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Item does not contain fulltext, BACKGROUND: Adverse effects (AE) to TB treatment cause morbidity, mortality and treatment interruption. The aim of these clinical standards is to encourage best practise for the diagnosis and management of AE.METHODS: 65/81 invited experts participated in a Delphi process using a 5-point Likert scale to score draft standards.RESULTS: We identified eight clinical standards. Each person commencing treatment for TB should: Standard 1, be counselled regarding AE before and during treatment; Standard 2, be evaluated for factors that might increase AE risk with regular review to actively identify and manage these; Standard 3, when AE occur, carefully assessed and possible allergic or hypersensitivity reactions considered; Standard 4, receive appropriate care to minimise morbidity and mortality associated with AE; Standard 5, be restarted on TB drugs after a serious AE according to a standardised protocol that includes active drug safety monitoring. In addition: Standard 6, healthcare workers should be trained on AE including how to counsel people undertaking TB treatment, as well as active AE monitoring and management; Standard 7, there should be active AE monitoring and reporting for all new TB drugs and regimens; and Standard 8, knowledge gaps identified from active AE monitoring should be systematically addressed through clinical research.CONCLUSION: These standards provide a person-centred, consensus-based approach to minimise the impact of AE during TB treatment.

Contains fulltext : 87815.pdf (publisher's version ) (Open Access), Cleft palate is a common congenital disorder that affects up to 1 in 2,500 live human births and results in considerable morbidity to affected individuals and their families. The etiology of cleft palate is complex, with both genetic and environmental factors implicated. Mutations in the transcription factor-encoding genes p63 and interferon regulatory factor 6 (IRF6) have individually been identified as causes of cleft palate; however, a relationship between the key transcription factors p63 and IRF6 has not been determined. Here, we used both mouse models and human primary keratinocytes from patients with cleft palate to demonstrate that IRF6 and p63 interact epistatically during development of the secondary palate. Mice simultaneously carrying a heterozygous deletion of p63 and the Irf6 knockin mutation R84C, which causes cleft palate in humans, displayed ectodermal abnormalities that led to cleft palate. Furthermore, we showed that p63 transactivated IRF6 by binding to an upstream enhancer element; genetic variation within this enhancer element is associated with increased susceptibility to cleft lip. Our findings therefore identify p63 as a key regulatory molecule during palate development and provide a mechanism for the cooperative role of p63 and IRF6 in orofacial development in mice and humans.

Dimethylsulfide (DMS), sulfur dioxide (SO2), dimethylesulfoxide (DMSO), sulfate (SO2-4) and methanesulfonate (MSA) were measured at a coastal site, Pointe de Penmarc’h, over a 25 day period during May and June 1993. Measurements were also performed to estimate the DMS flux from the algal beds around the Penmarc’h lighthouse and from the surrounding sea water. Similar atmospheric measurements were conducted at a second site approximately 2km inland from Penmarc’h. A comparison between the 2 sites indicates similar patterns of DMS concentration at each site, with values at the inland site being generally 10–15% lower. The concentrations of the aerosol phase products such as methanesulfonic acid and sulfate are examined in the light of air mass origins. The fraction of nss SO2-4 produced from biogenic sources is estimated to be less than 25%. The yield of MSA and DMSO from DMS oxidation are assessed from their relative concentrations and estimates of their atmospheric lifetime.

A database of 15,617 point measurements of dimethylsulfide (DMS) in surface waters along with lesser amounts of data for aqueous and particulate dimethylsulfoniopropionate concentration, chlorophyll concentration, sea surface salinity and temperature, and wind speed has been assembled. The database was processed to create a series of climatological annual and monthly 1°x1°latitude-longitude squares of data. The results were compared to published fields of geophysical and biological parameters. No significant correlation was found between DMS and these parameters, and no simple algorithm could be found to create monthly fields of sea surface DMS concentration based on these parameters. Instead, an annual map of sea surface DMS was produced using an algorithm similar to that employed by Conkright et al. [1994]. In this approach, a first-guess field of DMS sea surface concentration measurements is created and then a correction to this field is generated based on actual measurements. Monthly sea surface grids of DMS were obtained using a similar scheme, but the sparsity of DMS measurements made the method difficult to implement. A scheme was used which projected actual data into months of the year where no data were otherwise present