Guidelines and Safety Practices for Improving Patient Safety

AbstractThis chapter explains why clinical practice guidelines are needed to improve patient safety and how further research into safety practices can successfully influence the guideline development process. There is a description of the structured process by which guidelines that aim to increase the likelihood of a higher score are created. Proposals are made relating to (a) the live updating of individual guideline recommendations and (b) tackling challenges related to the improvement of guidelines

Perturbed adipose tissue hydrogen peroxide metabolism in centrally obese men: Association with insulin resistance.

Although adipose tissue hydrogen peroxide (H2O2) and its metabolizing enzymes have been linked to obesity and insulin resistance in animal studies, this relation remains to be evaluated in humans.Non-diabetic men (N = 43, median age, 49 (37, 54 y)) undergoing abdominal surgeries were studied. Participants were classified by body mass index (BMI) into normal-weight (N = 19), or overweight/obese (Ow/Ob; BMI ≥25; N = 24). Centrally obese men were identified by waist-height ratio ≥0.5. H2O2 and activities of superoxide dismutase, catalase and glutathione peroxidase enzymes were assayed in subcutaneous fat samples, and visceral fat (available from N = 33), and their associations with anthropometric parameters, fasting serum lipids, and the homeostasis model of insulin resistance (HOMA-IR) were tested using correlations and multivariate linear regression.H2O2 concentrations and catalase activity were increased in visceral fat from Ow/Ob men, compared to normal-weight subjects (+32%, P = 0.038 and +51%, P = 0.043 respectively). Centrally obese subjects had >2-fold higher superoxide dismutase activity (P = 0.005), 46% higher H2O2 (P = 0.028), and 89% higher catalase activity (P = 0.009) in visceral fat, compared to lean subjects. Central obesity did not alter these markers in subcutaneous fat, apart from a 50% increase in catalase, and did not affect glutathione peroxidase in either fat depot. H2O2 in visceral fat positively correlated with insulin resistance (r = 0.40, P = 0.032). Catalase activity in visceral fat was an independent determinant of HOMA-IR, explaining ~18% of the variance (ß = 0.42, P = 0.016), after adjustment for age and BMI.These findings suggest that adipose tissue catalase shows compensatory up-regulation in response to obesity-induced H2O2 accumulation, and that perturbed H2O2 metabolism in visceral fat is linked to insulin resistance in obese humans

H₂O₂ metabolism in visceral (left panel) and subcutaneous (right panel) adipose tissue from centrally obese (waist-height ratio ≥0.5, N = 30) and lean (waist-height ratio <0.5, N = 13) individuals.

<p><i>A</i>, <i>B</i>, higher H₂O₂ levels in visceral but not in subcutaneous adipose tissue of centrally obese individuals. <i>C</i>, <i>D</i>, Superoxide dismutase activity in visceral but not subcutaneous fat is higher in central obesity subjects. <i>E</i>, <i>F</i>, Visceral and subcutaneous fat catalase activities are higher in subjects with central obesity. <i>G</i>, <i>H</i>, No difference between the lean and centrally obese subjects in glutathione peroxidase activity in either fat depot. Values represent medians and 25^th and 75^th percentiles, *P < 0.05, **P <0.01, Mann Whitney <i>U</i> test.</p

Characteristics of the study population ¹.

<p>Characteristics of the study population <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0177268#t001fn001" target="_blank">¹</a>.</p

<i>A</i>, <i>B</i>, <i>C</i>, <i>D</i> Lack of associations of H₂O₂ <i>(A)</i> or activity of its metabolizing enzymes <i>(B-D)</i> in subcutaneous adipose tissue with the homeostasis model of insulin resistance (HOMA-IR) in the total population (N = 43).

<p>Each scatter plot shows the best-fit linear regression line and 95% confidence intervals, with Pearson correlation coefficients. All parameters are log-transformed apart from superoxide dismutase activity.</p

<i>A</i>, <i>B</i>, <i>C</i>, <i>D</i> Scatter plots for the associations of H₂O₂ <i>(A)</i> and activity of its metabolizing enzymes <i>(B-D)</i> in visceral adipose tissue with the homeostasis model of insulin resistance (HOMA-IR) in the total population (N = 33).

<p>Each plot shows the best-fit linear regression line and 95% confidence intervals, with Pearson correlation coefficients. All parameters are log-transformed apart from H₂O₂ concentrations.</p

Correlation of age and anthropometric and biochemical measures with markers of hydrogenperoxide metabolism¹.

<p>Correlation of age and anthropometric and biochemical measures with markers of hydrogenperoxide metabolism<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0177268#t003fn001" target="_blank">¹</a>.</p

Visceral adipose tissue parameters as independent predictors of HOMA-IR ¹.

<p>Visceral adipose tissue parameters as independent predictors of HOMA-IR <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0177268#t004fn001" target="_blank">¹</a>.</p

Assessment of DNA damage using chromosomal aberrations assay in lymphocytes of waterpipe smokers

OBJECTIVES: The aim of this study was to investigate the genotoxicity of waterpipe smoking in the lymphocytes of waterpipe smokers using chromosomal aberrations (CAs) assay. MATERIALS AND METHODS: Fifty waterpipe smokers and 18 healthy non-smokers volunteered to participate in the study. Additionally, 18 heavy cigarette smokers were recruited for comparison. Chromosomal aberrations (CAs) assay was used to evaluate DNA damage in the lymphocytes. RESULTS: The results showed that similarly to cigarette smoking, waterpipe smoking significantly increased the frequencies of CAs (p < 0.01). In addition, the frequencies of CAs increased with more waterpipe use. CONCLUSIONS: Waterpipe smoking causes DNA damage to lymphocytes and the damage increases with more waterpipe use