A quarter of patients admitted with a proximal femoral fracture suffer from an acute episode of delirium during their hospital *** it is often unrecognised,poorly managed,and rarely discussed by *** is important not o...
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A quarter of patients admitted with a proximal femoral fracture suffer from an acute episode of delirium during their hospital *** it is often unrecognised,poorly managed,and rarely discussed by *** is important not only to the affected individuals and their families,but also socioeconomically to the broader *** increases mortality and morbidity,leads to lasting cognitive and functional decline,and increases both length of stay and dependence on *** should be routinely and openly discussed by all members of the clinical team,including surgeons when gaining *** to do so may expose surgeons to claims of *** we present a concise review of the literature and discuss the epidemiology,causative factors,potential consequences and preventative strategies in the perioperative period.
AIM: To systematically evaluate the evidence-based literature on surgical treatment interventions for elite rugby players with anterior shoulder instability. METHODS: We conducted a systematic review according to the ...
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AIM: To systematically evaluate the evidence-based literature on surgical treatment interventions for elite rugby players with anterior shoulder instability. METHODS: We conducted a systematic review according to the PRISMA guidelines. A literature search was performed in PubM ed, EMBASE and Google Scholar using the following search terms: "rugby" and "shoulder" in combination with "instability" or "dislocation". All articles published from inception of the included data sources to January 1st 2014 that evaluated surgical treatment of elite rugby players with anterior shoulder instability were examined. RESULTS: Only five studies were found that met the eligibility criteria. A total of 379 shoulders in 376 elite rugby union and league players were included. All the studies were retrospective cohort or case series studies. The mean Coleman Methodological Score for the 5 studies was 47.4(poor). Owing to heterogeneity amongst the studies, quantitative synthesis was not possible, however a detailed qualitative synthesis is reported. The overall recurrence rate of instability after surgery was 8.7%, and the mean return to competitive play, where reported, was 13 ***: Arthroscopic stabilization has been performed successfully in acute anterior instability and there is a preference for open Latarjet-type procedures when instability is associated with osseous defects.
Alkaptonuria (AKU) is an inherited disorder of tyrosine metabolism caused by lack of active enzyme homogentisate 1,2-dioxygenase (HGD). The primary consequence of HGD deficiency is increased circulating homogentisic a...
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Alkaptonuria (AKU) is an inherited disorder of tyrosine metabolism caused by lack of active enzyme homogentisate 1,2-dioxygenase (HGD). The primary consequence of HGD deficiency is increased circulating homogentisic acid (HGA), the main agent in the pathology of AKU disease. Here we report the first metabolomic analysis of AKU homozygous Hgd knockout (Hgd−/−) mice to model the wider metabolic effects of Hgd deletion and the implication for AKU in humans. Untargeted metabolic profiling was performed on urine from Hgd−/− AKU (n = 15) and Hgd+/− non-AKU control (n = 14) mice by liquid chromatography high-resolution time-of-flight mass spectrometry (Experiment 1). The metabolites showing alteration in Hgd−/− were further investigated in AKU mice (n = 18) and patients from the UK National AKU Centre (n = 25) at baseline and after treatment with the HGA-lowering agent nitisinone (Experiment 2). A metabolic flux experiment was carried out after administration of 13C-labelled HGA to Hgd−/−(n = 4) and Hgd+/−(n = 4) mice (Experiment 3) to confirm direct association with HGA. Hgd−/− mice showed the expected increase in HGA, together with unexpected alterations in tyrosine, purine and TCA-cycle pathways. Metabolites with the greatest abundance increases in Hgd−/− were HGA and previously unreported sulfate and glucuronide HGA conjugates, these were decreased in mice and patients on nitisinone and shown to be products from HGA by the 13C-labelled HGA tracer. Our findings reveal that increased HGA in AKU undergoes further metabolism by mainly phase II biotransformations. The data advance our understanding of overall tyrosine metabolism, demonstrating how specific metabolic conditions can elucidate hitherto undiscovered pathways in biochemistry and metabolism.
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