50 research outputs found

    Systemic ototoxicity: a review

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    Background: Systemic ototoxicity is a significant cause of vestibulocochlear morbidity in sub-Saharan Africa. It may result in permanent hearing impairment and/or balance problems.Objectives: To review the literature pertaining to the ototoxic potential of three frequently prescribed systemic medications in the sub-Saharan setting; quinine, furosemide and aminoglycoside antibiotics. The pathophysiology, clinical manifestations and risk factors and risk minimisation strategies regarding the ototoxicity associated with these drugs are presented in order to highlight this problem and reduce the incidence of adverse outcomes.Data sources: The biomedical literature was systematically reviewed. This included a search of the National Library of Medicine's PubMed database (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed). The search was limited to the English language literature and used the following search terms: ototoxicity; aminoglycosides; quinine; furosemide; gentamicin; vestibular toxicity; auditory toxicity; and Africa. Study selection: Studies and reviews directly addressing clinical ototoxicity, experimental studies and studies regarding ototoxicity in sub-Saharan Africa were reviewed. The authors formed a consensus opinion regarding the most relevant articles considering factors including evidence level.Data extraction: Systematic data extraction was undertaken from relevant studies. Conclusions: Quinine, furosemide and aminoglycosides are potentially ototoxic. High doses, prolonged treatment and intravenous administration increase this risk. The clinical condition of the patient may further predispose patients to ototoxic damage. Lack of monitoring facilities and efficacious, cost effective alternatives increase the risks of ototoxicity in the African setting. Clinicians must be aware of these risks and those patients at increased risk, and be vigilant in recognising their clinical manifestations. East African Medical Journal Vol 82(10) 2005: 537-54

    An Unusual Case of Odynophagia

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    Chest CT and hospital outcomes in patients with omicron compared with delta variant SARS-CoV-2 infection

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    Background The SARS-Cov-2 Omicron variant demonstrates rapid spread but with reduced disease severity. Studies evaluating the lung imaging findings of Omicron infection versus non-Omicron variants remain lacking. Purpose To compare Omicron and Delta variants of SARS-CoV-2 by their chest CT radiological pattern, biochemical parameters, clinical severity and hospital outcomes after adjusting for vaccination status. Materials and Methods Retrospective study of hospitalized adult patients rt-PCR positive for SARS-CoV-2 with CT pulmonary angiography performed within 7 days of admission between December 1, 2021 and January 14, 2022. Blinded radiological analysis with multiple readers including RSNA CT classification, chest CT severity score (CT-SS, range 0 least severe to 25 most severe) and CT imaging features including bronchial wall thickening. Results 106 patients (Delta n=66, Omicron n=40) were evaluated (mean age, 58 years ± 18, 58 men). In the Omicron group, 37% (15/40) of CT pulmonary angiograms were categorized as normal compared with 15% (10/66) in the Delta group (p=.016). Using a generalized linear model to control for confounding variables, including vaccination status, Omicron variant infection was associated with a CT-SS that was lower by 7.2 points compared to infection with Delta variant (β=-7.2, 95%CI: -9.9, -4.5; p <.001). Bronchial wall thickening was more common with Omicron than with the Delta variant (odds ratio [OR] 2.4, 95%CI: 1.01, 5.92, p=.04). Vaccination with a booster shot was associated with a protective effect on chest infection compared with the unvaccinated (CT-SS median 5 (IQR 0-11), CT-SS median 11 (IQR 7.5-14), respectively; p = .03). The Delta variant was associated with a higher odds ratio of severe disease (OR 4.6, 95%CI: 1.2, 26, p=.01) and critical care admission (OR 7.0, 95%CI: 1.5, 66, p=.004) than the Omicron variant. Conclusion The SARS-COV-2 Omicron variant was associated with fewer and less severe changes on chest CT compared with the Delta variant. Patients with Omicron had greater frequency of bronchial wall thickening but lower clinical severity and improved hospital outcomes than those with Delta

    Equivalence of greenhouse-gas emissions for peak temperature limits

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    Climate policies address emissions of many greenhouse gases including carbon dioxide, methane, nitrous oxide and various halogen-containing compounds. These are aggregated and traded on a CO2-equivalent basis using the 100-year global warming potential (GWP100); however, the GWP100 has received scientific and economic criticism as a tool for policy. In particular, given international agreement to limit global average warming to 2 °C, the GWP100 does not measure temperature and does not clearly signal the need to limit cumulative CO2 emissions. Here, we show that future peak temperature is constrained by cumulative emissions of several long-lived gases (including CO2 and N2O) and emission rates of a separate basket of shorter-lived species (including CH4). For each basket we develop an emissions-equivalence metric allowing peak temperature to be estimated directly for any emissions scenario. Today’s emissions of shorter-lived species have a lesser impact on ultimate peak temperature than those nearer the time of peaking. The 2 °C limit could therefore be met by setting a limit to cumulative long-lived CO2-equivalent emissions while setting a maximum future rate for shorter-lived emissions

    Linearity between temperature peak and bioenergy CO2 emission rates

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    International audienceMany future energy and emission scenarios envisage an increase of bioenergy in the global primary energy mix(1-4). In most climate impact assessment models and policies, bioenergy systems are assumed to be carbon neutral, thus ignoring the time lag between CO2 emissions from biomass combustion and CO2 uptake by vegetation(5). Here, we show that the temperature peak caused by CO2 emissions from bioenergy is proportional to the maximum rate at which emissions occur and is almost insensitive to cumulative emissions. Whereas the carbon-climate response (CCR; ref. 6) to fossil fuel emissions is approximately constant, the CCR to bioenergy emissions depends on time, biomass turnover times, and emission scenarios. The linearity between temperature peak and bioenergy CO2 emission rates resembles the characteristic of the temperature response to short-lived climate forcers. As for the latter(7-9), the timing of CO2 emissions from bioenergy matters. Under the international agreement to limit global warming to 2 degrees C by 2100(3), early emissions from bioenergy thus have smaller contributions on the targeted temperature than emissions postponed later into the future, especially when bioenergy is sourced from biomass with medium(50-60 years) or long turnover times (100 years)
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