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Background: Outpatient laparoscopic cholecystectomy has proven to be a safe and cost-effective technique; however, it is not yet a universally widespread procedure. The aim of the study was to determine the predictive factors of outpatient laparoscopic cholecystectomy failure., Method: A systematic review and meta-analysis was performed according to Preferred Reporting Items for Systematic Reviews and Meta-analysis methodology. MEDLINE, Cochrane Library, Ovid, and ISRCTN Registry were searched. The main variables were demographic (age, sex), clinical (weight, American Society of Anesthesiologists classification, previous complicated biliary pathology, history of abdominal surgery in supramesocolic compartment, gallbladder wall thickness), and surgical factors (operative time, afternoon surgery). The secondary variables were the prevalence rates of outpatient laparoscopic cholecystectomy failure due to pain or postoperative nausea and vomiting., Results: Fourteen studies (4,194 patients) were included, with a mean outpatient laparoscopic cholecystectomy failure rate of 23.4%. The predictors of outpatient laparoscopic cholecystectomy failure were: age ≥65 years (odds ratio: 2.34; 95% confidence interval, 1.42-3.86; P = .0009), body mass index ≥30 (odds ratio: 1.6; 95% confidence interval, 1.05-2.45; P = .03), American Society of Anesthesiologists score ≥III (odds ratio: 2.89; 95% confidence interval, 1.72-4.87; P < .0001), previous complicated biliary pathology (odds ratio: 2.39; 95% confidence interval, 1.40-4.06; P = .001), gallbladder wall thickening (odds ratio: 2.33; 95% confidence interval, 1.34-4.04; P = .003), surgical time exceeding 60 minutes (mean difference: -16.03; 95% confidence interval,-21.25 to -10.81; P < .00001), and the beginning of surgery after 1:00 pm (odds ratio: 4.20; 95% confidence interval, 1.97-11.96; P = .007). Sex (odds ratio: 1.07; 95% confidence interval, 0.73-1.57, P = .73) and history of abdominal surgery in the supramesocolic compartment (odds ratio: 2.32; 95 confidence interval, 0.92-5.82, P = .07) were not associated with outpatient laparoscopic cholecystectomy failure., Conclusion: Our meta-analysis allowed us to identify the predictors of outpatient laparoscopic cholecystectomy failure. The knowledge of these factors could help surgeons in their decision-making process for the selection of patients who are suitable for outpatient laparoscopic cholecystectomy., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Listeria monocytogenes is riboflavin auxotrophic, but it has two genes envisaged to transform riboflavin into FMN and FAD after its uptaked by specialized transporters. One encodes a bifunctional type I FAD synthase (FADS, herein LmFADS-1), while the other produces a protein similar to type I at the FMN:ATP adenylyltransferase (FMNAT) site but with a shorter C-terminal that lacks any riboflavin kinase (RFK) motif. This second protein is rare among bacteria and has been named FADS type II (LmFADS-2). Here we present a biochemical and biophysical study of LmFADS-1 and LmFADS-2 by integrating kinetic and thermodynamic data together with sequence and structural prediction methods to evaluate their occurrence in Listeria, as well as their function and molecular properties. Despite LmFADS-1 similarities to other type I FADSs, (i) its RFK activity has not riboflavin substrate inhibition and occurs under reducing and oxidizing conditions, (ii) its FMNAT activity requires strong reducing environment, and (iii) binding of reaction products, but not substrates, favors binding of the second ligand. LmFADS-2 produces FAD under oxidizing and reducing environments, but its C-terminus module function remains unknown. Listeria species conserve both FADSs, being sequence identity high within L. monocytogenes strains. Our data exemplify alternative strategies for FMN and FAD biosynthesis and homeostasis, envisaging that in Listeria two FADSs might be required to fulfill the supply of flavin cofactors under niches that can go from saprophytism to virulence. As FADSs are attractive antimicrobial targets, understanding of FADSs traits in different species is essential to help in the discovery of specific antimicrobials., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Background: The knowledge and acceptance of the concept of brain death (BD) among health care personnel is fundamental., Objective: To analyze the level of understanding of the BD concept among personnel in Spanish and Latin American healthcare centers and to determine the factors affecting this attitude., Material and Methods: Data from 12 hospitals and 32 primary care centers in 4 countries within the International Collaborative Donor Project were selected (Spain, Mexico, Cuba and Costa Rica (n=4378))., Results: 62% of the personnel (n=2714) understood BD and believed that this was the death of an individual. Of the rest, 30% (n=1333) did not understand it and the remaining 8% (n=331) believed it did not mean the death of a patient. 83% (n=931) of physicians understood BD, compared to 75% (n=895) of nurses, 55% (n=299) of healthcare assistants, 53% (n=108) of non-healthcare university-educated personnel and 36% (n=481) of those without a university education (p<0.001). 68% (n=1084) of Mexicans understood BD compared to 66% (n=134) of Cubans, 58% (n=1411) of Spaniards, and 52% (n=85) (p<0.001) of Costa Ricans. There were significant relationships between knowledge of the concept and the following: type of healthcare center (p<0.001), clinical service (p<0.001), having spoken about organ donation within the family (p<0.001) and one's partner's attitude to the subject (p<0.001). A direct relationship has been found between understanding the concept and attitude toward deceased donation (p<0.001)., Conclusions: The understanding of BD by personnel from healthcare centers was not as good as expected. There were marked differences depending on job category.

Friedreich ataxia (FA), the most common form of hereditary ataxia, is caused by a deficit in the mitochondrial protein frataxin. While several hypotheses have been suggested, frataxin function is not well understood. Oxidative stress has been suggested to play a role in the pathophysiology of FA, but this view has been recently questioned, and its link to frataxin is unclear. Here, we report the use of RNA interference (RNAi) to suppress the Drosophila frataxin gene (fh) expression. This model system parallels the situation in FA patients, namely a moderate systemic reduction of frataxin levels compatible with normal embryonic development. Under these conditions, fh-RNAi flies showed a shortened life span, reduced climbing abilities, and enhanced sensitivity to oxidative stress. Under hyperoxia, fh-RNAi flies also showed a dramatic reduction of aconitase activity that seriously impairs the mitochondrial respiration while the activities of succinate dehydrogenase, respiratory complex I and II, and indirectly complex III and IV are normal. Remarkably, frataxin overexpression also induced the oxidative-mediated inactivation of mitochondrial aconitase. This work demonstrates, for the first time, the essential function of frataxin in protecting aconitase from oxidative stress-dependent inactivation in a multicellular organism. Moreover our data support an important role of oxidative stress in the progression of FA and suggest a tissue-dependent sensitivity to frataxin imbalance. We propose that in FA, the oxidative mediated inactivation of aconitase, which occurs normally during the aging process, is enhanced due to the lack of frataxin.