Modifying a method for human reliability assessment based on CREAM-BN: A case study in control room of a petrochemical plant.

BACKGROUND: Cognitive Reliability and Error Analysis Method (CREAM), as one of the second-generation methods, has been developed to overcome the shortcomings of the first-generation human reliability analysis methods. Although it is a useful tool for assessing the effects of context on human failure probability, namely common performance conditions (CPCs), there still exist some problems, such as lack of data about CPCs, and their unclear relationship with the operator control mode. OBJECTIVE: The current paper aimed at applying CREAM Bayesian Network (BN) in a real-world situation in order to identify the limitations associated to CPCs in estimating Human Error Probability (HEP). METHOD: In this paper, the data pertaining to CPCs were collected by a self-designed questionnaire. CREAM BN was then performed in a five-step methodology, including the identification of the primary effects of CPCs, adjustment of dependency of CPCs, new grouping of CPCs, determination of control modes, and HEP calculation. RESULTS: The results showed that there are varied values of control modes in CREAM BN in comparison with the basic CREAM. On the other hand, this method provides the grounds for incorporating various importance levels of CPCs in HEP estimation by changing the nature of prior conditional probabilities from the deterministic one into the probabilistic one. CONCLUSION: The methodology introduced in this study provides a simple method for the calculation of HEP in the complex industries.•This method provides the application of the CREAM BN in a real-environmental in practice.•This method provides a foundation for incorporating various importance levels of the CPCs in the HEP estimation by changing the nature of prior conditional probabilities from deterministic into probabilistic.•It could reduce the uncertainty in the calculation of HEP.

Supernumerary nostrils: a case report and review.

Supernumerary or accessory nostrils are a very rare type of congenital nasal anomaly, with only a few cases reported in the literature. They can be associated with such malformations as facial clefts and they can be unilateral or bilateral, with most cases reported being unilateral. The accessory nostril may or may not communicate with the ipsilateral nasal cavity, probably depending on the degree of embryological progression of the anomaly. A case of simple supernumerary left nostril with no nasal cavity communication and with a normally developed nose is presented. The surgical treatment is described and the different speculative theories related to the embryogenesis of supernumerary nostrils are also reviewed.

Contracture of the newborn myocardium after prolonged prearrest cooling.

Profound hypothermic circulatory arrest is frequently used to facilitate the surgical repair of congenital heart defects in neonates. Deep hypothermia is achieved by a period of core systemic cooling during cardiopulmonary bypass before cardioplegic arrest. There have been conflicting reports with respect to the consequence of perfusing a nonarrested newborn heart under hypothermic conditions. This in vitro study was designed to prolong the clinically simulated hypothermic perfusion sequence into an extreme condition and to test the hypothesis that prolonged cold perfusion of the nonarrested newborn myocardium could, in fact, be detrimental. Twenty-four newborn piglets (5 to 7 days old) were randomly assigned to four groups and studied in a crystalloid perfused Langendorff heart model. The first two groups of hearts (n = 6 per group) were subjected to either 30 minutes (group I) or 90 minutes (group II) of cold perfusion at 15 degrees C, followed by 90 minutes of ischemia and then 30 minutes of normothermic reperfusion. In a second experiment, group III hearts subjected to 30 minutes of cold perfusion were compared with group IV (90 minutes of cold perfusion) without ischemic insult in either case. Postischemic recovery of isovolumetric developed pressure was significantly impaired in group II (16.1% +/- 7.4% [II] versus 65.5% +/- 4.8% [I], p < 0.05), and 50% of the hearts had no spontaneous cardiac activity on reperfusion. End-diastolic pressure showed significant contracture with prolonged cold perfusion: group II 57.3 +/- 13.9 mm Hg versus group I 14.8 +/- 1.8 mm Hg, p < 0.05. In the absence of ischemia, a similar relationship was observed between groups IV and III (left ventricular developed pressure 68.5% +/- 3.6% versus 82.4% +/- 4.2%, p < 0.05, and left ventricular end-diastolic pressure 23.5 +/- 6.2 mm Hg versus 13.3 +/- 2.6 mm Hg, p = not significant. Ultrastructural examination revealed severe damage to the myocardial cells and contraction band necrosis in group II (prolonged cooling and ischemia). These results suggest that prolonged cold perfusion of the nonarrested newborn heart impairs functional recovery and is therefore detrimental. When followed by a period of ischemic arrest, it further potentiates the myocardial injury and induces severe contracture. This preceding adverse effect of prolonged myocardial cold perfusion before cardiac arrest may, in part, explain the suboptimal protective effect of cardioplegia in neonates.

Adverse effect of prearrest hypothermia in immature hearts: rate versus duration of cooling.

It has been suggested that rapid cooling before the induction of arrest may be harmful to the newborn myocardium. The objective of this study was twofold: (1) to evaluate whether prearrest rapid cooling is indeed detrimental to myocardial recovery and (2) if so, to evaluate whether the adverse effect of prearrest hypothermia is dependent on the rate of cooling or the total duration of cold perfusion. After an initial stabilization period isolated Langendorff hearts (n = 5 per group) from neonatal piglets (5 to 7 days old) were randomized to four groups: group 1, 5 minutes of rapid cooling to 15 degrees C; group 2, 20 minutes of slow cooling to 15 degrees C; group 3 and group 4, rapid and slow cooling, respectively, with the addition of St. Thomas cardioplegic solution. All groups were then subjected to 2 hours of ischemia at 15 degrees C followed by 30 minutes of reperfusion at 38.5 degrees C. Post-ischemic recovery of left ventricular developed pressure was significantly greater in group 1 versus group 2 (80% +/- 3% versus 61% +/- 2%; p less than 0.05) and in the presence of cardioplegia, group 3 versus group 4 (72% +/- 3% versus 57% +/- 3%; p less than 0.05). The increase in left ventricular end-diastolic pressure was significantly less in group 1 versus group 2 (8% +/- 5% versus 33% +/- 7%; p less than 0.01). Myocardial adenosine triphosphate content recovery correlated with ventricular recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Stimulation of growth hormone release and synthesis by estrogens in rat anterior pituitary cells in culture.

We have investigated the potential effect of estrogens in the control of GH secretion in rat anterior pituitary cells in primary culture. We have found that a 72-h preincubation with 17 beta-estradiol (E2) caused an approximately 2- to 3-fold stimulation of basal and GH-releasing factor (GRF)-induced GH release as well as cellular GH content at EC50 values of 44, 35, and 15 pM, respectively. Estrone and estriol also increased GH release at respective EC50 values of 100 and 250 pM. The stimulatory effects of these steroids on GH release and cellular GH content were competitively blocked by simultaneous incubation with the antiestrogen LY156758. In contrast to thyroid and glucocorticoid hormones, a 72-h pretreatment with E2 failed to potentiate GRF-induced cAMP accumulation or enhance the sensitivity of the GH response to GRF. However, E2 increased the stimulatory effect of submaximal concentrations of dexamethasone on spontaneous and GRF-induced GH release as well as on total GH, but did not further increase the effect of maximal dexamethasone concentrations. As determined by a 60-min pulse labeling with [35S]methionine performed after a 72-h preincubation with E2, GH and PRL synthesis were increased by about 50% above control values (P less than 0.005). The present data clearly indicate for the first time that E2, at physiological concentrations, exerts a stimulatory effect on spontaneous and GRF-induced GH release as well as on cellular GH content, probably resulting, at least in part, from stimulation of GH synthesis.