0; and the inhibitors proportion of participants achieving an HAI titre ≥40 is >60%. Local reactions (redness, swelling, pain, and limitation of arm movement) at the PCV13 injection site and systemic events, including fever (oral temperature ≥38 °C), chills, fatigue, headache, vomiting, decreased appetite, rash, and new and aggravated generalized muscle or joint pain, and the use of antipyretic and pain medications to treat symptoms, was recorded for 14 days in an electronic diary by the participants. Other adverse events, which

were collected by the investigator in response to direct questioning of the subject on his/her health since the last visit, were documented on the case report form at each visit throughout the study; the investigator PF-06463922 cost assessed each adverse event for severity, for serious criteria, and causality. Sample size estimation Doxorubicin mouse was based on the proportion of responders (achieving at least a 4-fold increase in HAI titre) in each group for TIV comparisons, and the GMCs

in each group for PCV13 comparisons. Sample sizes were calculated using nQuery Advisor® 6.0 (Statistical Solutions, Ltd., Cork, Ireland). This study was powered to show noninferiority of PCV13 + TIV relative to Placebo + TIV and PCV13 alone. For TIV comparisons, sample size calculations assumed power of at least 80%; a noninferiority criterion of −0.10 for the difference in proportions of responders; no difference in true responses between the groups ([PCV13 + TIV]−[Placebo + TIV alone]); a 2-sided, type-I error rate of 0.05; and a dropout rate of ≤7%. With these assumptions, 511 evaluable participants per group were needed for Fossariinae TIV comparisons.

A total of 1160 participants were randomly assigned to ensure 1022 evaluable participants for TIV comparisons. For IgG comparisons, sample size calculations assumed power of approximately 90%; 2-fold noninferiority criterion for GMCs; no difference in true responses between the groups ([PCV13 + TIV] − [PCV13 alone]); a 2-sided, type-I error of 0.05; and a dropout rate of ≤7%. With these assumptions, 281 evaluable participants per group were needed for pneumococcal comparisons. Eligible participants were randomly assigned in a 1:1 ratio to receive PCV13 + TIV/Placebo or Placebo + TIV/PCV13 through the sponsor’s internet-based enrollment system. This system was accessed through the internet or an interactive voice-response system by authorized site staff. The randomization schedule used a randomized block design in which treatment sequences were randomly ordered within each block. All participants, study staff, and those assessing outcomes were blinded to the group assignment. The selection for inclusion in the IgG subset analysis occurred after all participants were enrolled. Participants were randomly ordered within treatment groups and assigned a rank (1, 2, 3, etc.

[4] and ours may account for the fact that in their series only the sinus node artery was analyzed, while in our study we evaluated the largest atrial branch arising from the right coronary artery, independently of whether selleck products or not this was the sinus node artery. The mechanism by which atrial branches may be occluded during PTCA is not well known. However, if we Libraries extrapolate the information derived from studies on SBO [21], [22] and [23], possible causal mechanisms of ABO could be persistent coronary spasm or the displacement of the atherosclerotic plaque. Coronary vasospasm of the

atrial branch cannot be ruled out in our study because a second testing angiography was not further performed. However, our data reinforce the notion that displacement of an atherosclerotic plaque may be a plausible mechanism. Indeed, we have observed that ABO occurred more GDC-0941 price frequently in patients with bifurcations lesions with ostial AB atherosclerosis and when higher maximal inflation pressure during stenting is applied. These findings are in agreement

with the predictors reported previously in patients with SBO after PTCA such as the baseline reference diameter of SB and the presence of significant stenosis at the origin of the SB [1], [2], [3] and [21]. Due to the retrospective design, this study can be exposed to patient selection bias. However, the included patients were consecutive and were admitted to the hospital during a well defined 2-years period of time. The lack of a second coronariography after the index PTCA does not allow to exclude that ABO was indeed caused by a transient atrial

coronary spasm. However, a second testing angiography is not indicated since at present time there are no clinical guidelines for ABO. Finally, the large variety of the stent types implanted during this study does not allow to demonstrate any possible association between a particular stent model and the occurrence of ABO. The clinical consequences of acute occlusion of atrial arteries after PTCA have not been prospectively analyzed. However, there are several case-report studies showing that patients with ABO may develop atrial myocardial Tolmetin infarction, sinus node dysfunction and atrial fibrillation [4], [5], [11], [19] and [20]. The close association between the latter arrhythmia and atrial myocardial ischemia was demonstrated in an experimental study in situ dog hearts [24] where the electrophysiological effects of acute ligation of one atrial artery were assessed by epicardial mapping of local electrograms and continuous ECG loop recordings [25]. These studies have demonstrated that acute atrial ischemia creates a substrate capable to elicit and maintain atrial fibrillation. Our study reveals that the incidence of accidental ABO is relatively high and the consequences in terms of atrial arrhythmogenesis are expected to be of clinical relevance.

Carbon tetrachloride (CCl4), riboflavin, deoxyribose, carrageenan and silymarin were purchased from Sigma Chemicals, USA. Serum glutamate pyruvate transaminase (SGPT), Serum Glutamate Oxaloacetate Transaminase (SGOT), Serum Alkaline Phosphatase (ALP) and Serum Total Bilirubin (T. Bil) assay kits were purchased from Span diagnostics Ltd, Gujarat, India. All other chemicals used were of analytical B-Raf inhibitor drug grade. Adult albino Wistar rats (National Institute of Nutrition, Hyderabad, India) of either sex weighing 150–200 g were used in the studies.

The animals were maintained under standard laboratory conditions at an ambient temperature of 23 ± 2 °C having 50 ± 5% relative humidity with 12 h light and dark cycle. The use and care of the animals in the experimental protocol has been approved by the local Institutional Animal Ethics Committee (Regd. No. 516/01/A/CPCSEA) following the guidelines of the Committee for the Purpose of Control and Supervision of Experiments on Animals (CPCSEA), Government of India.

The acute toxicity study was conducted for hydroalcoholic, methanolic, ethyl acetate and hexane extracts of LY2157299 clinical trial G. gynandra as per OECD (Organisation for Economic Co-operation and Development) guidelines 420 (OECD.2001). Total phenolic content was determined using the Folin–Ciocalteu reagent7 using standard gallic acid calibration curve, measure the concentration of phenolic content in gallic acid total equivalents using unit’s mg/gm (GAE).8 The Fazel Shamsa et al, 2008 Libraries method using atropine calibration curve, measure the concentration of alkaloid content in atropine equivalents using unit’s mg/g.9 Superoxide scavenging activity10 of the plant extracts was determined by McCord & Fridovich method, which depends on light induced superoxide generation by riboflavin and the corresponding reduction of nitroblue tetrazolium.11 Hydroxyl radical scavenging activity was measured by

studying the competition between deoxyribose and the extracts for hydroxyl radicals generated from the Fe2+/EDTA/H2O2 system (Fenton reaction). The hydroxyl radical attacks deoxyribose, which found eventually results in the formation of thiobarbituric acid reacting substances (TBARS).12 The scavenging activity for DPPH free radicals was measured according to the procedure described by Braca et al, 2003.13 and 14 In the present work hepatoprotective activity of different extracts of G. gynandra were tested against carbon tetrachloride (CCl4) induced hepatotoxicity by measuring biochemical enzymes (SGOT, SGPT, ALP and T. BIL). An increase in the enzymes levels of these biochemical parameters is a sensitive index of hepatic damage. The standard and test group animals were treated with 50 mg/kg dose of silymarin and 100, 200, 400 mg/kg doses of different extracts of G. gynandra for 6 days. On 6th day, 1 h after treatment with standard drug and selected plant extracts, the animals were intoxicated with CCl4 in liquid paraffin (1:1 v/v, 0.75 ml of CCl4/kg, i.p.).

Depression during pregnancy is more common among women with a history of depression or a family history of

depression, those in single motherhood or with more than three children, cigarette smokers, low income earners, teenagers, and those in unsupportive social situations (Dietz et al 2007, Yonkers et al 2009). The importance of prenatal intervention is highlighted by studies showing that depression is associated with increased risk of prenatal and perinatal complications (Jablensky et al 2005, Nakano et al 2004). For example, depressed women are more likely to deliver prematurely (Field, 2011) and they often have neonates who require intensive care for postnatal complications including growth retardation and bronchopulmonary dysplasia (Chung et al 2001). Furthermore, Modulators although pregnant women typically report significantly GS-1101 supplier lower rates of tobacco, alcohol, and cannabis use than before pregnancy (Hotham et al 2008), depression increases vulnerability to caffeine, nicotine, drug, and alcohol use in pregnant women (De learn more Tychey et al 2005, Field et al 2009). Depression is also associated with failure to eat well and seek prenatal

care (Yonkers et al 2009). Prenatal interventions for depressed pregnant women have included antidepressants, psychotherapy, alternative therapies, and physical activity (Field et al 2009, Rethorst et al 2009). In recent years, accumulating evidence has supported the popular belief that physical activity is associated with psychological health in pregnant women. why Guidelines from the American College of Obstetricians and Gynecologists (Artal and O’Toole, 2003) recommend regular exercise for pregnant women, including those who are sedentary, for its

overall health benefits including improved psychological health. Physical activity during pregnancy appears to be beneficial to the maternal-foetal unit and may prevent the occurrence of maternal disorders, such as hypertension (Yeo et al 2000, Barakat et al 2009) and gestational diabetes (Dempsey et al 2004, Callaway et al 2010), as well as improving well-being and quality of life (Montoya Arizabaleta et al 2010). In addition, several studies over the last decade have reported that physical activity has few negative effects for many pregnant women (Alderman et al 1998, Artal and O’Toole, 2003, Barakat et al 2008, Barakat et al 2009). Pregnancy is a time of intense physical change and emotional upheaval in many women (Hueston and Kasik-Miller, 1998, Montoya Arizabaleta et al 2010). In addition to the obvious outward physical changes that accompany pregnancy, significant increases in mental health problems, including What is already known on this topic: Depression is common among pregnant women and is associated with increased risk of prenatal and perinatal complications.

Additionally, there were no supplementary immunization activities (vaccination campaigns) for measles conducted in Sri Lanka during the period of the trial. Ongoing transmission of measles is 5-FU mouse unlikely to have contributed to the increases

in seropositivity, as Sri Lanka has maintained very high rates of measles vaccination among infants since 2000 [8], and there were no known/reported outbreaks of measles in the District of Colombo during the study period. And finally, unrecognized measles transmission would have had to occur at very high community attack rates in infants (e.g. 90%), as we found long-term increases in anti-measles IgG after 28 days post-vaccination in nearly all infants in the study. Few studies have prospectively measured measles antibody responses so long after vaccination with a single dose of measles vaccine at 9 months of age, but studies in the Gambia [9] and [10] (measles vaccine co-administered with yellow fever vaccine) and Malawi check details [11] (measles vaccine given alone) have made similar Modulators findings of continually increasing measles immune responses at 9–15

months post-vaccination in the absence of identified measles outbreaks and with “no explanation for this trend” [10]. Regarding our findings for the immune response to JE, these results are similar to those obtained in a study among 9-month-old infants in the Philippines in which measles vaccine and LJEV were administered concomitantly [5] and [12]. The seropositivity to JE measured at one month was nearly identical in the Sri Lankan and Philippine infants (90.7% vs 90.5%, respectively), although the JE GMTs were somewhat lower in the Sri Lankan infants (111 vs 155, respectively). The significance

of the out lower GMTs are uncertain, given that GMTs in both populations are well above the WHO-recommended threshold of protection of a 1:10 dilution in a 50% PRNT assay [4]. It is reassuring that 1 year following administration of the vaccine, JE antibody concentrations were well-maintained in Sri Lankan children. In studies in infants and young children that have measured the response to LJEV alone, seropositivity rates post-vaccination have ranged from 86% in Bangladesh [13], to 92% in the Philippines [5], to 95% in Thailand [14] and 96% in Korea [15]. A key limitation of this study was that there was not a control group followed in parallel to strengthen interpretation of immunogenicity and safety. Additionally, we measured seropositivity for measles antibodies using ELISA, which does specifically measure neutralizing antibodies; only results from PRNT for measles are considered truly indicative of seroprotective responses to measles [16].

In presence of Ca (II) GSK126 ion the percentage of protein binding of drug increased (42–46) % at lower concentration range and (82–91) % at higher concentration zone. In brief, Ca2+ caused an increase in protein binding of Amlodipine Modulators besylate leading to the formation of stable 1:1 Amlodipine besylate–Ca 2+ complex. This means that the increase in percentage of protein binding may be due to capture of binding sites in the protein by Ca2+ or Amlodipine besylate

& Amlodipine besylate–Ca2+ complex. Thus possibility of adverse effect of Amlodipine besylate may become prominent in presence of Ca or similar drugs in the body system. The subsequent non-linear shape of the Scatchard plots (Fig. 14 and Fig. 15) describes both high and low affinity binding sites of the drug on protein molecules. There were at least two classes (Class 1 and Class II) of binding sites in BSA for Amlodipine besylate and its (1:1) complex with Ca (II) ion (Table 2). We saw that in class I binding sites, the value of affinity constant for Amlodipine besylate alone 1.02 was lower than its 1:1 complexes with Ca (II) ion 1.04 (Table 2), that is, the presence of Ca 2+ with Amlodipine besylate at physiological temperature and pH conditions, cause an increase in values of affinity constant. In class-I, the number of binding

site decrease in presence of Ca (II) ion 2.08 than that of alone Amlodipine besylate i.e. 8.03. Since it is almost exclusively limited to albumin and the number of available binding sites is limited, the binding properties of drugs depend on IPI-145 research buy plasma albumin concentration. So, due to increase in affinity of the Amlodipine besylate to plasma

protein in class I binding site in presence of Ca (II) ion, the volume of distribution (Vd) as well as bioavailability of the drug (Amlodipine besylate) may decrease.17 and 18 So the proposed drug–metal interactions could interfere substantially with the intestinal absorption Oxygenase of Amlodipine besylate owing to the lower solubility of the chelates in intestinal tract.19 So concomitant administration of Amlodipine besylate with food products containing Calcium, nutritional supplements and multivitamins containing Ca (II) ion could impair the clinical efficacy of the drug and reduce its bioavailability. More detailed research may reveal the mechanism of increase binding of drug to the protein in presence of calcium. All authors have none to declare. “
“In nineties solid lipid nanoparticles followed by nanostructured lipid formulations were introduced as an alternative to the conventional colloidal systems like emulsions, liposomes and microparticulate dispersions.1 The important merits of nanostructured lipid based systems includes its biocompatibility, its suitability for drug targeting, fabricated drug release, easy production process and suitability for the large scale production.2 and 3 However, it has few demerits also like drug loading and drug stability during storage.

9 × 107 pfu/mL prior to inactivation). As controls for the assay, additional suckling mice were intracranially

inoculated with live V3526 or PCM. The brains from mice surviving 14 days post-inoculation were removed upon euthanasia, homogenized and frozen. A second set of suckling mice were inoculated intracranially with the brain homogenate Volasertib from the corresponding group and observed for an additional 14 days. A sandwich ELISA was developed utilizing monoclonal antibody (Mab) 1A4A-1 for the capture of antigen and horse anti-V3526 polyclonal serum for the detection of bound antigen [19]. Mab 1A4A-1 recognizes the E2c epitope on the VEEV IAB E2 glycoprotein, which has been identified as a critical virus neutralization site within the E2 envelope

protein [27], and allows for detection of VEEV IAB viruses including V3526, VEEV TrD and C84 as well as VEEV subtypes IC and ID. The Mab was coated on a 96-well plate overnight at 4 °C at 0.5 μg/well. All subsequent incubations were performed at 37 °C. Libraries plates were then blocked with phosphate buffered saline (PBS) containing 0.5% Tween-20 and 5% skim milk (PBSTM) for 2 h. Samples were diluted in PBSTM containing 1% inactivated fetal bovine serum (FBS), serially diluted 1:2 and incubated for 2 h. Plates were washed six times with PBS containing Tween-20 (PBST) using the Bio-Rad 1550 Microplate washer. Bound virus was detected using horse anti-V3526 serum (1:1000) for 2 h [12]. Following incubation, plates were washed six times with PBST. Bound equine antibody was quantitated by addition of peroxidase-labeled goat anti-horse Crizotinib in vitro antibody (KPL, Inc.), incubated for 1 h, followed by six washes with PBST and the addition of ABTS substrate

(KPL, Inc). After 30 min at room temperature, the optical density (OD) was determined at 410 nm using the SpectraMax 340PC (Molecular Devices). The per well background value was determined at 490 nm and subtracted from the 410 nm value to normalize differences in the non-optical quality of plastic of the round-bottom plates. All data were collected using SoftMaxPro 3.1 (Molecular Devices). Alhydrogel™ was purchased from Accurate Chemical and Scientific Corporation, Westbury, NY and diluted the day of use to achieve a final concentration of 0.2% v/v dose with sterile PBS. CpG ODN2395 was purchased from InvivoGen, San Diego, CA and reconstituted the day of use and diluted isothipendyl in sterile, endotoxin-free water to achieve a final concentration of 20 μg/dose. Viprovex® was purchased from ImmuneRegen, Scottsdale, AZ and reconstituted in sterile PBS the day of use to achieve a final concentration of 76 μg/dose. The concentration of CpG and Alhydrogel™ when used in combination were the same as when the adjuvants were prepared in the single adjuvant formulations. Six-week old female BALB/c mice were purchased from the National Cancer Institute, Fort Detrick, MD. Mice were group housed in polycarbonate cages with microisolator lids.

Furthermore, many of the eating disorder measures Small Molecule Compound Library available were developed over 20 years ago when the study of males in non-athlete populations, not to mention male athletes, was not a common topic to be studying. Therefore, the eating disorder measures may not accurately

account for factors contributing to male patterns of ED. Although new eating disorder measures such as the eating disorder Assessment for Men49 (EDAM) are being developed to better account ED among men, this measure has yet to be used to examine ED among male athletes. All of the preceding factors suggest the study of ED among male athletes and the further validation of the EAT, EDI, QEDD, BULIT-R, and EDE-Q for assessment of ED in this population vital. The second major finding of this review was that the use of EAT, EDI, BULIT-R, QEDD, and EDE-Q was much more frequent when assessing ED in athletes than the use of measures developed specifically for CB-839 cost administration to athletes—WPSS-MA, AQ, and AMDQ. Only three studies, one for each questionnaire, used the WPSS-MA, AQ, and AMDQ. The lack of studies using the WPSS-MA, AQ, and AMDQ is not surprising considering these three eating disorder measures are much newer in relation to the EAT, EDI, BULIT-R, QEDD, and EDE-Q (e.g., the AQ and WPSS-MA were developed/validated 8 and 2 years ago, respectively)

and, thus, have not been used with enough frequency for researchers to realize these measures are available. Additionally, the lack of use of the WPSS-MA, AQ, and AMDQ might also be a result of the fact the EAT, EDI, BULIT-R, QEDD, and EDE-Q have always been available for use in the assessment of ED in athlete samples, despite the fact these eating disorder measures

may not be valid in this population. Given the isothipendyl EAT, EDI, BULIT-R, QEDD, and EDE-Q are most frequently used within the literature to assess ED in athletes, it is important to know which eating disorder measure are best suited (i.e., have adequate validity and reliability in assessing ED in athlete populations) for administration to male and female athletes. This review found approximately half the selected studies calculated a reliability coefficient within the athlete population (n = 26) and only seven studies calculated a validity coefficient, three of which were calculated for the infrequently used WPS-MA, ATHLETE, and AMDQ questionnaires. Not only have the EAT, EDI, BULIT-R, QEDD, and EDE-Q scarcely been validated in athlete populations, these five questionnaires have been validated almost exclusively in non-athlete populations with samples of women (EAT, 27 EDI, 19 and 28 BULIT-R, 50 QEDD, 25 EDE-Q 26). Only four studies found validity evidence for the EAT, EDI, BULIT-R, QEDD, and EDE-Q in an athlete population.

0001 CaCl2, 1 glucose, 4 NaCl, 5 ATP, 0.3 GTP, at pH 7.4. Shox2-GFP cells were visually patched (Supplemental Experimental Procedures). Biocytin filled cells were after processing (Supplemental Experimental Procedures) traced postexperimentally using camera-lucida, scanned in, and retraced in CorelDraw. NMDA (5–10 μM)

and 5-HT (8 μM) were bath-applied to induce locomotor-like activity. Brainstem-evoked locomotor-like activity was elicited as previously described (Talpalar et al., 2011). The locomotor frequency (cycles per second, Hz) was calculated PF-02341066 molecular weight from 3–5 min of activity, taken at least 10 min after the initial burst of drug-induced activity, when the locomotor-like activity was stable. Locomotor-like activity was analyzed using rectified and smoothed (time constant of 0.2 s) signals of ventral root activity in either Spike2 (Cambridge Electronic Design) or a custom-made program in R package. Left-right and flexor-extensor coordination

was assessed with circular DAPT cost statistic, where the vector direction gives the preferred phase of the activity and the length of the vector (r) the precision of the phase. p values larger than 0.05 determined by Rayleigh’s test were considered nonsignificant. The degree of rhythmicity of individual Shox2-INs based firing or voltage fluctuations was also evaluated using circular statistics (Supplemental Experimental Procedures). Transsynaptic virus experiments using coinjection of attenuated rabies viruses and complementing AAV-G protein were carried out as previously described (Stepien et al., 2010 and Tripodi

et al., 2011; Supplemental Experimental Procedures). For intraspinal injections, floxed-AAV-Synaptophysin-GFP was injected intraspinally and unilaterally at P3, followed by targeted hindlimb muscle injections 4-Aminobutyrate aminotransferase (TA and GS) of f-dextran at P8, and experiments were terminated at P17 for analysis. Values are reported as mean ± SEM. The level of significance was p < 0.05 for all statistical tests. This work was supported by the Swedish Research Council (to O.K.), ERC advanced grants (to O.K. and S.A.), the Torsten and Ragnar Söderberg Foundations (to O.K.), StratNeuro (to O.K.), a NINDS grant (to T.M.J.), ProjectALS (to T.M.J.), the HHMI (to T.M.J.), a Swiss National Science Foundation grant (to S.A. and D.S.), the Novartis Research Foundation (to S.A.), Kanton Basel-Stadt (to S.A.), National Science Foundation IRFP (to K.J.D.), the Helen Hay Whitney Foundation (to L.Z.), BRFAA (to L.Z.), and a Marie Curie Reintegration Grant (to L.Z.). We are grateful to Dr. Thomas Hnasko for providing the vGluT2lox/lox mice, to Kamal Sharma for providing Chx10lnlDTA mice, and to Ann-Charlotte Westerdahl and Natalie Sleiers for technical assistance. "
“Synaptic vesicles (SVs) within individual presynaptic nerve terminals are divided into distinct pools with respect to their relative propensities for fusion (Alabi and Tsien, 2012).

How may connectivity rearrangements promote long-term learning and memory in enriched mice? We suggest that environmental enrichment may facilitate synapse turnover and de novo synaptogenesis upon learning and that those learning-related changes in connectivity may mediate long-term LY294002 retention of specific

memories. Such a scenario implies that LTP at existing synapses may be but one synaptic mechanism to mediate learning and memory, that parallel pathways triggered by experience and involving structural rearrangements of connectivity can complement or even bypass a requirement for LTP, and that these pathways are augmented upon enriched environment (Figure 8; see also Ivanco et al.,

2000 and Rampon et al., 2000). In support of the notion that connectivity rearrangements Selleckchem AZD8055 underlie enhanced learning upon enrichment, learning was already enhanced at 2 weeks of enrichment, when remodeling was increased but no obvious net increases in synapse numbers were yet detectable. Accordingly, environmental enrichment may persistently elevate signals that promote the disassembly of labile synapses and induce filopodial and spine growth, thus facilitating long-term learning and memory and bypassing a requirement to induce these signals through LTP-related mechanisms. In conclusion, we have provided evidence that circuit remodeling and de novo synaptogenesis processes in the adult have important roles in learning and memory and that β-Adducin is critically important to establish new synapses under conditions of enhanced plasticity. Future studies will aim at elucidating how experience enhances synapse

turnover and synaptogenesis, how this potentiates memory processes, and how impairment of these processes may produce memory losses in disease. Transgenic mice expressing membrane-targeted GFP in a small subset of neurons (Thy1-mGFPSi1) were as described ( De Paola et al., 2003 and Galimberti et al., 2010). β-Adducin−/− mice (B6.129-β-Adducintm1Feb/Ibcm; Gilligan et al., 1999) were Suplatast tosilate generously provided by Luanne Peters (Jackson Labs). Rab3a−/− mice (B6;129S-Rab3atm1Sud/J) were obtained from the Jackson Laboratory. Both β-Adducin−/− and Rab3a−/− mice were backcrossed into Thy1-mGFPSi1 mice. Enriched environment (EE) procedures were as described (Gogolla et al., 2009). Organotypic slice cultures were based on the Stoppini method (Stoppini et al., 1991), as described (De Paola et al., 2003). All procedures were approved by the Cantonal Veterinary Office of Basel, Switzerland. Lentiviral constructs were a generous gift from Pavel Osten (Cold Spring Harbor Laboratories; Dittgen et al., 2004); cytosolic GFP was replaced in the expression cassette by the mGFP or the GFP-β-Adducin sequence.