58 research outputs found

    Assessment of human error contribution to container loss risk under fault tree analysis and interval type-2 fuzzy logic-based SLIM approach

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    Human is a key element of the safety of life on board ships and a significant contributing factor to most of the accidents and incidents in the maritime industry. At this point, risk analysis plays a critical role in ensuring operational safety and maritime transportation sustainability. This paper aims to systematically evaluate how human errors (HEs) contribute to operational risks. Based on this, Fault Tree Analysis (FTA) is combined under an Interval Type-2 Fuzzy Logic environment with Success Likelihood Index Method (SLIM). Whilst the FTA evaluates the criticality of the operational activities, the Interval Type-2 Fuzzy Sets (IT2FS) deals with vagueness and subjectivity in using experts’ judgments, and the SLIM estimates the probabilities for the human error-related basic events. Since container losses can lead to severe damage and catastrophic events in a container terminal, loading operation was investigated as a case study. Safety culture, experience, and fatigue were observed as highly effective factors in crew performance. The obtained results also indicate that this hybrid approach can effectively be applied to determine the operational vulnerabilities in high-risk industries. The paper intends to improve safety control levels and lower losses in the future of maritime container transport besides emphasizing the potential consequences of failures and crucial human errors in the operational process

    Gain of function mutation in K(ATP) channels and resulting upregulation of coupling conductance are partners in crime in the impairment of Ca<sup>2+</sup> oscillations in pancreatic ß-cells

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    Gain of function mutations in the pore forming Kir6 subunits of the ATP sensitive K+ channels (K(ATP) channels) of pancreatic β-cells are the major cause of neonatal diabetes in humans. In this study, we show that in insulin secreting mouse β-cell lines, gain of function mutations in Kir6.1 result in a significant connexin36 (Cx36) overexpression, which form gap junctional connections and mediate electrical coupling between β-cells within pancreatic islets. Using computational modeling, we show that upregulation in Cx36 might play a functional role in the impairment of glucose stimulated Ca2+ oscillations in a cluster of β-cells with Kir6.1 gain of function mutations in their K(ATP) channels (GoF-K(ATP) channels). Our results show that without an increase in Cx36 expression, a gain of function mutation in Kir6.1 might not be sufficient to diminish glucose stimulated Ca2+ oscillations in a β-cell cluster. We also show that a reduced Cx36 expression, which leads to loss of coordination in a wild-type β-cell cluster, restores coordinated Ca2+ oscillations in a β-cell cluster with GoF-K(ATP) channels. Our results indicate that in a heterogenous β-cell cluster with GoF-K(ATP) channels, there is an inverted u-shaped nonmonotonic relation between the cluster activity and Cx36 expression. These results show that in a neonatal diabetic β-cell model, gain of function mutations in the Kir6.1 cause Cx36 overexpression, which aggravates the impairment of glucose stimulated Ca2+ oscillations.</p

    Gain of function mutation in K(ATP) channels and resulting upregulation of coupling conductance are partners in crime in the impairment of Ca<sup>2+</sup> oscillations in pancreatic ß-cells

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    Gain of function mutations in the pore forming Kir6 subunits of the ATP sensitive K+ channels (K(ATP) channels) of pancreatic β-cells are the major cause of neonatal diabetes in humans. In this study, we show that in insulin secreting mouse β-cell lines, gain of function mutations in Kir6.1 result in a significant connexin36 (Cx36) overexpression, which form gap junctional connections and mediate electrical coupling between β-cells within pancreatic islets. Using computational modeling, we show that upregulation in Cx36 might play a functional role in the impairment of glucose stimulated Ca2+ oscillations in a cluster of β-cells with Kir6.1 gain of function mutations in their K(ATP) channels (GoF-K(ATP) channels). Our results show that without an increase in Cx36 expression, a gain of function mutation in Kir6.1 might not be sufficient to diminish glucose stimulated Ca2+ oscillations in a β-cell cluster. We also show that a reduced Cx36 expression, which leads to loss of coordination in a wild-type β-cell cluster, restores coordinated Ca2+ oscillations in a β-cell cluster with GoF-K(ATP) channels. Our results indicate that in a heterogenous β-cell cluster with GoF-K(ATP) channels, there is an inverted u-shaped nonmonotonic relation between the cluster activity and Cx36 expression. These results show that in a neonatal diabetic β-cell model, gain of function mutations in the Kir6.1 cause Cx36 overexpression, which aggravates the impairment of glucose stimulated Ca2+ oscillations.</p

    Emotional dysregulation in adolescents with functional gastrointestinal disorders

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    WOS: 000529355200005PubMed: 32179047Background and Study Aims: In various gastrointestinal system diseases, emotional dysregulation has been shown to reduce pain tolerance and increase the severity of the disease. Increased emotional dysregulation during the adolescence period causes gastrointestinal symptoms to be more frequent and severe. In this study, Child Depression Inventory (CDI) scores were investigated in patients admitted to our clinic with functional gastrointestinal disorders. Patients and Methods: According to Rome IV criteria, 200 patients with functional abdominal pain and dyspepsia aged 12-17 years were included in this study. 100 patients without a chronic disease were taken as control group. Patients completed the self-report questionnaires about symptoms, school performance, nutrition and sports habits. We used Child Depression Inventory (CDI) to assess the patients' depression. Results: The mean age of study group was 15.29 +/- 1.48 years (12-17 years), median 16 years; 80% (160/200) were girls. The mean age of control group was 14.96 +/- 1.66 years (12-17 years), median 15 years; 70% (70/100) were girls. There is no difference between the two groups for age and gender. Median depression score was 12.5 (range, 0-53) in the study group and 10.0 (range, 0-41) in the control group and a significant difference was found between the two groups (p = 0.014). School performance was revealed as 'very good' in 112 (56%) children in the study group and in 24 (24%) children in the control group and a significant difference was found between the two groups (p < 0.001). A negative correlation was found between school performance and depressive symptoms. Conclusion: It is not clear that emotional dysregulation induces FGIDs or FGIDs cause emotional dysregulation. But it is known that these diseases are common in the adolescent age group. Incorporating social and physical activities into the educational processes of adolescents will have favorable effects on their academic performance as well as emotional regulation. (C) 2020 Pan-Arab Association of Gastroenterology. Published by Elsevier B.V. All rights reserved

    Fatal Deep Inguinal Infection after Diagnostic Coronary Angiography

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    Herein we would like to share our case complicated with inguinal infection secondary to femoral haematoma after coronary angiography. A-79 years-old female underwent diagnostic coronary angiography suffered from a large haematoma in the right inguinal region where femoral artery puncture was performed at another hospital. She was treated at same hospital 16 days and discharged. She presented to our department with a deep ulcerative and ruptured wound in the femoral artery puncture site. The wound-site culture revealed E. coli. After appropriate antibiotic treatment and wound care, the deep inguinal infection began healed. Purulan material and swallowing decreased and patient discharged. After 8 days, she came back with shock presentation and hospitalised to intensive care unit, but she died within 3 hours. We emphasised that the importance of prevention and management of access site haematoma during percutaneous procedures is vital and should not be neglected in routine practice
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