Phenotypic Characterization of Multifungicide Resistance in Botrytis cinerea Isolates from Strawberry Fields in Florida.

Chemical control has always been essential for the management of gray mold, caused by Botrytis cinerea, to ensure sustainable strawberry production. However, lack of knowledge about actual resistance development may have disastrous consequences and lead to severe epidemics such as the one that affected several strawberry fields in 2012 in Florida. In this study, we tested 392 isolates collected from Florida strawberry fields between 2010 and 2012 for their sensitivity to boscalid (Bosc), a succinate dehydrogenase inhibitor (SdhI); pyraclostrobin, a quinone outside inhibitor (QoI); boscalid + pyraclostrobin (Pristine); fenhexamid, a hydroxyanilide (Hyd); pyrimethanil and cyprodinil, anilinopyrimidines; fludioxonil, a phenylpyrrole; and fludioxonil + cyprodinil (Switch). The respective resistance frequencies for boscalid, pyraclostrobin, Pristine, fenhexamid, cyprodinil, and pyrimethanil were 85.4, 86.5, 86.0, 44.4, 52.7, and 59.5%. Overall, 17.8 and 19.8% of isolates showed reduced sensitivity to fludioxonil and Switch, respectively. All fungicides sprayed preventively on detached strawberry fruit failed to control isolates with high levels of resistance to each fungicide except for fludioxonil and Switch. Four phenotypes with multifungicide resistance (MFR) were detected in B. cinerea populations from Florida. Isolates resistant to one fungicide (FR1), two (MFR2), three (MFR3), and four (MFR4) fungicides from different chemical groups represented 5.9, 28.6, 41.8, and 23.7% of the total resistant population, respectively. The MFR3 isolates were predominant and contained two subpopulations, the Bosc-QoI-APR isolates (56.5%) and the Bosc-QoI-HydR isolates (40.6%). In addition to reporting on very highly resistant populations to boscalid and QoI fungicides, we show evidence for a widespread multifungicide resistance to B. cinerea that warrants immediate implementation of novel management strategies to impede the development of more resistant populations.

Nurse initiated thrombolysis in the accident and emergency department: safe, accurate, and faster than fast track.

OBJECTIVE: To reduce the time between arrival at hospital of a patient with acute myocardial infarction and administration of thrombolytic therapy (door to needle time) by the introduction of nurse initiated thrombolysis in the accident and emergency department. METHODS: Two acute chest pain nurse specialists (ACPNS) based in A&E for 62.5 hours of the week were responsible for initiating thrombolysis in the A&E department. The service reverts to a "fast track" system outside of these hours, with the on call medical team prescribing thrombolysis on the coronary care unit. Prospectively gathered data were analysed for a nine month period and a head to head comparison made between the mean and median door to needle times for both systems of thrombolysis delivery. RESULTS: Data from 91 patients were analysed; 43 (47%) were thrombolysed in A&E by the ACPNS and 48 (53%) were thrombolysed in the coronary care unit by the on call medical team. The ACPNS achieved a median door to needle time of 23 minutes (IQR=17 to 32) compared with 56 minutes (IQR=34 to 79.5) for the fast track. The proportion of patients thrombolysed in 30 minutes by the ACPNS and fast track system was 72% (31 of 43) and 21% (10 of 48) respectively (difference=51%, 95% confidence intervals 34% to 69%, p<0.05). CONCLUSION: Diagnosis of acute myocardial infarction and administration of thrombolysis by experienced cardiology nurses in A&E is a safe and effective strategy for reducing door to needle times, even when compared with a conventional fast track system.

On the "specifics" of specific reading disability and specific language impairment.

The reading and oral language scores of 110 children with a specific reading disability (SRD) and 102 children with a specific language impairment (SLI) indicated that approximately 53% of children with an SRD and children with an SLI could be equally classified as having an SRD or an SLI, 55% of children with an SRD have impaired oral language, and 51% of children with an SLI have a reading disability. Finding that a large percentage of children can be equally classified as SRD or SLI has repercussions for the criteria used to define an SRD, for conceptualising subgroups of learning disability, and for estimates of the incidence of SRD. Further, it highlights the need for future studies to assess both the reading and oral language abilities of SRD and SLI participants to determine how specifically impaired and homogeneous samples really are.

Auditory temporal processing in disabled readers with and without oral language delay.

Inferior auditory temporal processing has been postulated as causally linked to phonological processing deficits in disabled readers with concomitant oral language delay (LDRDs), and absent in specifically disabled readers with normal oral language (SRDs). This investigation compared SRDs, LDRDs and normal readers aged 7-10 years on measures of auditory temporal processing (temporal order judgement) and phonological decoding (nonword reading). LDRDs exhibited deficits in temporal order judgement compared with normal readers, from whom SRDs did not differ significantly. These findings suggest that auditory temporal processing and oral language are related; however, very large within-group variability in the auditory temporal processing data further suggests that this relationship prevails in only a proportion of disabled readers with concomitant oral language weakness. In nonword reading, LDRDs performed worst of all, but SRDs also exhibited significant deficits compared with normal readers. Taken together, our results preclude the conceptualisation of temporal processing deficits as the unitary cause of phonological and language deficits in disabled readers.

Distribution of tin in brain subcellular fractions following the administration of trimethyl tin and triethyl tin to the rat.

The time course of tin distribution in homogenates and subcellular fractions of rat brain was determined following the acute administration of trimethyl tin (TMT) and triethyl tin (TET) to the rat. Exposure to TMT resulted in lower concentrations but greater persistence of tin in subcellular fractions compared to exposure to TET. A delayed accumulation of tin in the mitochondrial fraction was observed following the administration of TMT but not TET. Analysis of total protein and mitochondrial markers did not reveal differences between the compositions of mitochondrial fractions prepared from control and TMT-treated subjects.