Results: 5

1.
Figure 1

Figure 1. From: Sparing of neuronal function postseizure with gene therapy.

(A) Significant reduction in KA-induced neurotoxicity in cultured hippocampal neurons by overexpression of GT (Left) or Bcl-2 (Right). n = 20–30/group. (B) Significant reduction in KA-induced hippocampal neurotoxicity by GT or Bcl-2. n = 10–15/group. *, P < 0.05; **, P < 0.02; ***, P < 0.001, by t test.

John McLaughlin, et al. Proc Natl Acad Sci U S A. 2000 November 7;97(23):12804-12809.
2.
Figure 4

Figure 4. From: Sparing of neuronal function postseizure with gene therapy.

(A) Immunoblot of immunoprecipitated cell lysates from cultures infected with Bcl-2 vector (bcl-2 +) or β-gal control vector (Bgal + ). The arrow indicates the bcl-2 protein band at approximately 30 kDa. (B and C) Cells double labeled for Bcl-2 (B) and β-gal (IC). ×200 magnification.

John McLaughlin, et al. Proc Natl Acad Sci U S A. 2000 November 7;97(23):12804-12809.
3.
Figure 3

Figure 3. From: Sparing of neuronal function postseizure with gene therapy.

Effects of GT (Center) and Bcl-2 (Right) on retention impairment in a submerged (A) and visible platform test (B) in a water maze produced by KA-induced lesions. Data were from the same rats used for the lesion data in Fig. 1B. *, P < 0.05; **, P < 0.01, by post hoc test after ANOVA.

John McLaughlin, et al. Proc Natl Acad Sci U S A. 2000 November 7;97(23):12804-12809.
4.
Figure 2

Figure 2. From: Sparing of neuronal function postseizure with gene therapy.

(A) Effects of GT (Left) or Bcl-2 (Right) on ROS accumulation post-KA. Values are expressed as percentage above that in mock-infected control cultures without KA. In control vector-treated wells, KA significantly increased ROS accumulation (P < 0.05 and 0.01 in GT and Bcl-2 studies, respectively, post hoc test after two-way ANOVA). In GT-infected wells, KA did not significantly increase accumulation, and in either condition (±KA), there was significantly less accumulation than in cognate control wells (P < 0.01 for both). In contrast, KA significantly increased accumulation in Bcl-2-treated wells (P < 0.05), and values did not differ significantly from the cognate control wells. (B) Effects of GT or Bcl-2 on metabolism in primary hippocampal cultures under hypoglycemic conditions as assessed by proton efflux rates, measured by microphysiometry. vIE1GT (Left) attenuated the drop of metabolism posthypoglycemia (***, P < 0.001 by post hoc test after two-way ANOVA, comparing experimental vector versus control vector at the same time point), whereas vα22βgalα4bcl-2 (Right) had no effect. Data on the left previously published (7), making use of a related HSV vector expressing either GT (vIE1GT) or β-Gal as a reporter gene (vIE1βGal).

John McLaughlin, et al. Proc Natl Acad Sci U S A. 2000 November 7;97(23):12804-12809.
5.
Figure 5

Figure 5. From: Sparing of neuronal function postseizure with gene therapy.

Equivalent patterns of expression and of decreasing lesion size after treatment with GT and Bcl-2. (A) X-Gal-stained neurons (×100) in representative sections (counterstained with Cresyl violet) from a rat receiving GT (Upper) or Bcl-2 (Lower). Cell bodies and large diameter dendrites of granule cells in the superior blade of the dentate gyrus are visibly stained. (B) Percentage of total X-Gal-positive cells in 1-mm regions along the anterior/posterior (A/P) axis of the dentate gyrus (n = 9/group). Mean percentage of total lesion differed between areas [F(3,64) = 27.23, P < 0.001] but not between groups. Zero on the x axis refers to the injection site. (C) Percentage of X-Gal-positive cells on the superior blade of the dentate gyrus grouped into three equal regions along the medial/lateral (M/L) axis (n = 9/group). Mean percentage of total lesion differed between areas [F(2,48) = 10.01, P < 0.001] but not between groups. The number “1” on the x axis refers to the most medial third. (D) Percentage of total lesion in 1-mm regions along the A/P axis for hippocampi treated with KA and Glut-1 or Bcl-2 (n = 5/group). Mean percentage of total lesion differed between areas [F(3,32) = 18.22, P < 0.001], but not between groups. (E) Percentage of total lesion grouped into three equal regions along the M/L axis (n = 5/group). Mean percentage of total lesion differed between areas [F(2,24) = 51.93, P < 0.001], but not between groups. The number “1” on the x axis refers to the most medial third.

John McLaughlin, et al. Proc Natl Acad Sci U S A. 2000 November 7;97(23):12804-12809.

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