4 research outputs found

    STZ- WT mice depict significantly increased ROS levels that decrease in]SOD2-STZ mice.

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    <p>(A) The images depict nasal cavity sections showing genotypic differences in DHE fluorescence. (B) The graph depicts ratio of DHE and corresponding DAPI fluorescence, which was measured with ImageJ software. Significance was assessed by one way ANOVA with Dunnett's post-test. For WT, WT-STZ, SOD2, and SOD2-STZ nβ€Š=β€Š4, 6, 4, 4 respectively. ** p<0.01, * p<0.05 Barβ€Š=β€Š20 Β΅m.</p

    MEMRI experiments demonstrate that the axonal transport deficits in WT-STZ mice recover in SOD2-STZ mice.

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    <p>(A) Pseudo-color MRI images depicting changes in Mn<sup>2+</sup> signal intensities (yellow color) at the beginning (2minutes) and at the end of the imaging session (32 minutes) at a region of interest (ROI) identified as a circle on the outer olfactory neuronal layer (ONL). Note that the WT, SOD and SOD2-STZ mice exhibit a change from green (2 minute time point) to yellow (32 minute time point) whereas the WT-STZ animals exhibit a light green color at both time points indicating that Mn<sup>2+</sup> has not traveled to these areas at the same rate. (B) Gray-Scale Image of the same data set in (A). (C) The graph depicts normalized axonal transport rates (% control) in the WT and SOD2 mice treated with vehicle or STZ for a week before <i>in vivo</i> axonal transport studies. Twelve mice were used in the WT group and four mice were used in each of WT-STZ, SOD2, and SOD2-STZ groups. Statistical analysis: One way ANOVA, Dunnett's post-test. * p<0.05. SOD2 β€Š=β€Š SOD-2 overexpressing mice; SOD2-STZ β€Š=β€Š SOD-2 overexpressing mice treated with STZ.</p

    STZ-induced hyperglycemia impairs axonal transport in the olfactory receptor neurons.

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    <p>(A) Graph depicts axonal transport rates (depicted as Mn<sup>2+</sup> Ξ”SI/t on Y axis, where β€œSI” is signal intensity and β€œt” is time) of Mn<sup>2+</sup>at 1 week post-STZ treatment for WT(nβ€Š=β€Š3) and WT-STZ with fasting glucose levels 200–399 mg/dl (nβ€Š=β€Š3), and >400 mg/dl (nβ€Š=β€Š5). (B) Graph depicts the changes in axonal transport rates for WT (nβ€Š=β€Š4), WT-STZ (nβ€Š=β€Š3), and WT-STZ+insulin treated mice (nβ€Š=β€Š4). (C) The graph represents changes in axonal transport rates in a mouse model of WT-STZ (nβ€Š=β€Š5) as compared to WT mice (nβ€Š=β€Š4). Statistical analysis: One way ANOVA, Tukey's post test for more than 2 groups and Students t test to compare 2 groups. * p<0.05, ** p<0.01, *** p<0.001/WT β€Š=β€Š wildtype control. WT-STZ β€Š=β€Š Wildtype treated with streptozotocin.</p

    Phosphorylated Tau significantly increase in WT-STZ mice and recovers in SOD2-STZ mice, despite hyperglycemia.

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    <p>Western blotting analysis of OB tissues from WT, WT-STZ, SOD2, SOD2-STZ mice show: (A) changes in site-specific phosphorylation of tau (p-tau) at threonine 205, (seven mice in WT, WT-STZ groups and six in SOD2 and SOD2-STZ groups) (B) changes in total levels of tau protein, (seven mice in WT, WT-STZ groups and six in SOD2 and SOD2-STZ groups) (C) QPCR of brain homogenates depict relative changes in mRNA levels of tau, (six mice used in each of the four groups) and (D) representative western blot from OB homogenates from 1 week vehicle or STZ treated 2-4-month-old mice. The results are normalized to Ξ²-actin. Statistical analysis: One way ANOVA followed by Dunnett's post test. ** p<0.01, *p<0.05.</p
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