![]() Third, in regard to the induction of mutations, the greater current risk seems to result from exposure to chemical mutagens in the environment rather than from the exposure of populations to radiation. Second, the instruments and techniques used in medical radiation have improved significantly, so that the overall doses used in medical diagnoses are reduced and patient exposure in all but the targeted organs is lessened. First, it is now clear that the risk of cancer in individuals exposed to radiation is significant and that limiting exposure to radiation to reduce the risk of cancer also limits the genetically significant exposure. Scientific Committee on the Effects of Atomic Radiation ( UNSCEAR) has also addressed the genetic effects of radiation exposure on populations.Īlthough there is a continuing need to assess the genetic effects of radiation exposure, for several reasons the perspective has changed somewhat from that in the 1950s. In 1956 the National Academy of Sciences-National Research Council (NAS-NRC) established the Committee on the Biological Effects of Atomic Radiation (denoted the BEAR Committee), which was the forerunner of the subsequent NAS-NRC committees on the Biological Effects of Ionizing Radiation (BEIR committees of which this BEIR V report is one). These efforts were motivated by concern over the effects of extremely large sources of radiation that were being developed in the nuclear industry, of radioactive fallout from the atmospheric testing of atomic weapons and of the rapidly increasing use of radiation in medical diagnosis and therapy. Although occupational exposure to high levels of radiation has always been of concern, not until during and after World War II was there a concerted effort to evaluate the genetic effects of radiation on entire populations. The mutagenic effects of radiation were first recognized in the 1920s, and since that time radiation has been used in genetic research as an important means of obtaining new mutations in experimental organisms. C) Diagram of the kidney sections used for norepinephrine analysis, flow cytometry, cytokine analysis and histopathology.Ionizing radiation damages the genetic material in reproductive cells and results in mutations that are transmitted from generation to generation. Tissues were collected at the end of the protocol for norepinephrine analysis and for inflammatory profile. Fasting glucose was measured one week before RDNx/Sham surgery, a glucose tolerance test (GTT) and indirect calorimetry were conducted 3 and 4 weeks after RDNx/Sham respectively. B) In the Metabolic Protocol body weight (weekly), food intake (weekly) and body composition (monthly) were measured in LFD-Sham, LFD-RDNx, HFD-Sham, HFD-RDNx, (n=9/group). At 17 weeks of diet, kidneys were collected for norepinephrine analysis. After 12 weeks of diet and a 3 day control (C) recording of mean arterial pressure (MAP) and heart rate (HR), mice in LFD-Sham (n=7), LFD-RDNx (n=5), HFD-Sham (n=6), HFD-RDNx (n=5) groups underwent renal denervation (RDNx) or sham surgery. T cell cytokines glucose hypertension metabolic syndrome renal denervation.Ī) In the Cardiovascular Protocol, mice on low fat diet (LFD) or high fat diet (HFD) underwent telemetry surgery. These results indicate that although renal nerves play a role in obesity-induced hypertension, they do not contribute to impaired glucose metabolism or renal inflammation in this model. Also, RDNx had no significant effect on glucose metabolism or renal inflammation as measured by the number of CD8, CD4, and T helper cells or levels of inflammatory cytokines in the kidneys. RDNx had no significant effect on AP in low-fat diet mice. RDNx, but not Sham surgery, normalized AP in high-fat diet mice (115.8☑.5 mm Hg in sham versus 96.6☖.7 mm Hg in RDNx). High fat-fed C57BL/6J mice exhibited an inflammatory and metabolic syndrome phenotype, including increased fat mass, increased AP, and hyperglycemia compared with low-fat diet mice. In a parallel study, radiotelemeters were implanted in mice for AP measurement. ![]() Body weight, food intake, fasting blood glucose, and glucose metabolism (glucose tolerance test) were measured. Eight-week-old C57BL/6J mice were fed either a low-fat diet (10 kcal%) or a high-fat diet (45 kcal%) for 10 weeks. The present study tested the hypothesis that RDNx reduces AP and renal inflammation and improves glucose metabolism in obesity-induced hypertension. In addition, RDNx has been shown to reduce renal inflammation in the mouse model of angiotensin II hypertension. Renal denervation (RDNx) lowers arterial pressure (AP) and improves glucose metabolism in drug-resistant hypertensive patients with high body mass index. ![]() Hypertension often occurs in concurrence with obesity and diabetes mellitus, commonly referred to as metabolic syndrome. ![]()
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