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Risk Assessment Techniques and Methods of Approach
Published in D. Kofi Asante-Duah, Hazardous Waste Risk Assessment, 2021
The potential for failures of hazardous waste facilities, and the inherent uncertainties associated with such facilities, all pose some degree of hazard; failures are the result of facility breach, followed by the release and migration of potentially harmful chemical contaminants through the environment. Failures may range from design flaws and deficiencies or faults, to operational and traffic accidents, to natural and man-made disasters. PRA offers techniques used to identify possible hazards and potential consequences. Such analyses can be used to improve design or operation to reduce risks. For instance, probabilistic techniques may be applied to the assessment of the structural integrity of hazardous waste facilities and containments or for the evaluation of accident scenarios in the transportation of hazardous materials. Such approaches would be based on quantitative measures of the probability that a facility or containment failure will occur or that an accident will occur during transportation and/or equipment operation.
Effects of continuous and pulsatile flows generated by ventricular assist devices on renal function and pathology
Published in Expert Review of Medical Devices, 2018
Takuma Miyamoto, Jamshid H. Karimov, Kiyotaka Fukamachi
Welp et al. [64] examined the concomitant physiological effects on plasma renin activity of 20 patients supported with a CF LVAD (INCOR assist device; Berlin Heart, Berlin, Germany), compared with a PF LVAD (EXCOR; Berlin Heart) used as a BTT. Plasma renin activity fell significantly to near normal levels after 21 days of support in both CF- and PF-supported patients. However, after 3 weeks of support, plasma renin activity was significantly lower in patients supported with a PF device. This difference remained until POD 70 of support. As with plasma renin activity, after 3 weeks of support, aldosterone levels were significantly lower in PF patients.
Arsenic, cadmium, and mercury-induced hypertension: mechanisms and epidemiological findings
Published in Journal of Toxicology and Environmental Health, Part B, 2018
Airton da Cunha Martins, Maria Fernanda Hornos Carneiro, Denise Grotto, Joseph A Adeyemi, Fernando Barbosa
Similar to Hg, acute Cd exposure also induced endothelial dysfunction and contributed to increased peripheral resistance with consequent genesis and maintenance of hypertension, possibly by RAS activation (Angeli et al. 2013). The mechanism involving endothelial dysfunction may be attributed to increased local release of angiotensin II and elevated activity of COX-2 and NADPH oxidase, which contribute to establishment of hypertension (Angeli et al. 2013). Chronic CdCl2 exposure in rats also leads to upregulation of RAS and significant elevation of blood pressure (Choudhary and Bodakhe 2016). To assess the role of RAS in hypertension induced by Cd, Angeli et al. (2013), used the AT1 receptor antagonist losartan and ACE inhibitor enalapril and demonstrated that these drugs attenuated the hypertension and vascular dysfunction induced by this metal. However, Nath and Vivek (1997) observed that exposed male Sprague–Dawley rats to Cd acetate (1mg/kg) for 5 days exhibited increased blood pressure without significant changes in plasma renin activity, suggesting that Cd-induced hypertensive response may be renin independent. Satarug et al. (2005) proposed a Cd-induced nephropathy mechanism related to high blood pressure. Cd binds to serum albumin consequently accumulating in liver, where the metal forms a complex with high affinity metal proteins (Coyle et al. 2002). This complex reaches the kidney which filters and accumulates it in the proximal tubule, whose cells possess transporters for free and bound forms of Cd (Erfurt, Roussa, and Thévenod 2003), interfering with regular tubular function. Therefore, Cd-mediated nephropathy appears as a low molecular weight (LMW) proteinuria due to diminished intrarenal uptake and catabolism of filtered metal.
Baroreflex activation therapy systems: current status and future prospects
Published in Expert Review of Medical Devices, 2019
Gino Seravalle, Raffaella Dell’Oro, Guido Grassi
The first study was conducted in 11 patients undergoing carotid endoarterectomy [54]. The unilateral electrical stimulation of the carotid sinus induced a reduction of systolic blood pressure (SBP) of 13 mmHg. Starting from this evidence the first feasibility study with permanent implantation in humans was performed in the European multicenter DEBuT-HT (Device Based Therapy of Hypertension) study (Table 1) [55]. Of the 45 resistant hypertensive patients enrolled in the study, the 18 patients that completed the follow-up showed a persistent reduction in systolic and diastolic blood pressure (−33/−22 mmHg after 2 years). At 4 years a reduction of more than 30 mmHg of SBP was observed in 72% of these patients, and 67% showed a SBP<140 mmHg. Concomitantly, it has been observed a reduction in left ventricular mass index (−24.1 ± 18.7 g/m2), a small heart rate reduction, a decrease in plasma renin activity levels (about 20%), a tendency of heart rate variability to increase in the low-frequency component (an index of improvement in vagal control of the heart) and a substantially unchanged baroreflex modulation of heart rate [56,57]. The subsequent more rigorous study, the Rheos Pivotal Trial [58], a multicenter, randomized, double-blind, parallel-design, showed less enthusiastic results. No significant difference was reported in the primary efficacy end-point of ≥ 10 mmHg drop in SBP after 6 month follow-up but 42% in the ‘early’ (1 month post-implantation activation) vs. 24% of the ‘delayed’ (6 month post-implantation activation) group achieved SBP < 140 mmHg. Additionally, about 4.5% of patients developed transient or permanent facial nerve injury. It has been also shown that unilateral stimulation, particularly in the right-side, appears to be more effective [59,60]. Proof of mechanism studies have shown that depressor response of BAT was mediated through sympathetic inhibition and that physiologic regulation of the baroreflex remained unaffected [57].