Prevention and management of work-related cardiovascular disorders

Cardiovascular disorders (CVDs) constitute a major burden for health of working populations throughout the world with as much as 50% of all causes of death and at least 25% of work disability. There are some changes in CVD risk factors among occupational classes. This is mainly due to the new types of work-related causes of morbidity associated with the recent developments in global work life, particularly in the industrialized countries. Meanwhile, in the developing countries or those in transition (e.g., in Eastern Europe), CVD mortality is increasing due to major socioeconomic changes, the demographic transition and rapid industrialisation and urbanisation, all leading to growing challenges to cardiovascular health. Better control of known risk factors (i.e., smoking, obesity, physical inactivity, high cholesterol, high blood pressure, and high blood glucose) is effective to prevent CVD incidence. But the expected improvement has not been achieved. The obstacles of achieving such impact are due to lack of awareness, lack of policies and their implementation into practice and shortage of infrastructures and human resources. These are needed for wide-scale and long-term programme implementation. Considering the WHO Global Strategy on Occupational Health for All, the WHO Global Action Plan on Workers’ Health, the WHO Programme on Prevention of Non-communicable Diseases and the ILO Decent Work agenda, the 6th ICOH International Conference on Work Environment and Cardiovascular Diseases adopted the Tokyo Declaration

Aberrant Myeloid Differentiation Contributes to the Development of Osteoporosis in Neurofibromatosis Type 1

Neurofibromatosis type 1 (NF1), also known as von Recklinghausen disease, is a common autosomal dominant genetic disorder affecting approximately 1 in 3000 individuals worldwide. NF1 results from heritable or spontaneous mutations of the NF1 tumor suppressor gene. NF1 encodes the protein neurofibromin, which functions to negatively regulate Ras-activity. Approximately 50 % of NF1 patients develop osteopenia or osteoporosis, resulting in significantly increased rates of long-bone fracture and morbidity. While defective osteoblast bone anabolism has been implicated as a central factor in the pathogenesis of NF1 associated skeletal deficits, recent data suggest that NF1 (Nf1) haploinsufficiency within the hematopoietic compartment, particularly in osteoclasts and myeloid progenitors, plays a pivotal role in engendering NF1 osseous manifestations. In this chapter, we review the latest data from clinical studies and murine models delineating a critical role for hematopoietic compartment, myeloid progenitors of NF1 (Nf1) haploinsufficient and their progeny-osteoclasts, in the pathogenesis of NF1 associated osteopenia/osteoporosis and discuss putative targets for future therapeutics