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At least 397 records · Page 22Linked to original sources
PubMed2004

Organochlorine compounds in tissues of swordfish (Xiphias gladius) from Mediterranean Sea and Azores islands.

Polychlorobiphenyls (PCB) and organochlorine (OC) pesticides are endocrine-disrupting chemicals (EDCs). The Italian Ministry of Environment has undertaken a program (1999-2001) to measure levels of contaminants in top marine predators and to develop sensitive biomarkers for the evaluation of toxicological risk in these species. In 1999, 15 swordfishes (Xiphias gladius) taken from the Mediterranean Sea along the Sicilian coast (Strait of Messina, Italy) and in the Atlantic Ocean along the Azores Islands, and analysed for 34 congeners of PCBs and 27 organochlorine (OC) pesticides in gonad, muscle, liver and blubber tissues. In the tissues of Mediterranean swordfishes the sum of the determined PCBs congeners ranged from 4.61 to 4651.17 ng g(-1) on fresh tissue basis. Among organochlorine pesticides DDE, DDT and DDD (TDE) predominated with an overall range of 2.37-4734.56 ng(-1) w.w. In particular p,p'-DDE had concentrations appearing up to 3900 ng(-1), with the highest values found in fatty tissues, such as blubber. In the liver of Azores Island swordfishes lower levels of summation PCBs (8.43-294.17 ng/g w.w.) and summation DDTs (<0.01-217.44 ng/g w.w.) were determined.

Animals↗
PubMed2005

Methods for etiologic and early marker investigations in the PLCO trial.

With the rapid development of biomarkers and new technologies, large-scale biologically-based cohort studies present expanding opportunities for population-based research on disease etiology and early detection markers. The prostate, lung, colorectal and ovarian cancer (PLCO) screening trial is a large randomized trial designed to determine if screening for these cancers leads to mortality reduction for these diseases. Within the Trial, the PLCO etiology and early marker study (EEMS) identifies risk factors for cancer and other diseases and evaluates biologic markers for the early detection of disease. EEMS includes 155,000 volunteers who provide basic risk factor information. Serial blood samples are collected at each of six screening rounds (including one collection for cryopreserved whole blood) from screening arm participants (77,000 subjects) and buccal cells are collected from those in the control arm of the trial. Etiologic studies consider environmental (e.g., diet), biochemical, and genetic factors. Early detection studies focus on blood-based biologic markers of early disease. Clinical epidemiology is also an important component of the PLCO trial.

Biomarkers, Tumor↗
PubMedDate not supplied

Data input module for Birth Defects Systems Manager.

The need for a computational bioinformatics infrastructure to manage the vast digital information from functional genomics and proteomics motivated us to develop Birth Defects Systems Manager (BDSM) as an open resource to facilitate analysis and discovery in developmental biology and developmental toxicity. This report describes the design, development and implementation of the data loading module of BDSM, referred to as LoadBDSM. It includes a shared data directory resource that can be granted various levels of security for different research groups or investigators to manage experimental datasets individually or in groups. LoadBDSM allows the upload of data and experiment details using controlled semantics for developmental exposure (toxicant, dosing scenario, intervention), biological sample (species, tissue, stage) and disease outcome (time, risk, phenotype). It adheres to existing controlled vocabulary plus rules of inference (ontologies) for experiment, data and metadata annotations. LoadBDSM extends the capabilities of BDSM to support the emergence of "embryo-formatics" defined here as the data, information and knowledge from genomic sciences applied to, or derived from, an embryological context. This includes, but is not limited to, delineating pathways and biological regulatory networks for specific chemicals or classes of developmental toxicants, developing novel biomarkers indicative of exposure and/or predictive of adverse effects, and integrating modern computing and information technology with data from molecular biology.

Abnormalities, Drug-Induced↗
PubMed2006

Metabolism and disposition of 1-bromopropane in rats and mice following inhalation or intravenous administration.

Workplace exposure to 1-bromopropane (1-BrP) can potentially occur during its use in spray adhesives, fats, waxes, and resins. 1-BrP may be used to replace ozone depleting solvents, resulting in an increase in its annual production in the US, which currently exceeds 1 million pounds. The potential for human exposure to 1-BrP and the reports of adverse effects associated with potential occupational exposure to high levels of 1-BrP have increased the need for the development of biomarkers of exposure and an improved understanding of 1-BrP metabolism and disposition. In this study, the factors influencing the disposition and biotransformation of 1-BrP were examined in male F344 rats and B6C3F1 mice following inhalation exposure (800 ppm) or intravenous administration (5, 20, and 100 mg/kg). [1,2,3-(13)C]1-BrP and [1-(14)C]1-BrP were administered to enable characterization of urinary metabolites using NMR spectroscopy, LC-MS/MS, and HPLC coupled radiochromatography. Exhaled breath volatile organic chemicals (VOC), exhaled CO(2), urine, feces, and tissues were collected for up to 48 h post-administration for determination of radioactivity distribution. Rats and mice exhaled a majority of the administered dose as either VOC (40-72%) or (14)CO(2) (10-30%). For rats, but not mice, the percentage of the dose exhaled as VOC increased between the mid ( approximately 50%) and high ( approximately 71%) dose groups; while the percentage of the dose exhaled as (14)CO(2) decreased (19 to 10%). The molar ratio of exhaled (14)CO(2) to total released bromide, which decreased as dose increased, demonstrated that the proportion of 1-BrP metabolized via oxidation relative to pathways dependent on glutathione conjugation is inversely proportional to dose in the rat. [(14)C]1-BrP equivalents were recovered in urine (13-17%, rats; 14-23% mice), feces (<2%), or retained in the tissues and carcass (<6%) of rats and mice administered i.v. 5 to 100 mg/kg [(14)C]1-BrP. Metabolites characterized in urine of rats and mice include N-acetyl-S-propylcysteine, N-acetyl-3-(propylsulfinyl)alanine, N-acetyl-S-(2-hydroxypropyl)cysteine, 1-bromo-2-hydroxypropane-O-glucuronide, N-acetyl-S-(2-oxopropyl)cysteine, and N-acetyl-3-[(2-oxopropyl)sulfinyl]alanine. These metabolites may be formed following oxidation of 1-bromopropane to 1-bromo-2-propanol and bromoacetone and following subsequent glutathione conjugation with either of these compounds. Rats pretreated with 1-aminobenzotriazole (ABT), a potent inhibitor of P450 excreted less in urine (down 30%), exhaled as (14)CO2 (down 80%), or retained in liver (down 90%), with a concomitant increase in radioactivity expired as VOC (up 52%). Following ABT pretreatment, rat urinary metabolites were reduced in number from 10 to 1, N-acetyl-S-propylcysteine, which accounted for >90% of the total urinary radioactivity in ABT pretreated rats. Together, these data demonstrate a role for cytochrome P450 and glutathione in the dose-dependent metabolism and disposition of 1-BrP in the rat.

Animals↗
PubMed2001

Impact of bacteria in dairy products and of the intestinal microflora on the genotoxic and carcinogenic effects of heterocyclic aromatic amines.

This article gives a short overview on the present state of knowledge of the effects of the intestinal microflora on the health hazards of heterocyclic aromatic amines (HAs). Results of single cell gel electrophoresis assays with conventional, germ free and human flora associated rats indicate that the presence of intestinal microorganisms strongly enhances the induction of DNA-damage in colon and liver cells by IQ. Furthermore, it was found that supplementation of the feed with Lactobacilli attenuates the induction of colon cancer by this same amine. These recent findings suggest that the intestinal microflora and lactic acid bacilli in dairy products strongly affect the health risks of HAs. Nevertheless, most previous experiments with HAs focused on the involvement of mammalian enzymes in the biotransformation of these compounds and only a few articles are available which concern interactions of bacteria with HAs. Some of these studies suggested that the formation of directly mutagenic hydroxy-metabolites of the amines by fecal bacteria might be an important activation pathway but it turned out that the hydroxy-derivative of IQ is not genotoxic in mammalian cells and does not cause colon cancer in laboratory rodents. There is some evidence that hydrolysis of HA-metabolites by bacterial ss-glucuronidase might play a role in the activation of HAs but experimental data are scarce and no firm conclusions can be drawn at present. The most important detoxification mechanism appears to be the direct binding of the HAs to the cell walls of certain bacterial strains contained in fermented foods. It was shown that these effects do also take place under physiologically relevant conditions. Overall, it seems that intestinal bacteria play a key role in the activation and detoxification of HAs which has been an area of research long ignored. The elucidation of these mechanisms may enable the development of biomarkers for colon cancer risk and nutritional strategies of protection.

Amines↗
PubMed2006

Asthma: defining of the persistent adult phenotypes.

The common disease asthma is probably not a single disease, but rather a complex of multiple, separate syndromes that overlap. Although clinicians have recognised these different phenotypes for many years, they have remained poorly characterised, with little known about the underlying pathobiology contributing to them. Development of targeted therapies for asthma, and phenotype-specific clinical trials have raised interest in these phenotypes. Improved understanding of these phenotypes in complex diseases such as asthma will also improve our ability to link specific genotypes to their associated disease, which should help development of biomarkers. However, there is no standardised method to define asthma phenotypes. This Review analyses some of the methods that have been used to define asthma phenotypes and proposes an integrated method of classification to improve our understanding of these phenotypes.

Adrenal Cortex Hormones↗
PubMed2000

Biochemical and (ultra)structural hepatic perturbations of Brachydanio rerio (Teleostei, Cyprinidae) exposed to two sublethal concentrations of copper sulfate.

The aim of this study was to compare biochemical and (ultra)structural perturbations induced by Cu in the liver of Brachydanio rerio exposed for 14 days to sublethal concentrations of copper and then replaced for 14 days to clean water. Toxicity of Cu was clearly demonstrated: simultaneously to Cu accumulation, the liver developed large lysed areas and hepatocytic alterations. However, the majority of the parenchyma was composed of functional dark hepatocytes displaying typical feature of increased metabolism: development of rough reticulum, increase in size of nucleus and nucleolus, glycogenic depletion. Increase in hepatic protein content and of anti-oxidative defences (glutathione content, catalase and glutathione-S-transferase (GST) activities) indicated that the overall response of the liver was adaptative. In all hepatocytes a cord-like structure of the nucleoli was suspected to be associated to metal deposition. After 14 days depuration, the liver still contained high Cu concentrations and the hepatic alterations were not reversed. Such complementary studies are necessary for a better understanding of the deleterious effects of pollutants and for the development of biomarkers for metal toxicity.

Journal Article↗
PubMed2000

Changes in immune function with age.

Aging is associated with a decline in immune function in humans and animals. The primary defects appear to reside in the T-cell compartment. Improving understanding of the mechanisms underlying the general decline in immune functions with age may enhance our ability to prevent and treat age-associated illnesses. Development of biomarker(s) of immune senescence may eventually help clinicians to identify subpopulations of the elderly who are at risk for infections, malignancies, and possibly autoimmune diseases.

Aged↗
PubMed1999

Identification of modified tryptophan residues in apolipoprotein B-100 derived from copper ion-oxidized low-density lipoprotein.

Oxidative modifications of low-density lipoproteins (LDL) may contribute to the pathogenesis of atherosclerosis. Although the oxidation products of the lipid components of LDL have been studied extensively, less is known about the oxidation products of the apoprotein, apolipoprotein B-100. To identify the specific oxidative modifications, we oxidized LDL in the presence of Cu(2+), treated with DNPH, precipitated and delipidated the protein, digested the protein with trypsin, and analyzed the peptides by high-performance liquid chromatography. We isolated nine peptides that exhibited measurable absorbance at 365 nm, which is characteristic of hydrazones derived from DNPH and is not observed in peptides derived from unoxidized LDL. Unexpectedly, we obtained the same peptides with absorbance at 365 nm in Cu(2+)-oxidized LDL not treated with DNPH. N-terminal sequence analyses and mass spectrometry indicated that the peptides isolated from the Cu(2+)-oxidized LDL all contained kynurenine residues in place of Trp residues found in the native apoprotein. The product profile we observed in Cu(2+)-oxidized LDL was remarkably different from the profiles observed in LDL oxidized by HOCl or myeloperoxidase in vitro, and the preferential oxidation of Trp to kynurenine in Cu(2+)-catalyzed oxidation of LDL contrasts with the products observed following oxidation of LDL with HOCl or myeloperoxidase. Our studies to date support the working hypothesis that the specific products of protein oxidation are sufficiently distinct to be developed as biomarkers of proposed mechanisms of oxidation of LDL and biological molecules in other toxicities and diseases.

Amino Acid Sequence↗
PubMed2001

Metabonomic investigations into hydrazine toxicity in the rat.

The systemic biochemical effects of oral hydrazine administration (dosed at 75, 90, and 120 mg/kg) have been investigated in male Han Wistar rats using metabonomic analysis of (1)H NMR spectra of urine and plasma, conventional clinical chemistry, and liver histopathology. Plasma samples were collected both pre- and 24 h postdose, while urine was collected predose and daily over a 7 day postdose period. (1)H NMR spectra of the biofluids were analyzed visually and via pattern recognition using principal component analysis. The latter showed that there was a dose-dependent biochemical effect of hydrazine treatment on the levels of a range of low molecular weight compounds in urine and plasma, which was correlated with the severity of the hydrazine induced liver lesions. In plasma, increases in the levels of free glycine, alanine, isoleucine, valine, lysine, arginine, tyrosine, citrulline, 3-D-hydroxybutyrate, creatine, histidine, and threonine were observed. Urinary excretion of hippurate, citrate, succinate, 2-oxoglutarate, trimethylamine-N-oxide, fumarate and creatinine were decreased following hydrazine dosing, whereas taurine, creatine, threonine, N-methylnicotinic acid, tyrosine, beta-alanine, citrulline, Nalpha-acetylcitrulline and argininosuccinate excretion was increased. Moreover, the most notable effect was the appearance in urine and plasma of 2-aminoadipate, which has previously been shown to lead to neurological effects in rats. High urinary levels of 2-aminoadipate may explain the hitherto poorly understood neurological effects of hydrazine. Metabonomic analysis of high-resolution (1)H NMR spectra of biofluids has provided a means of monitoring the progression of toxicity and recovery, while also allowing the identification of novel biomarkers of development and regression of the lesion.

Administration, Oral↗
PubMedDate not supplied

Characterization of N1- and N6-adenosine adducts and N1-inosine adducts formed by the reaction of butadiene monoxide with adenosine: evidence for the N1-adenosine adducts as major initial products.

1,3-Butadiene is a known human mutagen and possible human carcinogen; however, the molecular mechanisms of its activity are poorly understood. We have previously shown that the primary metabolite, butadiene monoxide (BM), reacts with guanosine to form N1-, N2-, and N7-guanosine adducts. In this study we characterize the reaction of BM with adenosine; ten adducts identified as diastereomeric pairs of N1-(1-hydroxy-3-buten-2-yl)adenosine,N1-(2-hydroxy-3-buten-1 -yl)adenosine, N6-(1-hydroxy-3-buten-2-yl)adenosine,N6-(2-hydroxy-3-buten-+ ++1yl)adenosine, and N1-(1-hydroxy-3-buten-2-yl)inosine are characterized. The N6-adenosine and N1-inosine adducts were characterized by their UV spectra, 1H NMR, FAB/MS, and stability studies. The N6-adenosine and N1-inosine adducts were stable for up to 168 h at 37 degrees C in phosphate buffer (pH 7.4). The N1-adenosine adducts, which were unstable at pH 7.4 at 37 degrees C (half-life of 7 and 9.5 h for the two regioisomers), were characterized by their UV spectra and their ability to undergo the Dimroth rearrangement to yield the corresponding N6-adenosine adducts, or undergo deamination to yield the corresponding N1-inosine adducts. Upon the reaction of BM with adenosine in phosphate buffer (pH 7.4) at 37 degrees C, the N1-adenosine adducts were the first to be detected, with the N6-adenosine and N1-inosine adducts. showing a lag in formation possibly due to the time needed for rearrangement/deamination. Reaction of adenosine with an excess of BM in phosphate buffer (pH 7.4) at 37 degrees C, followed by extraction of the reaction mixture with ethyl ether to remove excess unreacted BM and incubation at 80 degrees C for 1 h, resulted in complete conversion of N1-adenosine adducts to the corresponding N6-adenosine and N1-inosine adducts. Under these conditions, adduct formation exhibited pseudo-first-order kinetics, with the combined N6-adenosine adducts being formed 3-fold more favorably than the combined N1-inosine adducts. When incubations were carried out at lower BM concentrations, the N6-adenosine adducts remained the major detectable adducts at all concentrations. These results show that adenosine, in addition to guanosine, can lead to multiple adducts when incubated with BM, and may be useful in development of biomarkers for exposure to 1,3-butadiene. Characterization of the N1-adenosine adducts and their rearrangement/deamination products may also contribute to the understanding of mutagenic and carcinogenic mechanisms of 1,3-butadiene.

Adenosine↗
PubMed2001

Chromosomal deletions and tumor suppressor genes in prostate cancer.

Chromosomal deletion appears to be the earliest as well as the most frequent somatic genetic alteration during carcinogenesis. It inactivates a tumor suppressor gene in three ways, that is, revealing a gene mutation through loss of heterozygosity as proposed in the two-hit theory, inducing haploinsufficiency through quantitative hemizygous deletion and associated loss of expression, and truncating a genome by homozygous deletion. Whereas the two-hit theory has guided the isolation of many tumor suppressor genes, the haploinsufficiency hypothesis seems to be also useful in identifying target genes of chromosomal deletions, especially for the deletions detected by comparative genomic hybridization (CGH). At present, a number of chromosomal regions have been identified for their frequent deletions in prostate cancer, including 2q13-q33, 5q14-q23, 6q16-q22, 7q22-q32, 8p21-p22, 9p21-p22, 10q23-q24, 12p12-13, 13q14-q21, 16q22-24, and 18q21-q24. Strong candidate genes have been identified for some of these regions, including NKX3.1 from 8p21, PTEN from 10q23, p27/Kip1 from 12p13, and KLF5 from 13q21. In addition to their location in a region with frequent deletion, there are functional and/or genetic evidence supporting the candidacy of these genes. Thus far PTEN is the most frequently mutated gene in prostate cancer, and KLF5 showed the most frequent hemizygous deletion and loss of expression. A tumor suppressor role has been demonstrated for NKX3.1, PTEN, and p27/Kip1 in knockout mice models. Such genes are important targets of investigation for the development of biomarkers and therapeutic regimens.

Animals↗
PubMed2006

The genetics of Parkinson disease: Implications for neurological care.

The identification of single genes linked to heritable forms of Parkinson disease (PD) has challenged the previously held view of a nongenetic etiology for this progressive movement disorder. Detailed analyses of individuals with mutations in SNCA, Parkin, PINK1, DJ1 or LRRK2 have greatly advanced our knowledge of preclinical and clinical, morphological, and pathological changes in PD. These genetic breakthroughs have had profound implications for scientists, neurologists and patients alike. Such advances have provided unique opportunities to pursue the mechanisms of neuronal degeneration in models of PD pathogenesis, thereby reinforcing the significance of oxidative stress and mitochondrial dysfunction. With emerging clues from familial variants, researchers have begun to explore factors that lead to the expression of the more common, sporadic disease phenotype (idiopathic PD), including interactions between various genes, modifying effects of susceptibility alleles and epigenetic factors, and the influence of environmental agents and aging on the expression of PD-linked genes. These genetic leads have added to the urgency of developing translational drug treatments, and neurologists and their patients are confronting considerations relating to DNA testing. In this article, we summarize recent progress in establishing a neurogenetic component of PD, emphasize the need for developing PD biomarkers to improve diagnostic accuracy (in both clinical practice and therapeutic trials), and discuss scenarios in which specific DNA tests might be considered for diagnostic purposes. In the absence of consensus guidelines for DNA testing in PD and of any neuroprotective treatment for this nonfatal disorder, we remind ourselves of the omnipresent mandate, 'Primum nil nocere!' ('First, do no harm!').

Genes, Dominant↗
PubMed2025

Genome-wide DNA methylation regulation analysis provides novel insights on post-radiation breast cancer.

Breast cancer (BC) is the most common malignancy with a poor prognosis. Radiotherapy is one of the leading traditional treatments for BC. However, radiotherapy-associated secondary diseases are severe issues for the treatment of BC. The present study integrated multi-omics data to investigate the molecular and epigenetic mechanisms involved in post-radiation BC. The differences in the expression of radiation-associated genes between post-radiation and pre-radiation BC samples were determined. Enrichment analysis revealed that these radiation-associated genes involved diverse biological functions and pathways in BC. Combining epigenetic data, we identified radiation-associated genes whose transcriptional changes might be associated with aberrant methylation. Then, we identified potential therapeutic targets and chemical drugs for post-radiation BC patient treatment by constructing a drug-target association network. Specifically, four radiation-associated genes (CD248, CCDC80, GADD45B, and MMP2) whose increased expression might be regulated by hypomethylation of the corresponding enhancer region were found to have excellent diagnostic effects and clinical prognostic value. Finally, we further used independent samples to verify CD248 expression and established a simple epigenetic regulatory model. In summary, this study provides novel insights for understanding the regulation of target genes mediated by DNA methylation and developing potential biomarkers for radiation-associated secondary diseases in BC.

Humans↗
PubMed1999

Milk cytokines and subclinical breast inflammation in Tanzanian women: effects of dietary red palm oil or sunflower oil supplementation.

Previously, we have found that subclinical breast inflammation, as indicated by raised breastmilk concentrations of sodium and the inflammatory cytokine, interleukin-8 (IL-8), was highly prevalent in Bangladesh and associated with poor infant growth. In order to investigate further the prevalence of subclinical breast inflammation and to assess the impact of dietary intervention, we studied rural Tanzanian women taking part in a study of dietary sunflower or red palm oil supplementation during late pregnancy and lactation. We measured breastmilk concentrations of IL-8, the anti-inflammatory cytokine, transforming growth factor-beta2 (TGF-beta) and the ratio of sodium to potassium. We also estimated systemic inflammation by plasma concentrations of the acute phase proteins, alpha1-acid glycoprotein and C-reactive protein. There were highly significant intercorrelations among milk Na/K ratio and concentrations of IL-8 and TGF-beta, the last only after treatment with bile salts which also improved TGF-beta recovery in the enzyme-linked immunosorbent assay (ELISA). Plasma acute phase protein concentrations tended to correlate with milk Na/K ratio and IL-8, suggesting that subclinical breast inflammation was related to systemic inflammation. Dietary supplementation with vitamin E-rich sunflower oil but not provitamin A-containing red palm oil decreased milk Na/K, IL-8 and TGF-beta at 3 months postpartum; however, the effect was significant only for Na/K ratio. The results suggest that milk Na/K ratio, IL-8, and TGF-beta all measure the same phenomenon of subclinical breast inflammation but that Na/K ratio, having the lowest assay variability, is the most useful. Subclinical breast inflammation may result in part from systemic inflammation and may be improved by increased dietary intake of vitamin E-rich sunflower oil.

Acute-Phase Proteins↗
PubMed2005

New biological agents in the treatment of advanced non-small cell lung cancer.

Molecularly targeted therapies that are more tumor specific in their efficacy, with associated fewer toxicities, are currently being developed. Specific biomarkers that may predict response or resistance to a particular agent are being sought. Several classes of compounds now target specific steps in cellular proliferation and apoptosis. These include epidermal growth factor receptor (EGFR) inhibitors, vascular endothelial cell targeting agents, matrix metalloproteinase inhibitors, farnesyltransferase inhibitors, retinoids, proteosome inhibitors, and raf/MAPkinase (mitogen-activated protein kinase) inhibitors. Many of these agents, such as bortezomib, have demonstrated promise in the fields of non-small cell lung cancer (NSCLC). However, a cautionary perspective must be maintained because agents such as bexarotene, which showed promise in early studies, have proved disappointing in randomized trials. As the number of therapeutic agents increases in NSCLC, there will be greater emphasis on the selection of an appropriate patient population in which to give specific, targeted therapies.

Angiogenesis Inhibitors↗
PubMed2007

Molecular markers of early Parkinson's disease based on gene expression in blood.

Parkinson's disease (PD) progresses relentlessly and affects five million people worldwide. Laboratory tests for PD are critically needed for developing treatments designed to slow or prevent progression of the disease. We performed a transcriptome-wide scan in 105 individuals to interrogate the molecular processes perturbed in cellular blood of patients with early-stage PD. The molecular multigene marker here identified is associated with risk of PD in 66 samples of the training set comprising healthy and disease controls [third tertile cross-validated odds ratio of 5.7 (P for trend 0.005)]. It is further validated in 39 independent test samples [third tertile odds ratio of 5.1 (P for trend 0.04)]. Insights into disease-linked processes detectable in peripheral blood are offered by 22 unique genes differentially expressed in patients with PD versus healthy individuals. These include the co-chaperone ST13, which stabilizes heat-shock protein 70, a modifier of alpha-synuclein misfolding and toxicity. ST13 messenger RNA copies are lower in patients with PD (mean +/- SE 0.59 +/- 0.05) than in controls (0.96 +/- 0.09) (P = 0.002) in two independent populations. Thus, gene expression signals measured in blood can facilitate the development of biomarkers for PD.

Biomarkers↗