catena-Poly[[bis­(2-hydr­oxy-2-phenyl­acetato-κ2 O 1,O 2)zinc(II)]-μ-1,2-di-4-pyridylethane-κ2 N:N′]

The title compound, [Zn(C8H6O3)2(C12H12N2)]n, consists of [Zn(Hopa)2] (H2opa = 2-hydr­oxy-2-phenyl­acetic acid or mandelic acid) units bridged by 1,2-di-4-pyridylethane (bpe) ligands, forming a polymeric chain developing parallel to the b axis. The bridging bpe ligand is arranged around a twofold axis passing through the middle of the ethane C—C bond. The geometry around the ZnII ion is distorted octa­hedral, constructed by four O atoms from two Hopa− ligands and two N atoms from two bridging bpe ligands. O—H⋯O hydrogen bonds link the chains, forming a three-dimensional network

Dirac solitons in optical microresonators

Mode-coupling-induced dispersion has been used to engineer microresonators for soliton generation at the edge of the visible band. Here, we show that the optical soliton formed in this way is analogous to optical Bragg solitons and, more generally, to the Dirac soliton in quantum field theory. This optical Dirac soliton is studied theoretically, and a closed-form solution is derived in the corresponding conservative system. Both analytical and numerical solutions show unusual properties, such as polarization twisting and asymmetrical optical spectra. The closed-form solution is also used to study the repetition rate shift in the soliton. An observation of the asymmetrical spectrum is analysed using theory. The properties of Dirac optical solitons in microresonators are important at a fundamental level and provide a road map for soliton microcomb generation in the visible band

Loss of androgen signaling in mesenchymal sonic hedgehog responsive cells diminishes prostate development, growth, and regeneration.

Prostate embryonic development, pubertal and adult growth, maintenance, and regeneration are regulated through androgen signaling-mediated mesenchymal-epithelial interactions. Specifically, the essential role of mesenchymal androgen signaling in the development of prostate epithelium has been observed for over 30 years. However, the identity of the mesenchymal cells responsible for this paracrine regulation and related mechanisms are still unknown. Here, we provide the first demonstration of an indispensable role of the androgen receptor (AR) in sonic hedgehog (SHH) responsive Gli1-expressing cells, in regulating prostate development, growth, and regeneration. Selective deletion of AR expression in Gli1-expressing cells during embryogenesis disrupts prostatic budding and impairs prostate development and formation. Tissue recombination assays showed that urogenital mesenchyme (UGM) containing AR-deficient mesenchymal Gli1-expressing cells combined with wildtype urogenital epithelium (UGE) failed to develop normal prostate tissue in the presence of androgens, revealing the decisive role of AR in mesenchymal SHH responsive cells in prostate development. Prepubescent deletion of AR expression in Gli1-expressing cells resulted in severe impairment of androgen-induced prostate growth and regeneration. RNA-sequencing analysis showed significant alterations in signaling pathways related to prostate development, stem cells, and organ morphogenesis in AR-deficient Gli1-expressing cells. Among these altered pathways, the transforming growth factor β1 (TGFβ1) pathway was up-regulated in AR-deficient Gli1-expressing cells. We further demonstrated the activation of TGFβ1 signaling in AR-deleted prostatic Gli1-expressing cells, which inhibits prostate epithelium growth through paracrine regulation. These data demonstrate a novel role of the AR in the Gli1-expressing cellular niche for regulating prostatic cell fate, morphogenesis, and renewal, and elucidate the mechanism by which mesenchymal androgen-signaling through SHH-responsive cells elicits the growth and regeneration of prostate epithelium

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

Loss of the tumor suppressor, Tp53, enhances the androgen receptor-mediated oncogenic transformation and tumor development in the mouse prostate.

Recent genome analysis of human prostate cancers demonstrated that both AR gene amplification and TP53 mutation are among the most frequently observed alterations in advanced prostate cancer. However, the biological role of these dual genetic alterations in prostate tumorigenesis is largely unknown. In addition, there are no biologically relevant models that can be used to assess the molecular mechanisms for these genetic abnormalities. Here, we report a novel mouse model, in which elevated transgenic AR expression and Trp53 deletion occur simultaneously in mouse prostatic epithelium to mimic human prostate cancer cells. These compound mice developed an earlier onset of high-grade prostatic intraepithelial neoplasia and accelerated prostate tumors in comparison with mice harboring only the AR transgene. Histological analysis showed prostatic sarcomatoid and basaloid carcinomas with massive squamous differentiation in the above compound mice. RNA-sequencing analyses identified a robust enrichment of the signature genes for human prostatic basal cell carcinomas in the above prostate tumors. Master regulator analysis revealed SOX2 as a transcriptional regulator in prostatic basal cell tumors. Elevated expression of SOX2 and its downstream target genes were detected in prostatic tumors of the compound mice. Chromatin immunoprecipitation analyses implicate a coregulatory role of AR and SOX2 in the expression of prostatic basal cell signature genes. Our data demonstrate a critical role of SOX2 in prostate tumorigenesis and provide mechanistic insight into prostate tumor aggressiveness and progression mediated by aberrant AR and p53 signaling pathways

The usefulness of soluble transferrin receptor in the diagnosis and treatment of iron deficiency anemia in children

PurposeSoluble transferrin receptor (sTfR) is a truncated extracellular form of the membrane transferrin receptor produced by proteolysis. Concentrations of serum sTfR are related to iron status and erythropoiesis in the body. We investigated whether serum sTfR levels can aid in diagnosis and treatment of iron deficiency anemia (IDA) in children.MethodsNinety-eight patients with IDA were enrolled and were classified according to age at diagnosis. Group 1 comprised 78 children, aged 6-59 months, and group 2 comprised 20 adolescents, aged 12-16 years.ResultsIn group 1, patients' serum sTfR levels correlated negatively with mean corpuscular volume; hemoglobin (Hb), ferritin, and serum iron levels; and transferrin saturation and positively with total iron binding capacity (TIBC) and red cell distribution width. In group 2, patients' serum sTfR levels did not correlate with ferritin levels and TIBC, but had a significant relationship with other iron indices. Hb and serum sTfR levels had a significant inverse relationship in both groups; however, in group 1, there was no correlation between Hb and serum ferritin levels. In 30 patients of group 1, serum sTfR levels were significantly decreased with an increase in Hb levels after iron supplementation for 1 month.ConclusionSerum sTfR levels significantly correlated with other diagnostic iron parameters of IDA and inversely correlated with an increase in Hb levels following iron supplementation. Therefore, serum sTfR levels can be a useful marker for the diagnosis and treatment of IDA in children