DOCSLIB.ORG

Supporting Information

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Supporting Information Supporting Information Lee et al. 10.1073/pnas.1309293111 SI Materials and Methods performing independent random permutation of the signature Genome Sequence and Annotation. We obtained mouse genome values for each gene. The FDR corresponding to a given P value sequence via the BSgenome.Mmusculus.UCSC.mm9 package in threshold was computed as the ratio of the number of GO cate- BioConductor (1). We downloaded the corresponding genome gories with a P value below threshold, averaged over 50 ran- annotation coordinates directly from www.genome.ucsc.edu (ver- domized data sets, and the number of GO categories with a P value below threshold. A 1% FDR based on the empirical sion mm9). − permutation test corresponds to a WMW test P < 10 4. Information Content of Locus Expression Signatures. To assess how much information about downstream transcriptional regulation Low-Complexity Sequence Features (Fig. S4). To eliminate the po- was contained in a given signature, without the need to specify tential confounding contribution from low-complexity sequence a particular regulatory mechanism, we summed the squares of the features to LESs, we calculated the frequency of each base and the CpG dinucleotide across the transcribed region for each gene. t-values tgm corresponding to the regression coefficients βgm: X Next, we computed the residuals from a multiple linear regression χ2 = 2 : of each LES on these five frequencies (without an intercept). m tgm g We calculated DNA base composition and CpG content for 1-kb windows up to 200 kb upstream or downstream. The base up 2 To determine the statistical significance of the χ statistic, we composition indicator variable Ngbi for base b, gene g, and dis- constructed a null distribution as follows. We performed 100 tance i from TSS was defined as follows: independent permutations by randomizing expression level of 1if base at locus i is b gene across genes for each tumor. We did not permute insertion Nup = : loci because we want to preserve the correlation structure be- gbi 0 otherwise tween insertion loci. For the randomized data sets, we performed down multiple linear regression to calculate the t-value and corre- The base composition Ngbi for the downstream sequence sponding χ2 statistic for each locus with the same method as is calculated with the same procedure using the downstream χ2 up down the actual data set. The mean statistic averaged over 100 sequence. The CpG content Ng;CpG;i, Ng;CpG;i for upstream and randomized data sets for each locus is shown in Fig. S1C as downstream sequences was calculated using the same procedure. purple bar. To calculate the base composition of upstream sequence for To investigate the fraction of the variance in expression levels window;up each window Ngbw , we divided the 200-kb sequence up- of each tumor that is accounted for by our locus expression stream into 1-kb window intervals. For each such window, we signatures, we performed multiple linear regression of the mRNA calculated the upstream base composition as follows: expression levels for each held-out tumor on the locus expression X signature (LES) matrix constructed using all other tumors and window;up = up : 2 Ngbw Ngbi calculated coefficients of determination (R ). We used either (i) i∈w the 13 insertion loci that occur in at least 10 tumors or (ii) the 87 insertion loci that occur in at least 3 tumors. For comparison, we Here, w represents the wth window of the upstream sequence for also performed multiple linear regression using only the 25% most gene g. We also calculated the downstream base composition variable genes. To construct a null distribution, we used 100 in- window;down window;up window;down Ngbw and CpG content Ng;CpG;w and Ng;CpG;w using dependent random permutations of all genes for each tumor. the same procedure. We measured coefficients of determination (R2) by regressing the LESs on all low sequence complexity for Permutation to Calculate False Discovery Rate. To calculate false window w (without an intercept). We used the residuals of this discovery rates (FDR) in each analysis, we performed permu- model fit in further transcription factor (TF)-locus association tations of locus expression signatures across genes for each locus. analyses. Then, we applied the same procedure as used in each analysis to calculate statistics such as t-value or P value for the randomized TF Binding Affinity Profiles. We used the convert2psam utility from data sets. The FDR corresponding to a given P value threshold REDUCE Suite version 2.0 software package (www.bussemakerlab. was computed as the ratio of the number of associations with the org) to convert each of position weight matrix (PWM) from P value below threshold averaged over 1,000 randomized data JASPAR to a position-specific affinity matrix or position-specific sets and the number of associations with the P value below affinity matrix (PSAM) (2); pseudocounts equal to 1 were added to threshold for the real data set. For the t-value, we computed the the PWM at each position, and the resulting base counts were number of associations whose absolute t-value is bigger than a divided by that of the most frequent base at each position to get an given t-value threshold instead. estimate for the relative affinity associated with each point muta- tion away from the optimal binding sequence. The resulting PSAM Forward Selection of Gene Ontology Categories. For each gene collection was used to compute a weighted promoter affinity ontology (GO) category, we applied the Wilcoxon–Mann–Whitney for each gene. All putative individual binding sites in the ge- (WMW) test to detect differences in distribution between the nomic region from 200 kb upstream to 200 kb downstream of locus expression signature value of genes within the GO category the TSS of each gene with a predicted relative affinity of at least and that of the other genes. At each step, we subtracted the mean 0.1 were identified and scored using the AffinityProfile utility in signature value of the genes in the gene set with the lowest P value the REDUCE Suite. from all genes in that gene set. The P values were then recalcu- lated, and the procedure was repeated until even the most sig- Inferring Length Scale Parameters. For each choice of the regula- − nificantly regulated gene group had P > 10 5, which corresponds tory scale parameter λ in the range from 1,000 to 100,000 base to an FDR < 0.1%. Statistical significance was determined by pairs, we obtained a total weighted upstream affinity by summing Lee et al. www.pnas.org/cgi/content/short/1309293111 1of12 the affinity of all upstream or downstream binding sites using probes mapping to the same mouse RefSeq ID, resulting in 9,757 a weight exp(−d/λ), where d is the (absolute) distance of a given genes shared between both data sets. binding site from the transcription start site (TSS). Then, we To obtain robust results, we filtered out noninformative genes λup computed TF-specific and locus-specific parameters φm that using two criteria. First, only mouse genes showing a high variance maximized the correlation coefficients between a total weighted across tumors (upper 50th percentile) were retained. Second, we upstream affinity and each LES, resulting in an optimized total deleted human genes whose expression was detected in neither weighted affinity. An analogous procedure was performed for treatment nor control. Next, we calculated averages of gene the downstream sequence. The sum of upstream and down- expression levels across profiles for the same drug in different cell stream total weighted affinities was used for mapping the locus- types, resulting in 1,309 drug signatures. Genome-wide linear TF network and drug-TF-locus network. regression of each of these on the locus expression signatures was performed. To determine the statistical significance of each pu- Myc Validation of Result. We downloaded gene expression profiles tative drug-locus association, we performed 100 random permu- obtained by ref. 3 for transgenic mice that conditionally express tations of drug signatures and repeated the analysis. A 1% FDR the human MYC cDNA in T-cell lymphocytes (GEO accession corresponded to a regression coefficients whose t-value has an number GSE10200). In this transgenic mouse, doxycycline treat- absolute value >7. ment suppresses MYC expression. We used the two most extreme Statistical significance for TF-drug associations was also de- doxycycline concentrations of 0 and 20 ng/mL. To obtain an es- termined by performing 100 independent random permutations of timate for the differential expression level in response to inac- drug response profiles, resulting in a 5% FDR for family-level and tivation of Myc, we subtracted the treatment/reference log2-ratio − − individual PSAMs at P < 3.0 × 10 3 < × 5 at 0 ng/mL from that at 20 ng/mL. These values served as the de- and 6.3 10 , respectively. pendent variable in the regression on TF affinity profiles. We adopted the same statistical significance criterion for the drug- locus association and TF-locus associations as in previous analyses. Mapping Drug-Locus Associations. Genome-wide mRNA expres- Human Mutation Expression Signatures. The acute myeloid leuke- sion data for cultured human cells treated with bioactive small “ ” molecules were downloaded from the Connectivity Map website mia data set was downloaded from The Cancer Genome Atlas (www.broadinstitute.org/cmap/). This collection contains 7,056 data portal (https://tcga-data.nci.nih.gov/tcga/tcgaHome2.jsp). We expression profiles for 1,309 distinct compounds. The experi- downloaded level 3 gene expression levels (Affymetrix HG-U133 ments were carried out on two different Affymetrix GeneChip platform) and level 2 somatic mutation data for 197 acute myeloid designs (HG-U133A and HT-HG_U133A) and in four different leukemia tumor samples and found that both data types were cell lines (the breast cancer epithelial cell line MCF7, the pros- available for 194 tumor samples.
Load more

Recommended publications
  • Anaphylactic Microshock of the Guinea-Pig by H
    Brit. J. Pharmacol. (1963), 21, 414-418. THE EFFECT OF SOME NEW ANTIHISTAMINES ON THE ANAPHYLACTIC MICROSHOCK OF THE GUINEA-PIG BY H. HERXHEIMER AND E. STRESEMANN From the Asthmapoliklinik, Free University, West Berlin, Germany (Received May 14, 1963) The dose/response curves for the protective effects of the new antihistamine compounds trimeprazine, 10-(3-diethylamino-2-methylpropyl)phenothiazine 1,1-dioxide hydrochloride (oxomemazine hydrochloride), cyproheptadine, homochlorcyclizine and methotrimeprazine against the anaphylactic microshock of the guinea-pig were similar to that of promethazine. The first three compounds, however, protected at lower doses than promethazine (5 to 10 ug/kg). The protective effect of cyproheptadine lasted longer than 24 hr. The antianaphylactic effects of promethazine, mepyramine, chlorcyclizine, tri- pelennamine and diphenhydramine have been investigated by Armitage, Herxheimer & Rosa (1952). In this paper we describe investigations of a few of the newer antihistamines. METHODS The microshock method (Herxheimer, 1952) was used and the protection against anaphylactic shock was calculated according to Armitage et al. (1952) with the formula p=100(1-c/t), in which p is the percentage of full protection, c the control preconvulsion time and t the preconvulsion time of the animal under the influence of the drug. The compounds investigated were trimeprazine, methotrimeprazine, cyproheptadine, homo- chlorcyclizine and 10(-3-diethylamino-2-methylpropyl)phenothiazine 1,1-dioxide hydrochloride (oxomemazine hydrochloride, 6847 R.P.). They were injected intramuscularly in aqueous solution; the exposure to the antigen (an aerosol of 5% albumen solution) was done 1 hr later. For cyproheptadine, the exposure was delayed by between 1 and 48 hr in order to investigate the duration of the effect.
    [Show full text]
  • PROZAC Product Monograph Page 1 of 49 Table of Contents
    PRODUCT MONOGRAPH PrPROZAC® fluoxetine hydrochloride 10 mg and 20 mg Capsules Antidepressant / Antiobsessional / Antibulimic © Eli Lilly Canada Inc. Date of Revision: January, 25 Exchange Tower 2021 130 King Street West, Suite 900 PO Box 73 Toronto, Ontario M5X 1B1 1-888-545-5972 www.lilly.ca Submission Control No: 192639 PROZAC Product Monograph Page 1 of 49 Table of Contents PART I: HEALTH PROFESSIONAL INFORMATION .......................................................3 SUMMARY PRODUCT INFORMATION...........................................................................3 INDICATIONS AND CLINICAL USE ................................................................................3 CONTRAINDICATIONS .....................................................................................................4 WARNINGS AND PRECAUTIONS ....................................................................................5 ADVERSE REACTIONS ...................................................................................................13 DRUG INTERACTIONS....................................................................................................22 DOSAGE AND ADMINISTRATION ................................................................................27 OVERDOSAGE..................................................................................................................28 ACTION AND CLINICAL PHARMACOLOGY ...............................................................30 STORAGE AND STABILITY............................................................................................32
    [Show full text]
  • Specifications of Approved Drug Compound Library
    Annexure-I : Specifications of Approved drug compound library The compounds should be structurally diverse, medicinally active, and cell permeable Compounds should have rich documentation with structure, Target, Activity and IC50 should be known Compounds which are supplied should have been validated by NMR and HPLC to ensure high purity Each compound should be supplied as 10mM solution in DMSO and at least 100µl of each compound should be supplied. Compounds should be supplied in screw capped vial arranged as 96 well plate format.
    [Show full text]
  • Pericardial, Retroperitoneal, and Pleural Fibrosis Induced by Pergolide
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.66.1.79 on 1 January 1999. Downloaded from J Neurol Neurosurg Psychiatry 1999;66:79–81 79 SHORT REPORT Pericardial, retroperitoneal, and pleural fibrosis induced by pergolide S Shaunak, A Wilkins, J B Pilling, D J Dick Abstract 1992, the emergence of motor fluctuations led Three patients with Parkinson’s disease to the introduction of pergolide, and the dose are described who developed pericardial, of this was gradually increased to a maximum retroperitoneal, and pleural fibrosis asso- of 1mg/day. 1n 1994, 2 years after the ciated with pergolide treatment. Surgical introduction of pergolide, the patient devel- intervention was required in all three oped left flank pain with weight loss, and was cases, either to reach a tissue diagnosis or found to have a mild anaemia (haemoglobin for potentially life threatening complica- 10.4 g/dl), with indices suggesting iron defi- tions. Symptoms emerged on average 2 ciency, and an ESR of 40 mm/h. Upper gastro- years after the institution of treatment, intestinal endoscopy and barium enema gave and were suYciently non-specific to cause negative results. Seven months later right sided significant delays in diagnosis in all cases. chest pain and a non-productive cough devel- The erythrocyte sedimentation rate (ESR) oped; investigations confirmed persistent anae- was raised in the two patients in whom it mia, an ESR of 55 mm/h, and bilateral pleural was measured. Serosal fibrosis is a rarely thickening on chest radiography and CT. Lung reported adverse eVect of pergolide treat- function tests showed a reduction in total lung ment, although it is well described with capacity of 36% with no fall in transfer factor, other dopamine agonists.
    [Show full text]
  • What Are the Acute Treatments for Migraine and How Are They Used?
    2. Acute Treatment CQ II-2-1 What are the acute treatments for migraine and how are they used? Recommendation The mainstay of acute treatment for migraine is pharmacotherapy. The drugs used include (1) acetaminophen, (2) non-steroidal anti-inflammatory drugs (NSAIDs), (3) ergotamines, (4) triptans and (5) antiemetics. Stratified treatment according to the severity of migraine is recommended: use NSAIDs such as aspirin and naproxen for mild to moderate headache, and use triptans for moderate to severe headache, or even mild to moderate headache when NSAIDs were ineffective in the past. It is necessary to give guidance and cautions to patients having acute attacks, and explain the methods of using medications (timing, dose, frequency of use) and medication use during pregnancy and breast-feeding. Grade A Background and Objective The objective of acute treatment is to resolve the migraine attack completely and rapidly and restore the patient’s normal functions. An ideal treatment should have the following characteristics: (1) resolves pain and associated symptoms rapidly; (2) is consistently effective; (3) no recurrence; (4) no need for additional use of medication; (5) no adverse effects; (6) can be administered by the patients themselves; and (7) low cost. Literature was searched to identify acute treatments that satisfy the above conditions. Comments and Evidence The acute treatment drugs for migraine generally include (1) acetaminophens, (2) non-steroidal anti-inflammatory drugs (NSAIDs), (3) ergotamines, (4) triptans, and (5) antiemetics. For severe migraines including status migrainosus and migraine attacks refractory to treatment, (6) anesthetics, and (7) corticosteroids (dexamethasone) are used (Tables 1 and 2).1)-9) There are two approaches to the selection and sequencing of these medications: “step care” and “stratified care”.
    [Show full text]
  • Upregulation of Peroxisome Proliferator-Activated Receptor-Α And
    Upregulation of peroxisome proliferator-activated receptor-α and the lipid metabolism pathway promotes carcinogenesis of ampullary cancer Chih-Yang Wang, Ying-Jui Chao, Yi-Ling Chen, Tzu-Wen Wang, Nam Nhut Phan, Hui-Ping Hsu, Yan-Shen Shan, Ming-Derg Lai 1 Supplementary Table 1. Demographics and clinical outcomes of five patients with ampullary cancer Time of Tumor Time to Age Differentia survival/ Sex Staging size Morphology Recurrence recurrence Condition (years) tion expired (cm) (months) (months) T2N0, 51 F 211 Polypoid Unknown No -- Survived 193 stage Ib T2N0, 2.41.5 58 F Mixed Good Yes 14 Expired 17 stage Ib 0.6 T3N0, 4.53.5 68 M Polypoid Good No -- Survived 162 stage IIA 1.2 T3N0, 66 M 110.8 Ulcerative Good Yes 64 Expired 227 stage IIA T3N0, 60 M 21.81 Mixed Moderate Yes 5.6 Expired 16.7 stage IIA 2 Supplementary Table 2. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of an ampullary cancer microarray using the Database for Annotation, Visualization and Integrated Discovery (DAVID). This table contains only pathways with p values that ranged 0.0001~0.05. KEGG Pathway p value Genes Pentose and 1.50E-04 UGT1A6, CRYL1, UGT1A8, AKR1B1, UGT2B11, UGT2A3, glucuronate UGT2B10, UGT2B7, XYLB interconversions Drug metabolism 1.63E-04 CYP3A4, XDH, UGT1A6, CYP3A5, CES2, CYP3A7, UGT1A8, NAT2, UGT2B11, DPYD, UGT2A3, UGT2B10, UGT2B7 Maturity-onset 2.43E-04 HNF1A, HNF4A, SLC2A2, PKLR, NEUROD1, HNF4G, diabetes of the PDX1, NR5A2, NKX2-2 young Starch and sucrose 6.03E-04 GBA3, UGT1A6, G6PC, UGT1A8, ENPP3, MGAM, SI, metabolism
    [Show full text]
  • Hygroscopicity of Pharmaceutical Crystals
    HYGROSCOPICITY OF PHARMACEUTICAL CRYSTALS A DISSERTATION SUBMITTED TO THE FACULTY OF GRADUATE SCHOOL OF THE UNIVERSITY OF MINNESOTA BY DABING CHEN IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY RAJ SURYANARAYANAN (ADVISER) JANUARY, 2009 © Dabing Chen, January / 2009 ACKNOWLEDGEMENTS I am very grateful to my thesis advisor, Prof. Raj Suryanarayanan, for his constant guidance, support, and encouragement throughout my research. Without his help, the completion of this thesis would be impossible. His friendship and advices are precious to my professional and personal growth and will help me overcome many difficulties in my future career. I would like to take the opportunity to thank Prof. David J.W. Grant, who was my advisor during the first three years in graduate school and led me into the research area of physical pharmacy. It was my great honor to have worked for him, and he will always live as a role model in my life. Many thanks to Dr. Zheng Jane Li at Boehringer Ingelheim Pharmaceuticals (BI) for her invaluable advice as an industrial mentor and also for agreeing to serve on my committee. I sincerely appreciate her helpful discussions, revision of the manuscripts, and supervision of my research. I also want to thank her for providing me the internship opportunity at BI. I thank Dr. Timothy S. Wiedmann and Dr. Theodore P. Labuza for serving on my committee and for critically reviewing my thesis. I also want to thank Dr. Timothy S. Wiedmann for allowing me the use of the HPLC instruments in his lab and also for his advice as the Director of Graduate Studies.
    [Show full text]
  • Oxytocin Versus Methylergometrine in the Active Management of Third Stage of Labour
    Open Journal of Obstetrics and Gynecology, 2014, 4, 666-671 Published Online August 2014 in SciRes. http://www.scirp.org/journal/ojog http://dx.doi.org/10.4236/ojog.2014.411093 Oxytocin versus Methylergometrine in the Active Management of Third Stage of Labour Ajantha Boopathi1*, Sujir Radhakrishnan Nayak2, Arun Rao2, Bharathi Rao2 1Andal Hospital, Cuddalore, India 2Department of Obstetrics and Gynecology, Kasturba Medical College (A Constituent of Manipal University), Mangalore, India Email: *[email protected] Received 19 June 2014; revised 15 July 2014; accepted 10 August 2014 Copyright © 2014 by authors and Scientific Research Publishing Inc. This work is licensed under the Creative Commons Attribution International License (CC BY). http://creativecommons.org/licenses/by/4.0/ Abstract Objective: To compare the efficacy of Oxytocin versus Methylergometrine in active management of third stage of labour in reducing risk of postpartum hemorrhage. Methods: This study was carried out by randomly assigning into two groups with 150 women in each group. Group 1 included pa- tients who received injection Oxytocin 10 IU intramuscular within one minute of the birth of the baby. Injection Methylergometrine (0.2 mg) was given intravenously at the delivery of anterior shoulder of the baby to women in Group 2. Outcome measures were the duration of third stage, blood loss, pre and post-delivery hematocrit, side effects and incidence of PPH. Statistical analysis was done using Chi square test, Fischers test, Mann Whitney test, and t test. p < 0.05 was consi- dered significant. Results: Mean duration of third stage of labour, mean blood loss, post-delivery fall in hematocrit and need for additional uterotonics were significantly less in the Group 2.
    [Show full text]
  • (12) Patent Application Publication (10) Pub. No.: US 2010/0221245 A1 Kunin (43) Pub
    US 2010O221245A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2010/0221245 A1 Kunin (43) Pub. Date: Sep. 2, 2010 (54) TOPICAL SKIN CARE COMPOSITION Publication Classification (51) Int. Cl. (76) Inventor: Audrey Kunin, Mission Hills, KS A 6LX 39/395 (2006.01) (US) A6II 3L/235 (2006.01) A638/16 (2006.01) Correspondence Address: (52) U.S. Cl. ......................... 424/133.1: 514/533: 514/12 HUSCH BLACKWELL SANDERS LLP (57) ABSTRACT 4801 Main Street, Suite 1000 - KANSAS CITY, MO 64112 (US) The present invention is directed to a topical skin care com position. The composition has the unique ability to treat acne without drying out the user's skin. In particular, the compo (21) Appl. No.: 12/395,251 sition includes a base, an antibacterial agent, at least one anti-inflammatory agent, and at least one antioxidant. The (22) Filed: Feb. 27, 2009 antibacterial agent may be benzoyl peroxide. US 2010/0221 245 A1 Sep. 2, 2010 TOPCAL SKIN CARE COMPOSITION stay of acne treatment since the 1950s. Skin irritation is the most common side effect of benzoyl peroxide and other anti BACKGROUND OF THE INVENTION biotic usage. Some treatments can be severe and can leave the 0001. The present invention generally relates to composi user's skin excessively dry. Excessive use of some acne prod tions and methods for producing topical skin care. Acne Vul ucts may cause redness, dryness of the face, and can actually garis, or acne, is a common skin disease that is prevalent in lead to more acne. Therefore, it would be beneficial to provide teenagers and young adults.
    [Show full text]
  • (12) Patent Application Publication (10) Pub. No.: US 2006/0110428A1 De Juan Et Al
    US 200601 10428A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2006/0110428A1 de Juan et al. (43) Pub. Date: May 25, 2006 (54) METHODS AND DEVICES FOR THE Publication Classification TREATMENT OF OCULAR CONDITIONS (51) Int. Cl. (76) Inventors: Eugene de Juan, LaCanada, CA (US); A6F 2/00 (2006.01) Signe E. Varner, Los Angeles, CA (52) U.S. Cl. .............................................................. 424/427 (US); Laurie R. Lawin, New Brighton, MN (US) (57) ABSTRACT Correspondence Address: Featured is a method for instilling one or more bioactive SCOTT PRIBNOW agents into ocular tissue within an eye of a patient for the Kagan Binder, PLLC treatment of an ocular condition, the method comprising Suite 200 concurrently using at least two of the following bioactive 221 Main Street North agent delivery methods (A)-(C): Stillwater, MN 55082 (US) (A) implanting a Sustained release delivery device com (21) Appl. No.: 11/175,850 prising one or more bioactive agents in a posterior region of the eye so that it delivers the one or more (22) Filed: Jul. 5, 2005 bioactive agents into the vitreous humor of the eye; (B) instilling (e.g., injecting or implanting) one or more Related U.S. Application Data bioactive agents Subretinally; and (60) Provisional application No. 60/585,236, filed on Jul. (C) instilling (e.g., injecting or delivering by ocular ion 2, 2004. Provisional application No. 60/669,701, filed tophoresis) one or more bioactive agents into the Vit on Apr. 8, 2005. reous humor of the eye. Patent Application Publication May 25, 2006 Sheet 1 of 22 US 2006/0110428A1 R 2 2 C.6 Fig.
    [Show full text]
  • Regulatory Effects of Caffeic Acid Phenethyl Ester on Neuroinflammation in Microglial Cells
    Int. J. Mol. Sci. 2015, 16, 5572-5589; doi:10.3390/ijms16035572 OPEN ACCESS International Journal of Molecular Sciences ISSN 1422-0067 www.mdpi.com/journal/ijms Article Regulatory Effects of Caffeic Acid Phenethyl Ester on Neuroinflammation in Microglial Cells Cheng-Fang Tsai 1,†, Yueh-Hsiung Kuo 1,2,†, Wei-Lan Yeh 3, Caren Yu-Ju Wu 4, Hsiao-Yun Lin 5, 4 4 4 1 5,6, Sheng-Wei Lai , Yu-Shu Liu , Ling-Hsuan Wu , Jheng-Kun Lu and Dah-Yuu Lu * 1 Department of Biotechnology, Asia University, Taichung 413, Taiwan; E-Mails: [email protected] (C.-F.T.); [email protected] (Y.-H.K.); [email protected] (J.-K.L.) 2 Department of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung 404, Taiwan 3 Department of Cell and Tissue Engineering, Changhua Christian Hospital, Changhua 500, Taiwan; E-Mail: [email protected] 4 Graduate Institute of Basic Medical Science, College of Medicine, China Medical University, Taichung 404, Taiwan; E-Mails: [email protected] (C.Y.-J.W.); [email protected] (S.-W.L.); [email protected] (Y.-S.L.); [email protected] (L.-H.W.) 5 Graduate Institute of Neural and Cognitive Sciences, China Medical University, Taichung 404, Taiwan; E-Mail: [email protected] 6 Department of Photonics and Communication Engineering, Asia University, Taichung 413, Taiwan † These authors contributed equally to this work. * Author to whom correspondence should be addressed; E-Mail: [email protected]; Tel.: +886-4-2205-3366 (ext. 8206); Fax: +886-4-2207-1507. Academic Editor: Guido R.
    [Show full text]
  • Classification of Medicinal Drugs and Driving: Co-Ordination and Synthesis Report
    Project No. TREN-05-FP6TR-S07.61320-518404-DRUID DRUID Driving under the Influence of Drugs, Alcohol and Medicines Integrated Project 1.6. Sustainable Development, Global Change and Ecosystem 1.6.2: Sustainable Surface Transport 6th Framework Programme Deliverable 4.4.1 Classification of medicinal drugs and driving: Co-ordination and synthesis report. Due date of deliverable: 21.07.2011 Actual submission date: 21.07.2011 Revision date: 21.07.2011 Start date of project: 15.10.2006 Duration: 48 months Organisation name of lead contractor for this deliverable: UVA Revision 0.0 Project co-funded by the European Commission within the Sixth Framework Programme (2002-2006) Dissemination Level PU Public PP Restricted to other programme participants (including the Commission x Services) RE Restricted to a group specified by the consortium (including the Commission Services) CO Confidential, only for members of the consortium (including the Commission Services) DRUID 6th Framework Programme Deliverable D.4.4.1 Classification of medicinal drugs and driving: Co-ordination and synthesis report. Page 1 of 243 Classification of medicinal drugs and driving: Co-ordination and synthesis report. Authors Trinidad Gómez-Talegón, Inmaculada Fierro, M. Carmen Del Río, F. Javier Álvarez (UVa, University of Valladolid, Spain) Partners - Silvia Ravera, Susana Monteiro, Han de Gier (RUGPha, University of Groningen, the Netherlands) - Gertrude Van der Linden, Sara-Ann Legrand, Kristof Pil, Alain Verstraete (UGent, Ghent University, Belgium) - Michel Mallaret, Charles Mercier-Guyon, Isabelle Mercier-Guyon (UGren, University of Grenoble, Centre Regional de Pharmacovigilance, France) - Katerina Touliou (CERT-HIT, Centre for Research and Technology Hellas, Greece) - Michael Hei βing (BASt, Bundesanstalt für Straßenwesen, Germany).
    [Show full text]