2 is upregulated in the oocytes of primordial follicles post CPA exposure. Activated follicles resist gonadotoxic agents, even though p63 is expressed inside their oocytes. Therefore, CPA induces depletion of oocytes in primordial follicles through the CHK2-TAp63 apoptotic pathway.https://digitalcommons.unmc.edu/chri_forum/1054/thumbnail.jp

MOMENT RESISTANCE PERFORMANCE OF LARCH LAMINATED TIMBER BEAM-COLUMN JOINTS REINFORCED WITH CFRP

This study evaluates the moment resisting capacity of the drift pin larch beam-column joint with slotted-in steel plates of larch laminated timber. It is reinforced with carbon fiber reinforced plastic (CFRP) to suppress the brittle fracture of the beam-column joint and improve the joint capacity using larch laminated timber, a wood material manufactured by multi-layering of timber as a structural member of heavy timber.The average maximum moment capacity of the control specimen was 16.9 kN·m and the average maximum moments of the Type-A (volume ratio of joint reinforced with CFRP: 3.6%) and Type-B (volume ratio of joint reinforced with CFRP: 5.4%) were increased by 46% and 62%, respectively, compared to that of the control specimen. The capacity of the joint, such as the average yield capacity, ultimate moment capacity, and ductility ratio, of the control, Type-A, and Type-B specimens increased as the reinforcement ratio of the CFRP increased. For the failure mode of the control specimen, splitting failure occurred in both the column and beam members in the end distance direction. However, the splitting failure did not occur in the beam member due to the improvement of the joint and ductility of the specimens reinforced with the CFRP. The Type-A specimen had improved joint capacity and ductility compared to the control specimen; however, brittle failure occurred owing to the external force exceeding the joint capacity. However, in some of the Type-B specimens, the splitting failure did not occur in the column and beam members due to the CFRP reinforcement. Particularly, the Type-B3 specimen exhibited ductility

Muscle 4EBP1 activation modifies the structure and function of the neuromuscular junction in mice

Dysregulation of mTOR complex 1 (mTORC1) activity drives neuromuscular junction (NMJ) structural instability during aging; however, downstream targets mediating this effect have not been elucidated. Here, we investigate the roles of two mTORC1 phosphorylation targets for mRNA translation, ribosome protein S6 kinase 1 (S6K1) and eukaryotic translation initiation factor 4E-binding protein 1 (4EBP1), in regulating NMJ structural instability induced by aging and sustained mTORC1 activation. While myofiber-specific deletion of S6k1 has no effect on NMJ structural integrity, 4EBP1 activation in murine muscle induces drastic morphological remodeling of the NMJ with enhancement of synaptic transmission. Mechanistically, structural modification of the NMJ is attributed to increased satellite cell activation and enhanced post-synaptic acetylcholine receptor (AChR) turnover upon 4EBP1 activation. Considering that loss of post-synaptic myonuclei and reduced NMJ turnover are features of aging, targeting 4EBP1 activation could induce NMJ renewal by expanding the pool of post-synaptic myonuclei as an alternative intervention to mitigate sarcopenia