24 research outputs found

    Identifying the learning development of students who are refugees

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    Students who are refugees need understanding and support to settle successfully into mainstream Australian classrooms. Teachers not aware of students’ prior learning and the process of second language acquisition may have difficulty providing the most appropriate learning environments to meet these students’ needs. This study found that, with no coordination of information on students’ learning backgrounds nor of their learning needs and development, students were in danger of being identified as at-risk of having a learning disability, with little support to substantiate such claims

    Characteristics of a Brucella species from a bottlenose dolphin (Tursiops truncatus

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    Abstract. A culture isolated from an aborted fetus of a bottlenose dolphin (Tursiops truncatus) was characterized. The isolate was a gram-negative coccobacillus, and the colonial morphology was typical of a smooth Brucella. The isolate was positive for catalase, oxidase, nitrate reduction, and urease. Hydrogen sulfide was not produced. It grew in air at 37 C but required 72 hours for good growth. There was growth on media containing basic fuchsin, thionin, thionin blue, penicillin, and erythritol. The M antigen was dominant, and the isolate was lysed by 4 of 10 brucellaphages tested. The oxidative metabolic profile of the isolate was similar to that for B. abortus but differed in utilization of L-asparagine, L-glutamic acid, and DL-citrulline. Whole-cell lysates were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The protein profiles were markedly different from the protein profiles of reference strains of Brucella species. Biochemical and oxidative metabolism profiles indicated that the isolate belongs in the genus Brucella but did not match the profiles of any established species or biovars. This isolate may be an atypical strain of a recognized Brucella species or a new biovar or species of Brucella. Brucella species have been isolated from numerous animal species, including cattle, swine, goats, sheep, dogs, bison, and elk. 7,22 These bacteria cause abortion in the majority of infected hosts. There are no reports of Brucella infection in marine mammals. A bacterium was isolated from an aborted fetus of a bottlenose dolphin (Tursiops truncatus) at the Balboa Hospital, San Diego, California. The isolate was tentatively identified as a Brucella species and submitted for identification to the National Veterinary Services Laboratories (NVSL), Ames, Iowa. This report describes the characterization of this isolate using tests recommended for identification of species and biovars of the genus Brucella

    Node/paranode complexes in ventral ON after partial transection.

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    <p>(a) Representative images of Caspr<sup>+ve</sup> paranodes (green) flanking the β-III tubulin<sup>+ve</sup> (red) paranodal gap, and β-III tubulin<sup>+ve</sup> areas (red) colocalised with Na<sub>v</sub>1.6<sup>+ve</sup> nodes (blue) in normal ventral ON and at 1 day post injury; colocalised areas are yellow and purple respectively (examples indicated by arrows), scale  = 20 μm. Mean ± SEM length of the paranodal gap (b), paranode length (c) and the ratio of node to paranode lengths (e) in ventral ON of normal animals and 1, 3, 7 days, 1 and 3 months after injury; representative images (d), scale bar  = 1 μm. Orthogonal projection of a representative z stack illustrating a large atypical node/paranode complex well within the stack of images (f, boxed), scale bar  = 5 μm; Caspr<sup>+ve</sup> paranodes are green, β-III tubulin<sup>+ve</sup> axons are red (note: only projections in the z plane of the identified node/paranode complex are shown in the panels adjacent to the main image). Mean ± SEM percentages of node/paranode complexes that were atypical (hemi – nodes, single paranodes) (g), * significantly different from normal for each complex type (p≤0.05) (n = 6 animals/time point)</p

    Effects of 670 nm light on RGC numbers and visual function.

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    <p>Mean ± SEM retrograde labelled RGC numbers (central or ventral retinal regions) (a) and responses in the optokinetic nystagmus test of visual function (smooth pursuits or fast resets) (b), in 670 nm treated or control animals 3 months after injury, * significant differences indicated (p≤0.05) (n = 4–5 animals / group), PT is partial ON transection injury.</p

    Oxidative stress indicators in ON after partial transection.

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    <p>(a) Mean ± SEM ROS/RNS assessed as DCF fluorescence in homogenates of ON including both the dorsal injury site and the ventral region vulnerable to secondary degeneration, from normal animals and 1, 3, 7 days, 1 and 3 months after injury, or (b) from ventral ON only from normal animals and 1 or 7 days after injury (6 animals pooled per time point, assayed in duplicate). (c) Semi – quantification of mean ± SEM intensity of CML immunoreactivity in olig1<sup>+ve</sup> oligodendrocytes in ventral ON, assessed by tracing identified cells in single images in the z axis; representative images at 1 day (d), scale bar  = 10 μm, (n = 4–5 animals/time point). Similarly, semi – quantification of mean ± SEM intensity of DHE staining in olig1<sup>+ve</sup> (e) or CC1<sup>+ve</sup> (f) oligodendrocytes in ventral ON; * significantly different from normal (p≤0.05).</p

    Effects of 670 nm light treatment on oxidative stress indicators.

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    <p>(a) Mean ± SEM ROS/RNS assessed as DCF fluorescence in pooled homogenates from dorsal or ventral ON from PT handled or PT 670 nm treated animals, 1 day after injury (6 animals pooled per time point, assayed in duplicate). Semi – quantification of maximum (b) or mean (c) ± SEM intensity of DHE staining in CC1<sup>+ve</sup> oligodendrocytes in ventral ON of PT handled or PT 670 nm treated animals, 1 day after injury, assessed by tracing identified cells in single images in the z axis; with (d) representative images, example of identified cells indicated, scale bar  = 10 μm. Similarly, mean ± SEM intensity of CML immunoreactivity in CC1<sup>+ve</sup> (e) or olig1<sup>+ve</sup> (f) oligodendrocytes in ventral ON of PT handled or PT 670 nm treated animals, 1 day after injury. PT is partial ON transection injury.</p

    Cytochrome<i>c</i> oxidase activity after injury, +/− 670 nm light.

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    <p>Semi – quantification of mean ± SEM cytochrome <i>c</i> oxidase activity in ON including both the dorsal injury site and the ventral region vulnerable to secondary degeneration (a) or in ventral ON only (b) from normal animals and 1, 3, 7 days, 1 and 3 months after injury. Similarly, mean ± SEM cytochrome <i>c</i> oxidase activity in handled normal, PT handled or PT 670 nm treated animals, encompassing the dorsal injury site and ventral ON (c), or in ventral ON only, 1 day after injury (d). Mean ± SEM cytochrome <i>c</i> oxidase activity encompassing the dorsal injury site and ventral ON (defined by region enclosed in dotted lines in F) in PT handled or PT 670 nm treated ON compared to handled normal, 3 months after injury (e); representative images of cytochrome <i>c</i> oxidase activity histochemistry at 3 months (f), scale bar  = 100 μm (n = 4–5 animals/group), * significant differences indicated (p≤0.05), PT is partial ON transection injury.</p

    Representative TEM images from normal ventral ON (a) and from day 1 after injury (b–d).

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    <p>Note the disorganisation, lack of definition (arrow head) and multi – layering (arrows) in the paranodal loops from ON vulnerable to secondary degeneration (b, c) and the complete breakdown in structure of one paranode in a node/paranode complex (d), scale bar  = 0.5 μm.</p

    Effects of 670 nm light on node/paranode complexes of ventral ON.

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    <p>Mean ± SEM paranode length (a) and length of the paranodal gap (b) in ventral ON of 670 nm treated and control animals, 1 day after injury; representative images (c). Mean ± SEM percentage of single paranodes in the same groups (d); Caspr<sup>+ve</sup> paranodes are green, β-III tubulin<sup>+ve</sup> paranodal gaps are red, scale bar  = 5 μm, * significant differences indicated (p≤0.05), PT is partial ON transection injury. Representative TEM images of PT injured (e) and PT 670 nm light treated (f) node/paranode complexes in ventral ON 1 day after injury. Note the increased definition of the paranodal loops in 670 nm light treated animals, but continued disorganisation (arrows). Representative example of a putative hemi – node in ventral ON from 670 nm light treated animal, with one half of the node/paranode complex clearly defined and the other disorganised (g), scale bars for TEM images  = 0.5 μm.</p
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