Effect of Edwardsiella ictaluri Infection on Plasma Corticosterone Levels in Channel Catfish (Ictalurus punctatus)

Channel catfish (Ictalurus punctatus) were innoculated with a new host specific bacterium, Edwardsiella ictaluri, to observe the influence of bacterial infection on plasma corticosterone levels at various temperatures. The fish were innoculated intraperitoneally. The infected fish were separated from the controls. Plasma corticosterone concentrations were determined by radioimmunoassay. The plasma corticosterone concentrations in non-innoculated catfish were about 6.15 ng/ml and nearly 5.63 ng/ml in the infected fish. The lower level of the hormone in the infected catfish was not significantly different from the control level. High temperature was a stress factor which increased plasma corticosterone levels whereas E. ictaluri retarded the response of corticosterone secreting cells of the fish kidneys

Flip, feedback and fly: Using LOOP to Enhance the Professional Experience of Initial Teacher Education

The Australian Professional Teaching Standards require pre-service teachers to complete a minimum number of days of professional experience in order to graduate. Problems can arise, however, when the evaluation of their professional experience against the Standards shifts from the providers of teacher education programmes to school-based supervising teachers. The Lesson Observation On-line Platform (LOOP) begins to address these problems by utilising a secure, shared digital platform to facilitate evidence-based evaluation of the performance of pre-service teachers. In this research, we evaluated the potential of LOOP to assess pre-service teachers against the Standards as well as to enhance the professional development of both pre-service teachers and their supervising teachers. The responses from two pre-service teachers and their supervising teachers demonstrate that the methodological matters can be easily overcome. Nevertheless our findings indicate that there are several practical issues that need to be overcome if LOOP were to be fully successful

Is the NIH policy for sharing GWAS data running the risk of being counterproductive?

Through their current policy on data sharing, the National Institutes of Health (NIH) are inadvertently placing a serious and potentially insuperable burden upon non-US researchers who perform patient-based genomics studies in collaboration with US institutions. Because this policy could adversely affect future transnational scientific collaborations, we explore some of its likely consequences and suggest possible courses of remedial action wherever feasible

LINE-1 Endonuclease-Dependent Retrotranspositional Events Causing Human Genetic Disease: Mutation Detection Bias and Multiple Mechanisms of Target Gene Disruption

LINE-1 (L1) elements are the most abundant autonomous non-LTR retrotransposons in the human genome. Having recently performed a meta-analysis of L1 endonuclease-mediated retrotranspositional events causing human genetic disease, we have extended this study by focusing on two key issues, namely, mutation detection bias and the multiplicity of mechanisms of target gene disruption. Our analysis suggests that whereas an ascertainment bias may have generally militated against the detection of autosomal L1-mediated insertions, autosomal L1 direct insertions could have been disproportionately overlooked owing to their unusually large size. Our analysis has also indicated that the mechanisms underlying the functional disruption of target genes by L1-mediated retrotranspositional events are likely to be dependent on several different factors such as the type of insertion (L1 direct, L1 trans-driven Alu, or SVA), the precise locations of the inserted sequences within the target gene regions, the length of the inserted sequences, and possibly also their orientation

Emerging genotype-phenotype relationships in patients with large NF1 deletions.

The most frequent recurring mutations in neurofibromatosis type 1 (NF1) are large deletions encompassing the NF1 gene and its flanking regions (NF1 microdeletions). The majority of these deletions encompass 1.4-Mb and are associated with the loss of 14 protein-coding genes and four microRNA genes. Patients with germline type-1 NF1 microdeletions frequently exhibit dysmorphic facial features, overgrowth/tall-for-age stature, significant delay in cognitive development, large hands and feet, hyperflexibility of joints and muscular hypotonia. Such patients also display significantly more cardiovascular anomalies as compared with patients without large deletions and often exhibit increased numbers of subcutaneous, plexiform and spinal neurofibromas as compared with the general NF1 population. Further, an extremely high burden of internal neurofibromas, characterised by >3000 ml tumour volume, is encountered significantly, more frequently, in non-mosaic NF1 microdeletion patients than in NF1 patients lacking such deletions. NF1 microdeletion patients also have an increased risk of malignant peripheral nerve sheath tumours (MPNSTs); their lifetime MPNST risk is 16–26%, rather higher than that of NF1 patients with intragenic NF1 mutations (8–13%). NF1 microdeletion patients, therefore, represent a high-risk group for the development of MPNSTs, tumours which are very aggressive and difficult to treat. Co-deletion of the SUZ12 gene in addition to NF1 further increases the MPNST risk in NF1 microdeletion patients. Here, we summarise current knowledge about genotype–phenotype relationships in NF1 microdeletion patients and discuss the potential role of the genes located within the NF1 microdeletion interval whose haploinsufficiency may contribute to the more severe clinical phenotyp

Resolving the Surfaces of Extrasolar Planets With Secondary Eclipse Light Curves

We present a method that employs the secondary eclipse light curves of transiting extrasolar planets to probe the spatial variation of their thermal emission. This technique permits an observer to resolve the surface of the planet without the need to spatially resolve its central star. We evaluate the feasibility of this technique for the HD 209458 system [..]. We consider two representations of the planetary thermal emission; a simple model parameterized by a sinusoidal dependence on longitude and latitude, as well as the results of a three-dimensional dynamical simulation of the planetary atmosphere previously published by Cooper & Showman. We find that observations of the secondary eclipse light curve are most sensitive to a longitudinal offset in the geometric and photometric centroids of the hemisphere of the planet visible near opposition. To quantify this signal, we define a new parameter, the ``uniform time offset,'' which measures the time lag between the observed secondary eclipse and that predicted by a planet with a uniform surface flux distribution. We compare the predicted amplitude of this parameter for HD 209458 with the precision with which it could be measured with IRAC. We find that IRAC observations at 3.6um a single secondary eclipse should permit sufficient precision to confirm or reject the Cooper & Showman model of the surface flux distribution for this planet. We quantify the signal-to-noise ratio for this offset in the remaining IRAC bands (4.5um, 5.8um, and 8.0um), and find that a modest improvement in photometric precision (as might be realized through observations of several eclipse events) should permit a similarly robust detection.Comment: AASTeX 5.2, 24 pages, 5 figures, accepted for publication in ApJ; v2: clarifications, updated to version accepted by ApJ; v3: try to reduce spacin

Measuring atomic NOON-states and using them to make precision measurements

A scheme for creating NOON-states of the quasi-momentum of ultra-cold atoms has recently been proposed [New J. Phys. 8, 180 (2006)]. This was achieved by trapping the atoms in an optical lattice in a ring configuration and rotating the potential at a rate equal to half a quantum of angular momentum . In this paper we present a scheme for confirming that a NOON-state has indeed been created. This is achieved by spectroscopically mapping out the anti-crossing between the ground and first excited levels by modulating the rate at which the potential is rotated. Finally we show how the NOON-state can be used to make precision measurements of rotation.Comment: 14 preprint pages, 7 figure

The DEEP2 Galaxy Redshift Survey: Redshift Identification of Single-Line Emission Galaxies

We present two methods for determining spectroscopic redshifts of galaxies in the DEEP2 survey which display only one identifiable feature, an emission line, in the observed spectrum ("single-line galaxies"). First, we assume each single line is one of the four brightest lines accessible to DEEP2: Halpha, [OIII] 5007, Hbeta, or [OII] 3727. Then, we supplement spectral information with BRI photometry. The first method, parameter space proximity (PSP), calculates the distance of a single-line galaxy to galaxies of known redshift in (B-R), (R-I), R, observed wavelength parameter space. The second method is an artificial neural network (ANN). Prior information, such as allowable line widths and ratios, rules out one or more of the four lines for some galaxies in both methods. Based on analyses of evaluation sets, both methods are nearly perfect at identifying blended [OII] doublets. Of the lines identified as Halpha in the PSP and ANN methods, 91.4% and 94.2% respectively are accurate. Although the methods are not this accurate at discriminating between [OIII] and Hbeta, they can identify a single line as one of the two, and the ANN method in particular unambiguously identifies many [OIII] lines. From a sample of 640 single-line spectra, the methods determine the identities of 401 (62.7%) and 472 (73.8%) single lines, respectively, at accuracies similar to those found in the evaluation sets.Comment: 11 pages, 6 figures, accepted to Ap

Challenges in the diagnosis of neurofibromatosis type 1 (NF1) in young children facilitated by means of revised diagnostic criteria including genetic testing for pathogenic NF1 gene variants

Neurofibromatosis type 1 (NF1) is the most frequent disorder associated with multiple café-au-lait macules (CALM) which may either be present at birth or appear during the first year of life. Other NF1-associated features such as skin-fold freckling and Lisch nodules occur later during childhood whereas dermal neurofibromas are rare in young children and usually only arise during early adulthood. The NIH clinical diagnostic criteria for NF1, established in 1988, include the most common NF1-associated features. Since many of these features are age-dependent, arriving at a definitive diagnosis of NF1 by employing these criteria may not be possible in infancy if CALM are the only clinical feature evident. Indeed, approximately 46% of patients who are diagnosed with NF1 later in life do not meet the NIH diagnostic criteria by the age of 1 year. Further, the 1988 diagnostic criteria for NF1 are not specific enough to distinguish NF1 from other related disorders such as Legius syndrome. In this review, we outline the challenges faced in diagnosing NF1 in young children, and evaluate the utility of the recently revised (2021) diagnostic criteria for NF1, which include the presence of pathogenic variants in the NF1 gene and choroidal anomalies, for achieving an early and accurate diagnosis

Classification of NF1 microdeletions and its importance for establishing genotype/phenotype correlations in patients with NF1 microdeletions

An estimated 5–11% of patients with neurofibromatosis type-1 (NF1) harbour large deletions encompassing the NF1 gene and flanking regions. These NF1 microdeletions are subclassified into type 1, 2, 3 and atypical deletions which are distinguishable from each other by their extent and by the number of genes included within the deletion regions as well as the frequency of mosaicism with normal cells. Most common are type-1 NF1 deletions which encompass 1.4-Mb and 14 protein-coding genes. Type-1 deletions are frequently associated with overgrowth, global developmental delay, cognitive disability and dysmorphic facial features which are uncommon in patients with intragenic pathogenic NF1 gene variants. Further, patients with type-1 NF1 deletions frequently exhibit high numbers of neurofibromas and have an increased risk of malignant peripheral nerve sheath tumours. Genes located within the type-1 NF1 microdeletion interval and co-deleted with NF1 are likely to act as modifiers responsible for the severe disease phenotype in patients with NF1 microdeletions, thereby causing the NF1 microdeletion syndrome. Genotype/phenotype correlations in patients with NF1 microdeletions of different lengths are important to identify such modifier genes. However, these correlations are critically dependent upon the accurate characterization of the deletions in terms of their extent. In this review, we outline the utility as well as the shortcomings of multiplex ligation-dependent probe amplification (MLPA) to classify the different types of NF1 microdeletion and indicate the importance of high-resolution microarray analysis for correct classification, a necessary precondition to identify those genes responsible for the NF1 microdeletion syndrome