Interpreting multisource feedback: online study of consensus and variation among GP appraisers.

BACKGROUND: GPs collect multisource feedback (MSF) about their professional practice and discuss it at appraisal. Appraisers use such information to identify concerns about a doctor's performance, and to guide the doctor's professional development plan (PDP). AIM: To investigate whether GP appraisers detect variation in doctors' MSF results, and the degree of consensus in appraisers' interpretations of this information. DESIGN AND SETTING: Online study of GP appraisers in north-east England. METHOD: GP appraisers were invited to review eight anonymised doctors' MSF reports, which represented different patterns of scores on the UK General Medical Council's Patient and Colleague Questionnaires. Participants provided a structured assessment of each doctor's report, and recommended actions for their PDP. Appraiser ratings of each report were summarised descriptively. An 'agreement score' was calculated for each appraiser to determine whether their assessments were more lenient than those of other participants. RESULTS: At least one report was assessed by 101/146 appraisers (69%). The pattern of appraisers' ratings suggested that they could detect variation in GPs' MSF results, and recommend reasonable actions for the doctors' PDP. Increasing appraiser age was associated with more favourable interpretations of MSF results. CONCLUSION: Although preliminary, the finding of broad consensus among GP appraisers in their assessment of MSF reports should be reassuring for GPs, appraisers, and employing organisations. However, if older appraisers are more lenient than younger appraisers in their interpretation of MSF and in the actions they suggest to their appraisees as a result, organisations need to consider what steps could be taken to address such differences.

Three-year-olds express suspense when an agent approaches a scene with a false belief.

Research on early false belief understanding has entirely relied on affect-neutral measures such as judgments (standard tasks), attentional allocation (looking duration, preferential looking, anticipatory looking), or active intervention. We used a novel, affective measure to test whether preschoolers affectively anticipate another's misguided acts. In two experiments, 3-year-olds showed more expressions of suspense (by, e.g. brow furrowing or lip biting) when they saw an agent approach a scene with a false as opposed to a true belief (Experiment 1) or ignorance (Experiment 2). This shows that the children anticipated the agent's surprise and disappointment when encountering reality. The findings suggest that early implicit knowledge of false beliefs includes anticipations of the affective implications of erring. This vital dimension of beliefs should no longer be ignored in research on early theory of mind.

FGF2 delays tectal neurogenesis, increases tectal cell numbers, and alters tectal lamination in embryonic chicks.

Intraventricular injections of the fibroblast growth factor 2 (FGF2) are known to increase the size of the optic tectum in embryonic chicks. Here we show that this increase in tectum size is due to a delay in tectal neurogenesis, which by definition extends the proliferation of tectal progenitors. Specifically, we use cumulative labeling with the thymidine analog EdU to demonstrate that FGF2 treatment on embryonic day 4 (ED4) reduces the proportion and absolute number of unlabeled cells in the rostroventral tectum when EdU infusions are begun on ED5, as one would expect if FGF2 retards tectal neurogenesis. We also examined FGF2's effect on neurogenesis in the caudodorsal tectum, which is born 2-3 days after the rostroventral tectum, by combining FGF2 treatment on ED4 with EDU infusions beginning on ED8. Again, FGF2 treatment reduced the proportion and number of EdU-negative (i.e., unlabeled) cells, consistent with a delay in neurogenesis. Collectively, these data indicate FGF2 in embryonic chicks delays neurogenesis throughout much of the tectum and continues to do so for several days after the FGF2 injection. One effect of this delay in neurogenesis is that tectal cell numbers more than double. In addition, tectal laminae that are born early in development become abnormally thin and cell-sparse after FGF2 treatment, whereas late-born layers remain unaffected. Combined with the results of prior work, these data indicate that FGF2 delays tectal neurogenesis and, thereby, triggers a cascade of changes in tectum size and morphology.

Expansion, folding, and abnormal lamination of the chick optic tectum after intraventricular injections of FGF2.

Comparative research has shown that evolutionary increases in brain region volumes often involve delays in neurogenesis. However, little is known about the influence of such changes on subsequent development. To get at this question, we injected FGF2--which delays cell cycle exit in mammalian neocortex--into the cerebral ventricles of chicks at embryonic day (ED) 4. This manipulation alters the development of the optic tectum dramatically. By ED7, the tectum of FGF2-treated birds is abnormally thin and has a reduced postmitotic layer, consistent with a delay in neurogenesis. FGF2 treatment also increases tectal volume and ventricular surface area, disturbs tectal lamination, and creates small discontinuities in the pia mater overlying the tectum. On ED12, the tectum is still larger in FGF2-treated embryos than in controls. However, lateral portions of the FGF2-treated tectum now exhibit volcano-like laminar disturbances that coincide with holes in the pia, and the caudomedial tectum exhibits prominent folds. To explain these observations, we propose that the tangential expansion of the ventricular surface in FGF2-treated tecta outpaces the expansion of the pial surface, creating abnormal mechanical stresses. Two alternative means of alleviating these stresses are tectal foliation and the formation of pial holes. The latter probably alter signaling gradients required for normal cell migration and may generate abnormal patterns of cerebrospinal fluid flow; both abnormalities would generate disturbances in tectal lamination. Overall, our findings suggest that evolutionary expansion of sheet-like, laminated brain regions requires a concomitant expansion of the pia mater.

Species differences in early patterning of the avian brain.

The telencephalon is proportionately larger in parrots than in galliformes (chicken-like birds), whereas the midbrain tectum is proportionately smaller. We here test the hypothesis that the adult species difference in midbrain proportion is due to an evolutionary change in early brain patterning. In particular, we compare the size of the early embryonic midbrain between parakeets (Melopsittacus undulatus) and bobwhite quail (Colinus virgianus) by examining the expression domains of transcription factors Pax6 and Gbx2, which are expressed in the forebrain and hindbrain, respectively. Because these expression domains form rostral and caudal borders with the presumptive midbrain when this region is specified (Hamburger-Hamilton stages 9-11), they allow us to measure and compare the sizes of a molecularly defined presumptive midbrain in the two species. Based on published data from older embryos, we predicted that the molecularly defined midbrain territory is significantly larger in quail than parakeets. Indeed, our data show that normalized midbrain length is 33% greater in quail and that the midbrain to forebrain ratio is 28% greater. This is strong evidence of a significant species difference in early brain patterning.