ABSTRACT
The vast majority of non-melanoma skin cancer (NMSC) is attributable to excessive exposure to ultraviolet radiation (UVR). Outdoor workers are exposed to an UVR dose at least 2 to 3 times higher than indoor workers and often to daily UVR doses 5 times above internationally recommended limits. The risk of UVR workplace exposure is vastly neglected, and the evident future challenges presented in this statement are contrasted with the current situation regarding legal recognition, patient care and compensation. While prevention is crucial to reduce cancer risks for outdoor workers, it is as much of relevance to better protect them through legally binding rules and regulations. Specific actions are outlined in five recommendations based on a Call to Action (table 1). The role of health professionals, including dermatologists, in this context is crucial.
Subject(s)
Occupational Exposure , Skin Neoplasms , Humans , Skin Neoplasms/etiology , Skin Neoplasms/prevention & control , Ultraviolet Rays/adverse effects , WorkplaceABSTRACT
Although cap-dependent translation initiation is the prevalent mode of ribosome binding to mRNAs in eukaryotes, some mRNAs exhibit the ability to bypass the requirement for the cap structure. The translation of X-chromosome-linked inhibitor of apoptosis protein (XIAP) mRNA is controlled by an internal ribosome entry site (IRES) element, which requires the interaction of the heterogeneous nuclear ribonucleoprotein C1-C2 (hnRNP-C1/C2). We analyze, at the protein level, the time course and distribution of XIAP and hnRNP-C1/C2 upon ischemia in mice or staurosporine (STP)-induced apoptosis in HT22 cells. Both ischemia and STP induced a parallel upregulation of XIAP and hnRNP-C1/C2 protein levels in the penumbra and in HT22 cells. These results suggest that the increased levels of hnRNP C1/C2 may modulate XIAP translation, probably by interacting with the XIAP-IRES. The up-regulation of hnRNP-C1/C2 may foster the synthesis of XIAP as a protective pathway by which neurons try to counteract the initial deleterious effects of apoptosis.
Subject(s)
Apoptosis/physiology , Heterogeneous-Nuclear Ribonucleoprotein Group C/metabolism , Neurons/physiology , X-Linked Inhibitor of Apoptosis Protein/metabolism , Animals , Brain Ischemia/metabolism , Caspase 3/metabolism , Cell Line , Cell Survival , Cytochromes c/metabolism , Enzyme Inhibitors/metabolism , Gene Expression Regulation , Heterogeneous-Nuclear Ribonucleoprotein Group C/genetics , Male , Mice , Mice, Inbred C57BL , Neurons/cytology , Staurosporine/metabolism , X-Linked Inhibitor of Apoptosis Protein/geneticsABSTRACT
As already shown, a single bolus injection of heparin is sufficient to perform extracorporeal circulation (ECC) for long-term lung support if bioactive surfaces (HBS) are used. In the present study whether complete avoidance of systemic heparinization using HBS is possible was studied. Seven conscious sheep (50-60 kg) underwent venovenous bypass under standardized conditions using a Maxima capillary membrane oxygenator. Drug administration, surgery, and other conditions, such as priming volume and blood flow rates, were identical in all experiments. All blood contacting surfaces (oxygenator, catheters, etc.) were HBS. The ECC periods were set for 24 hr (n = 3) and 5 days (n = 4). At no time was heparin administered. No complications occurred in any experiment. Partial thromboplastin time, activated clotting time, and other coagulation parameters remained within physiologic ranges. Platelets did not drop below 80% of baseline values, and hemolysis rates were negligible. Blood gas data and other vital parameters were normal during the entire ECC period. Results show that HBS can be applied to long-term ECC, without the necessity for heparin administration.