Analysis of Occupational Accidents in Underground and Surface Mining in Spain Using Data-Mining Techniques.

An analysis of occupational accidents in the mining sector was conducted using the data from the Spanish Ministry of Employment and Social Safety between 2005 and 2015, and data-mining techniques were applied. Data was processed with the software Weka. Two scenarios were chosen from the accidents database: surface and underground mining. The most important variables involved in occupational accidents and their association rules were determined. These rules are composed of several predictor variables that cause accidents, defining its characteristics and context. This study exposes the 20 most important association rules in the sector-either surface or underground mining-based on the statistical confidence levels of each rule as obtained by Weka. The outcomes display the most typical immediate causes, along with the percentage of accidents with a basis in each association rule. The most important immediate cause is body movement with physical effort or overexertion, and the type of accident is physical effort or overexertion. On the other hand, the second most important immediate cause and type of accident are different between the two scenarios. Data-mining techniques were chosen as a useful tool to find out the root cause of the accidents.

Plasma tissue inhibitor of matrix metalloproteinase-1 a predictor of long-term mortality in patients treated with cardiac resynchronization therapy.

AIMS: Matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) are involved in cardiac remodelling. Available information regarding their prognostic utility in heart failure (HF) and cardiac resynchronization therapy (CRT) is controversial. The aim of this study was to analyse MMP-2 and TIMP-1 levels as predictors of long-term mortality in HF patients treated with CRT. METHODS AND RESULTS: We prospectively included 42 consecutive patients with successfully implanted CRT. Matrix metalloproteinase-2 and TIMP-1 assays were performed prior to implant. Patients were evaluated at baseline and at the outpatient clinic at 6-month intervals. Clinical response, left ventricular (LV) remodelling, and mortality were analysed. During a mean follow-up of 60 ± 34 months, long-term mortality from any cause was 36% (15 patients). The cause of death was end stage of HF in 12 patients, sudden death in 2 patients, and 1 unknown. After adjustment using a Cox regression model, the independent predictors of long-term mortality were baseline TIMP-1, hazard ratio (HR) 1.18 (95% confidence interval (95% CI) [1.05-1.33], P = 0.007), baseline glomerular filtration rate (GFR), HR 0.97 (95% CI [0.94-1.00], P = 0.05), and permanent atrial fibrillation (AF), HR 3.14 (95% CI [1.02-9.67], P = 0.04). Area under receiver operating characteristic curve for TIMP-1 was 0.79 (95% CI [0.63-0.94]). Tissue inhibitor of matrix metalloproteinase-1 ≥ 248 ng/mL predicts mortality with 80% sensitivity and 71% specificity. CONCLUSION: Tissue inhibitor of matrix metalloproteinase-1 is a powerful predictor of long-term mortality in HF patients treated with CRT.

Losartan prevents heart fibrosis induced by long-term intensive exercise in an animal model.

RATIONALE: Recently it has been shown that long-term intensive exercise practice is able to induce myocardial fibrosis in an animal model. Angiotensin II is a profibrotic hormone that could be involved in the cardiac remodeling resulting from endurance exercise. OBJECTIVE: This study examined the antifibrotic effect of losartan, an angiotensin II type 1 receptor antagonist, in an animal model of heart fibrosis induced by long-term intense exercise. METHODS AND RESULTS: Male Wistar rats were randomly distributed into 4 experimental groups: Exercise, Exercise plus losartan, Sedentary and Sedentary plus losartan. Exercise groups were conditioned to run vigorously for 16 weeks. Losartan was orally administered daily before each training session (50 mg/kg/day). Time-matched sedentary rats served as controls. After euthanasia, heart hypertrophy was evaluated by histological studies; ventricular collagen deposition was quantified by histological and biochemical studies; and messenger RNA and protein expression of transforming growth factor-ß1, fibronectin-1, matrix metalloproteinase-2, tissue inhibitor of metalloproteinase-1, procollagen-I and procollagen-III was evaluated in all 4 cardiac chambers. Daily intensive exercise caused hypertrophy in the left ventricular heart wall and originated collagen deposition in the right ventricle. Additionally long-term intensive exercise induced a significant increase in messenger RNA expression and protein synthesis of the major fibrotic markers in both atria and in the right ventricle. Losartan treatment was able to reduce all increases in messenger RNA expression and protein levels caused by exercise, although it could not completely reverse the heart hypertrophy. CONCLUSIONS: Losartan treatment prevents the heart fibrosis induced by endurance exercise in training animals.

Inappropriate shocks or inappropriate programming? A review of Guidant's reconfirmation algorithm.

Ventricular tachycardia episodes terminating during or immediately after device charging are not expected to be treated by current implantable cardioverter defibrillators as shocks are non-committed. For proper troubleshooting, the reconfirmation algorithm will be reviewed.