PubMed · 14522791
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David R Hardten. 2003. Interface fluid after LASIK.. https://doi.org/10.1016/s0161-6420(03)00903-5
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In 1951 and 1952 specialists from the Mayak production association investigated the radiological situation in the area of the Metlinski reservoir that was located 5-7 km from the site of liquid radioactive waste (LRW) discharge. Based on their measurements of both the specific radioactivity in the water and the dose-rate above the water surface, the gamma-field above the water surface in 1951 was demonstrated to be mainly due to (95)Zr+(95)Nb. The dose-rate at the shore of the reservoir was calculated for the period 1949-1951. In November and December 1951, the gamma-field at the shore was mainly due to (140)Ba+(140)La. For the period 1949-1951, the external exposure of the Metlino population due to the decay of these radionuclides was about 200 R (2 Sv), most of the dose having been produced in 1951. The contribution of (137)Cs to external doses did at that time probably not exceed a fraction of several percent. This finding is in contradiction to the assumptions made in the most recent TRDS-2000 system that was developed to reconstruct the doses to the residents of the Techa river. The results presented here demonstrate that the reconstruction of external doses received by the Metlino population as well as by the Techa river residents can be improved for the most critical period between 1949 and 1954.
During the past few years, it has become increasingly evident that residual renal function (RRF) is an important and independent predictor of poor outcome in patients with chronic kidney disease (CKD). Although the causes of this observation are not fully understood, it appears that the loss of RRF impairs both fluid removal and clearance of solutes, which in turn leads to uremic toxicity and increased morbidity and mortality. There is increasing evidence that patients with CKD develop signs of fluid overload already in the early phases of the disease, and this may be a stimulus for inflammatory activation. Recently, an inflammatory component was identified in uremic atherosclerotic and non-atherosclerotic cardiovascular disease (CVD), which have been consistently associated with poor clinical outcome in patients with CKD. Signs of systemic inflammation occur in parallel to the impairment in renal function, and the pathophysiology is most likely multifactorial, including a decrease in cytokine clearance, advanced glycation end-product accumulation, oxidative stress, and principal fluid overload. Additionally, inflammation seems to be a predictor of accelerated loss of renal function. In this article, we discuss the evidence showing that patients with CKD generally have fluid overload, the mechanisms by which impaired renal function may lead to a chronic inflammatory state, and the available information linking fluid overload to accelerated loss of renal function and CVD through inflammation. Inflammation may lead to the development of complications of CKD, in particular CVD, but on the other hand may also lead to a faster progression of renal disease. Strategies aiming to reduce fluid overload may be useful to reduce cardiovascular morbidity and mortality, but also preserve RRF.