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In peer-mediated intervention (PMI), peers act as agents of intervention. Previous reviews in this area have not addressed the effectiveness of using PMI with children with autism who are minimally verbal. Following a systematic search, we reviewed 25 studies where PMI was used to increase communication in minimally verbal participants. The majority of these (n= 23) were single-case experimental design studies in settings that included preschools, elementary schools, and high schools. PMIs varied in the amounts of training offered to peers and the types of activities in which children engaged. Social communication increased across studies, with alternative and augmentative communication and spoken language measured in seven studies, respectively. We offer recommendations for future research in this area.

AbstractObjectivesInfant mental health (IMH), an area which focuses on the social and emotional development of infants in the context of the parent-infant relationship, has become an increasingly prominent field of both research and clinical practice worldwide. IMH network groups are initiatives which aim to facilitate continuous learning in the IMH approach, provide an opportunity for case discussion and encourage reflective practice. This study aimed to explore the experiences of staff working within an adult mental health (AMH) service and their participation in a perinatal IMH network group (PIMH-NG).MethodsThis study had a qualitative research design and the data were collected using a focus group methodology. Participants were recruited from a PIMH-NG which aimed to provide staff working within an AMH setting with the opportunity for continuous development of IMH knowledge. The data were analysed using thematic analysis.ResultsThe data gathered from the focus group indicated that staff participating in a PIMH-NG enhanced their clinical skill, reflective practice and supported the dissemination of IMH knowledge throughout their respective teams. The PIMH-NG facilitated this work by providing the opportunity for continuous learning, reflective group discussion and ongoing peer support.ConclusionsThe findings of this study indicate that incorporating elements of an IMH model into AMH services can be beneficial for staff, service users and overall service delivery and development. These findings may be used to develop the structure and content of future network groups of this nature.

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The description of the heterotrophic dinoflagellate Pfiesteriapiscicidaas the causative agent of fish lesions and deaths alongthemid-Atlantic estuaries has revealed the need for bioassays to assess itspotential toxigenicity. We designed a bioassay in which fish are exposed toclonal dinoflagellate strains or environmental consortia (e.g. environmentalwater or sediment samples) in 750-mL culture flasks, and examinedthe relationships among dinoflagellate proliferation profiles, the presence ofP. piscicidaand fish deaths. Assay development andcharacterization were accomplished with dinoflagellate clonal cultures(P. piscicida, Karlodinium micrum,Prorocentrum minimum, CCMP1828, CCMP1829, and CCMP1834)co-incubated with sets of two young adult sheepshead minnows(Cyprinodon variegatus). Variables characterized includedwater quality (pH, dissolved oxygen, ammonia, nitrate and nitriteconcentrations), the effect of the presence of fish on the proliferation andcompositions of protist (dinoflagellate, protozoa, diatom) and bacterialpopulations, and time of fish death. The presence of fish in experimentalflasksinduced proliferation of P. piscicidaandCryptoperidiniopsissp. (but not K.micrumor P. minimum) with populationsrising between days 6 and 10, and declining 4 to 5 days later. Some fish deathsoccurred when or soon after P. piscicidacell numberswere maximal. We conclude that this assay enables the assessment of acuteeffects of ichthyocidal dinoflagellates on fish during the first 10 days (StageA) of the experimental course. Fish deaths during the subsequent 10 to 20 days(Stage B) may be attributed to the proliferation of ichthyocidaldinoflagellates, pathogenic bacteria and/or deteriorating water quality,whereasthose beyond a period of approximately three weeks (Stage C) can be mostcertainly attributed to deteriorated water quality. Application of the flaskassay to environmental samples [n=53] yielded fish deaths in all three stages:A, 78%; B, 11%, and C, 2%, with fish still living in 9% of the sample waterstested at the conclusion of the experiment beyond three weeks. The majority ofsamples that resulted in fish death in stage A tested positive for P.piscicidaby PCR. If implemented with cautious interpretation, thisassay should prove useful in monitoring blooms for the presence of P.piscicidaand other dinoflagellate s pecies potentially harmful tofish.

The naturally occurring plant growth substance elicited by triacontanol was found to be 9-ß-L(+) adenosine by physical and spectral methods. At picomolar concentrations, 9-ß-L(+) adenosine stimulated growth as determined by dry weight measurements of several plant species. Reaction of adenosine deaminase with adenosine from rice showed that small quantities of 9-ß-L(+) adenosine exist in plants. We believe this is the first report of 9-ß-L(+) adenosine as a natural product.

Traditionally external quality assessment schemes (EQAS) distribute samples spectrally similar to a normal serum. This does not allow laboratories to assess the performance of their methods at measuring lipaemic samples. The Irish EQAS distributed a sample with a supplied lipid diluent. A sample of the same batch had previously been circulated as a normal distribution to obtain baseline values.Most analytes were affected by the lipaemia. The degree of interference was instrument/method dependent and a wide range of values was reported for each analyte: total protein 51–134 g/L (baseline 65 g/L); albumin 33–56 g/L (baseline 42 g/L); calcium 2·12–6·10 mmol/L (baseline 2·34 mmol/L); urate 38–1100μmol/L (baseline 195μmol/L); creatinine 6–199μmol/L (baseline 140μmol/L); glucose 4·2–9·5 mmol/L (baseline 4·8 mmol/L); total bilirubin 1–192μmol/L (baseline 36μmol/L); urea 1·1–8·1 mmol/L (baseline 3·8 mmol/L); aspartate aminotransferase (AST) 12–105 iu/L (baseline 44 iu/L); iron 4·3–107μmol/L (baseline 26·8μmol/L); inorganic phosphorus 1·12–4·96 mmol/L (baseline 1·59 mmol/L); and cholesterol 2·5–17·1 mmol/L (baseline 4·1 mmol/L).In situations where no clearing of the lipid occurs in the reagent, interference can be minimized by taking a sample blank reading or using a kinetic procedure. If clearing of the lipid does occur, time must be allowed for this to be completed before analytical readings are taken.