Orthodontic Approach to Hemifacial Microsomia

Aim and objective: To present a growing patient with unilateral mandibular hypoplasia and microtia involved in the first and second branchial arch syndrome (FSBAS) treated with functional appliance. Background: The FSBAS comprises several developmental facial hypoplasia in ear and maxillofacial bones, resulting in hemifacial microsomia. Treatment for hemifacial microsomia varies greatly depending on the grade of mandibular deformities. Functional appliance treatment during growth period is available for mild to moderate mandibular deformities. However, there are few reports of hemifacial microsomia treated with functional appliance. Case description: The patient, an 8-year-and-5-month-old girl, had a chief complaint of mandibular deviation. She had been diagnosed with the FSBAS at birth. Her facial profile was straight and panoramic radiograph indicated that the mandibular ramal height of the affected side was about 60.4% compared to the unaffected side. The occlusal cant was 6°, and the right maxilla and mandible showed severe growth deficiency. At the age of 10 years, functional appliance with expander was used; for 2 years 6 months, the maxillomandibular growth was controlled and from panoramic radiograph, the ramus height of the affected side was increased to 65.0% compared to the unaffected left mandibular ramus. At the age of 12 years and 8 months, multibracket treatment was initiated. After 32 months of active treatment, proper occlusion with functional Class I canine and molar relationships was obtained, although facial asymmetry associated with the difference of ramus heights still existed. The resulting occlusion was stable during 1.5-year retention period. Conclusion: Our results indicated the importance of orthopedic treatment during growth period in the patient with hemifacial macrosomia involving the FSBAS. Clinical significance: This report proposes an efficacy of conventional orthodontic treatment for growing patients with hemifacial macrosomia involved in the FSBAS

シークワシャー果実中のシネフリン：分析法とカンキツ品種における分布

中村学園大学平成20年

Musashi and Plasticity of Xenopus and Axolotl Spinal Cord Ependymal Cells

The differentiated state of spinal cord ependymal cells in regeneration-competent amphibians varies between a constitutively active state in what is essentially a developing organism, the tadpole of the frog Xenopus laevis, and a quiescent, activatable state in a slowly growing adult salamander Ambystoma mexicanum, the Axolotl. Ependymal cells are epithelial in intact spinal cord of all vertebrates. After transection, body region ependymal epithelium in both Xenopus and the Axolotl disorganizes for regenerative outgrowth (gap replacement). Injury-reactive ependymal cells serve as a stem/progenitor cell population in regeneration and reconstruct the central canal. Expression patterns of mRNA and protein for the stem/progenitor cell-maintenance Notch signaling pathway mRNA-binding protein Musashi (msi) change with life stage and regeneration competence. Msi-1 is missing (immunohistochemistry), or at very low levels (polymerase chain reaction, PCR), in both intact regeneration-competent adult Axolotl cord and intact non-regeneration-competent Xenopus tadpole (Nieuwkoop and Faber stage 62+, NF 62+). The critical correlation for successful regeneration is msi-1 expression/upregulation after injury in the ependymal outgrowth and stump-region ependymal cells. msi-1 and msi-2 isoforms were cloned for the Axolotl as well as previously unknown isoforms of Xenopus msi-2. Intact Xenopus spinal cord ependymal cells show a loss of msi-1 expression between regeneration-competent (NF 50–53) and non-regenerating stages (NF 62+) and in post-metamorphosis froglets, while msi-2 displays a lower molecular weight isoform in non-regenerating cord. In the Axolotl, embryos and juveniles maintain Msi-1 expression in the intact cord. In the adult Axolotl, Msi-1 is absent, but upregulates after injury. Msi-2 levels are more variable among Axolotl life stages: rising between late tailbud embryos and juveniles and decreasing in adult cord. Cultures of regeneration-competent Xenopus tadpole cord and injury-responsive adult Axolotl cord ependymal cells showed an identical growth factor response. Epidermal growth factor (EGF) maintains mesenchymal outgrowth in vitro, the cells are proliferative and maintain msi-1 expression. Non-regeneration competent Xenopus ependymal cells, NF 62+, failed to attach or grow well in EGF+ medium. Ependymal Msi-1 expression in vivo and in vitro is a strong indicator of regeneration competence in the amphibian spinal cord

トリガーポイント治療の適用後における僧帽筋上部線維の筋硬度、圧痛閾値および頸部可動域の即時変化 : 単一盲検ランダム化プラセボ対照試験

東京都立大

Impaired bone quality characterized by apatite orientation under stress shielding following fixing of a fracture of the radius with a 3D printed Ti-6Al-4V custom-made bone plate in dogs

Custom-made implants have recently gained attention in veterinary medicine because of their ability to properly fit animal bones having a wide variety of shapes and sizes. The effect of custom-made implants on bone soundness and the regeneration process is not yet clear. We fabricated a 3D printed Ti-6Al-4V custom-made bone plate that fits the shape of the dog radius, and placed it into the radius where an osteotomy had been made. The preferential orientation of the apatite c-axis contributes to the mechanical integrity of the bone and is a reliable measure of bone quality. We determined this parameter as well as the bone shape and bone mineral density (BMD). The bone portion which lies parallel to the bone plate exhibited bone resorption, decreased BMD, and significant degradation of apatite orientation, relative to the portion outside the plate, at 7 months after the operation. This demonstrates the presence of stress shielding in which applied stress is not transmitted to bone due to the insertion of a stiff bone plate. This reduced stress condition clearly influences the bone regeneration process. The apatite orientation in the regenerated site remained different even after 7 months of regeneration, indicating insufficient mechanical function in the regenerated portion. This is the first study in which the apatite orientation and BMD of the radius were evaluated under conditions of stress shielding in dogs. Our results suggest that assessment of bone repair by radiography can indicate the degree of restoration of BMD, but not the apatite orientation.Impaired bone quality characterized by apatite orientation under stress shielding following fixing of a fracture of the radius with a 3D printed Ti-6Al-4V custom-made bone plate in dogs. Keiichiro Mie et al. PLOS ONE. 2020. 9(2) doi.org/10.1371/journal.pone.023767

ISR-DEPENDENT METABOLIC REGULATION

The eukaryotic translation initiation factor 2α (eIF2α) phosphorylation‐dependent integrated stress response (ISR), a component of the unfolded protein response, has long been known to regulate intermediary metabolism, but the details are poorly worked out. We report that profiling of mRNAs of transgenic mice harboring a ligand‐activated skeletal muscle–specific derivative of the eIF2α protein kinase R‐like ER kinase revealed the expected up‐regulation of genes involved in amino acid biosynthesis and transport but also uncovered the induced expression and secretion of a myokine, fibroblast growth factor 21 (FGF21), that stimulates energy consumption and prevents obesity. The link between the ISR and FGF21 expression was further reinforced by the identification of a small‐molecule ISR activator that promoted Fgf21 expression in cell‐based screens and by implication of the ISR‐inducible activating transcription factor 4 in the process. Our findings establish that eIF2α phosphorylation regulates not only cell‐autonomous proteostasis and amino acid metabolism, but also affects non‐cell‐autonomous metabolic regulation by induced expression of a potent myokine.—Miyake, M., Nomura, A., Ogura, A., Takehana, K., Kitahara, Y., Takahara, K., Tsugawa, K., Miyamoto, C., Miura, N., Sato, R., Kurahashi, K., Harding, H. P., Oyadomari, M., Ron, D., Oyadomari, S. Skeletal muscle‐specific eukaryotic translation initiation factor 2α phosphorylation controls amino acid metabolism and fibroblast growth factor 21‐mediated non‐cell‐autonomous energy metabolism

Skeletal muscle–specific eukaryotic translation initiation factor 2α phosphorylation controls amino acid metabolism and fibroblast growth factor 21–mediated non–cell-autonomous energy metabolism

The eukaryotic translation initiation factor 2α (eIF2α) phosphorylation-dependent integrated stress response (ISR), a component of the unfolded protein response, has long been known to regulate intermediary metabolism, but the details are poorly worked out. We report that profiling of mRNAs of transgenic mice harboring a ligand-activated skeletal muscle-specific derivative of the eIF2α protein kinase R-like ER kinase revealed the expected up-regulation of genes involved in amino acid biosynthesis and transport but also uncovered the induced expression and secretion of a myokine, fibroblast growth factor 21 (FGF21), that stimulates energy consumption and prevents obesity. The link between the ISR and FGF21 expression was further reinforced by the identification of a small-molecule ISR activator that promoted Fgf21 expression in cell-based screens and by implication of the ISR-inducible activating transcription factor 4 in the process. Our findings establish that eIF2α phosphorylation regulates not only cell-autonomous proteostasis and amino acid metabolism, but also affects non-cell-autonomous metabolic regulation by induced expression of a potent myokine.Ministry of Education, Culture, Sports, Science and Culture (MEXT) of Japan Inoue Foundation for Science Mitsubishi Foundation Uehara Memorial Foundation Naito Foundation Cell Science Research Foundation Takeda Science Foundation Sankyo Foundation Ono Medical Research Foundation Mochida Memorial Foundation Ube Foundation Kowa Life Science Foundation Suzuken Memorial Foundation Kanae Foundation Japan Diabetes Foundation Japan Society for Promotion of Science (JSPS) EU FP7. Grant Number: 277713 Wellcome Trust. Grant Number: 084812/Z/08/