13 results match your criteria Human Genomics and Proteomics [Journal]

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Plasma Proteomic Signature in Overweight Girls Closely Correlates with Homeostasis Model Assessment (HOMA), an Objective Measure of Insulin Resistance.

Hum Genomics Proteomics 2011 6;2011:323629. Epub 2011 Oct 6.

Department of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences, Bethesda, MD 20814-4799, USA.

Obesity is known to be associated with a large number of long-term morbidities, and while in some cases the relationship of obesity and the consequences is clear (for example, excess weight and lower extremity orthopedic problems) in others the mechanism is not as clear. One common system of categorizing overweight in terms of the likelihood of negative consequences involves using the concept of "metabolic syndrome". We hypothesized that the development of a plasma protein profile of overweight adolescents with and without the metabolic syndrome might give a more precise and informative picture of the disease process than the current clinical categorization and permit early targeted intervention. Read More

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http://dx.doi.org/10.4061/2011/323629DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3308678PMC
August 2012
10 Reads

Genome-wide linkage and association scans for quantitative trait Loci of serum lactate dehydrogenase-the framingham heart study.

Hum Genomics Proteomics 2010 Sep 1;2010:905237. Epub 2010 Sep 1.

Office of Biostatistics Research, Division of Cardiovascular Sciences, National Heart, Lung and Blood Institute, NIH 6701 Rockledge Dr. Suite 9196, Bethesda, MD 20892-7913, USA.

Serum lactate dehydrogenase (LDH) is used in diagnosing many diseases and is significantly determined by genetic factors. Three genes coding for LDH isoenzymes were mapped to chromosome 11q15 and 12p12. We used 330 Framingham Heart Study largest families for microsatellite linkage scan and 100K SNPs association scan to determine quantitative trait loci of LDH level. Read More

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http://mr.crossref.org/iPage?doi=10.4061%2F2010%2F905237
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http://dx.doi.org/10.4061/2010/905237DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2958689PMC
September 2010
8 Reads

Genetic variations in human glutathione transferase enzymes: significance for pharmacology and toxicology.

Authors:
P David Josephy

Hum Genomics Proteomics 2010 Jun 13;2010:876940. Epub 2010 Jun 13.

Department of Molecular and Cellular Biology, University of Guelph, Guelph, ON, Canada N1G 2W1.

Glutathione transferase enzymes (GSTs) catalyze reactions in which electrophiles are conjugated to the tripeptide thiol glutathione. While many GST-catalyzed transformations result in the detoxication of xenobiotics, a few substrates, such as dihaloalkanes, undergo bioactivation to reactive intermediates. Many molecular epidemiological studies have tested associations between polymorphisms (especially, deletions) of human GST genes and disease susceptibility or response to therapy. Read More

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http://mr.crossref.org/iPage?doi=10.4061%2F2010%2F876940
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http://dx.doi.org/10.4061/2010/876940DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2958679PMC
June 2010
4 Reads

Pharmacogenetics of anticoagulants.

Hum Genomics Proteomics 2010 Sep 13;2010:754919. Epub 2010 Sep 13.

Division of Clinical Pharmacology, Karolinska Institutet, 17177 Stockholm, Sweden.

Warfarin, acenocoumarol, and phenprocoumon are among the major anticoagulant drugs worldwide. Because of their low therapeutic index and serious adverse reactions (ADRs), their wide use, and their varying kinetics and pharmacogenetic dependence, it is of great importance to explore further possibilities to forecast the dose beyond conventional INR measurements. Here, we describe particulars of the relative pharmacogenetic influence on the kinetics of these agents, the population distribution of genetics risk groups, and novel data on clinical features with influence on dose requirement and ADR risk. Read More

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http://mr.crossref.org/iPage?doi=10.4061%2F2010%2F754919
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http://dx.doi.org/10.4061/2010/754919DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2958670PMC
September 2010
8 Reads

Developmental pharmacogenetics in pediatric rheumatology: utilizing a new paradigm to effectively treat patients with juvenile idiopathic arthritis with methotrexate.

Hum Genomics Proteomics 2010 Jun 22;2010:257120. Epub 2010 Jun 22.

Division of Clinical Pharmacology and Toxicology, Children's Mercy Hospitals and Clinics, University of Missouri Kansas City, 2401 Gillham Road, Kansas City, MO 64108, USA.

Although methotrexate is widely used in clinical practice there remains significant lack of understanding of its mechanisms of action and the factors that contribute to the variability in toxicity and response seen clinically. In addition to differences in drug administration, factors that affect pharmacokinetics and pharmacodynamics such as genetic variation may explain individual differences in drug biotransformation. However, the pediatric population has an additional factor to consider, namely the ontogeny of gene expression which may result in variation throughout growth and development. Read More

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http://mr.crossref.org/iPage?doi=10.4061%2F2010%2F257120
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http://dx.doi.org/10.4061/2010/257120DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2958653PMC
June 2010
7 Reads

Gender dependence for a subset of the low-abundance signaling proteome in human platelets.

Hum Genomics Proteomics 2010 Apr 13;2010:164906. Epub 2010 Apr 13.

Department of Anatomy, Physiology and Genetics, USU Center for Medical Proteomics, Uniformed Services University, School of Medicine, USUHS, 4301 Jones Bridge Road, Bethesda, MD 20814, USA.

The incidence of cardiovascular diseases is ten-times higher in males than females, although the biological basis for this gender disparity is not known. However, based on the fact that antiplatelet drugs are the mainstay for prevention and therapy, we hypothesized that the signaling proteomes in platelets from normal male donors might be more activated than platelets from normal female donors. We report here that platelets from male donors express significantly higher levels of signaling cascade proteins than platelets from female donors. Read More

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http://dx.doi.org/10.4061/2010/164906DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2958630PMC
April 2010
13 Reads

Pharmacogenomics of mood stabilizers in the treatment of bipolar disorder.

Hum Genomics Proteomics 2010 Aug 3;2010:159761. Epub 2010 Aug 3.

Laboratory of Molecular Genetics, Unit of Clinical Pharmacology, Department of Neuroscience "B.B. Brodie", University of Cagliari, sp8 Sestu-Monserrato, km. 0,700, Monserrato 09042, Cagliari, Italy.

Bipolar disorder (BD) is a chronic and often severe psychiatric illness characterized by manic and depressive episodes. Among the most effective treatments, mood stabilizers represent the keystone in acute mania, depression, and maintenance treatment of BD. However, treatment response is a highly heterogeneous trait, thus emphasizing the need for a structured informational framework of phenotypic and genetic predictors. Read More

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https://pdfs.semanticscholar.org/282a/738651de8f7d0c0fe62dd6
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http://www.crossref.org/iPage?doi=10.4061%2F2010%2F159761
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http://dx.doi.org/10.4061/2010/159761DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2958627PMC
August 2010
9 Reads

Gene Expression and Serum Cytokine Profiling of Low Stage CLL Identify WNT/PCP, Flt-3L/Flt-3 and CXCL9/CXCR3 as Regulators of Cell Proliferation, Survival and Migration.

Hum Genomics Proteomics 2009 Jun 24;2009:453634. Epub 2009 Jun 24.

Department of Hematology/Oncology, Arizona Cancer Center, Tucson, AZ 85724, USA.

Gene expression profiling (GEP) of 8 stage 0/I untreated Chronic Lymphocytic Leukemia (CLL) patients showed over-expression of Frizzled 3 (FZD3)/ROR-1 receptor tyrosine kinase (RTK), FLT-3 RTK and CXCR3 G-protein coupled receptor (GPCR). RT-PCR of 24 genes in 21 patients of the WNT pathway corroborated the GEP. Transforming growth factorβ, fibromodulin, TGFβRIII and SMAD2 are also over-expressed by GEP. Read More

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http://dx.doi.org/10.4061/2009/453634DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2958625PMC
June 2009
15 Reads

Proteomics: challenges, techniques and possibilities to overcome biological sample complexity.

Hum Genomics Proteomics 2009 Dec 8;2009. Epub 2009 Dec 8.

Department of Biology, The Hong Kong University of Science and Technology, Kowloon, Hong Kong.

Proteomics is the large-scale study of the structure and function of proteins in complex biological sample. Such an approach has the potential value to understand the complex nature of the organism. Current proteomic tools allow large-scale, high-throughput analyses for the detection, identification, and functional investigation of proteome. Read More

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http://mr.crossref.org/iPage?doi=10.4061%2F2009%2F239204
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http://dx.doi.org/10.4061/2009/239204DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950283PMC
December 2009
3 Reads

Development of Potential Pharmacodynamic and Diagnostic Markers for Anti-IFN-α Monoclonal Antibody Trials in Systemic Lupus Erythematosus.

Hum Genomics Proteomics 2009 Nov 17;2009. Epub 2009 Nov 17.

MedImmune, LLC., One MedImmune Way, Gaithersburg, MD 20878, USA.

To identify potential pharmacodynamic biomarkers to guide dose selection in clinical trials using anti-interferon-alpha (IFN-α) monoclonal antibody (mAb) therapy for systemic lupus erythematosus (SLE), we used an Affymetrix human genome array platform and identified 110 IFN-α/β-inducible transcripts significantly upregulated in whole blood (WB) of 41 SLE patients. The overexpression of these genes was confirmed prospectively in 54 additional SLE patients and allowed for the categorization of the SLE patients into groups of high, moderate, and weak overexpressers of IFN-α/β-inducible genes. This approach could potentially allow for an accurate assessment of drug target neutralization in early trials of anti-IFN-α mAb therapy for SLE. Read More

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http://mr.crossref.org/iPage?doi=10.4061%2F2009%2F374312
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http://dx.doi.org/10.4061/2009/374312DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950308PMC
November 2009
19 Reads

Prediction of disease severity in patients with early rheumatoid arthritis by gene expression profiling.

Hum Genomics Proteomics 2009 Apr 27;2009. Epub 2009 Apr 27.

Division of Rheumatology, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.

In order to test the ability of peripheral blood gene expression profiles to predict future disease severity in patients with early rheumatoid arthritis (RA), a group of 17 patients (1 ± 0.2 years disease duration) was evaluated at baseline for gene expression profiles. Disease status was evaluated after a mean of 5 years using an index combining pain, global and recoded MHAQ scores. Read More

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http://dx.doi.org/10.4061/2009/484351DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950309PMC
April 2009
8 Reads

A new scientific journal linked to a genetic database: towards a novel publication modality.

Hum Genomics Proteomics 2009 17;2009. Epub 2008 Nov 17.

MGC-Department of Cell Biology and Genetics, Center for Biomedical Genetics, Erasmus MC, Faculty of Medicine and Health Sciences, Erasmus University Rotterdam, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands.

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http://dx.doi.org/10.4061/2009/597478DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950282PMC
July 2011
3 Reads

Data integration in genetics and genomics: methods and challenges.

Hum Genomics Proteomics 2009 Jan 12;2009. Epub 2009 Jan 12.

Biostatistics Methodology Unit, The Hospital for Sick Children Research Institute, 555 University Avenue, Toronto, ON, Canada M5G 1X8.

Due to rapid technological advances, various types of genomic and proteomic data with different sizes, formats, and structures have become available. Among them are gene expression, single nucleotide polymorphism, copy number variation, and protein-protein/gene-gene interactions. Each of these distinct data types provides a different, partly independent and complementary, view of the whole genome. Read More

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http://dx.doi.org/10.4061/2009/869093DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950414PMC
January 2009
7 Reads
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