Reverse engineering field-derived vertical distribution profiles to infer larval swimming behaviors.

Biophysical models are well-used tools for predicting the dispersal of marine larvae. Larval behavior has been shown to influence dispersal, but how to incorporate behavior effectively within dispersal models remains a challenge. Mechanisms of behavior are often derived from laboratory-based studies and therefore, may not reflect behavior in situ. Here, using state-of-the-art models, we explore the movements that larvae must undertake to achieve the vertical distribution patterns observed in nature. Results suggest that behaviors are not consistent with those described under the tidally synchronized vertical migration (TVM) hypothesis. Instead, we show (i) a need for swimming speed and direction to vary over the tidal cycle and (ii) that, in some instances, larval swimming cannot explain observed vertical patterns. We argue that current methods of behavioral parameterization are limited in their capacity to replicate in situ observations of vertical distribution, which may cause dispersal error to propagate over time, due to advective differences over depth and demonstrate an alternative to laboratory-based behavioral parameterization that encompasses the range of environmental cues that may be acting on planktic organisms.

Anaphylaxis to muscle relaxants: an audit of ten years of allergy testing at the Royal Adelaide Hospital.

We audited patients with anaphylaxis to muscle relaxants during anaesthesia referred to the Department of Anaesthesia at the Royal Adelaide Hospital between the start of 2000 and the end of 2009. Of the 220 patients tested during this period, 43 had a positive intradermal test to the muscle relaxant given during their anaesthetic. The majority of these were to rocuronium and suxamethonium. Where rocuronium was the index agent, 65% of patients cross-reacted with another relaxant and 29% of patients with suxamethonium as their index agent demonstrated cross-reaction with another relaxant.

A deficit in shifting attention present in high-functioning autism but not Asperger's disorder.

The aim of this study was to examine executive functioning, in particular, attentional set-shifting deficits in high-functioning autism (n = 12) and Asperger's disorder (n = 12). A large or global digit composed of smaller or local digits was presented during each trial. The participants indicated the presence of 1s or 2s by pressing the appropriate button. These targets could appear globally or locally Relative to IQ, sex and age matched controls, reaction time to global targets in individuals with autism was retarded when the previous target appeared locally. This deficiency in shifting from local to global processing, however, was not observed in individuals with Asperger's disorder. The theoretical and neurobiological significance of this dissociation in executive functioning in these clinically related disorders was explored.

Movement preparation in high-functioning autism and Asperger disorder: a serial choice reaction time task involving motor reprogramming.

Autism and Asperger disorder have long been associated with movement abnormalities, although the neurobehavioural details of these abnormalities remain poorly defined. Clumsiness has traditionally been associated with Asperger disorder but not autism, although this is controversial. Others have suggested that both groups demonstrate a similar global motor delay. In this study we aimed to determine whether movement preparation or movement execution was atypical in these disorders and to describe any differences between autism and Asperger disorder. A simple motor reprogramming task was employed. The results indicated that individuals with autism and Asperger disorder have atypical movement preparation with an intact ability to execute movement. An atypical deficit in motor preparation was found in Asperger disorder, whereas movement preparation was characterized by a "lack of anticipation" in autism. The differences in movement preparation profiles in these disorders were suggested to reflect differential involvement of the fronto-striatal region, in particular the supplementary motor area and anterior cingulate.

Seasonal changes in circadian grazing patterns of Kerry cows (Bos Taurus) in semi-feral conditions in Killarney National Park, Co. Kerry, Ireland.

Domestic cattle generally graze during the day although some night-time grazing also occurs. However, questions remain as to the effect of management on circadian grazing patterns. This study provides for the first time a quantification of seasonal, circadian and animal variation in grazing behaviour and grazing time in cattle in semi-wild conditions.The objectives of the study were to examine how daily grazing times and the temporal distribution of grazing activity changed with season and to examine the extent to which grazing patterns were influenced by day-length. A group of 12 heifers of the Kerry breed continuously grazed a lowland field of 4.7ha. The old permanent pasture sward was dominated by Holcus spp. and Agrostis spp. Feed availability was never limiting. Length and periodicity of grazing were recorded using vibracorders attached to the necks of seven animals.Results showed that daily grazing times remained constant over most of the grazing season (circa 10-11h per day), however, some variation occurred late in the season. The temporal distribution of grazing activity changed as the season advanced so that by October grazing patterns became significantly different to those of July. The time interval between grazing bouts at dawn and dusk decreased with decreasing day-length. An increased percentage of night-time grazing occurred at shorter day-lengths.It is concluded that there is a significant seasonal effect of day-length on temporal distribution of grazing activity with night-time grazing featuring more as day-length decreases. The maintenance of similar total daily grazing times in the face of changing day-length (with the exception of late in the season) suggests that daily grazing times are a function of the attainment of a relatively constant nutritional requirement by the animal.

Atypical interference of local detail on global processing in high-functioning autism and Asperger's disorder.

This study explored the claim that individuals with autism and Asperger's disorder tend to process locally rather than holistically. Participants observed a large or "global" number composed of smaller or "local" numbers. The response was contingent upon the identification of either the large stimulus or the small stimuli. Relative to age, sex, and IQ matched controls, global processing in children and adolescents with autism (N = 12) and Asperger's disorder (N = 12) was more vulnerable when the local stimuli were incongruent. The autism group made more global errors than their matched control group, regardless of whether there was local incongruence. In contrast, the Asperger's disorder group made a similar number of global errors as their respective control group. These results were discussed in relation to an "absence of global precedence" notion, "weak central coherence" theory, and right-hemisphere dysfunction. The neurobiological significance of these findings were discussed in the context of a fronto-striatal model of dysfunction.

Autism: fifty years on from Kanner.

It is now 50 years since Leo Kanner first described autism as a distinctive pattern of symptoms in some children with severe developmental problems. Since then the assessment and diagnosis of children with pervasive disorders of development has been refined and much is known about the phenomenology and epidemiology. Autism is a biological disorder of the central nervous system (CNS) of unknown cause. It is associated with a number of organic disorders such as epilepsy and has comorbidity with other psychiatric disorders such as tic disorder. Cognitive abnormalities in social interactions, affect and language are present but there is still debate regarding which of these, if any, is the primary cognitive deficit. Special education and behavioral management has led to modest but important developmental improvement in many children with autism. Autism remains a life-long condition but patterns of symptoms change and skills develop from childhood into adult life.

Molecular and cytogenetic analysis of tumors in von Recklinghausen neurofibromatosis.

Von Recklinghausen neurofibromatosis (NF1) is a common autosomal dominant disorder mapped to 17q11.2 and typically characterized by the occurrence of neural crest-derived tumors. The gene has recently been cloned using reverse genetics or "positional cloning" approaches. Its function, however, remains unknown. We have performed cytogenetic and molecular analyses on 9 malignant tumors from NF1 patients to look for loss of alleles or chromosome rearrangements involving chromosome 17 to test the hypothesis that the NF1 gene acts as a recessive "tumor suppressor" gene. Loss of alleles on this chromosome was detected for 3 of 9 malignant tumors. Two peripheral nerve sheath tumors showed allele loss at informative loci on both the long and short arms of chromosome 17. In contrast, a glioblastoma with focal gliosarcoma showed loss of heterozygosity on the short arm of chromosome 17 only, and not at loci on the long arm. One nerve sheath tumor was previously shown by direct sequence analysis to have a point mutation at the TP53 locus at 17p13. These data support a role for the TP53 gene or other genes on the short arm of chromosome 17 in at least some malignancies in NF1. Six other neurofibrosarcomas showed no allele loss at informative loci on chromosome 17. Cytogenetic analysis was performed on 7 tumors, including 2 with allele loss. The two tumors with allele loss showed abnormal karyotypes while all others were normal. Southern blot and pulsed-field gel analysis using probes within or closely linked to the NF1 locus detected no gross deletions or rearrangements in the tumors studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Type 1 neurofibromatosis gene: identification of a large transcript disrupted in three NF1 patients.

Von Recklinghausen neurofibromatosis (NF1) is a common autosomal dominant disorder characterized by abnormalities in multiple tissues derived from the neural crest. No reliable cellular phenotypic marker has been identified, which has hampered direct efforts to identify the gene. The chromosome location of the NF1 gene has been previously mapped genetically to 17q11.2, and data from two NF1 patients with balanced translocations in this region have further narrowed the candidate interval. The use of chromosome jumping and yeast artificial chromosome technology has now led to the identification of a large (approximately 13 kilobases) ubiquitously expressed transcript (denoted NF1LT) from this region that is definitely interrupted by one and most likely by both translocations. Previously identified candidate genes, which failed to show abnormalities in NF1 patients, are apparently located within introns of NF1LT, on the antisense strand. A new mutation patient with NF1 has been identified with a de novo 0.5-kilobase insertion in the NF1LT gene. These observations, together with the high spontaneous mutation rate of NF1 (which is consistent with a large locus), suggest that NF1LT represents the elusive NF1 gene.

Direct construction of a chromosome-specific NotI linking library from flow-sorted chromosomes.

A linking library consists of genomic DNA fragments which contain a specific rare restriction enzyme site; such clones are very useful as probes in pulsed field gel electrophoresis and in mapping and cloning large regions of DNA. However, identifying those linking clones which map to a certain chromosomal region can be laborious. Therefore, we have developed a straightforward procedure for constructing a linking library directly from flow-sorted chromosomes. As a test of the approach, a NotI linking library was constructed from the chromosome 17 fraction of a flow-sort of human chromosomes, using only 70 ng of DNA. Thirteen of sixteen linking clones were mapped to chromosome 17, suggesting that the library is highly enriched for this chromosome. This method should be generally applicable to other chromosomes and enzymes as well.

Physical mapping of the von Recklinghausen neurofibromatosis region on chromosome 17.

The von Recklinghausen neurofibromatosis (NF1) locus has been linked to chromosome 17, and recent linkage analyses place the gene on the proximal long arm. NF1 probably resides in 17q11.2, since two unrelated NF1 patients have been identified who possess constitutional reciprocal translocations involving 17q11.2 with chromosomes 1 and 22. We have used a somatic-cell hybrid from the t(17;22) individual, along with other hybrid cell lines, to order probes around the NF1 locus. An additional probe, 17L1, has been isolated from a NotI linking library made from flow-sorted chromosome 17 material and has been mapped to a region immediately proximal to the translocation breakpoint. While neither NF1 translocation breakpoint has yet been identified by pulse-field gel analysis, an overlap between two probes, EW206 and EW207, has been detected. Furthermore, we have identified the breakpoint in a non-NF1 translocation, SP-3, on the proximal side of the NF1 locus. This breakpoint has been helpful in creating a 1,000-kb pulsed-field map, which includes the closely linked NF1 probes HHH202 and TH17.19. The combined somatic-cell hybrid and pulsed-field gel analysis we report here favors the probe order D17Z1-HHH202-TH17.19-CRYB1-17L1-NF1- (EW206, EW207, EW203, L581, L946)-(ERBB2, ERBA1). The agreement in probe ordering between linkage analysis and physical mapping is excellent, and the availability of translocation breakpoints in NF1 should now greatly assist the cloning of this locus.