MS and MO coded all responses. A third coder (LV) coded five items independent of the other coders, to reassure reliability. Interrater reliability was considered satisfactory (k = 0.85; range = 0.25–1.0) [51]. This study was approved by the Medical Ethical Committee of Utrecht University. All participants were blind to the study aims and the condition they were assigned to via alternating enrolment. Upon registration, selleck participants completed an online questionnaire at home assessing background characteristics. The experiment took place at the Netherlands Institute for Health Services Research (NIVEL) and lasted approximately 1 h. First, participants

were welcomed and informed about the study procedures. Informed consent was obtained.

After hands and wrists were cleaned with soap, electrodes were attached to measure SCL and participants were connected to the BIOPAC equipment. Participants were instructed to not move their hands, as this may affect measurement of SCL. Before and during video-viewing, SCL was obtained. When baseline measurement was completed (4 min), participants watched one www.selleckchem.com/products/MLN-2238.html of the two videos (approximately 10 min). After video-viewing, participants were disconnected from the BIOPAC equipment and received the recall questionnaire (approximately 20 min), followed by the manipulation check questionnaire (approximately 10 min). Finally, participants were debriefed and thanked for ALOX15 their contribution. The videos contained four important time points for data-analyses. At 150 s (T1) the clinician disclosed the bad

news; this section of the consultation ended at 176 s (T2). Clinicians’ affective communication differed between 320 s (T3) and the end of the consultation (T4) in both videos. All statistical analyses were preformed at a significance level of a = 0.05 (two-tailed), using STATA 11. T-tests and chi-squared tests were used to assess differences in background characteristics. The conditions were compared using chi-squared tests, to analyse the effectiveness of the manipulation. SCL of all 50 subjects was analysed. Individual data was freed from obvious artefacts (mostly due to movement) and corrected for participants’ own baseline SCL (150 s before start of the video), using Microsoft Excel. The first part of the video (before T3) consisted of breaking the bad news and was identical in both conditions. Therefore, the effect of breaking bad news on participants’ physiological arousal was calculated for the total sample by testing the difference between mean SCL at T1 and T2, using a paired t-test. To explore the effect of clinician’s communication, all data were plotted to explore the direction of the slopes of SCL before and after T3, using Microsoft Excel.

The most used device for PFO closure was Amplatzer (∼70% of cases). The procedure was successful in all patients. They occurred in 24/1035 (2.3%) patients in the peri-procedural phase. 12/24 (50%) subjects experienced

cardiac arrhythmia: 5 patients had transient atrial fibrillation (AF), one patient a transient bradycardia, one patient a I° atrioventricular block, 4 had AF and 1 had a wide QRS tachycardia, before starting the procedure, and needed electrical cardioversion. 2/24 (8.3%) patients had a femoral arteriovenous Z VAD FMK fistula, thus needing vascular surgery. 4/24 (16.6%) subjects had respiratory problems after general anesthesia. One patient experienced a device embolization, retrieved percutaneously. One patient had a transient visual loss and 4 patients had a vagal reaction,

allergy to antibiotics, right coronary spasm and mild pericardial effusion. Both clinical and cardio-neurosonological follow-ups were assessed in 444/1035 (43%), 243/1035 (23.5%) and in 31/1035 (3%) subjects, at the 6- 12- 24-month follow-up, respectively. Up to the 12-month follow-up, fourteen neurological recurrences were observed in 12/444 (2.7%) patients: 8 TIA and 2 hemorrhagic and 4 ischemic strokes. 10/14 (71.5%) neurological recurrences occurred within the 6-month follow-up. 41 cardiac and extra-cardiac complications occurred in 40/444 (9%) subjects, up to the 12th month. 34/41 (83%) complications were related to arrhythmias, 16 of Everolimus price them had AF, one atrial flutter, 10 supraventricular many paroxysmal tachycardia and the remaining 7 patients non specific arrhythmic patterns. 7/41 (17%) complications were related to myocardial ischemia, atrial erosion, device malposition, gluteal hematoma, apical thrombus, pericardial effusion and

dyspnoea. Most cardiac complications (34/41, 83%) occurred within the 6-month follow-up. Neither neurological recurrences nor cardiac-extra-cardiac complications were observed at the 24-month follow-up. Data concerning residual RLS were available in 401/444 (90.3%) and in 198/243 (81.5%) subjects, at the 6- and 12-month follow-up, respectively. A large permanent residual RLS was observed in 1/401 (0.25%) and 1/198 (0.5%) patient at the 6- and 12-month follow-up, respectively. cTTE was the most utilized diagnostic technique during the follow-up (47.1%, 42.4% and 74.2% at the 6- 12- 24-month follow-up, respectively); successively, in a lesser extent, were the data obtained by cTTE plus cTCD (23.2%, 24.3% and 16.1% at the 6- 12- 24-month follow-up, respectively). The aim of our study was to analyse the clinical practice regarding PFO closure in Italy by a prospective, observational and multi-centric survey using a web-based database. The number of the entire population that underwent PFO closure was, to our knowledge, one of the highest among similar studies.

MIKE 3 has hydrostatic and non-hydrostatic options, and we applied the former in order to make a straightforward comparison with POM. The substantial difference between POM and MIKE 3 in our case is that the latter is used in a z-level formulation with either the Smagorinsky subgrid scale model turbulent closure (Smagorinsky 1963) for both vertical and lateral mixing or a second moment k-ε turbulence closure for vertical mixing. The Słupsk Furrow overflow is expected to depend strongly on the existing irregularities of bottom

topography, which can bias the flow performance and complicate the interpretation of the numerical simulation results on the transverse secondary circulation. For this reason it seemed worth starting with the Selleckchem BTK inhibitor numerical simulations of a channelized Doxorubicin solubility dmso gravity current in an idealized sloping channel, the size, geometry and initial salinity stratification of which are comparable to those of the Słupsk Furrow (Figure 3). For the sake of clarity, the x axis of the channel is directed eastwards, like the Słupsk Furrow. The channel is 300 km long, 40 km wide, and 150 m deep; its cross-section is parabolic in shape. The channel consists of 3 parts, each 100 km long, and only the central

part has a slope of 5 × 10−4. The channel is closed at x = 0 and x = 300 km. The finite difference grid cell size is 2/3 km in the x and y directions. Vertically there are 63 sigma layers in POM and 75 equal z-layers in MIKE 3, so that both models provide an identical vertical resolution in the mid cross-section of the channel (63 sigma or z layers being no more than 2 m thick). To achieve a more detailed vertical resolution of possible density inversions in BBL under the gravity current, the final runs of the sigma

coordinate POM acetylcholine and the z-coordinate POM were performed with 129 sigma layers and 150 z-layers, so that the vertical grid size did not exceed 1 m. The temperature distribution in an initially motionless channel was taken to be uniform at T = 5°C; the initial salinity field is shown in Figure 3. Heat and salt fluxes across the sea surface and bottom are absent, as is wind forcing; bottom friction is controlled by the roughness parameter (0.01 m). Note that the simulation of ocean overflows using an idealized topography of the model domain has been undertaken by several researchers. For instance, Ezer (2006) used an idealized topography of the Faroe Bank Channel (FBC) to simulate the FBC Overflow, and Umlauf et al. (2010) performed 2D numerical experiments in an infinitely long and deep channel with an idealized cross-section of parabolic shape and a constant down-channel tilt to simulate the bottom gravity current of saline water of North Sea origin passing through a small, 10 m deep and 10 km wide, channel-like constriction north of the Kriegers Shoal in the Arkona Basin, (western Baltic Sea) ( Umlauf & Arneborg 2009a).

1%) was added to each well after 6, 24, and 48 h of hormone treatment. The cells remained for 4 h at 37 °C and 5% CO2 humidified atmosphere. The MTT solution was aspirated, and isopropanol (100 μL per well) was added. The plate was then stirred for 30 min at room temperature, to solubilize the blue formazan crystals that stained the mitochondria. Colorimetric quantification Dapagliflozin manufacturer was determined by spectrophotometry set to the wavelength of 570 nm. The experiments were carried out in six replicates and were repeated three times. To evaluate whether NE-induced OSCC proliferation is mediated

by IL-6, anti-IL-6 ab (R&D Systems, Minneapolis, MN) was employed to neutralize the action of IL-6. Briefly, after SCC9 cells had reached 20% confluence, cells were cultured for 24 h in serum-reduced medium (0.1% FBS). Then, the SCC9 cells were pre-treated with IL-6 neutralizing ab (1 and 10 μg/mL) for 30 min prior to the addition of NE (10 μM). Cells were further incubated for 6 h, and proliferation was evaluated by MTT assay. To assess whether OSCC cells express β1- and β2-AR, 20 tumor specimens were collected from patients with OSCC who had not received any treatment yet. All the OSCC cases had the diagnosis confirmed histologically. Once removed from the surgery site, the specimens were washed in saline solution, placed in

a tube containing TRIzol reagent (Invitrogen Life Technologies, Carlsbad, CA), and immediately stored in liquid nitrogen. For comparative analysis, 17 specimens of oral leukoplakia (considered a precursor lesion

of OSCC) and 15 samples of normal oral mucosa were collected and stored following the Ribociclib solubility dmso same protocol. The samples were then thawed and ground in TRIzol with an electric homogenizer. The total RNA was then extracted, cDNA was synthesized, and real-time PCR assay was performed as previously described. Data were checked for normality, and statistical analysis was performed by one-way analysis of variance (ANOVA) followed by the Bonferroni’s multiple-comparison test. P values <0.05 were considered significant. In all the evaluated times (1, 6, and 24 h), treatment of SCC9, SCC15, and SCC25 cells with physiological Buspirone HCl stress levels of NE (10 μM) elevated IL-6 mRNA expression. Maximum IL-6 expression peaked 1 h after stimulation with 10 μM NE, leading to an increase of 501.5 ± 34.8%, 317.1 ± 32.65%, and 237.7 ± 37.6% in IL-6 mRNA expression in SCC9 (p < 0.001), SCC15 (p < 0.05), and SCC25 cells (p < 0.05), respectively ( Fig. 1A–C). A smaller but significant enhancement in IL-6 mRNA levels in the SCC9 and SCC25 cell lines was also observed after 6 h of stimulation with NE, which did not continue after 24 h ( Fig. 1A and B). The synthetic β-adrenergic receptor agonist isoproterenol also induced a significant rise in IL-6 mRNA expression in SCC9 and SCC25 cells (SCC15 cells were not tested for isoproterenol). Specifically, after 1 h of treatment of SCC9 cells with 1 and 10 μM isoproterenol, IL-6 RNAm levels increased 269.7 ± 16.

The study was approved by the Research Ethics Committee of UFPI with the number 0153.0.045.000-10, and informed consent was obtained from recipients and relatives prior to Linsitinib solubility dmso inclusion, according to the Declaration of Helsinki. A 55-year-old man with CDC assay negative received a kidney transplant from his mother (Table 1). Eight years after transplantation he lost the kidney by chronic rejection. A serum screen of this recipient using single class I and II allele SPA Luminex panels (Labscreen; OneLambda, Canoga Park, CA) revealed the presence of anti-class II donor specific antibodies (anti-DRB5*02:02) as well as non-donor specific antibodies (Fig. 4).

We asked why the recipient developed antibodies against antigens to which he was never exposed. In order to solve this problem we used the EpHLA software. A closer view of results in the EpHLA’s Histocompatibility Map report showed that

all HLA molecules to which the recipient developed antibodies share eplets with DRB5*02:02 from the immunizer. Interestingly, the DRB5*02:02 molecule has three potentially immunogenic eplets: 6C, 71QAA, 108T3. We noted that while 6C eplet appears only on DRB5*02:02 molecule, the 71QAA eplet is shared by molecules of serum group DR15 (DRB1*15:01, DRB1*15:02, DRB1*15:03) and the 108T3 eplet is shared by DRB5*01:01 (Fig. 4). Thus, we were able to identify the epitopes targeted by the recipient’s Selleckchem PD0332991 HLA antibodies using the EpHLA software, and the alleles DRB5*02:02, DRB5*01:01, DRB1*15:01, DRB1*15:02, DRB1*15:03 are the unacceptable mismatches for this case; they are associated to a 28% cPRA. A 35-year-old female in chronic hemodialysis, enrolled in the related renal transplantation program Carnitine palmitoyltransferase II with two potential donors (brothers). The donors were typed as identical HLA each other and distinct as regards the recipient (Table 2). The result of the T and B CDC assays were positive to both donors. Four years later, the CDC assays performed with the same donors were negative and flow cytometry crossmatches were positive for T and B cells. The SPA results using current serum showed preformed antibodies directed to a myriad of different

class I and II HLA antigens (cPRA = 91%). The possible immunization events were blood transfusions and three gestations from the same husband, whose HLA typing is shown in Table 2. A closer examination of the SPA results revealed: (i) specific antibodies against the husband’s HLA mismatches, including allele A*02:01 (MFI = 8,994), and (ii) antibodies against potential donors’ HLA antigens, including allele A*68:02 (MFI = 12,353). Because A*02:01 and A*68:02 alleles belong to the same CREG, we reasoned that such alleles could share the same eplet targeted by the recipient’s HLA antibodies. We tested our hypothesis using the EpHLA software analyzing recipient versus immunizer, and then versus potential donors (Fig. 5 and Fig. 6). We found that the recipient HLA antibodies recognize the pair of eplets 142MT + 145KHA.

Furthermore, in animals treated with L. obliqua venom it was also observed accumulation and extravasation of leukocytes, in parallel with E-selectin and VCAM-1 enrichment on the vessel wall, suggesting that venom exerts a direct selleckchem effect on leukocyte and endothelial cells, activating and increasing the expression of crucial molecules for the onset of inflammatory responses. Cell shape is governed by the cytoskeleton, which acts as a mechanical supporting framework, and alterations in actin dynamics

is a hallmark of cell activation (Prasain and Stevens, 2009). To evaluate L. obliqua venom effect on endothelial cell morphology we determined a time course JAK inhibitor review of actin stress fiber formation in endothelial cells stimulated with the venom in vitro. After different times of incubation with the venom (3 μg/ml), cells were fixed and stained with rhodamine-conjugated

phalloidin to visualize F-actin distribution. As seen in Fig. 3A, immediately after contact with cells (1–3 min) L. obliqua venom induces rapid and profound alterations in actin cytoskeleton reorganization, when the membrane skeleton and the cortical actin rim crowned the cell border and stress fibers course through the cytosol. After 5 min, actin fibers rearrangement lead to the spreading and polarity of endothelial cells, which show spiky, thin cell protrusions extended at the cell periphery. This phenotype, characteristic of contracting or migrating cells is maintained throughout the observation (15 min) ( Fig. 3A). Focal adhesion kinase (FAK) is a non-receptor protein tyrosine kinase that localizes at focal adhesion complexes, mediating integrin, growth factor, and mechanical stress signaling (Schlaepfer et al., 2004). The phosphorylation at Tyr397 residues correlates with increasing

catalytic activity and induces FAK interaction with actin cytoskeleton, controlling adhesion, proliferation and cell migration (Schaller, 2010). Endothelial Ergoloid FAK is essential for vascular network stability, regulating cell survival and morphology (Braren et al., 2006). Fig. 3 shows that in parallel with the changes in cytoskeleton, L. obliqua venom induces FAK activation ( Fig. 3B) and its association to actin ( Fig. 3C) in endothelial cells. Increasing FAK phosphorylation at Tyr397 occurs just after 1 min of treatment and was maintained for 5 min ( Fig. 3B), diminishing after 15 min. It was also observed a close correlation between the kinetics of FAK phosphorylation and its subsequent association to polymerized actin in the first 3 min after treatment ( Fig. 3C), suggesting a direct link between these two events. At the 5th min, although pFAK was increased, its association to actin declined, reaching control level after 15 min.

3c. Finally, the MODIS-A Local Area Coverage (LAC) data with 1 km nominal resolution are displayed in Fig. 3d. Note that the AMT data click here are not included in Fig. 3. The error statistics for data shown in Fig. 3 are summarized in Table 2. The categorization of data into 3 subsets (GAC, MLAC, LAC) does not show any evidence that either of the subsets has a much better statistics than the other data subsets. The R2 coefficient for all data subsets is about 0.8 if AMT data are not included. The lowest mean

absolute percentage error (MPE) of about 22% is for the MODIS-A LAC data set, while the lowest percentage of model bias (PBIAS) is for the SeaWiFS GAC data (about 1%). The results shown in Figure 2 and Figure 3 indicate that the performance of satellite POC algorithms is acceptable and comparable to the performance of the standard correlational satellite algorithms for chlorophyll (Chl) concentration (Bailey and Werdell, 2006). Similar conclusion has been reached by Duforet-Gaurier et al. (2010), but these authors used more limited data sets (27 data points). Allison selleck chemical et al. (2010) also concluded that the band ratio algorithm is currently the best option for estimating POC from ocean color remote sensing in the Southern Ocean, although they recommended a slightly modified version of the regional algorithm. In spite of

these results one has to recognize that the POC database (260 data points) is still modest when compared to global Chl matchup database (∼2500 data points in Siegel et al., 2013), and more efforts are needed to carry out global POC measurements to increase this database in the future. In addition, historically much less efforts have been devoted

to establishing robust POC in situ data selleck kinase inhibitor collection protocols, and there have been no round robin or intercomparison experiments between different laboratories. More research efforts should be focused on this issue. In recent years, satellite-derived Chl data improved substantially our understanding of phytoplankton biomass and primary production distributions within the world’s oceans. However, of particular interest to ocean biogeochemistry and its role in climate change is not Chl, but carbon. It is therefore important to continue the experimental and conceptual work to improve the reliability of in situ and satellite POC determinations. Another challenging task for the ocean color methods is development of the capability to partition the POC stock into the living and non-living components (Behrenfeld et al., 2005). In our final word we would like to stress that even if scientists continue to strive to decrease errors and improve satellite methods, the substantial scientific benefits from use of large scale ocean color satellite observations are unquestionable. None declared. The authors would like to thank all the people who were involved in the programs providing free access to the data sets used in this study. The historical field data were obtained from the U.S.

Then, cell cultures were pretreated for 24 hours before XRT with 1 μM simvastatin alone, C225

alone (10 nM C225 for FaDu cells or 30 nM for A431 cells), or with the two drugs. Next, cell cultures were either irradiated (2 Gy) or subjected to mock irradiation in the presence or absence of the drugs. Colonies were stained with crystal violet. Clonogenic cell survival was calculated as the ratio between the number Apoptosis inhibitor of colonies presented after irradiation and the number of cells plated, which was then normalized by the clonogenic efficiency of the untreated controls. Note that when XRT was applied, clonogenic cell survival was the survival after 2 Gy, which is the most useful clinical marker of intrinsic radiosensitivity. To generate tumor xenografts, 106 cells suspended in 100 μl of medium were injected into subcutaneous tissues on the right hind limb of 6- to 8-week-old female athymic Swiss nu/nu mice (Harlan, Gannat, selleckchem France). Cells were injected on a Monday and left to grow for 7 days, moment when the treatments began. Tumor growth was measured—π/6 × (large diameter) × (small diameter)2—twice weekly. Mice were killed when the tumor volume reached 1200 mm3, when the mice showed moderate to severe toxicities, or when significant differences between groups were observed. All experimental procedures were approved by the Institutional Animal

Care and Ethics Committee. The mice received fractionated XRT, C225, and simvastatin. XRT was selectively delivered from Monday to Friday for 2 weeks using the 6-MV X-ray beams at doses of 20 to 30 Gy depending on type of experiment, in 10 fractions, 1 fraction each day. On the first day of treatment, C225 was intraperitoneally injected 6 hours before

irradiation at doses of 1 mg per animal to allow the antibody to have time to saturate the EGFR. Next, C225 was administered on days 3, 7, and 10 at doses of 0.5 mg per animal 2 hours (together with simvastatin or its vehicle) before irradiation as a maintenance C225 dose. Simvastatin (50 mg/kg) was administered orally on a daily basis for 12 days 2 hours before irradiation. Mice were randomly allocated to receive XRT plus C225 or XRT, C225, and simvastatin as well as to receive single treatments with XRT, C225, or simvastatin alone. In addition, a group Tolmetin of mice treated in parallel was killed on day 4 to obtain tumor samples for immunofluorescence. Semi-confluent cell cultures were pretreated for 48 hours with C225 and simvastatin in FBS-free medium and then irradiated with a single dose of 5 Gy. Twenty minutes after irradiation, cell cultures were rinsed in ice-cold phosphate-buffered saline (PBS) and lysed in radioimmunoprecipitation assay buffer with protease and phosphatase inhibitors. Vehicle and mock irradiation were provided as controls. Protein concentration in the lysates was determined by the Pierce BCA Protein Assay Kit (Thermo Scientific, Rockford, IL).

Later papers associated the scattering coefficient b with scattering into a much smaller angle of 4°. The first correlation based on measurements was presented by Mankovsky (1971). Morel (1974), who used the Mie model (an analytical http://www.selleckchem.com/products/LDE225(NVP-LDE225).html solution of electromagnetic wave interaction with spherical particles), showed that the ratio βp(4°)/bp changes only slightly with the refractive index and the particle size distribution. Recent measurements by Chami et al. (2005) show a linear correlation between the values of βp(4°) and the scattering coefficient bp. As with the scattering coefficient b, links between the backscattering

coefficient bb and scattering functions β were sought. One of the first to address the problem was Oishi (1990), who used modelling methods to show that the scattering function for an angle of 120° gave the best linear correlation with bb. Modelling was carried out with Mie algorithms for various refractive indices and different particle size distributions. In his paper, Oishi published some measurements that confirmed

the Crenolanib results of calculations. The optical scheme of an instrument for determining the backscattering coefficient on the basis of β(140°) measurements was presented by Maffione et al. (1991) and Maffione & Dana (1997). The designs of the latter authors were incorporated into commercially available instruments. In response to that latter paper Boss & Pegau (2001) supplied new arguments to justify Oishi’s ideas. Like Maffione & Dana (1997) they used the non-dimensional quantity χ(θ, λ), the definition of which includes the ratio of the backscattering coefficient bb to the volume scattering function for various scattering angles: equation(1) χθλ=bbλ2πβθλ. Boss & Pegau (2001) analysed the variability of χ(θ) for clean sea water and for suspensions. They also used new measurements and stated that the most accurate approximation of the backscattering coefficient could be obtained with measured β(117°). Other instruments were designed, enabling bbp to be obtained on the basis of the measurement of light scattered into angles around 117°. Sullivan

& Twardowski (2009) recently carried out research based on a very large number of measurements. They showed that the strongest correlation between backscattering coefficient and volume FER scattering function was obtained for scattering angles in the 110°–120° range. An interesting spectral analysis of the function χ(θ, λ), based on measurements made with the previous version of a prototypical volume scattering meter for Black Sea water and selected phytoplankton cultures, was presented by Chami et al. (2006). They considered the particle-affected function χ for scattering angles 120° and 140°, concluding that χp(120°) was spectrally less dependent than χp(140°); the former is therefore recommended, especially during phytoplankton blooms.

Slides were evaluated APO866 cell line using a Leica DMR upright microscope equipped for epifluorescence microscopy. ST sections were stained for TH immunoreactivity (IR) using nickel enhancement and slides were scanned as 600 dpi, 8 bit grayscale tiff images

using a CanoScan8400F flatbed scanner with automatic settings disabled. One section at the level of the anterior commissure (−0.26 mm from Bregma) was chosen from each brain for fiber density measurement. Using Fiji software (http://imageJ.nih.gov/ij), each ST was outlined using the freehand tool, processed to correct for background and brightness, converted to a binary image and the number of pixels in the ST determined as a measure of TH-IR fiber density. ST fiber density data are expressed as a percentage of injected vs control ST for each treatment group. Sections of SN were stained for TH-IR without nickel enhancement. For the dose response study, the number of TH-IR neurons was counted in both injected and control SNs in one section from each brain at the level of the medial terminal nucleus accessory optic tract (−5.3 mm from Bregma) using Neurolucida software (Micro Bright Field Biosciences). AZD4547 molecular weight For the efficacy study, unbiased stereology was used to determine the total number of TH-IR neurons in each SN. Seven sections at similar anterior to posterior levels were chosen throughout

the anterior-posterior extent of the SN in every brain. The number of TH-IR cells was counted in injected and control SN using StereoInvestigator™ software (Micro Bright Field Biosciences). Parameters were as follows: grid size (80×80), frame size (175×175), guard zones (3 μm), optical dissector height (10 μm). The Gundersen coefficient of error was ≤0.07 for TH neuronal counts in the

control SN and ≤0.11 for Branched chain aminotransferase TH neuronal counts in experimental SN. For both counting methods, only large TH-IR neurons (greater than ~15 μm in diameter) were counted to avoid counting interneurons or dying neurons. Histology images were collected using a Retiga 4000R digital camera on a Leica DMR upright microscope. Adobe Photoshop CS5 was used to compile multi-photo plate figures. Data were analyzed using Prism software. Kruskal–Wallis one-way ANOVAs followed by Dunn’s post hoc tests were used to compare treatment groups for forelimb behavior analysis. All other data were analyzed using a parametric one-way ANOVA followed by Tukey’s post hoc tests. Statistically significant differences were set at p≤0.05. Data are expressed as mean±SEM. This study was supported by the Department of Defense Neurotoxicology Program (NO06079001) and NIH grants (NS31957 and NS054989 to M.C.B. and T32 NS041234 to C.E.K.), the Harry F. and Elaine M. Chaddick Foundation and the Medical Research Institute Council of Ann and Robert H. Lurie Children’s Hospital of Chicago. The University of Pennsylvania Viral Vector Core is acknowledged for AAV production. The technical assistance of Jianping Xie and Brian Corstange (Ann and Robert H.