Healthcare is a major emitter of environmental pollutants that adversely affect health. Within the healthcare community, awareness of these effects is low, and recognition of the duty to address them ...is only beginning to gain traction. Healthcare sustainability science explores dimensions of resource consumption and environmental emissions associated with healthcare activities. This emerging field provides tools and metrics to quantify the unintended consequences of healthcare delivery and evaluate effective approaches that improve patient safety while protecting public health. This narrative review describes the scope of healthcare sustainability research, identifies knowledge gaps, introduces a framework for applications of existing research methods and tools to the healthcare context, and establishes research priorities to improve the environmental performance of healthcare services. The framework was developed through review of the current state of healthcare sustainability science and expert consensus by the Working Group for Environmental Sustainability in Clinical Care. Key recommendations include: development of a comprehensive life cycle inventory database for medical devices and drugs; application of standardized sustainability performance metrics at the clinician, hospital/health system, and national levels; revision of infection control standards driving non-evidence-based uptake of single-use disposable devices; call for increased federal research funding; and formation of a Global Commission on the Advancement of Environmental Sustainability in Healthcare. There is an urgent need for research that informs policy and practice to address the public health crisis arising from healthcare pollution. A transformational vision is required to align research priorities to achieve a sustainable healthcare system that advances quality, safety and value.
Chronic idiopathic thrombocytopenic purpura is an autoimmune disorder in which the destruction of autologous platelets is mediated by autoantibodies directed against platelet-surface constituents.
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...Glycoproteins IIb and IIIa, which exist in the platelet membrane in a 1:1 complex (IIb-IIIa), appear to be the main target molecules for these autoantibodies.
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The destruction of autologous platelets is thought to result from the ingestion of autoantibody-coated platelets by phagocytic cells in the spleen and other organs.
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The functional state of the reticuloendothelial system may influence the rate of cell destruction in individual patients.
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We recently encountered a patient who had severe, life-threatening thrombocytopenia after . . .
An anti-idiotype serum was raised in a chimpanzee (A) by immunization with autologous lymphocytes primed in vitro against an unrelated chimp (B). This autoantiserum in the presence of complement was ...cytotoxic for 5 to 7% of the resting lymphocytes from chimp A and for 30 to 45% of the mixed lymphocyte culture (MLC) primed cells (A X Bx), but was not reactive against the lymphocytes of the priming chimp (B). Anti-idiotype antibody and complement treatment of autologous resting or primed cells blocked the ability of these cells to respond in MLC or primed lymphocyte test (PLT) to the stimulator cells from chimp B, but not to cells from a third chimp. When cells from the immunized animal (A) were incubated with the autologous antiserum in vitro, they were stimulated, thus producing cells which had the same activity in PLT as did cells primed against stimulator cells of chimp B. Thus, an autoanti-idiotype serum has been raised in a primate system which identifies the recognition structure on autologous T cells directed against antigeneic determinants on the stimulator cells of a histoincompatible donor.
