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            "abstractNote": "Background\nThe present study sought to investigate erythrocyte glutathione S-transferases (GST), NADH-Methaemoglobin reductase (NADH-MR) and Na+/K+-ATPase activities of hypoglycemic rats treated with ethanol/water (1:2 v/v) extract of A. sativa as agent of glycemic control.\n\nMethods\nHyperglycemia was induced by a single intra-peritoneal injection of 0.1 mol/L alloxan monohydrate in phosphate buffer saline (PBS) solution (pH = 7.4); dosage = 140 mg/kg. At the end of the experimental time (t = 76 h), erythrocyte GST, NADH-MR and Na+/K+-ATPase activities as well as serum fasting blood sugar (FBS) levels were measured by spectrophotometric methods.\n\nResults\nSerum FBS levels of control/normal (C/N) rats ranged between 72.93 ± 0.82–95.12 ± 0.92 mg/dL, whereas experimental rats without glycemic control gave: 249.41 ± 1.03–256.11 ± 1.23 mg/dL. Hyperglycemic rats treated with ethanol/water (1:2 v/v) extract of A. sativa exhibited comparative reduced serum levels of FBS alongside with erythrocyte GST, NADH-MR and Na+/K+-ATPase activities. The average relative activities of the three enzymes and corresponding order of enzyme activity in hyperglycemic rats treated with ethanol/water (1:2 v/v) extract of A. sativa was: NADH-MR = 60.99% > GST = 47.81% > Na+/K+-ATPase = 46.81%. In the same order, relative activities of the three enzymes in rats without glycemic control were: NADH-MR = 49.65% > GST = 23.69% > Na+/K+-ATPase = 17.02%.\n\nConclusion\nErythrocyte GST, NADH-MR and Na+/K+-ATPase activities gave insights into the pathophysiology of diabetic state and served as biomarkers for ascertaining therapeutic control in Type 1 diabetes mellitus.",
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            "creatorSummary": "Sternberg and Mitchell",
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            "title": "Plasma neuronal specific enolase: a potential stage diagnostic marker in human African trypanosomiasis",
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                    "creatorType": "author",
                    "firstName": "Jeremy M.",
                    "lastName": "Sternberg"
                },
                {
                    "creatorType": "author",
                    "firstName": "Julia A.",
                    "lastName": "Mitchell"
                }
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            "abstractNote": "Background This study was carried out to determine the potential of neuronal specific enolase (NSE) as a stage diagnostic marker in human African trypanosomiasis.\nMethods Plasma and cerebrospinal fluid were obtained from a cohort of Trypanosoma brucei rhodesiense infected patients and non-infected controls. Neuronal specific enolase concentrations were measured by ELISA and analysed in relation to diagnosis and disease-stage data.\nResults Plasma NSE concentration was significantly increased in late-stage patients (median 21 ng/ml), compared to the control (median 11 ng/ml), but not in early-stage patients (median 5.3 ng/ml). Cerebrospinal fluid NSE concentration did not vary between stages.\nConclusion Plasma NSE is a potential stage diagnostic in this cohort and merits further investigation.",
            "publicationTitle": "Transactions of The Royal Society of Tropical Medicine and Hygiene",
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            "shortTitle": "Plasma neuronal specific enolase",
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                    "lastName": "Reeves"
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            "title": "Repeated exposure to Ochratoxin A generates a neuroinflammatory response, characterized by neurodegenerative M1 microglial phenotype",
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                    "firstName": "Jenny Sandström",
                    "lastName": "von Tobel"
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            "abstractNote": "Neurotoxic effects of the environmentally abundant mycotoxin Ochratoxin A (OTA) were studied in histotypic 3D rat brain cell cultures, comprising all brain cell types. Cultures were exposed to nanomolar OTA concentrations and samples were collected 48 h after a single exposure, or after 10 days of repeated administration. OTA-induced changes in gene- and protein expression, as well as alterations in cell morphology were assessed.\n\nForty-eight-hour OTA exposure resulted in a disruption of the neuronal cytoskeleton and reduced expression of several oligodendrocyte-specific markers indicative of demyelination. Astrocyte disturbances were revealed by a decrease in two astrocytic proteins involved in regulation of inflammatory responses, metallothioneins I and II. Repeated OTA administration induced a neuroinflammatory response, as visualized by an increase of isolectin B4 labelled cells, increased expression of pro-inflammatory cytokines, and detection of macrophagic ED1/CD68 positive cells, as well as an upregulation of neurodegenerative M1 microglial phenotype markers.\n\nPartial recovery from OTA-induced deleterious effects on oligodendrocytes and astrocytes was achieved by co-treatment with sonic hedgehog (SHH). In addition, metallothionein I and II co-treatment partially restored OTA-induced effects on oligodendrocytes after 48 h, and modulated microglial reactivity after 10 days. These results suggest that OTA-exposure affects Shh-signalling, which in turn may influence both oligodendrocytes and astrocytes. Furthermore, the primarily astrocytic proteins MTI/MTII may affect microglial activation. Thus the neuroinflammatory response appears to be downstream of OTA-induced effects on demyelination, axonal instabilities and astrocytes disturbances. In conclusion, repeated OTA-exposure induced a secondary neuroinflammatory response characterized by neurodegenerative M1 microglial activation and pro-inflammatory response that could exacerbate the neurodegenerative process.",
            "publicationTitle": "NeuroToxicology",
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            "title": "Characterization of the platelet granule proteome: Evidence of the presence of MHC1 in alpha-granules",
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                    "firstName": "Anne",
                    "lastName": "Zufferey"
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                    "lastName": "Schvartz"
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                    "lastName": "Reny"
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                    "creatorType": "author",
                    "firstName": "Pierre",
                    "lastName": "Fontana"
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            ],
            "abstractNote": "In the present study, we performed an extensive qualitative characterization of the platelet granule proteome using subcellular fractionation followed by mass spectrometry analysis and functional annotation. Eight-hundred-and-twenty-seven proteins were identified, most of them being associated to granules and to the granule's secretory machinery. Functional pathway analysis revealed 30 pathways, including the major histocompatibility complex class 1 (MHC I) presenting antigen pathway. This pathway was of particular interest for its potential interrelation between platelets and the immune system. Key proteins belonging to this metabolic route such as β-2-microglobulin, 26S protease regulatory subunit 10B from the proteasome and proteins 1 and 2 of the transporter associated with antigen processing were shown to co-localize with von Willebrand factor in resting platelets and to be located on the plasma membrane when platelets were activated. Key proteins of the MHC1 antigen-presenting pathway are located in platelet alpha-granules. These results suggest a possible functional role of platelet granules in platelet-related immune modulation.\nBiological significance\nIn this study, we described the largest dataset related to platelet granule proteins. We performed a functional pathway analysis that evidenced several expected granule-related pathways. We also highlighted the “Antigen processing and presentation” pathway that has drawn our attention. Using immunofluorescence technique, we confirmed the presence of several key proteins for antigen presentation in platelet granules. This study suggests a putative functional role of MHC1 and platelet granules in the immune modulation.",
            "publicationTitle": "Journal of Proteomics",
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                },
                {
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            "itemType": "journalArticle",
            "title": "Assessment of phosphorylation in Toxoplasma glideosome assembly and function",
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                    "firstName": "Damien",
                    "lastName": "Jacot"
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                    "lastName": "Frénal"
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                }
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            "abstractNote": "Members of the phylum Apicomplexa possess a highly conserved molecular motor complex anchored in the parasite pellicle and associated with gliding motility, invasion and egress from infected cells. This machinery, called the glideosome, is structured around the acylated gliding-associated protein GAP45 that recruits the motor complex composed of myosin A and two associated myosin light chains (TgMLC1 and TgELC1). This motor is presumably firmly anchored to the inner membrane complex underneath the plasma membrane via an interaction with two integral membrane proteins, GAP50 and GAP40. To determine if the previously mapped phosphorylation sites on TgGAP45 and TgMLC1 have a direct significance for glideosome assembly and function, a series of phospho-mimetic and phospho-null mutants were generated. Neither the overexpression nor the allelic replacement of TgMLC1 with phospho-mutants impacted on glideosome assembly and parasite motility. TgGAP45 phosphorylation mutants were functionally investigated using a complementation strategy in a TgGAP45 inducible knockout background. The loss of interaction with TgGAP50 by one previously reported GAP45-mutant appeared to depend only on the presence of a remaining competing wild type copy of TgGAP45. Accordingly, this mutant displayed no phenotype in complementation experiments. Unexpectedly, GAP45 lacking the region encompassing the cluster of twelve phosphorylation sites did not impact on its dual function in motor recruitment and pellicle integrity. Despite the extensive phosphorylation of TgMLC1 and TgGAP45, this post-translational modification does not appear to be critical for the assembly and function of the glideosome.",
            "publicationTitle": "Cellular Microbiology",
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            "journalAbbreviation": "Cell Microbiol",
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            "itemType": "journalArticle",
            "title": "Post-Acute Brain Injury Urinary Signature: A New Resource for Molecular Diagnostics",
            "creators": [
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                    "firstName": "Andrew K.",
                    "lastName": "Ottens"
                },
                {
                    "creatorType": "author",
                    "firstName": "Jillian E.",
                    "lastName": "Stafflinger"
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                    "lastName": "Griffin"
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                    "lastName": "Kunz"
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                    "firstName": "David X.",
                    "lastName": "Cifu"
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                {
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                    "firstName": "Janet P.",
                    "lastName": "Niemeier"
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            ],
            "abstractNote": "Heterogeneity within brain injury presents a challenge to the development of informative molecular diagnostics. Recent studies show progress, particularly in cerebrospinal fluid, with biomarker assays targeting one or a few structural proteins. Protein-based assays in peripheral fluids, however, have been more challenging to develop, in part because of restricted and intermittent barrier access. Further, a greater number of molecular variables may be required to inform on patient status given the multi-factorial nature of brain injury. Presented is an alternative approach profiling peripheral fluid for a class of small metabolic by-products rendered by ongoing brain pathobiology. Urine specimens were collected for head trauma subjects upon admission to acute brain injury rehabilitation and non-traumatized matched controls. An innovative data-independent mass spectrometry approach was employed for reproducible molecular quantification across osmolarity-normalized samples. The postacute human traumatic brain injury urinary signature encompassed 2476 discriminant variables reproducibly measured in specimens for subject classification. Multiple subprofiles were then discerned in correlation with injury severity per the Glasgow Comma Scale and behavioral and neurocognitive function per the Patient Competency Rating Scale and Frontal Systems Behavioral Scale. Identified peptide constituents were enriched for outgrowth and guidance, extracellular matrix, and post-synaptic density proteins, which were reflective of ongoing post-acute neuroplastic processes demonstrating pathobiological relevance. Taken together, these findings support further development of diagnostics based on brain injury urinary signatures using either combinatorial quantitative models or pattern-recognition methods. Particularly, these findings espouse assay development to address unmet diagnostic and theragnostic needs in brain injury rehabilitative medicine.",
            "publicationTitle": "Journal of Neurotrauma",
            "publisher": "",
            "place": "",
            "date": "décembre 29, 2013",
            "volume": "31",
            "issue": "8",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "782-788",
            "series": "",
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            "journalAbbreviation": "Journal of Neurotrauma",
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            "PMID": "",
            "PMCID": "",
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            "shortTitle": "Post-Acute Brain Injury Urinary Signature",
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            "libraryCatalog": "online.liebertpub.com (Atypon)",
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                "CNN5THP7"
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                    "firstName": "Jiangyong",
                    "lastName": "Gu"
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                {
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                    "firstName": "Fang",
                    "lastName": "Luo"
                },
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                    "firstName": "Lirong",
                    "lastName": "Chen"
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                    "firstName": "Xiaojie",
                    "lastName": "Xu"
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            "abstractNote": "Chemogenomics focuses on the interactions between biologically active molecules and protein targets for drug discovery. Carbohydrates are the most abundant compounds in natural products. Compared with other drugs, the carbohydrate drugs show weaker side effects. Searching for multi-target carbohydrate drugs can be regarded as a solution to improve therapeutic efficacy and safety. In this work, we collected 60344 carbohydrates from the Universal Natural Products Database (UNPD) and explored the chemical space of carbohydrates by principal component analysis. We found that there is a large quantity of potential lead compounds among carbohydrates. Then we explored the potential of carbohydrates in drug discovery by using a network-based multi-target computational approach. All carbohydrates were docked to 2389 target proteins. The most potential carbohydrates for drug discovery and their indications were predicted based on a docking score-weighted prediction model. We also explored the interactions between carbohydrates and target proteins to find the pathological networks, potential drug candidates and new indications.",
            "publicationTitle": "Molecular BioSystems",
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            "abstractNote": "Numerous clinical trials are currently evaluating new strategies to halt the progression of renal damage in patients with chronic kidney diseases (CKDs). Unfortunately, none of them have considered that the lack of response to new therapies may be due to the pharmacogenetics/pharmacogenomics profile of the patient. The recent impact of high-throughput technologies used in genomics, proteomics and metabolomics may open a new way for discovering biomarkers that can provide us information about the mechanisms on the progression of renal damage. However, they can also be used for diagnosis and for selecting drugs, leading to personalized tailored therapy. The uses of classifiers formed by a list of genes, proteins and metabolites have been introduced into oncology and organ transplantation. These new approaches have recently also been used in the care of human glomerulonephritis. Integrating the large omic data sets with drug and disease databases could give the prediction of drug efficacy and side effects in CKDs.",
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