Reconciling IMF rules and international investment agreements: An innovative derogation for capital controls

In the absence of an international framework governing capital controls, a conflict has developed due to the different approaches towards such controls taken by various international organizations and international investment agreements (IIAs). IIAs should incorporate derogations for countries when treaty obligations conflict with IMF recommendations to impose controls in response to severe economic hardship

协调IMF规定与IIAs：资本控制的一种创新性免责条款

目前，对于资本控制的管理问题还没有形成一个统一的框架。不同的国际组织与国际协定（IIAs）采取不同的做法，由此产生了冲突。当协议责任与IMF应对严重经济困难的建议相冲突时，IIAs应该加入免责条款

Large deflection, nonlinear loads analysis, with application to large winglets

The inclusion of static aeroelastic effects is essential to the accurate calculation of the aerodynamic properties of a wing, the resulting wing loads, and ultimately the mass of the wing. Within an industrial aircraft design cycle, the computational time required for structurally coupled nonlinear flow solvers is impractical for the many different solutions required, even with the current development in computing power. The process currently used by most civilian aircraft manufacturers therefore makes use of time efficient linear panel methods for calculating the aerodynamics and modal data for calculating structural movements.University of Bristol.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

A quantitative investigation of the skeletal kinetics of the radionuclide tracer Tc-99m methylene diphosphonate (Tc-99m MDP) using gamma camera imaging and blood sampling

EThOS - Electronic Theses Online ServiceGBUnited Kingdo

CD169+ macrophages mediate pathological formation of woven bone in skeletal lesions of prostate cancer

Skeletal metastases present a major clinical challenge for prostate cancer patient care, inflicting distinctive mixed osteoblastic and osteolytic lesions that cause morbidity and refractory skeletal complications. Macrophages are abundant in bone and bone marrow and can influence both osteoblast and osteoclast function in physiology and pathology. Herein, we examined the role of macrophages in prostate cancer bone lesions, particularly the osteoblastic response. First, macrophage and lymphocyte distributions were qualitatively assessed in patient's prostate cancer skeletal lesions by immunohistochemistry. Second, macrophage functional contributions to prostate tumour growth in bone were explored using an immune-competent mouse model combined with two independent approaches to achieve in vivo macrophage depletion: liposome encapsulated clodronate that depletes phagocytic cells (including macrophages and osteoclasts); and targeted depletion of CD169+ macrophages using a suicide gene knock-in model. Immunohistochemistry and histomorphometric analysis were performed to quantitatively assess cancer-induced bone changes. In human bone metastasis specimens, CD68+ macrophages were consistently located within the tumour mass. Osteal macrophages (osteomacs) were associated with pathological woven bone within the metastatic lesions. In contrast, lymphocytes were inconsistently present in prostate cancer skeletal lesions and when detected, had varied distributions. In the immune-competent mouse model, CD169+ macrophage ablation significantly inhibited prostate cancer-induced woven bone formation, suggesting that CD169+ macrophages within pathological woven bone are integral to tumour-induced bone formation. In contrast, pan-phagocytic cell, but not targeted CD169+ macrophage depletion resulted in increased tumour mass, indicating that CD169− macrophage subset(s) and/or osteoclasts influenced tumour growth. In summary, these observations indicate a prominent role for macrophages in prostate cancer bone metastasis that may be therapeutically targetable to reduce the negative skeletal impacts of this malignancy, including tumour-induced bone modelling

CD169+ macrophages mediate pathological formation of woven bone in skeletal lesions of prostate cancer

Skeletal metastases present a major clinical challenge for prostate cancer patient care, inflicting distinctive mixed osteoblastic and osteolytic lesions that cause morbidity and refractory skeletal complications. Macrophages are abundant in bone and bone marrow and can influence both osteoblast and osteoclast function in physiology and pathology. Herein, we examined the role of macrophages in prostate cancer bone lesions, particularly the osteoblastic response. First, macrophage and lymphocyte distributions were qualitatively assessed in patient's prostate cancer skeletal lesions by immunohistochemistry. Second, macrophage functional contributions to prostate tumour growth in bone were explored using an immune-competent mouse model combined with two independent approaches to achieve in vivo macrophage depletion: liposome encapsulated clodronate that depletes phagocytic cells (including macrophages and osteoclasts); and targeted depletion of CD169(+) macrophages using a suicide gene knock-in model. Immunohistochemistry and histomorphometric analysis were performed to quantitatively assess cancer-induced bone changes. In human bone metastasis specimens, CD68(+) macrophages were consistently located within the tumour mass. Osteal macrophages (osteomacs) were associated with pathological woven bone within the metastatic lesions. In contrast, lymphocytes were inconsistently present in prostate cancer skeletal lesions and when detected, had varied distributions. In the immune-competent mouse model, CD169(+) macrophage ablation significantly inhibited prostate cancer-induced woven bone formation, suggesting that CD169(+) macrophages within pathological woven bone are integral to tumour-induced bone formation. In contrast, pan-phagocytic cell, but not targeted CD169(+) macrophage depletion resulted in increased tumour mass, indicating that CD169(-) macrophage subset(s) and/or osteoclasts influenced tumour growth. In summary, these observations indicate a prominent role for macrophages in prostate cancer bone metastasis that may be therapeutically targetable to reduce the negative skeletal impacts of this malignancy, including tumour-induced bone modelling. Copyright (C) 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd