Simmons Lykkegaard (glasschef05)

s and preferences of the Swedish population, providing a rationale for developing complementary healthcare-assisted communication pathways to realise the full potential of targeted prevention of hereditary CRC. In this study a majority of respondents wanted to be informed about a potential hereditary risk of CRC and preferred healthcare professionals to communicate this information. The two presented levels of CRC lifetime risk did not significantly affect the interest in being informed. Our data offer insights into the needs and preferences of the Swedish population, providing a rationale for developing complementary healthcare-assisted communication pathways to realise the full potential of targeted prevention of hereditary CRC.In bone tissues, metabolic turnover through bone resorption by osteoclasts and bone formation by osteoblasts, termed bone remodeling, is strictly controlled and maintains homeostasis. Fibrinolytic factors are expressed in osteoclasts and osteoblasts, and are involved in bone remodeling through bone resorption and formation. The repair/regeneration process after bone injury is divided into the acute inflammatory, repair, and remodeling stages. Osteoblasts, osteoclasts, chondrocytes, and macrophages involved in the bone repair process originate from hematopoietic stem/progenitor cells (HSPCs) and mesenchymal stem cells (MSCs) in the bone marrow. Therefore, stem cells in the bone marrow may be strongly influenced by bone injury. The urokinase-type PA (u-PA)/plasminogen (Plg) system functions in macrophage accumulation/phagocytosis through chemokines in the acute inflammatory stage, and Plg increases blood vessel-related growth factor expression, being involved in vascularization in mice. Plasminogen activator inhivitor-1 (PAI-1) causes bone loss and delayed bone repair through the inhibition of osteoblast differentiation in a drug-induced diabetes model in mice. Plg is considered to induce transforming growth factor-β (TGF-β) production in macrophages in the bone repair process, TGF-β release from the extracellular matrix through the activation of matrix metalloproteinase-9 (MMP-9), and stromal cell-derived factor-1 (SDF-1) expression in endosteal preosteoblasts, leading to the induction of bone marrow HSPCs in mice. Based on the above, establishment of a fibrinolytic factor-targeting method efficiently promoting bone repair/regeneration and fracture healing, and development of a new osteoporosis treatment method and diagnostic marker are awaited.Rheumatoid arthritis is an autoimmune inflammatory disease primarily characterized by synovitis which is accompanied by extra-articular organ involvement, such as interstitial pneumonia, in addition to clinical symptoms including pain, swelling, stiffness of multiple joints, fever, and malaise. Joint destruction progresses soon after the onset, and once the affected joints are deformed, the development of irreversible physical dysfunction is noted. Thus, proper diagnosis and treatment are required from the early stages of the disease. Although palliative therapy with glucocorticoids and anti-inflammatory drugs had been used, disease-modifying antirheumatic drugs (DMARDs) are currently used to suppress immune abnormalities and to control disease activity. DMARDs are classified into different groups, such as conventional synthetic DMARD, targeted synthetic DMARD, and biologic DMARD. The appropriate use of these drugs has allowed remission to be the therapeutic goal in all patients. By maintaining remission, these drugs have also been shown to prevent the progression of joint destruction and physical dysfunction over a long period. The advent of molecular-targeted therapies has allowed for the use of treatments based on pathological mechanisms, and such therapeutic strategies have also been applied to the treatment of various autoimmune inflammatory diseases. In the future, safer and more effective treatments, therapeutic strategies aimed at drug holidays or