Immune response and new tissue formation are important aspects of tissue repair. However, only a single aspect is generally considered in previous biomedical interventions, and the synergistic effect is unclear. Here, a dual-effect coating with immobilized immunomodulatory metal ions (e.g., Zn2+) and osteoinductive growth factors (e.g., BMP-2 peptide) is designed via mussel adhesion-mediated ion coordination and molecular clicking strategy. Compared to the bare TiO2 group, Zn2+ can increase M2 macrophage recruitment by up to 92.5% in vivo and upregulate the expression of M2 cytokine IL-10 by 84.5%; while the dual-effect of Zn2+ and BMP-2 peptide can increase M2 macrophages recruitment by up to 124.7% in vivo and upregulate the expression of M2 cytokine IL-10 by 171%. These benefits eventually significantly enhance bone-implant mechanical fixation (203.3 N) and new bone ingrowth (82.1%) compared to the bare TiO2 (98.6 N and 45.1%, respectively). Taken together, the dual-effect coating can be utilized to synergistically modulate the osteoimmune microenvironment at the bone-implant interface, enhancing bone regeneration for successful implantation.
In this review, an overview of itinerant magnets without magnetic elements is presented, beginning with a comparison of the local and itinerant moment pictures, the two extremes of magnetism. Then, the theoretical developments leading up to the self-consistent renormalization theory of spin fluctuations will be discussed, followed by an introduction to quantum criticality and the experimental signatures associated with systems near a quantum critical point. Three itinerant magnets without magnetic elements, ZrZn, ScIn, and TiAu are the focus of this review, as their empty d shells set them apart in their purely itinerant character, while several enhanced Pauli paramagnets and intermediate moment magnets are also discussed to put the overall comparison into perspective.
SUMMARYThe effect of angiotensin IL on blood pressure and perfusion of blood through the cortex and papilla regions of the kidney was determined in pentobarbitone-anaesthetized rats which were subjected to laser-Doppler flowmetry to estimate regional renal haemodynamics. Angiotensin II was infused at 10, 45 and 150 ng (kg body weight-1 min-m) which caused dose-related increases in blood pressure of 3, 12 and 24 %, respectively, and decreases in cortical perfusion of 9, 15 and 24 %, respectively. Papillary perfusion did not change at any dose of angiotensin II. This pattern and magnitude of responses to angiotensin II in blood pressure, cortical and papillary perfusions was essentially unaffected (a) following blockade of cyclo-oxygenase activity with indomethacin (1 3 mg kg-' plus 2 mg kg-' h-1), (b) during infusion of a bradykinin antagonist, at 1 3 ug minm , (c) when renal perfusion pressure was regulated at control levels and (d) following Methylene Blue administration to inhibit potential endothelial-derived relaxing factor production. By contrast, infusion of phenylephrine at 5, 10 and 20 ,ug kg-1 min-' caused dose-related increases in blood pressure and decreases in both cortical and papillary perfusions reaching some 28, 7 and 17 % respectively at the highest dose of phenylephrine used. These results showed that both cortex and papilla were sensitive to vasoconstrictor agents. They are compatible with the suggestion that angiotensin II regulates cortical but not papillary perfusion in the kidney, and that these responses do not depend on prostaglandin, bradykinin, renal perfusion pressure or endothelium-derived relaxing factor.
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