We have engineered a scaffold constructed of synthetic octacalcium phosphate (OCP) and porcine collagen sponge (OCP/Col), and reported that OCP/Col drastically enhanced bone regeneration. In this study, we investigated whether OCP/Col would enhance bone regeneration more than beta-tricalcium phosphate (beta-TCP) collagen composite (beta-TCP/Col) or hydroxyapatite (HA) collagen composite (HA/Col). Discs of OCP/Col, beta-TCP/Col, or HA/Col were implanted into critical-sized defects in rat crania and fixed at 4 or 12 weeks after implantation. The newly formed bone and the remaining granules of implants in the defect were determined by histomorphometrical analysis, and radiographic and histological examinations were performed. Statistical analysis showed that the newly formed bone by the implantation of OCP/Col was significantly more than that of beta-TCP/Col or HA/Col. In contrast, the remaining granules in OCP/Col were significantly lower than those in beta-TCP/Col or HA/Col. Bone regeneration by OCP/Col was based on secured calcified collagen and bone nucleation by OCP, whereas bone regeneration by beta-TCP/Col or HA/Col was initiated by poorly calcified collagen and osteoconductivity by beta-TCP or HA. This study showed that the implantation of OCP/Col in a rat cranial defect enhanced more bone regeneration than beta-TCP/Col and HA/Col.
Preoperative use of hypnotic medication, the thoracotomy approach, and duration of surgery ≥2.5 hours are associated with increased risk of neuropathic pain after thoracic surgery. The complete VATS approach could decrease the incidence of postoperative neuropathic pain, regardless of the duration of surgery.
If dangerous climatic change is to be avoided, all countries will need to contribute to reductions in greenhouse gas emissions on the basis of equity and in accordance with their common but differentiated responsibilities and respective capabiiities. This articie discusses the gap between the past (ideai) modei analysis for emission reductions and reaiistic policies. A key requirement for successfui policies is their acceptance by as many countries as possibie and their ease of practical implementation. The sectoral intensity approach has been proposed for its focus on tangible, practical actions; however, its emission reduction effects have been said to be ambiguous and difficult to evaluate quantitativeiy. The effects of global emission reduction based upon a sectoral approach to energy and carbon intensity targets are evaiuated using an energy systems model with a high regionai resolution and a detailed description of technology. This anaiysis found that deep emission cuts can be achieved by a sectorai approach, provided that deveioped and deveioping countries coiiaborate towards emission cuts under the proposed framework. This framework has a higher potentiai for agreement by both developed and developing countries. Si le changement clitnatique dangereux peut être évité, tous les pays devront oontribuer à la réduction des émissions de gaz à effet de serre sur la base du principe de l'équité et en accord avec leur responsabilités communes mais différenciées et leurs capacités respectives. Ce papier discute de l'écart entre l'analyse sur l'ancien modèle (idéal) de réduction des émissions et ies politiques réalistes. Une exigence clé pour ie succès des politiques est leur reconnaissance par le plus grand nombre de pays possible et leur facilité de mise en place en pratique. L'approche sectorielle d'intensité a éié proposée pour son axe sur des actions tangibles et concrètes, cependant ses effets en terme de réductions en émissions ont été interprétés comme étant ambigus et difficiles à évaluer de manière quantitative. L'effet des réductions des émissions mondiales basée sur une approche sectorielle d'objectifs d'intensité en énergie ou en carbone est évalué à travers un modèle de systèmes énergétiques à haute résolution régionaie et une description technologique détaillée. Cette analyse montre que d'importantes réductions d'émissions peuvent être réaiisées par une approche sectorielle à condition que les pays développés et les pays en développement collaborent dans le but de réduire les émissions à l'intérieur du cadre proposé. Ce cadre présente un plus fort potentiei d'accord entre pays développés et pays en développement. eiaritihsicain Global emission reductions through a sectoral intensity target scheme 847 CLIMATE POLICY • I S48 Akimoto et ai.
Acute onset of organ failure in heatstroke is triggered by rhabdomyolysis of skeletal muscle. Here, we showed that elevated temperature increases free cytosolic Ca2+ [Ca2+]f from RYR (ryanodine receptor)/UNC-68 in vivo in the muscles of an experimental model animal, the nematode Caenorhabditis elegans. This subsequently leads to mitochondrial fragmentation and dysfunction, and breakdown of myofilaments similar to rhabdomyolysis. In addition, treatment with an inhibitor of RYR (dantrolene) or activation of FoxO (Forkhead box O)/DAF-16 is effective against heat-induced muscle damage. Acute onset of organ failure in heatstroke is triggered by rhabdomyolysis of skeletal muscle. To gain insight into heat-induced muscle breakdown, we investigated alterations of Ca2+ homeostasis and mitochondrial morphology in vivo in body-wall muscles of C. elegans exposed to elevated temperature. Heat stress for 3 hr at 35° increased the concentration of [Ca2+]f, and led to mitochondrial fragmentation and subsequent dysfunction in the muscle cells. A similar mitochondrial fragmentation phenotype is induced in the absence of heat stress by treatment with a calcium ionophore, ionomycin. Mutation of the unc-68 gene, which encodes the ryanodine receptor that is linked to Ca2+ release from the sarcoplasmic reticulum, could suppress the mitochondrial dysfunction, muscle degeneration, and reduced mobility and life span induced by heat stress. In addition, in a daf-2 mutant, in which the DAF-16/FoxO transcription factor is activated, resistance to calcium overload, mitochondrial fragmentation, and dysfunction was observed. These findings reveal that heat-induced Ca2+ accumulation causes mitochondrial damage and consequently induces muscle breakdown.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.