Process hazard analysis, hazard identification and scenario definition: are the conventional tools sufficient, or should and can we do much better?

Hazard identification is the first and most crucial step in any risk assessment. Since the late 1960s it has been done in a systematic manner using hazard and operability studies (HAZOP) and failure mode and effect analysis (FMEA). In the area of process safety these methods have been successful in that they have gained global recognition. There still remain numerous and significant challenges when using these methodologies. These relate to the quality of human imagination in eliciting failure events and subsequent causal pathways, the breadth and depth of outcomes, application across operational modes, the repetitive nature of the methods and the substantial effort expended in performing this important step within risk management practice. The present article summarizes the attempts and actual successes that have been made over the last 30 years to deal with many of these challenges. It analyzes what should be done in the case of a full systems approach and describes promising developments in that direction. It shows two examples of how applying experience and historical data with Bayesian network, HAZOP and FMEA can help in addressing issues in operational risk management

Role of Rac GTPase activating proteins in regulation of NADPH oxidase in human neutrophils

Precise spatiotemporal regulation of O2 --generating NADPH oxidases (Nox) is a vital requirement. In the case of Nox1-3, which depend on the small GTPase Rac, acceleration of GTP hydrolysis by GTPase activating protein (GAP) could represent a feasible temporal control mechanism. Our goal was to investigate the molecular interactions between RacGAPs and phagocytic Nox2 in neutrophilic granulocytes. In structural studies we revealed that simultaneous interaction of Rac with its effector protein p67phox and regulatory protein RacGAP was sterically possible. The effect of RacGAPs was experimentally investigated in a cell-free O2 --generating system consisting of isolated membranes and recombinant p47phox and p67phox proteins. Addition of soluble RacGAPs decreased O 2 - production and there was no difference in the effect of four RacGAPs previously identified in neutrophils. Depletion of membrane-associated RacGAPs had a selective effect: a decrease in ARHGAP1 or ARHGAP25 level increased O2 - production but a depletion of ARHGAP35 had no effect. Only membrane-localized RacGAPs seem to be able to interact with Rac when it is assembled in the Nox2 complex. Thus, in neutrophils multiple RacGAPs are involved in the control of O2 - production by Nox2, allowing selective regulation via different signaling pathways. © 2013 Elsevier Inc

Prediction-based diagnosis and loss prevention using model-based reasoning

A diagnostic expert system established on model-based reasoning for on-line diagnosis and loss prevention is described in the paper. Its diagnostic cause-effect rules and possible actions (suggestions) are extracted from the results of standard HAZOP analysis. Automatic focusing as well as what-if type reasoning for testing hypothetical actions have been also implemented. The diagnostic system is tested on a granulator drum of a fertilizer plant in a simulation test-bed

Is there a connection between postprandial hyperglycemia and IGT related sensory nerve dysfunction?

BACKGROUND AND AIMS: To assess the risk factors for sensory nerve dysfunction in subjects with isolated impaired glucose tolerance (IGT). METHODS AND RESULTS: Seventy-two people with isolated IGT (WHO 1999 criteria) and 39 gender and age-matched healthy volunteers underwent detailed clinical and neurological assessment including quantitative sensory testing using the Neurometer device (current perception threshold measurement on four limbs at three different frequencies). Sensory nerve dysfunction was defined as at least two abnormalities on any frequencies on the upper or lower limbs. Sensory nerve dysfunction was more prevalent among subjects with IGT compared to controls (58.3 vs. 10.3%, OR: 11.23, 95%CI: 3.57-35.35). This association was not influenced by BMI, systolic and diastolic blood pressure, heart rate and autonomic neuropathy (multiple adjusted OR: 13.87, 95%CI: 3.18-60.58), but further adjustment for glycaemic measures abolished the association (OR: 1.58, 95%CI: 0.07-35.68). Assessing the components of glycaemic measures separately, the association between sensory nerve dysfunction and IGT was not affected by HbA1c (OR: 13.94, 95%CI: 1.84-105.5). It was, however, substantially attenuated by fasting plasma glucose (OR: 6.75, 95%CI: 1.33-34.27) while the significance was lost after adjustment for 120 min postload glucose level (OR: 3.76, 95%CI: 0.26-54.10). In the pooled population assessed, independent determinants of sensory nerve dysfunction were older age, 120 min glucose, higher height and cardiovascular autonomic neuropathy at near significance. CONCLUSIONS: Sensory nerve dysfunction amongst subjects with IGT was not explained by cardiovascular covariates, only by glycaemic measures. In addition to 120 min glucose, cardiovascular autonomic neuropathy at borderline significance, age, and height were the independent determinants of sensory nerve dysfunction