Schwartz S

References (13)

Title : Deciphering the m(6)A Code via Antibody-Independent Quantitative Profiling - Garcia-Campos_2019_Cell_178_731
Author(s) : Garcia-Campos MA , Edelheit S , Toth U , Safra M , Shachar R , Viukov S , Winkler R , Nir R , Lasman L , Brandis A , Hanna JH , Rossmanith W , Schwartz S
Ref : Cell , 178 :731 , 2019
Abstract : N6-methyladenosine (m(6)A) is the most abundant modification on mRNA and is implicated in critical roles in development, physiology, and disease. A major limitation has been the inability to quantify m(6)A stoichiometry and the lack of antibody-independent methodologies for interrogating m(6)A. Here, we develop MAZTER-seq for systematic quantitative profiling of m6A at single-nucleotide resolution at 16%-25% of expressed sites, building on differential cleavage by an RNase. MAZTER-seq permits validation and de novo discovery of m(6)A sites, calibration of the performance of antibody-based approaches, and quantitative tracking of m(6)A dynamics in yeast gametogenesis and mammalian differentiation. We discover that m6A stoichiometry is "hard coded" in cis via a simple and predictable code, accounting for 33%-46% of the variability in methylation levels and allowing accurate prediction of m(6)A loss and acquisition events across evolution. MAZTER-seq allows quantitative investigation of m(6)A regulation in subcellular fractions, diverse cell types, and disease states.
ESTHER : Garcia-Campos_2019_Cell_178_731
PubMedSearch : Garcia-Campos_2019_Cell_178_731
PubMedID: 31257032

Title : Use of FDA approved medications for Alzheimer's disease in mild dementia is associated with reduced informal costs of care - Behrens_2018_Int.Psychogeriatr__1
Author(s) : Behrens S , Rattinger GB , Schwartz S , Matyi J , Sanders C , DeBerard MS , Lyketsos CG , Tschanz JT
Ref : Int Psychogeriatr , :1 , 2018
Abstract : BACKGROUND: The use of FDA approved medications for Alzheimer's disease [AD; FDAAMAD; (cholinesterase inhibitors and N-methyl-D-aspartate receptor antagonists)] has been associated with symptomatic benefit with a reduction in formal (paid services) and total costs of care (formal and informal costs). We examined the use of these medications and their association with informal costs in persons with dementia. METHOD: Two hundred eighty participants (53% female, 72% AD) from the longitudinal, population-based Dementia Progression Study in Cache County, Utah (USA) were followed up to ten years. Mean (SD) age at baseline was 85.6 (5.5) years. Informal costs (expressed in 2015 dollars) were calculated using the replacement cost method (hours of care multiplied by the median wage in Utah in the visit year) and adjusted for inflation using the Medical Consumer Price Index. Generalized Estimating Equations with a gamma log-link function were used to examine the longitudinal association between use of FDAAMAD and informal costs. RESULTS: The daily informal cost for each participant at baseline ranged from $0 to $318.12, with the sample median of $9.40. Within the entire sample, use of FDAAMAD was not significantly associated with informal costs (expbeta = 0.73, p = 0.060). In analyses restricted to participants with mild dementia at baseline (N = 222), use of FDAAMAD was associated with 32% lower costs (expbeta = 0.68, p = 0.038). CONCLUSIONS: Use of FDAAMAD was associated with lower informal care costs in those with mild dementia only.
ESTHER : Behrens_2018_Int.Psychogeriatr__1
PubMedSearch : Behrens_2018_Int.Psychogeriatr__1
PubMedID: 29559029

Title : A Dose-Ranging Study of the DPP-IV Inhibitor PF-734200 Added to Metformin in Subjects With Type 2 Diabetes* - Terra_2011_Exp.Clin.Endocrinol.Diabetes_119_401
Author(s) : Terra SG , Somayaji V , Schwartz S , Lewin AJ , Teeter JG , Dai H , Nguyen TT , Calle RA
Ref : Experimental & Clinical Endocrinology & Diabetes Diabetes , 119 :401 , 2011
Abstract : The purpose of this phase 2, multicentre, randomized, double-blind, placebo-controlled, 12-week dose-ranging study was to assess the efficacy, safety, and tolerability of the dipeptidyl peptidase-IV (DPP-IV) inhibitor PF-734200 in adult subjects with type 2 diabetes who were on a stable dose of metformin. Men and women with inadequate glycaemic control with metformin as their sole diabetes medication were randomized to placebo or PF-734200 2 mg, 5 mg, 10 mg, or 20 mg every day. A population subset underwent mixed meal tolerance tests (MMTT) at baseline and week 12. A total of 301 subjects were treated. At week 12, PF-734200 doses of >/=5 mg produced a statistically significant reduction in haemoglobin A (1C) (HbA (1c)) compared with placebo. The mean (95% confidence interval) placebo-adjusted changes in HbA (1c) were -0.31% (-0.70 to 0.08), -0.74% (-1.12 to -0.36), -0.70% (-1.02 to -0.38), and -0.75% (-1.07 to -0.43) for the 2 mg, 5 mg, 10 mg, and 20 mg doses, respectively. PF-734200 20 mg significantly reduced glucose area under the curve following MMTT (-12.8% [-22.9 to -2.7]; p=0.003) compared with placebo. The reductions observed with other doses were not statistically significant. PF-734200 was safe and well tolerated at all doses tested when added to metformin. PF-734200 safely and effectively lowered HbA (1c) in subjects receiving metformin. The 20 mg dose provided the greatest improvements in post-prandial glucose.
ESTHER : Terra_2011_Exp.Clin.Endocrinol.Diabetes_119_401
PubMedSearch : Terra_2011_Exp.Clin.Endocrinol.Diabetes_119_401
PubMedID: 21472661

Title : Evaluation of pharmacokinetic and pharmacodynamic interaction between the dipeptidyl peptidase IV inhibitor vildagliptin, glyburide and pioglitazone in patients with Type 2 diabetes - Serra_2008_Int.J.Clin.Pharmacol.Ther_46_349
Author(s) : Serra D , He YL , Bullock J , Riviere GJ , Balez S , Schwartz S , Wang Y , Ligueros-Saylan M , Jarugula V , Dole WP
Ref : Int J Clinical Pharmacology & Therapeutics , 46 :349 , 2008
Abstract : BACKGROUND: Vildagliptin is a selective inhibitor of dipeptidyl peptidase IV (DPP-4) that improves glycemic control and pancreatic b-cell function in patients with Type 2 diabetes. Vildagliptin may be an appropriate agent to combine with other antihyperglycemic agents in patients requiring combination therapy to achieve optimal glycemic control. Two studies were performed to determine the potential for pharmacokinetic and pharmacodynamic interactions between vildagliptin and the sulfonylurea, glyburide, or pioglitazone in patients with Type 2 diabetes.
METHODS: Two open-label, multiple-dose, 3-period, randomized, crossover studies in patients with Type 2 diabetes were carried out. Steady state drug pharmacokinetics and postprandial plasma glucose and insulin responses were assessed during treatment with vildagliptin 100 mg b.i.d. alone and in combination with glyburide 10 mg q.d. (n = 17) or with vildagliptin 100 mg q.d. alone or in combination with pioglitazone 45 mg q.d. (n = 15).
RESULTS: Coadministration of vildagliptin with either glyburide or pioglitazone had no clinically significant effect on the pharmacokinetics of any of the 3 drugs. Changes in AUC and Cmax during combination treatment were small ( pound 15%), and 90% confidence intervals for the geometric mean ratios (drug coadministration/monotherapy) were generally contained within the acceptance range for bioequivalence (0.80 - 1.25). Vildagliptin/glyburide coadministration significantly reduced the area under the plasma glucose-time curve compared with glyburide alone (AUE0-5h reduced by 12% (p = 0.005) and AUE0-15h by 13% (p = 0.003)), and increased the area under the plasma insulin-time curve (AUE0-15h increased by 12% (p = 0.041)). Vildagliptin/pioglitazone coadministration also significantly reduced postprandial glucose exposure compared with pioglitazone alone (AUE0.5-5.5h reduced by 11% (p = 0.029) and AUE0-15.5h by 10% (p = 0.019)). Vildagliptin was generally well tolerated whether administered alone or in combination with glyburide or pioglitazone, and was not associated with hypoglycemia.
CONCLUSIONS: Coadministration of vildagliptin with either glyburide or pioglitazone in patients with Type 2 diabetes improves postprandial glycemic control without notable effects on drug pharmacokinetics.
ESTHER : Serra_2008_Int.J.Clin.Pharmacol.Ther_46_349
PubMedSearch : Serra_2008_Int.J.Clin.Pharmacol.Ther_46_349
PubMedID: 18793589

Title : Genome sequence of the Brown Norway rat yields insights into mammalian evolution - Gibbs_2004_Nature_428_493
Author(s) : Gibbs RA , Weinstock GM , Metzker ML , Muzny DM , Sodergren EJ , Scherer S , Scott G , Steffen D , Worley KC , Burch PE , Okwuonu G , Hines S , Lewis L , DeRamo C , Delgado O , Dugan-Rocha S , Miner G , Morgan M , Hawes A , Gill R , Celera , Holt RA , Adams MD , Amanatides PG , Baden-Tillson H , Barnstead M , Chin S , Evans CA , Ferriera S , Fosler C , Glodek A , Gu Z , Jennings D , Kraft CL , Nguyen T , Pfannkoch CM , Sitter C , Sutton GG , Venter JC , Woodage T , Smith D , Lee HM , Gustafson E , Cahill P , Kana A , Doucette-Stamm L , Weinstock K , Fechtel K , Weiss RB , Dunn DM , Green ED , Blakesley RW , Bouffard GG , de Jong PJ , Osoegawa K , Zhu B , Marra M , Schein J , Bosdet I , Fjell C , Jones S , Krzywinski M , Mathewson C , Siddiqui A , Wye N , McPherson J , Zhao S , Fraser CM , Shetty J , Shatsman S , Geer K , Chen Y , Abramzon S , Nierman WC , Havlak PH , Chen R , Durbin KJ , Egan A , Ren Y , Song XZ , Li B , Liu Y , Qin X , Cawley S , Cooney AJ , D'Souza LM , Martin K , Wu JQ , Gonzalez-Garay ML , Jackson AR , Kalafus KJ , McLeod MP , Milosavljevic A , Virk D , Volkov A , Wheeler DA , Zhang Z , Bailey JA , Eichler EE , Tuzun E , Birney E , Mongin E , Ureta-Vidal A , Woodwark C , Zdobnov E , Bork P , Suyama M , Torrents D , Alexandersson M , Trask BJ , Young JM , Huang H , Wang H , Xing H , Daniels S , Gietzen D , Schmidt J , Stevens K , Vitt U , Wingrove J , Camara F , Mar Alba M , Abril JF , Guigo R , Smit A , Dubchak I , Rubin EM , Couronne O , Poliakov A , Hubner N , Ganten D , Goesele C , Hummel O , Kreitler T , Lee YA , Monti J , Schulz H , Zimdahl H , Himmelbauer H , Lehrach H , Jacob HJ , Bromberg S , Gullings-Handley J , Jensen-Seaman MI , Kwitek AE , Lazar J , Pasko D , Tonellato PJ , Twigger S , Ponting CP , Duarte JM , Rice S , Goodstadt L , Beatson SA , Emes RD , Winter EE , Webber C , Brandt P , Nyakatura G , Adetobi M , Chiaromonte F , Elnitski L , Eswara P , Hardison RC , Hou M , Kolbe D , Makova K , Miller W , Nekrutenko A , Riemer C , Schwartz S , Taylor J , Yang S , Zhang Y , Lindpaintner K , Andrews TD , Caccamo M , Clamp M , Clarke L , Curwen V , Durbin R , Eyras E , Searle SM , Cooper GM , Batzoglou S , Brudno M , Sidow A , Stone EA , Payseur BA , Bourque G , Lopez-Otin C , Puente XS , Chakrabarti K , Chatterji S , Dewey C , Pachter L , Bray N , Yap VB , Caspi A , Tesler G , Pevzner PA , Haussler D , Roskin KM , Baertsch R , Clawson H , Furey TS , Hinrichs AS , Karolchik D , Kent WJ , Rosenbloom KR , Trumbower H , Weirauch M , Cooper DN , Stenson PD , Ma B , Brent M , Arumugam M , Shteynberg D , Copley RR , Taylor MS , Riethman H , Mudunuri U , Peterson J , Guyer M , Felsenfeld A , Old S , Mockrin S , Collins F
Ref : Nature , 428 :493 , 2004
Abstract : The laboratory rat (Rattus norvegicus) is an indispensable tool in experimental medicine and drug development, having made inestimable contributions to human health. We report here the genome sequence of the Brown Norway (BN) rat strain. The sequence represents a high-quality 'draft' covering over 90% of the genome. The BN rat sequence is the third complete mammalian genome to be deciphered, and three-way comparisons with the human and mouse genomes resolve details of mammalian evolution. This first comprehensive analysis includes genes and proteins and their relation to human disease, repeated sequences, comparative genome-wide studies of mammalian orthologous chromosomal regions and rearrangement breakpoints, reconstruction of ancestral karyotypes and the events leading to existing species, rates of variation, and lineage-specific and lineage-independent evolutionary events such as expansion of gene families, orthology relations and protein evolution.
ESTHER : Gibbs_2004_Nature_428_493
PubMedSearch : Gibbs_2004_Nature_428_493
PubMedID: 15057822
Gene_locus related to this paper: rat-abhea , rat-abheb , rat-cd029 , rat-d3zaw4 , rat-dpp9 , rat-d3zhq1 , rat-d3zkp8 , rat-d3zuq1 , rat-d3zxw8 , rat-d4a4w4 , rat-d4a7w1 , rat-d4a9l7 , rat-d4a071 , rat-d4aa31 , rat-d4aa33 , rat-d4aa61 , rat-dglb , rat-f1lz91 , rat-Kansl3 , rat-nceh1 , rat-Tex30 , ratno-1hlip , ratno-1neur , ratno-1plip , ratno-2neur , ratno-3neur , ratno-3plip , ratno-ABH15 , ratno-ACHE , ratno-balip , ratno-BCHE , ratno-cauxin , ratno-Ces1d , ratno-Ces1e , ratno-Ces2f , ratno-d3ze31 , ratno-d3zp14 , ratno-d3zxi3 , ratno-d3zxq0 , ratno-d3zxq1 , ratno-d4a3d4 , ratno-d4aa05 , ratno-dpp4 , ratno-dpp6 , ratno-est8 , ratno-FAP , ratno-hyep , ratno-hyes , ratno-kmcxe , ratno-lmcxe , ratno-LOC246252 , ratno-MGLL , ratno-pbcxe , ratno-phebest , ratno-Ppgb , ratno-q4qr68 , ratno-q6ayr2 , ratno-q6q629 , ratno-SPG21 , ratno-thyro , rat-m0rc77 , rat-a0a0g2k9y7 , rat-a0a0g2kb83 , rat-d3zba8 , rat-d3zbj1 , rat-d3zcr8 , rat-d3zxw5 , rat-d4a340 , rat-f1lvg7 , rat-m0r509 , rat-m0r5d4 , rat-b5den3 , rat-d3zxk4 , rat-d4a1b6 , rat-d3zmg4 , rat-ab17c

Title : Comparative analysis of the gene-dense ACHE\/TFR2 region on human chromosome 7q22 with the orthologous region on mouse chromosome 5 - Wilson_2001_Nucleic.Acids.Res_29_1352
Author(s) : Wilson MD , Riemer C , Martindale DW , Schnupf P , Boright AP , Cheung TL , Hardy DM , Schwartz S , Scherer SW , Tsui LC , Miller W , Koop BF
Ref : Nucleic Acids Research , 29 :1352 , 2001
Abstract : Chromosome 7q22 has been the focus of many cytogenetic and molecular studies aimed at delineating regions commonly deleted in myeloid leukemias and myelodysplastic syndromes. We have compared a gene-dense, GC-rich sub-region of 7q22 with the orthologous region on mouse chromosome 5. A physical map of 640 kb of genomic DNA from mouse chromosome 5 was derived from a series of overlapping bacterial artificial chromosomes. A 296 kb segment from the physical map, spanning ACHE: to Tfr2, was compared with 267 kb of human sequence. We identified a conserved linkage of 12 genes including an open reading frame flanked by ACHE: and Asr2, a novel cation-chloride cotransporter interacting protein Cip1, Ephb4, Zan and Perq1. While some of these genes have been previously described, in each case we present new data derived from our comparative sequence analysis. Adjacent unfinished sequence data from the mouse contains an orthologous block of 10 additional genes including three novel cDNA sequences that we subsequently mapped to human 7q22. Methods for displaying comparative genomic information, including unfinished sequence data, are becoming increasingly important. We supplement our printed comparative analysis with a new, Web-based program called Laj (local alignments with java). Laj provides interactive access to archived pairwise sequence alignments via the WWW. It displays synchronized views of a dot-plot, a percent identity plot, a nucleotide-level local alignment and a variety of relevant annotations. Our mouse-human comparison can be viewed at http://web.uvic.ca/~bioweb/laj.html. Laj is available at http://bio.cse.psu.edu/, along with online documentation and additional examples of annotated genomic regions.
ESTHER : Wilson_2001_Nucleic.Acids.Res_29_1352
PubMedSearch : Wilson_2001_Nucleic.Acids.Res_29_1352
PubMedID: 11239002
Gene_locus related to this paper: human-ACHE , mouse-ACHE

Title : Cerebrospinal fluid neuropeptide Y in Alzheimer's disease - Alom_1990_Eur.Neurol_30_207
Author(s) : Alom J , Galard R , Catalan R , Castellanos JM , Schwartz S , Tolosa E
Ref : Eur Neurol , 30 :207 , 1990
Abstract : The cerebrospinal fluid neuropeptide Y level was measured by radioimmunoassay in 20 patients with probable Alzheimer's disease and in 19 controls. The mean level was lower in patients (69.5 +/- 36.7 pg/ml) than in controls (103 +/- 21.8 pg/ml; p less than 0.001). Patients with a disease duration of greater than 2 years had cerebrospinal fluid neuropeptide Y levels lower than those with shorter disease duration (p less than 0.02). These results suggest that neuropeptide Y containing cells may be involved in Alzheimer's disease. No correlation was found between neuropeptide Y levels and degree of cognitive impairment or age at disease onset.
ESTHER : Alom_1990_Eur.Neurol_30_207
PubMedSearch : Alom_1990_Eur.Neurol_30_207
PubMedID: 2209674

Title : Patterns of firing in cuneate neurones and some effects of Flaxedil -
Author(s) : Galindo A , Krnjevic K , Schwartz S
Ref : Experimental Brain Research , 5 :87 , 1968
PubMedID: 4971059

Title : Penetration of blood-brain barrier by gamma-aminobutyric acid at sites of freezing -
Author(s) : Strasberg P , Krnjevic K , Schwartz S , Elliott KA
Ref : Journal of Neurochemistry , 14 :755 , 1967
PubMedID: 6028292

Title : Micro-iontophoretic studies on neurones in the cuneate nucleus - Galindo_1967_J.Physiol_192_359
Author(s) : Galindo A , Krnjevic K , Schwartz S
Ref : The Journal of Physiology , 192 :359 , 1967
Abstract : 1. Cuneate cells in anaesthetized cats were strongly excited by L-glutamate, and somewhat less by D-glutamate; cells which receive afferents from hair receptors were particularly sensitive.2. Glutamate could be used to demonstrate post-synaptic inhibitory inputs from the dorsal column, the medial lemniscus and the frontal cortex.3. Many cuneate cells were also strongly excited by adenosinetriphosphate (ATP); this was probably due to the chelating action of ATP, as citric acid was also quite effective.4. gamma-Aminobutyric acid (GABA) readily blocked all forms of spontaneous and evoked activity, except antidromic invasion of cuneothalamic neurones; cells which receive proprioceptive afferents were particularly sensitive to GABA. Glycine had a comparable effect.5. Acetylcholine (ACh), catecholamines, histamine, 5-hydroxytryptamine (5-HT) and an extract containing substance P mostly had only weak depressant actions. Cholinergic and mono-aminergic mechanisms are probably not very significant in the cuneate.6. These results are consistent with the possibility that glutamate and GABA (or glycine), or some closely related compounds, are the main excitatory and inhibitory transmitters in the cuneate nucleus.7. If ATP is released from afferent nerve endings, it could also play a significant role in excitation.
ESTHER : Galindo_1967_J.Physiol_192_359
PubMedSearch : Galindo_1967_J.Physiol_192_359
PubMedID: 4292909

Title : The action of gamma-aminobutyric acid on cortical neurones -
Author(s) : Krnjevic K , Schwartz S
Ref : Experimental Brain Research , 3 :320 , 1967
PubMedID: 6031164

Title : Some properties of unresponsive cells in the cerebral cortex -
Author(s) : Krnjevic K , Schwartz S
Ref : Experimental Brain Research , 3 :306 , 1967
PubMedID: 6031163

Title : Is gamma-aminobutyric acid an inhibitory transmitter? -
Author(s) : Krnjevic K , Schwartz S
Ref : Nature , 211 :1372 , 1966
PubMedID: 5969831