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Articles by A Jones
Total Records ( 5 ) for A Jones
  J. M Weller , A Jones , A. F Merry , B Jolly and D. Saunders
  Background

The mini-Clinical Evaluation Exercise (mini-CEX) is a workplace-based assessment which may be useful in anaesthesia training. However, its value depends on how supervisors use it with their trainees. This study analyses experience with the mini-CEX after its introduction into anaesthesia departments in our institution.

Methods

We conducted surveys, focus groups, and interviews with trainees and specialists. Data were recorded, transcribed, and entered into NVivo 8. Themes were identified and data coded into these themes.

Results

We identified six themes: assessor factors included skills needed to perform the assessments, influences on scoring decisions, and effects on the specialist–trainee relationship; trainee factors related to impact on trainee performance and value at the different training levels; teaching and learning included the effect of focused observation on structuring workplace learning; feedback described how the mini-CEX changed feedback and what was considered useful; mini-CEX process included implementation, initiation of assessments and case selection; and use in assessment included comparisons with existing assessments and the ability to identify poor performers.

Conclusions

Mini-CEX formalized the supervisory relationship, promoting educational interactions. During the observation period, trainees took responsibility for decisions, and specialists learnt more about their abilities. The structured format broadened the scope of feedback and made it easier to address performance gaps. We identified factors that facilitated or hindered implementation, or limited effective feedback and the ability to address poor performance. From this analysis, we propose strategies for the implementation of mini-CEX, and recommendations for assessor training to improve the quality and value of the assessments.

  A Jones , R Deb , E Torsney , F Howe , M Dunkley , Y Gnaneswaran , D Gaze , H Nasr , I. M Loftus , M. M Thompson and G. W. Cockerill
 

Background— Development and rupture of aortic aneurysms involve a combination of complex biological processes. Rosiglitazone, a peroxisome proliferator-activated receptor- agonist, has been shown to have a broad spectrum of effects in vivo. The hypothesis that rosiglitazone would reduce aneurysm expansion or rupture was tested in the angiotensin II (Ang II)-induced hypercholesterolemic mouse model.

Methods and Results— Apolipoprotein E-deficient mice, 12 months of age, were allocated to 4 groups. Three groups were infused with Ang II (1 µg · min–1 · kg–1), and the fourth was infused with saline. Rosiglitazone was given 1 week before infusion and 1 week after infusion. At day 28, aortic size was measured, and tissues were collected for analyses. Both pretreatment and posttreatment with rosiglitazone inhibited the occurrence of fatal rupture (11 of 30 versus 0 of 30 versus 0 of 15; P=0.0013) and reduced maximal dilatation of the aorta (4.6±0.13 versus 2.4±0.48 versus 2.15±0.46 mm2; P<0.0001). Blood glucose, total cholesterol, body weight, and atherosclerosis did not differ between groups. Pretreatment with rosiglitazone inhibited the Ang II-induced expression of angiotensin type 1a Ang II receptor while having no effect on the angiotensin type 2 Ang II receptor, in addition to reducing Ang II-induced expression of E-selectin, tumor necrosis factor-, and interleukin-6.

Conclusions— Pretreatment or posttreatment with RGZ reduced aortic expansion and rupture in this mouse model. Reduction of lesions in animals pretreated with rosiglitazone is concomitant with decreased expression of inflammatory mediators. Further studies are needed to elucidate the precise mechanism.

  A. E Teschendorff , U Menon , A Gentry Maharaj , S. J Ramus , D. J Weisenberger , H Shen , M Campan , H Noushmehr , C. G Bell , A. P Maxwell , D. A Savage , E Mueller Holzner , C Marth , G Kocjan , S. A Gayther , A Jones , S Beck , W Wagner , P. W Laird , I. J Jacobs and M. Widschwendter
 

Polycomb group proteins (PCGs) are involved in repression of genes that are required for stem cell differentiation. Recently, it was shown that promoters of PCG target genes (PCGTs) are 12-fold more likely to be methylated in cancer than non-PCGTs. Age is the most important demographic risk factor for cancer, and we hypothesized that its carcinogenic potential may be referred by irreversibly stabilizing stem cell features. To test this, we analyzed the methylation status of over 27,000 CpGs mapping to promoters of ~14,000 genes in whole blood samples from 261 postmenopausal women. We demonstrate that stem cell PCGTs are far more likely to become methylated with age than non-targets (odds ratio = 5.3 [3.8–7.4], P < 10–10), independently of sex, tissue type, disease state, and methylation platform. We identified a specific subset of 69 PCGT CpGs that undergo hypermethylation with age and validated this methylation signature in seven independent data sets encompassing over 900 samples, including normal and cancer solid tissues and a population of bone marrow mesenchymal stem/stromal cells (P < 10–5). We find that the age-PCGT methylation signature is present in preneoplastic conditions and may drive gene expression changes associated with carcinogenesis. These findings shed substantial novel insights into the epigenetic effects of aging and support the view that age may predispose to malignant transformation by irreversibly stabilizing stem cell features.

  L Lindahl , A Bommankanti , X Li , L Hayden , A Jones , M Khan , T Oni and J. M. Zengel
 

RNase MRP is a nucleolar RNA–protein enzyme that participates in the processing of rRNA during ribosome biogenesis. Previous experiments suggested that RNase MRP makes a nonessential cleavage in the first internal transcribed spacer. Here we report experiments with new temperature-sensitive RNase MRP mutants in Saccharomyces cerevisiae that show that the abundance of all early intermediates in the processing pathway is severely reduced upon inactivation of RNase MRP. Transcription of rRNA continues unabated as determined by RNA polymerase run-on transcription, but the precursor rRNA transcript does not accumulate, and appears to be unstable. Taken together, these observations suggest that inactivation of RNase MRP blocks cleavage at sites A0, A1, A2, and A3, which in turn, prevents precursor rRNA from entering the canonical processing pathway (35S > 20S + 27S > 18S + 25S + 5.8S rRNA). Nevertheless, at least some cleavage at the processing site in the second internal transcribed spacer takes place to form an unusual 24S intermediate, suggesting that cleavage at C2 is not blocked. Furthermore, the long form of 5.8S rRNA is made in the absence of RNase MRP activity, but only in the presence of Xrn1p (exonuclease 1), an enzyme not required for the canonical pathway. We conclude that RNase MRP is a key enzyme for initiating the canonical processing of precursor rRNA transcripts, but alternative pathway(s) might provide a backup for production of small amounts of rRNA.

  M. T Howes , M Kirkham , J Riches , K Cortese , P. J Walser , F Simpson , M. M Hill , A Jones , R Lundmark , M. R Lindsay , D. J Hernandez Deviez , G Hadzic , A McCluskey , R Bashir , L Liu , P Pilch , H McMahon , P. J Robinson , J. F Hancock , S Mayor and R. G. Parton
 

Quantitative ultrastructural analysis and proteomics detail CLIC structure, composition, and function.

 
 
 
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