1% [95% CI: 66.0–87.5] than in Vietnamese infants Selleck RAD001 (97.0% [95% CI: 89.6–99.6]) (Table 1) and was accompanied by substantially lower PD3 GMT levels among Bangladeshi infants (29.1 units/mL) compared to that among Vietnamese infants (158.5 units/mL) (Table 1). In the placebo group, 24 out of 132 infants (18%) showed a ≥3-fold rise in anti-rotavirus IgA titer between pD1 and PD3, with a PD3 GMT level of 2.9 units/mL, indicating natural rotavirus infection among some infants during the first 6 months of life. Among those

infants in Bangladesh and Vietnam who received placebo, the proportion with a ≥3-fold rise in anti-rotavirus IgA titer between pD1 and PD3, or the PD3 GMT level, was comparable between countries. The SNA responses were shown to vary by the individual serotypes contained in PRV as shown in previous clinical trials of PRV [12], [13], [18], [21], [22], [23] and [24]. In the per-protocol analysis, the SNA sero-responses were highest to serotype G1, followed by G3, P1A[8], G4, and G2 in the combined population of two Asian infant subjects (Table 2). The sero-response in SNA titers ranged from 11.9% (G2) to 41.8% (G1) in Vietnam, approximately 1.5- to 2.5-fold higher than those measured in Bangladesh (Fig. 1). The higher SNA responses among infants in Vietnam compared to Bangladesh BTK inhibitor were also noted in the comparison of PD3 SNA GMT

levels (Fig. 2). The baseline (pD1) GMT levels of the SNA to each of the individual rotavirus serotypes contained in PRV were considerably higher than those obtained in clinical trials conducted in developed countries [12], [13], [18], [21], [22], [23] and [24], ranging from 24.2 units/mL (G3) to 79.1 units/mL (P1A[8]) in Bangladesh and from 18.4 units/mL (G3) to 51.5 units/mL (P1A[8]) in Vietnam (Fig. 3). In both countries, the pD1 SNA GMT levels were highest to serotypes P1A[8] and G1, followed by serotypes G4, G2, and G3 (Fig. 3). In both the PRV and placebo groups, the pD1 SNA GMTs were higher in Bangladesh than in Vietnam against all five human rotavirus serotypes,

possibly indicating higher levels of maternal antibodies present in Bangladeshi infants than those in Vietnam (Fig. 3 and Fig. 4). By PD3 (measured approximately at 14–26 weeks of age), the SNA GMT titers declined substantially; the PD3 SNA GMTs to all 5 human serotypes of were 2- to 4-fold lower than those GMTs at pD1 (approximately 4–12 weeks of age) among the placebo subjects, and were comparable between the two countries (Fig. 4). Although the trial was designed to administer PRV concomitantly with routine EPI vaccines, including OPV and DTwP, not all subjects received each dose of PRV/placebo and OPV on the same day (Fig. 5). However, 91–92% of the Bangladeshi and Vietnamese subjects, respectively, in the immunogenicity cohort received each of the 3 doses of OPV on the same day as each of the 3 doses of PRV/placebo.

Surprisingly, the occurrence of prefrontal activity did not linearly decrease with the size of hippocampal lesion, but as soon as the NMDA-induced cavity reached a certain volume (∼0.5 mm3) over the Hipp, the occurrence

of SB and NG stabilized at a decreased level. The main caveat of excitotoxic lesions, especially when performed in small-size neonatal animals, is their relative poor selectivity. To decide whether the diminishment of prelimbic NG is due, at least in part, to side-effect lesion of the EC or other neighboring areas, we used a second approach to impair the hippocampal drive. Discharge of the medial septum (MS) that has been reported to be one of the generators of CA1 theta rhythms in adult (Mizumori et al., 1989) was reversibly blocked by microinjections of lidocaine. Low volume (10–20 nl) of lidocaine was slowly applied in 4 P6–8 rats (Figure 8E). learn more As consequence the occurrence of neonatal hippocampal theta bursts significantly (p < 0.05) and

reversibly Entinostat supplier decreased from 2.5 ± 0.5 to 1.5 ± 0.2 bursts/min, indicating that the MS represents one generator also of neonatal theta bursts. Neither SPWs nor fast hippocampal rhythms were affected by lidocaine. The prefrontal patterns of activity were recorded simultaneously with the hippocampal activity before and after lidocaine treatment. Whereas SB were not influenced by lidocaine-induced diminishment of hippocampal theta activity, the occurrence of prelimbic NG decreased (p < 0.05) from 0.36 ± 0.11 to 0.16 ± 0.09 bursts/min (Figure 8F). The amplitude, duration and main

frequency of prefrontal oscillations did not change after lidocaine injection. Despite small injected volume and controlled application, lidocaine may spread from the injection site and nonselectively affect neighboring areas. To selectively impair the septal drive to the Hipp, we used a Oxalosuccinic acid third experimental approach. As previously shown, septal GABAergic neurons contribute to the generation of adult hippocampal theta rhythm (Yoder and Pang, 2005). To identify their role for the immature theta bursts we selectively lesioned the septal GABAergic neurons by using the GABAergic neurotoxin GABA-transporter-saporin (GAT1-SAP) that combines a rabbit polyclonal antibody to the GABA-transporter-1 with the ribosomal toxin saporin. Newborn rats (n = 8) received intraseptally a small volume (20–40 nl) of GAT-1 (325 ng/μl, 20 nl/min) or of vehicle (artificial cerebrospinal fluid, ACSF) according to a previously described protocol (Pang et al., 2010). Seven days later, the density of septal parvalbumin (PV)-positive neurons decreased from 123 ± 52.4 cells/mm2 in ACSF-treated pups to 54.8 ± 8.6 cells/mm2 in GAT1-SAP-treated pups (Figure 8G).

17 Ahmad et al reported that synthesis of triheterocyclic 4H-pyrimido[2,1-b]benzothiazole ring systems by using one pot three component

mTOR inhibitor reaction. 18 Compounds were prepared as shown in Scheme 1. Substituted pyrimido[2,1-b][1,3]benzothiazole-3-carboxylate was prepared by condensation of substituted benzaldehyde, ethyl cynoacetate and substituted benzothiazole in microwave by MCR (multi-component reaction). Substituted benzothiazole were prepared by reported procedure. Melting points were determined in open capillaries. Reactions were monitored by thin layer chromatography using silica gel-G as adsorbent using benzene as mobile phase. IR spectra (KBr pellet) were recorded on Bruker α FT-IR spectrometer, at Amrutvahini College of Pharmacy, Sangamner. 1H NMR spectra (DMSO-d6) were taken on NMR Bruker (Swiss) Avance II 400 MHz spectrometer from Punjab University,

Chandigarh. Equimolar mixture of ethyl cynoacetate, (0.01 mol) substituted benzaldehyde (0.01 mol); substituted 2-amino benzothiazole (0.01 mol) and 25 ml ethanol in RBF were Selleckchem XAV939 irradiated independently inside microwave oven at 640 W for 5 min (TLC control). The crystalline product was started to separate out just after cooling the reaction mixture at room temperature. The crystalline solid that separated out was filtered and found to be pure by TLC. Recrystallization was done with ethanol. Physicochemical properties of all synthesized compounds depicted in Table 1. FT-IR (KBr): 3425(N–H str), 3036(C–H str), 1723(C O str), 1610(C N str), 1534(C C str),1266(C–S

str), 727(C–Cl str).1H NMR (DMSO-d6) δ ppm:, 1.34–1.38(t,3H,CH3), δ3.35(s,2H,NH2), δ4.29–4.35(q,2H,CH2), δ6.12(s,1H,CH), δ7.71–7.93(m,3H,Ar H), δ7.48(m,4H,Ar H)., EI–MS: (m/z:, %RA): 419(M+ 92%),418(M+2 56%); % Anal.: calculated: Ketanserin C 54.29,H 3.60%,N 10.00%,O 7.61% Found: C 54.32%,H 3.46%,N 9.06%,O 7.52%. FT-IR (KBr): 3418(N–H str), 3030(C–H str), 1719(C O str), 1606(C N str), 1540(C C str), 1528(–NO2str), 1267(C–S str). 1H NMR (DMSO-d6) δ ppm:, δ 1.33–1.37(t,3H,CH3), δ 4.12(s,2H,NH2), δ4.32(q,2H,CH2), δ 6.16(s,1H,CH), δ 7.61–7.73(m,4H,Ar H), δ 7.94(m,3H,Ar H)., EI–MS: (m/z:RA): 429(M+ 87%),427(M+2 48%); % Anal.: calculated for C 52.96%,H 3.51%,N 13.00%,O 14.85%,Found: C 52.78%,H 3.72%, N 13.06%,O 14.56%. FT–IR (KBr): 3455(N–H str), 3324(–OH str), 3021(C–H str), 1714(C O str), 1645(C N str), 1540(C C str),1270(C–S str). 1H NMR (DMSO-d6) δ ppm:, δ 1.31–1.36 δ(t,3H,CH3), δ 3.35(s,2H,NH2), δ 4.27–4.32(q,2H,CH2), δ 6.21(s,1H,CH), δ 5.1(s,1H,OH), δ 7.70–7.85(m,3H,Ar H), δ 7.90(m,4H,Ar H).

It also

provides interfaces for data retrieval, analysis and visualization. SMD has its source code fully and freely available to others under an Open Source Licence, enabling other groups to create a local installation of SMD (www.ncbi.nih.gov/pubmed). The DEG holds information on essential genes from a number of organisms.16 and 17 The current release 6.3 contains information on 11,392 essential genes from various organisms both prokaryotes and eukaryotes. A typical entry includes a database specific accession number, the common gene name. GI reference, function, organism, reference and nucleotide sequence (www.essentialgene.org). FRAX597 concentration With the explosion of microarray data there is an emerging need to develop tools that PARP inhibitor can statistically analyze the gene expression data. There are many tools available on net for the same. Cluster is a tool for data clustering of genes on the basis of gene expression data. It is available at Eisen Lab and can run on Windows. It uses many clustering algorithms which include

K-means, hierarchical, self-organizing map. The genes were clustered assuming the fact that genes that co-express along with the known virulent genes may also be responsible for the virulence.15 Basic Local Alignment Search Tool, or BLAST, was used for primary biological sequence information comparison. BLAST2 was used for the identification of paralogs for virulent genes. BLASTP was used for protein sequence comparison available on the home page of DEG and also was done for human genome and microbial genome BLAST (www.blastncbi.nlm.nih.gov.in). In the study well-reported virulent genes for S. pneumoniae were taken from VFDB. Next the gene expression data was downloaded with a time gap of 8–12 h. Data was normalized for further study. already To predict probable virulent genes normalized gene expression data was

analyzed by the help of cluster software using K-mean clustering algorithm and found 450 clusters. In K-means clustering, the numbers of clusters are designated (450), and then each gene is assigned to one of the K clusters by this algorithm before calculating distances. When a gene is found to be closer to the centroid of another cluster, it is reassigned. This is a very fast algorithm, but the number of clusters reported will be the K that was predetermined and it will not link them together as in the hierarchical clustering. Output of the clustering comes as a file containing different gene id(s) in 450 clusters. The genes that are co-expressed along with the virulent genes previously known are then isolated from the output file and their corresponding sequences of their product were downloaded from the NCBI. To predict more virulent genes search for paralogous genes was also done. This was done by using BLAST2 from NCBI. Essential genes are those indispensable for the survival or organism, and therefore their products are considered as a foundation of life.

Safety was analyzed on the total vaccinated cohort which included all infants

who had received at least one dose of the HRV vaccine/placebo. The sample size of 200 infants (100 twin pairs) was planned to provide at least 87% power to observe one case of transmission, for a true transmission rate of ≥2%. The percentage of twins receiving placebo with the presence of vaccine strain in at least one stool sample by ELISA was calculated with exact 95% CI [14]. The occurrence of genetic variation in the HRV vaccine strain in the vaccine and placebo recipients was described. As the stool samples were collected three times a week (every two days), the duration of antigen Akt inhibitor drugs shedding in days was derived as twice the number of rotavirus positive stools and was summarized by group. Live viral load in the twins receiving placebo in the case of transmission was also summarized.

Anti-rotavirus IgA seroconversion rate (anti-rotavirus antibody concentration ≥ 20 U/ml in infants initially negative for rotavirus) and geometric mean concentrations (GMCs) were calculated with their 95% CI [14]. The 95% CI for the mean of log-transformed concentration was first obtained assuming that log-transformed values were normally distributed with unknown variance. The 95% CI for the GMCs were then Ku-0059436 obtained by exponential-transformation TCL of the 95% CI for the mean of log-transformed titer/concentration. Gastroenteritis episodes including severe rotavirus gastroenteritis and serious adverse events were tabulated all through the study period. This study was sponsored and funded by GSK Biologicals. The sponsor was involved in all stages of the study, i.e. from study

design to data analysis and writing of the report, and also performed rotavirus ELISA testing. The corresponding author had full access to all the data in the study and had final responsibility for the decision to submit for publication. One hundred pairs of twins were enrolled to receive at least one dose of HRV vaccine/placebo. Fig. 1 describes the reasons for withdrawal and elimination of infants from the study at each stage. Mean age of the twins at the time of Dose 1 of HRV vaccine/placebo (total vaccinated cohort) was 8.2 weeks (standard deviation: 1.80 weeks). The distribution of male (47.5%) and female (52.5%) infants was similar in the study groups and all infants belonged to the American Hispanic or Latino ethnicity. Of the 80 evaluable placebo-recipient twins, 15 cases of transmission were identified. The percentage of placebo-recipient twins with HRV vaccine strain isolated in at least one stool sample collected at pre-defined time points was 18.8% (95% CI: 10.9–29.0%).

Electrical stimulation appears to be effective regardless

of the initial level of strength or the time after stroke and the benefits are maintained beyond the intervention period. Clinicians should therefore be confident in prescribing daily electrical stimulation for people after a stroke, when the primary objective of the intervention is to increase muscle strength. In particular, it may be a useful intervention in the presence of cognitive impairments or profound weakness Bcl-2 inhibitor when it is difficult for the person to carry out strengthening exercises independently. In addition, the results of this systematic review are valuable since they show that electrical stimulation can have a beneficial effect not only on strength but also on activity, with improvements maintained beyond the

intervention selleck inhibitor period. Further studies are necessary to investigate whether electrical stimulation is more effective than other strengthening interventions. What is already known on this topic: After a stroke, many people are unable to generate normal amounts of force, which restricts participation in daily activities. Cyclical electrical stimulation can be used to strengthen muscles, even when the patient cannot voluntarily generate adequate force for resistance exercise. What this study adds: Cyclical electrical stimulation increases strength and activity in people who have had a stroke. These effects are maintained beyond the intervention period, suggesting that the increased strength is utilised in daily life and is therefore maintained by ongoing increased activity. eAddenda: Figures 3a, 3b, 5a, 5b and Appendix 1 and 2 can be found online at doi:10.1016/j.jphys.2013.12.002 Competing interests: Nil. Acknowledgements: Brazilian Government Funding Agencies (CAPES, CNPq, and

FAPEMIG) for the financial support. Correspondence: Louise Ada, Discipline of Physiotherapy, Faculty of Health Sciences, The University of Sydney, Australia. Email: [email protected] “
“Kinesio Taping has become a very popular treatment for several much health conditions over the last decade. This method of taping was created by a Japanese chiropractor in the 1970s.1 Kinesio Taping uses elastic tape that is fixed onto the skin. Kinesio Tape is thinner and more elastic than conventional tape, which is hypothesised to allow greater mobility and skin traction.2 and 3 Kinesio Taping involves a combination of applying tension along the tape and placing the target muscle in a stretched position, so that convolutions in the tape occur after the application.1 During assessment, the therapist decides what level of tension will generate an appropriate level of traction on the skin. According to the Kinesio Taping Method manual, this traction promotes an elevation of the epidermis and reduces the pressure on the mechanoreceptors that are situated below the dermis, thus reducing the nociceptive stimuli.

Comparisons between the two groups in terms of the ELISA and SBA results were performed by Student’s t-test or the Mann–Whitney this website test. Mean

pre- and post-vaccination titers (ELISA and SBA) were compared by paired Student’s t-test or the Wilcoxon test. Intragroup differences between pre- and post-vaccination values were considered statistically significant at a level of 5%. In addition, a difference between two groups of similar size and similar variance whose 95% CIs do not overlap was considered significant at a level of approximately 5%, thus enabling significant differences between groups to be assessed by non-overlapping CIs. Chi-square tests (χ2) or Fisher’s exact tests were used to compare the groups in terms of the proportions GW786034 of patients with SBA titers ≥8, patients

showing a 4-fold rise in SBA titers, patients who responded to the vaccine, and patients who experienced side effects. The remaining variables of the study, including sociodemographic and clinical variables, were analyzed by descriptive statistics – mean (standard deviation) or median (minimum and maximum) – when quantitative and by proportions when qualitative. A level of significance of 5% was considered for all statistical tests. The statistical software used in all analysis was the Statistical Package for the Social Sciences, version 14.0 (SPSS Inc., Chicago, IL, USA). We included a total of 92 individuals in the study (mean age = 13.9 years, range 10–19 years), from May to December 2009: 43 in the HIV+ group (mean age = 13.8 years; range 10–19 years); and 49 in the HIV− group (mean age = 13.9 years; range 10–19 years). In the sample as a whole and in each

of the two groups, 52.7% of the patients were female and 47.3% were male. All of the patients in the HIV+ group were under treatment with highly active antiretroviral therapy (HAART). There were no losses in either of the study groups. As shown in Table 1, the mean level of post-vaccination Parvulin response was higher in the HIV− group than in the HIV+ group, whether evaluated by ELISA (p = 0.001) or by SBA (p < 0.001). The differences between groups are evidenced by the non-overlapping 95% CIs. Before vaccination, the percentage of patients with SBA titers ≥8 was higher in the HIV− group than in the HIV+ group (34.7% vs. 16.3%). There were significant differences between the two groups in terms of these titers (Table 1). In the HIV+ group, 35 (81.4%) of the patients had a post-vaccination SBA titer ≥8, compared with 100% of those in the HIV− group. A 4-fold increase in the SBA titer after vaccination was observed in 31 (72.1%) of the HIV+ group patients, again compared with 100% of those in the HIV− group (Table 1). We defined a positive antibody response to the vaccine as the combination of the established protective criteria (a post-vaccination SBA titer ≥8 and a 4-fold increase over the initial titer). Of the 43 HIV+ group patients, 31 (72.

Elle est très prurigineuse et retentit fortement sur la qualité de vie. Elle constitue un problème de santé publique [1]. Elle est contagieuse par contact cutané.

Il existe une forme particulière ou gale norvégienne survenant chez des personnes à l’état général altéré, de contagiosité extrême, responsable d’épidémies particulièrement dans les maisons de retraite. La gale est toujours restée présente dans l’histoire, avec des augmentations périodiques du nombre de cas, elle est actuellement en augmentation progressive en France. Depuis quelques années, il semble en effet que les cas se multiplient, en particulier chez des adultes mais aussi chez des jeunes enfants, y compris des nourrissons. On doit bien sûr se poser des questions concernant les raisons de cette see more recrudescence. Il faut noter cependant qu’il ne s’agit pas d’une maladie à déclaration obligatoire, UMI-77 in vitro aussi le nombre réel des cas en France est imprécis. Des estimations fondées sur les ventes de médicaments scabicides (benzoate de benzyle et ivermectine) indiquaient une moyenne

annuelle d’au moins 328 traitements pour 100 000 personnes entre 2005 et 2009. Cela constitue un coût non négligeable restant à la charge des patients puisque seule l’ivermectine est remboursée (partiellement) [2]. Nous sommes frappés du grand nombre de jeunes enfants atteints de formes profuses de gale. Les nourrissons ont des lésions particulières qui ne sont pas toujours bien identifiées (vésicules des mains et des pieds, nodules axillaires, eczéma profus y compris du visage) si bien que le diagnostic n’est pas toujours fait et même souvent un traitement intempestif par dermocorticoïdes est institué. La première raison de cette recrudescence de la gale peut être la difficulté du diagnostic. Il existe de nombreuses causes de prurit. L’eczématisation, l’impétiginisation modifient la séméiologie des lésions cutanées. La gale norvégienne, la gale du nourrisson ont une présentation différente de la gale habituelle.

Il n’existe pas de confirmation biologique. Il s’agit d’un diagnostic essentiellement clinique, il peut cependant être aidé par l’examen dermatoscopique qui permet de Idoxuridine visualiser le parasite, mais cette technique reste utilisée essentiellement par les dermatologues. Une autre raison est la difficulté du traitement. Il faut traiter en même temps toutes les personnes vivant au même domicile, désinfecter les vêtements, la literie… Des mauvaises conditions économiques, la promiscuité rendent difficile un traitement efficace. En conséquence, des recontaminations sont fréquentes. Le nombre de personnes ayant un immuno-déficit spontané ou thérapeutique, ou grabataires a augmenté avec la prolongation de la vie de ces personnes.

Limitations were applied as described above to match

the reported CLint,P-gp(efflux) values ( Troutman and Thakker, 2003). A Simcyp “compound file” was created based on the reported physicochemical characteristics, protein Epigenetics Compound Library cell assay binding and blood-to-plasma ratio for the compound buspirone (Gammans et al., 1986, Gertz et al., 2011 and Shibata et al., 2002). The “compound file” was then modified and used as a template to generate a set of virtual compounds from the combinations of the aforementioned parameters. The ionic class of the virtual compounds was set to be neutral in order to simplify the analysis and to reduce the number of combinations that could be derived from accounting for the different ionic classes. The drug’s C59 dissolution rate was estimated using the diffusion layer model built-into the Simcyp® ADAM model, where the drug was assumed to be a monodispersed powder with an initial particle radius of 30 μm. Peff values were estimated from the calculated Papp,Caco-2 values using the default method in the Simcyp® simulator for passively absorbed drugs ( Sun et al., 2002), Peff was kept constant throughout all the intestinal segments. Elimination was assumed to occur only by means of CYP3A4-mediated metabolism, both in the liver and the GI tract, which was estimated from the aforementioned enzyme kinetics parameters of CYP3A4. The fraction of drug unbound

in the enterocytes (fu,gut) was assumed to be

1 as per Yang et al. (2007). The rest of the parameters were kept as Simcyp® default values. The input parameters are summarized in Table S1 of the Supplementary Material. The virtual trials were simulated assuming a representative population. The values employed were those from the “healthy volunteers” population library within Liothyronine Sodium Simcyp®, assuming no variability for the system parameters. A “minimal” PBPK model was used to describe the disposition and systemic elimination of the simulated compounds (Rowland Yeo et al., 2010). The oral dose was set to 30 mg, administered under fasted conditions together with 250 mL of water; with sampling up to 36 h post dose (Sakr and Andheria, 2001a and Sakr and Andheria, 2001b). Simulations were carried out using the Simcyp® Batch processor on a Dell OptiPlex 7010 PC (Intel Core i7-3770, 16 GB Ram) running Microsoft Windows 7 Enterprise (Dell Corp. Ltd., Berkshire, UK). In order to analyse the simulated data the study tree was sub-categorized into the four classes described in the BCS, thus leading to a reduction in the number of combinations analysed (from 78,125 to 12,500) by limiting the values for solubility and permeability from five to two values each. Selection of the solubility and permeability values was based on the BCS cut-off criteria for high/low soluble and permeable compounds.

6 The compound (3) (0.21 g, 1 mmol, 1.00 equiv) was taken in a round-bottomed flask containing mixture (1:1) of demineralized water, and 4-bromophenol (4d) (0.15 g, Selleckchem PS 341 1 mmol) was added. 145° (hexane/MeOH). FTIR (KBr): 1724, 1599, 1520, 1344, 1H NMR (500 MHz, DMSO), 3.45 (DMSO solvent); 2.55 (s, 3H); 3.11 (s, J = 5, 1H); 5.3 (s, J = 10, 1H), 6.64–8.17 (m, 7H), 7.32 (dd, J = 15, 1H), 7.34 (dd, J = 15, 2H). 13C NMR (500 MHz, DMSO) 22, 32, 80.8, 103, 120, 120.1, 121.9, 125, Torin 1 in vitro 126, 127, 129, 133, 134, 145, 170.9, 191 δ ppm; ESIMS m/z 359 (M + ) Anal. Calc. for C22H17NO4 (359.37): C, 73.53; H, 4.77; N, 3.90 Found: C, 73.51; H, 4.75; N, 3.88. 1-(4-acetylphenyl)-3-(2-Napthyloxy)-pyrrolidine-2,5-dione

5b. Brown solid. Yield 86%; M.p. 147° (hexane/MeOH). FTIR (KBr): 1724, 1599, 1520, 1344, 1H NMR (500 MHz, DMSO), 3.45 (DMSO solvent); 2.55 (s, 3H); 3.11 (s, J = 5, 1H); 5.3 (s, J = 10, 1H), 6.52–8.20 (m, those 7H), 7.32 (dd, J = 15, 1H), 7.34 (dd, J = 15, 2H). 13C NMR (500 MHz, DMSO) 22.8, 31.1, 80.8, 103.6, 120, 120.3, 121.9, 125, 126, 127, 128.8,

133, 134, 145, 171, 187 δ ppm; ESIMS m/z 360 (M + H) Anal. Calc. for C22H17NO4 (359.37): C, 73.53; H, 4.77; N, 3.90 Found: C, 73.52; H, 4.78; N, 3.91. 1-(4-acetylphenyl)-3-(4-Chlorophenyloxy)-pyrrolidine-2,5-dione 5c. Yellow solid. Yield 88%; M.p. 164° (hexane/MeOH). FTIR (KBr): 1724, 1599, 1520, 1344, 1H NMR (500 MHz, DMSO), 3.45 (DMSO solvent); 2.04 (s, 3H); 2.5 (s, J = 5, 1H); 5.3 (s, J = 10, 1H), 6.52 (dd, J = 10, 1H), 6.55 (dd, J = 10, 1H), 7.32 (dd, J = 10, 1H), 7.34 (dd, J = 10, 2H). 13C NMR (500 MHz, DMSO) 22, 71, 82, 114.8, 118, 120, 128, 132.4, 133, 144, 160, 161, 189 δ ppm; ESIMS m/z 300 (M) – 1; 221, (M) – 2; 144 (M) – 3; 128 (M − 4) Anal. Calc. for C18H14ClNO4 (343.76): C, 62.89; H, 4.10; N, 4.07 Found: C, 62.86; H, 4.1; N, 4.01. 1-(4-acetylphenyl)-3-(4-Bromophenyloxy)-pyrrolidine-2,5-dione 5d. Brown solid. Yield 91%; M.p. 166° (hexane/MeOH). FTIR (KBr): 1724, 1599, 1344, 1H NMR (500 MHz, DMSO), 3.45 (DMSO solvent); 2.04 (s, 3H); 2.5 (s, J = 5, 1H); 5.3 (s, J = 10, 1H), 6.52 (dd, J = 10, 1H), 6.55 (dd, J = 10, 1H), 7.32 (dd, J = 10, 1H), 7.34 (dd, J = 10, 2H). 13C NMR (500 MHz, DMSO) 22.8, 72.2, 83.2, 115.4, 116.3, 120.3, 128, 132.4, 133, 145, 159, 161,195 δ ppm; ESIMS m/z 348 (M) – 1; 270, (M) – 2; 187 (M) – 3; 172 (M − 4) Anal. Calc. for C18H14BrNO4 (388.21): C, 55.69; H, 3.63; N, 3.61 Found: C, 55.63; H, 3.62; N, 3.63.