Knowledge and attitudes of healthcare professionals and the impact on willingness to donate organs: a tertiary hospital survey.

INTRODUCTION: Healthcare professionals (HCPs) working in critical care areas play an important role in the organ donation (OD) process. We studied HCPs' own willingness to be organ donors and its association with sociodemographic factors as well as their knowledge and attitudes about OD and transplantation. METHODS: A cross-sectional survey of HCPs working in four critical care units in a major transplant centre in Malaysia was undertaken using a validated structured questionnaire. Responses were analysed using multivariable analysis with willingness to donate as the dependent variable. RESULTS: Of the 412 respondents (response rate 98.1%), the majority were nurses (60.4%), Malay (71.1%) and female (77.2%). Overall, 68.0% were willing to donate. The independent predictors of willingness to donate were profession (p < 0.001) and the Hindu religion (p = 0.001). Ethnicity (p = 0.003), religious belief (p < 0.001), knowledge (p = 0.016), belief in brain death (p = 0.018) and confidence in transplantation (p < 0.001) also independently correlated with willingness to donate, while attitudes to OD did not. Of those willing to donate, only 37.3% were carrying a donor card and only 63.1% had informed their family of their intention to donate. CONCLUSION: Although willingness to donate was higher in critical care HCPs than HCPs in general, significant knowledge gaps as well as certain beliefs and perceptions that could pose a barrier to OD were identified in this group. Measures to improve OD rates in Malaysia should include targeted educational programmes for HCPs working in critical care areas.

Are we reaping what we sow? Gender diversity in surgery: a survey of medical students.

BACKGROUND: A survey of medical students from the Royal College of Surgeons in Ireland (RCSI) at Dublin, Perdana and Penang in Malaysia was undertaken in an attempt to explore attitudes towards a career in surgery and document potential differences between male and female students' perceptions of a surgical career. METHOD: A hyperlink to an online, anonymised questionnaire was distributed to medical students in 3rd, 4th and final year at three RCSI campuses. Basic descriptive statistics were used to describe the responses to individual questions and appropriate statistical tests used to compare male and female responses to questions. RESULTS: A total of 464 completed questionnaires were analysed. Almost 40% (n=185) were male and 60% (n=279) were female. Males were significantly more influenced by remuneration than females (p<0.001) towards a choice of surgical career. Females were significantly more influenced in their choice of surgical career by part-time work (p<0.001), parental leave (p<0.001), working hours (p<0.001) and length of residency (p=0.003). During surgical attachments, females were significantly more likely to admit feeling intimidated than males (p=0.002) and males more likely to report feeling confident (p<0.001). Ninety-six per cent of students felt they would be more likely to pursue a career in which they had identified a positive role model, with female medical students three times more likely to have identified a female role model than males. CONCLUSION: According to our study, preference for a career in surgery declines with advancing years in medical school for both males and females. Medical students report high levels of feeling intimidated or ignored during their surgical placements, and enthusiasm for surgery reduces during medical school with exposure to this. These findings, along with the importance of role modelling, add further urgency to the need to address factors which make surgery less appealing to female medical graduates.

Management of Symmetrical Peripheral Gangrene.

Symmetrical peripheral gangrene (SPG) is a rare, debilitating disease that deserves more widespread concern among the medical fraternities. The objective of this review is to outline the etiology, pathology findings, and management practices of SPG. About 18%-40% mortality rate was reported, and survivors have high frequency of multiple limb amputations. SPG is the hallmark of disseminated intravascular coagulation (DIC). The main pathogenesis theory, to date, is microthrombosis associated with disturbed procoagulant-anticoagulant balance. The treatment of SPG is largely anecdotal and theoretically involves heparin-based anticoagulation and substitution of natural anticoagulants. Early recognition, prompt management of DIC, and underlying conditions may halt the progression of the disease. The multicenter randomized controlled trial should be set up to formulate the proper treatment guidelines.

Reoxygenation-specific activation of the antioxidant transcription factor Nrf2 mediates cytoprotective gene expression in ischemia-reperfusion injury.

Tissue reoxygenation following hypoxia is associated with ischemia-reperfusion injury (IRI) and may signal the development of ischemic preconditioning, an adaptive state that is protective against subsequent IRI. Here we used microarray RNA analysis of in vivo and in vitro models of IRI to delineate the underlying molecular mechanisms. Microarray analysis of renal tissue after ischemia-reperfusion revealed a number of highly up-regulated antioxidant genes including aldehyde dehydrogenases (ALDH1A1 and ALDH1A7), glutathione S-transferases (GSTM5, GSTA2 and GSTP1), and NAD(P)H quinone oxidoreductase (NQO1). The transcription factor NF-E2-related factor-2 (Nrf2), a master regulator of this antioxidant response, is also elevated in IRI. Furthermore, microarray analysis of renal epithelial cells exposed to hypoxia/reoxygenation identified Nrf2 to be up-regulated on reoxygenation. We also reveal a reoxygenation-specific nuclear accumulation of Nrf2 protein and subsequent activation of a NQO1 promoter reporter construct. Attenuating reactive oxygen species (ROS) in reoxygenation using the antioxidant N-acetyl cysteine results in inhibition of Nrf-2 activation. mRNA levels for Nrf2-dependent genes were detected in human liver biopsy 1 h after transplantation. These results indicate that reoxygenation-dependent Nrf-2 activity facilitates ischemic preconditioning through the induction of antioxidant gene expression and that ROS may be critical in signaling this event.

Nitric oxide in early ischaemia reperfusion injury during human orthotopic liver transplantation.

BACKGROUND: Altered nitric oxide (NO) metabolism has been shown to contribute to ischemia-reperfusion (IR) injury in animal models. However, similar studies have not been performed in human liver transplantation (LT). In this study, we examined nitrate, nitrite, and nitrosothiols (NOx), NO synthases (endothelial [constitutive] nitric oxide synthase [eNOS] and inducible nitric oxide synthase [iNOS]), and nitrotyrosine in early IR injury after human LT. METHODS: Paired biopsies were obtained from nine donor livers before cold ischemia (retrieval biopsy) and after reimplantation (reperfusion biopsy). Sections were graded for reperfusion injury using the Suzuki score. NO was detected by chemiluminescence after reduction of NOx. Expression of eNOS and iNOS was by Western blot and reverse transcriptase polymerase chain reaction and peroxynitrite by immunodetection of 3-nitrotyrosine. RESULTS: Reperfusion biopsies showed histologic evidence of injury (median Suzuki score: retrieval 2, reperfusion 6, P=0.008) and neutrophil infiltration. NOx was reduced after reperfusion from 5.41 microM/100 mg (median, range 2.17-13.39 microM) to 3.51 microM (1.45-5.66 microM, P=0.05). eNOS protein was reduced after reperfusion from 0.6 units (median, range 0.45-1 unit) in retrieval biopsies to 0.39 units in reperfusion biopsies (range 0.2-0.79 units, P=0.007). There was no change in eNOS or iNOS mRNA expression or iNOS protein. Western blotting showed increased nitrotyrosine formation after reperfusion, median 0.42 (range 0.16-0.87) units in retrieval biopsies and 0.68 (0.29-1.06) units in reperfusion samples (P=0.007) and localized to periportal regions. CONCLUSIONS: iNOS protein may not contribute to early reperfusion injury during human LT. However, reduced NO bioavailability caused by reduced eNOS may contribute significantly to damage at this time point.