Postauditing in the EIA process

ABSTACT Environmental impact assessment (EIA) is an integral part of the protection of the environment. Although it is a tool which considers the impact on many different elements of the environment, the process also has many deficiencies. Because of its limitations, an audit has been forming since the beginning of EIA. An EIA audit evaluates the performance of an EIA by comparing actual impacts detected after the realization of the project to those that were predicted, those that were listed in the environmental impact statement. This paper will offer an insight into the EIA and the post-auditing process and contains three basic parts of these areas. The first part explores the EIA, its historical evolution and application in the Czech Republic. The second part will discuss the post-audit itself. In this part, the different post-auditing processes, which were carried out in different parts of the world, were chosen. Within the selected post-auditing, the predicted data from the environmental impact statements are statistically compared with resultant data from reality. It is therefore necessary to analyze the percentage given for how many predictions were wrong in a positive way, accurate or wrong in negative way. From different results of post-auditing, we can tell that only a small percentage of the..

Effect of BNN27 treatment on stride length and width in male and female mice.

<p>Male Tg vehicle-treated mice exhibited a decrease in stride length (a, left) at p115 (p = 0.0136, Mann-Whitney <i>U</i> test) and stride width (b, left) at p95 (p = 0.0202, Mann-Whitney <i>U</i> test) relative to Wt vehicle-treated mice. Female Tg vehicle-treated mice showed a decrease in stride length (c, left) at p95 (p = 0.0155, Mann-Whitney <i>U</i> test), p115 (p = 0.0024, Mann-Whitney <i>U</i> test), and p135 (p = 0.0010, Mann-Whitney <i>U</i> test) but no change in stride width (d, left) (p>0.05, Mann-Whitney <i>U</i> test) compared to Wt vehicle-treated mice. There was no significant effect of BNN27 treatment (10 mg/kg or 50 mg/kg) on stride length or width in either male or female Tg mice compared to vehicle treatment (p>0.05, Kruskal-Wallis test) (a-d, right). Wt-vehicle (male: n = 10, female: n = 9; grey), Tg-vehicle (male: n = 8, female: n = 11; grey), Tg-BNN27 10 mg/kg (male: n = 9, female: n = 9; black), Tg-BNN27 50 mg/kg (male: n = 9, female: n = 9; red). Data are presented as median ± interquartile ranges. * p<0.05, ** p<0.01, ***p<0.001.</p

Effect of BNN27 treatment on paw grip endurance (PaGE) and rotarod in male and female mice.

<p>Male Tg vehicle-treated mice demonstrated a significant decrease in time spent on the PaGE test (a, left) at p95 (p = 0.0023, Mann-Whitney <i>U</i> test), p115 (p = 0.0003, Mann-Whitney <i>U</i> test), and p135 (p = 0.0385, Mann-Whitney <i>U</i> test) and the rotarod test (b, left) at p55 (p = 0.0089, Mann-Whitney <i>U</i> test), p95 (p = 0.0192, Mann-Whitney <i>U</i> test), and p135 (p = 0.0152, Mann-Whitney <i>U</i> test) relative to Wt vehicle-treated mice. Female Tg vehicle-treated mice demonstrated a decrease in time spent on the PaGE test (c, left) at p95 (p = 0.0128, Mann-Whitney <i>U</i> test), p115 (p<0.0001, Mann-Whitney <i>U</i> test), and p135 (p<0.0001, Mann-Whitney <i>U</i> test) and the rotarod test (d, left) at p55 (p = 0.0379, Mann-Whitney <i>U</i> test), p95 (p = 0.0026, Mann-Whitney <i>U</i> test), and p135 (p = 0.0002, Mann-Whitney <i>U</i> test) relative to Wt vehicle-treated mice. In Tg female mice, BNN27 10 mg/kg treatment significantly increased the time spent on the PaGE (c, right) (p<0.05, Dunn’s multiple comparison test) and rotarod (d, right) (p<0.01, Dunn’s multiple comparison test) tests compared to vehicle treatment at p95. Wt-vehicle (male: n = 10, female: n = 9; grey), Tg-vehicle (male: n = 11, female: n = 11; grey), Tg-BNN27 10 mg/kg (male: n = 9, female: n = 9; black), Tg-BNN27 50 mg/kg (male: n = 9, female: n = 9; red). Data are presented as median ± interquartile ranges. * p<0.05, ** p<0.01, ***p<0.001, ****p<0.0001.</p

Effect of BNN27 treatment on motor neuron survival in male and female mice.

<p>There was no change in motor neuron counts in a) male and b) female mice following BNN27 treatment. Top, representative H&E stained longitudinal sections (10μM) of lumbar spinal cord from Wt vehicle-treated mice and Tg mice treated with vehicle, BNN27 10 mg/kg, or BNN27 50 mg/kg. Arrows indicate motor neurons; scale bar = 150μM. Bottom, quantification of motor neuron counts from Tg mice treated with vehicle (male: n = 7, female: n = 11; grey), BNN27 10 mg/kg (male: n = 8, female: n = 10; black), and BNN27 50 mg/kg (male: n = 9, female: n = 12; red) normalized to Wt vehicle-treated mice (male: n = 12, female: n = 9; white). Tg vehicle-treated mice showed a decrease in the relative motor neuron number compared to Wt vehicle-treated mice in both males (a; p = 0.0095, Mann-Whitney <i>U</i> test) and females (b; p = 0.0042, Mann-Whitney <i>U</i> test). BNN27 treatment (10 mg/kg or 50 mg/kg) had no effect on motor neuron counts in male (a; p>0.05, Kruskal-Wallis test) or female (b; p>0.05, Kruskal-Wallis test) mice. Data are presented as median and 10-90th percentiles. ** p<0.01.</p

MNTs attenuated survival of mouse motor neurons co-cultured with human astrocytes from SOD1 ALS patients.

<p>a) Survival of mouse motor neurons (MNs), expressing GFP under the Hb9 promoter, was significantly decreased in co-cultures with human astrocytes (iAstrocytes) from an ALS patient a SOD1 mutation (Patient 2/SOD1 210; light grey) compared to those from 3 compiled control patients (3 compiled; white) (p<0.0001, unpaired t-test). BNN20, BNN27, and BNN23 were each tested at 1 μM (dark grey), 10 μM (black), and 30 μM (medium grey) in iAstrocyte-mouse MN co-cultures. At 10 μM, BNN20 (p<0.01, Tukey’s test) and BNN27 (p<0.001, Tukey’s test) significantly increased the survival of MNs co-cultured with SOD1 iAstrocytes relative to untreated samples. b) The effects of BNN27 (red) were tested, along with Riluzole (dark grey), on iAstrocytes from 3 control patients (compiled) and 2 individual ALS patients each carrying a distinct SOD1 mutation (Patient 1/SOD1 91 and Patient 2/SOD1 210). Left, BNN27 (10 μM) treatment yielded a significant increase in MN survival in co-cultures with iAstrocytes from Patient 1 (p<0.0001, Tukey’s test) and Patient 2 (p<0.0001, Tukey’s test) relative to untreated co-cultures (light grey). Similarly, Riluzole (10 μM) treatment also significantly increased MN survival in co-cultures with Patient 1 (p<0.0001, Tukey’s test) and Patient 2 (p<0.0001, Tukey’s test) iAstroctyes. Right, representative images of mouse MNs co-cultured with iAstrocytes from control untreated (control), SOD1 210 untreated (untreated), SOD1 210 Riluzole (Riluzole), and SOD1 210 BNN27 (BNN27). Scale bar = 20μM. c) Oxidative stress levels were significantly increased in iAstrocytes from 2 ALS patients containing a SOD1 mutation (Patient 1/SOD1 91 and Patient 2/SOD1 210; light grey) compared to those from 2 control patients (white) (p<0.0001, Tukey’s test). BNN27 treatment (red) produced a significant decrease in oxidative stress levels from SOD1 iAstrocytes relative to untreated cells (p<0.001, Tukey’s test). Scale bar = 10μM. Experiments were performed in triplicate (a, c) and quadruplicate (b). Data are presented as mean ± SEMs. ** p<0.01, ***p<0.001, ****p<0.0001.</p

Effect of BNN27 treatment on neuromuscular junction integrity in male and female mice.

<p>There was no change in neuromuscular junction (NMJ) integrity in a) male and b) female mice following BNN27 treatment. Top, representative tibialis anterior sections (20μM) from Wt vehicle-treated mice and Tg mice treated with vehicle, BNN27 10 mg/kg or 50 mg/kg. Sections were stained for α-Bungarotoxin (left: TMR-α-Bungarotoxin 1:750; red) and the vesicular acetylcholine transporter (middle: VAChT 1:10,000; green). Overlay images (right) show overlap of α-Bungarotoxin and VAChT. Scale bar = 20μM. Bottom, quantification of the percent overlay between α-Bungarotoxin and VAChT from Tg mice treated with vehicle (male: n = 8, female: n = 11; grey), BNN27 10 mg/kg (male: n = 10, female: n = 10; black) or BNN27 50 mg/kg (male: n = 11, female: n = 13; red) normalized to Wt vehicle-treated mice (male: n = 10, female: n = 9; white). Tg vehicle-treated mice showed a decrease in the relative overlap compared to Wt vehicle-treated males (p = 0.0005, Mann-Whitney <i>U</i> test) and females (p = 0.0018, Mann-Whitney <i>U</i> test). Data are presented as median and 10-90th percentiles. ** p<0.01, *** p<0.001.</p

Effect of BNN27 treatment on paresis onset and survival in male and female mice.

<p>There was no significant effect of BNN27 (10 mg/kg or 50 mg/kg) treatment on paresis onset or survival compared to vehicle treatment in either male (p>0.05, Kruskal-Wallis test) or female (p>0.05, Kruskal-Wallis test) Tg mice. However, BNN27 10mg/kg treatment in Tg female mice produced a trend (p = 0.0523, Mann-Whitney <i>U</i> test) towards an increase in the age of paresis onset relative to Tg vehicle-treated female (b, left). Tg-vehicle (male: n = 8, female: n = 11; grey), Tg-BNN27 10 mg/kg (male: n = 10, female: n = 10; black), Tg-BNN27 50 mg/kg (male: n = 9, female: n = 9; red). Data are presented as percent values.</p