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- Ademuyiwa, Adesoji O., et al.
(author)
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Determinants of morbidity and mortality following emergency abdominal surgery in children in low-income and middle-income countries
- 2016
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In: BMJ Global Health. - : BMJ Publishing Group Ltd. - 2059-7908. ; 1:4
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Journal article (peer-reviewed)abstract
- Background: Child health is a key priority on the global health agenda, yet the provision of essential and emergency surgery in children is patchy in resource-poor regions. This study was aimed to determine the mortality risk for emergency abdominal paediatric surgery in low-income countries globally.Methods: Multicentre, international, prospective, cohort study. Self-selected surgical units performing emergency abdominal surgery submitted prespecified data for consecutive children aged <16 years during a 2-week period between July and December 2014. The United Nation's Human Development Index (HDI) was used to stratify countries. The main outcome measure was 30-day postoperative mortality, analysed by multilevel logistic regression.Results: This study included 1409 patients from 253 centres in 43 countries; 282 children were under 2 years of age. Among them, 265 (18.8%) were from low-HDI, 450 (31.9%) from middle-HDI and 694 (49.3%) from high-HDI countries. The most common operations performed were appendectomy, small bowel resection, pyloromyotomy and correction of intussusception. After adjustment for patient and hospital risk factors, child mortality at 30 days was significantly higher in low-HDI (adjusted OR 7.14 (95% CI 2.52 to 20.23), p<0.001) and middle-HDI (4.42 (1.44 to 13.56), p=0.009) countries compared with high-HDI countries, translating to 40 excess deaths per 1000 procedures performed.Conclusions: Adjusted mortality in children following emergency abdominal surgery may be as high as 7 times greater in low-HDI and middle-HDI countries compared with high-HDI countries. Effective provision of emergency essential surgery should be a key priority for global child health agendas.
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| 4. |
- Thomas, HS, et al.
(author)
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- 2019
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swepub:Mat__t
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| 5. |
- Tabiri, S, et al.
(author)
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- 2021
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swepub:Mat__t
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| 7. |
- Bravo, L, et al.
(author)
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- 2021
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swepub:Mat__t
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| 9. |
- Hassanin, Abdallah A., et al.
(author)
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Emergence, evolution, and vaccine production approaches of SARS-CoV-2 virus : benefits of getting vaccinated and common questions
- 2022
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In: Saudi Journal of Biological Sciences. - : Elsevier. - 1319-562X. ; 29:4, s. 1981-1997
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Research review (peer-reviewed)abstract
- The emergence of coronavirus disease 2019 (COVID-19) pandemic in Wuhan city, China at the end of 2019 made it urgent to identify the origin of the causal pathogen and its molecular evolution, to appropriately design an effective vaccine. This study analyzes the evolutionary background of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2 or SARS-2) in accordance with its close relative SARS-CoV (SARS-1), which was emerged in 2002. A comparative genomic and proteomic study was conducted on SARS-2, SARS-1, and Middle East respiratory syndrome coronavirus (MERS), which was emerged in 2012. In silico analysis inferred the genetic variability among the tested viruses. The SARS-1 genome harbored 11 genes encoding 12 proteins, while SARS-2 genome contained only 10 genes encoding for 10 proteins. MERS genome contained 11 genes encoding 11 proteins. The analysis also revealed a slight variation in the whole genome size of SARS-2 comparing to its siblings resulting from sequential insertions and deletions (indels) throughout the viral genome particularly ORF1AB, spike, ORF10 and ORF8. The effective indels were observed in the gene encoding the spike protein that is responsible for viral attachment to the angiotensin-converting enzyme 2 (ACE2) cell receptor and initiating infection. These indels are responsible for the newly emerging COVID-19 variants αCoV, βCoV, γCoV and δCoV. Nowadays, few effective COVID-19 vaccines developed based on spike (S) glycoprotein were approved and become available worldwide. Currently available vaccines can relatively prevent the spread of COVID-19 and suppress the disease. The traditional (killed or attenuated virus vaccine and antibody-based vaccine) and innovated vaccine production technologies (RNA- and DNA-based vaccines and viral vectors) are summarized in this review. We finally highlight the most common questions related to COVID-19 disease and the benefits of getting vaccinated.
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| 10. |
- Ahmed, Osman Salih Osman
(author)
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Role of cholesterol metabolism in hepatic steatosis and glucose tolerance
- 2019
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Doctoral thesis (other academic/artistic)abstract
- The liver is the central organ for lipid, lipoprotein and glucose homeostasis, thus hepatic metabolic disturbances can predispose individuals to develop cardiometabolic disorders (CMD) such as atherosclerotic cardiovascular diseases (ASCVD), type 2 diabetes mellitus (T2DM), and nonalcoholic fatty liver disease (NAFLD).The overall aim of this thesis was to expand the knowledge on how genetic and pharmacological interventions on hepatic and intestinal cholesterol metabolism could affect the pathophysiology of CMD. Papers I and II: Acyl-Coenzyme A:cholesterol acyltransferase 2 (ACAT2, encoded by the Soat2 gene) is exclusively expressed in hepatocytes and enterocytes and catalyzes the biosynthesis of cholesteryl esters from cholesterol and long-chain fatty acids. Previous studies in mice model have shown that loss of ACAT2 activity protects from atherosclerosis, diet-induced hypercholesterolemia, and dietary cholesterol-driven hepatic steatosis. Here, we aimed to dissect the potential molecular mechanisms by which genetic depletion of Soat2 could affect the pathophysiology of hepatic steatosis and insulin sensitivity, independently of dietary regimens. We found that depletion of Soat2 significantly reduces hepatic steatosis and improves glucose tolerance, independently of high levels of cholesterol in the diet. We proposed the downregulation of hepatic de novo lipogenesis; DNL (lipid synthesis from glucose), GLUT2 membrane protein and Cd36 mRNA levels, as main mechanisms by which Soat2 depletion improves CMD. Dampening induction of CIDEC/FSP27 mRNA and protein levels in the severe fatty liver is another potential mechanism. Thus, cholesterol esterification by ACAT2 seems to be linked to hepatic steatosis and glucose homeostasis. Taken together, our study strongly supports ACAT2 inhibition as a promising target to treat CMD. Papers III and IV: Ezetimibe and simvastatin inhibit cholesterol absorption and cholesterol synthesis, respectively. Adding ezetimibe to simvastatin therapy has been shown to result in an additional absolute risk reduction of death from ASCVD, particularly among patients with T2DM (IMPROVE-IT trial). In Paper III, we aimed to investigate the potential positive effects of cholesterol absorption and/or cholesterol synthesis inhibition on remnant particles, the binding to arterial proteoglycans (PG), and biliary lipid compositions as well as hepatic sterol regulatory element-binding protein 2 (SREBP2) target genes. Combined therapy resulted in athero-protective changes on remnant and apoB-lipoprotein particles, and on the affinity for arterial PG. In Paper IV, we aimed to further characterize the effects by the addition of ezetimibe to simvastatin therapy on the hepatic transcriptional signature to uncover potential beneficial responses on different metabolic pathways in humans. We identified a total of 260 reliable genes to be altered during the different treatments. Gene ontology and pathways analysis displayed involvement of the combined therapy in classical antibody-mediated complement activation. In view of individual genes, adding ezetimibe to simvastatin seems to affect the predisposition to hepatic steatosis and NAFLD, and improve the glucose tolerance; however functional validation in bigger cohorts is needed. Collectively, our data might explain the decrease of ASCVD events reported in the IMPROVE-IT and SHARP trials, especially in T2DM patients. Hence, we propose the addition of ezetimibe to simvastatin therapy as an optimal intervention for lipid disorders characterized by elevated remnant-cholesterol (such as T2DM) to improve the outcome of CMD.
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