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[PMID]: 25819077
[Au] Autor:Agarwal S; Ghanty P; Pal NR
[Ad] Address:Electronics and Communication Sciences Unit, Indian Statistical Institute, Calcutta 700108 and.
[Ti] Title:Identification of a small set of plasma signalling proteins using neural network for prediction of Alzheimer's disease.
[So] Source:Bioinformatics;31(15):2505-13, 2015 Aug 1.
[Is] ISSN:1367-4811
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:MOTIVATION: Alzheimer's disease (AD) is a dementia that gets worse with time resulting in loss of memory and cognitive functions. The life expectancy of AD patients following diagnosis is ∼7 years. In 2006, researchers estimated that 0.40% of the world population (range 0.17-0.89%) was afflicted by AD, and that the prevalence rate would be tripled by 2050. Usually, examination of brain tissues is required for definite diagnosis of AD. So, it is crucial to diagnose AD at an early stage via some alternative methods. As the brain controls many functions via releasing signalling proteins through blood, we analyse blood plasma proteins for diagnosis of AD. RESULTS: Here, we use a radial basis function (RBF) network for feature selection called feature selection RBF network for selection of plasma proteins that can help diagnosis of AD. We have identified a set of plasma proteins, smaller in size than previous study, with comparable prediction accuracy. We have also analysed mild cognitive impairment (MCI) samples with our selected proteins. We have used neural networks and support vector machines as classifiers. The principle component analysis, Sammmon projection and heat-map of the selected proteins have been used to demonstrate the proteins' discriminating power for diagnosis of AD. We have also found a set of plasma signalling proteins that can distinguish incipient AD from MCI at an early stage. Literature survey strongly supports the AD diagnosis capability of the selected plasma proteins. AVAILABILITY AND IMPLEMENTATION: The FSRBF code is available at https://sites.google.com/site/agarwalswapna/publications. CONTACT: agarwal.swapna@gmail.com or swapna_r@isical.ac.in SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1093/bioinformatics/btv173

  2 / 264667 MEDLINE  
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[PMID]: 25707913
[Au] Autor:Yang Q; Lai SK
[Ad] Address:Division of Molecular Pharmaceutics, University of North Carolina, Chapel Hill, NC, USA.
[Ti] Title:Anti-PEG immunity: emergence, characteristics, and unaddressed questions.
[So] Source:Wiley Interdiscip Rev Nanomed Nanobiotechnol;7(5):655-77, 2015 Sep.
[Is] ISSN:1939-0041
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The modification of protein and nanoparticle therapeutics with polyethylene glycol (PEG), a flexible, uncharged, and highly hydrophilic polymer, is a widely adopted approach to reduce RES clearance, extend circulation time, and improve drug efficacy. Nevertheless, an emerging body of literature, generated by numerous research groups, demonstrates that the immune system can produce antibodies that specifically bind PEG, which can lead to the 'accelerated blood clearance' of PEGylated therapeutics. In animals, anti-PEG immunity is typically robust but short-lived and consists of a predominantly anti-PEG IgM response. Rodent studies suggest that the induction of anti-PEG antibodies (α-PEG Abs) primarily occurs through a type 2 T-cell independent mechanism. Although anti-PEG immunity is less well-studied in humans, the presence of α-PEG Abs has been correlated with reduced efficacy of PEGylated therapeutics in clinical trials. The prevalence of anti-PEG IgG and reports of memory immune responses, as well as the existence of α-PEG Abs in healthy untreated individuals, suggests that the mechanism(s) and features of human anti-PEG immune responses may differ from those of animal models. Many questions, including the incidence rate of pre-existing α-PEG Abs and immunological mechanism(s) of α-PEG Ab formation in humans, must be answered in order to fully address the potential complications of anti-PEG immunity. WIREs Nanomed Nanobiotechnol 2015, 7:655-677. doi: 10.1002/wnan.1339 For further resources related to this article, please visit the WIREs website.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150726
[Lr] Last revision date:150726
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1002/wnan.1339

  3 / 264667 MEDLINE  
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[PMID]: 25722384
[Au] Autor:Murea M; Hsu FC; Cox AJ; Hugenschmidt CE; Xu J; Adams JN; Raffield LM; Whitlow CT; Maldjian JA; Bowden DW; Freedman BI
[Ad] Address:Internal Medicine-Nephrology, Wake Forest School of Medicine, Winston-Salem, NC, USA....
[Ti] Title:Structural and functional assessment of the brain in European Americans with mild-to-moderate kidney disease: Diabetes Heart Study-MIND.
[So] Source:Nephrol Dial Transplant;30(8):1322-9, 2015 Aug.
[Is] ISSN:1460-2385
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Advanced chronic kidney disease (CKD) is associated with altered cerebral structure and function. Relationships between mild-to-moderate CKD and brain morphology and cognitive performance were evaluated in European Americans (EAs). METHODS: A total of 478 EAs with estimated glomerular filtration rate (eGFR) >45 mL/min/1.73 m(2) and urine albumin:creatinine ratio (UACR) < 300 mg/g, most with type 2 diabetes (T2D), were included. Measures of total intracranial volume (TICV), cerebrospinal fluid volume, total white matter volume (TWMV), total gray matter volume (TGMV), total white matter lesion volume (TWMLV), hippocampal white matter volume (HWMV) and hippocampal gray matter volume (HGMV) were obtained with magnetic resonance imaging. Cognitive testing included memory (Rey Auditory Visual Learning Test), global cognition (Modified Mini-Mental State Examination) and executive function (Stroop Task, Semantic Fluency, Digit Symbol Substitution Test). Associations with CKD were assessed using log-transformed eGFR and UACR, adjusted for age, sex, body mass index, smoking, hemoglobin A1c, blood pressure, diabetes duration, cardiovascular disease and education. RESULTS: Participants were 55.2% female, 78.2% had T2D; mean SD age 67.6 9.0 years, T2D duration 16.4 6.5 years, eGFR 92.0 22.3 mL/min/1.73 m(2) and UACR 23.8 39.6 mg/g. In adjusted models, eGFR was negatively associated with TICV only in participants with T2D [parameter estimate (): -72.2, P = 0.002]. In non-diabetic participants, inverse relationships were observed between eGFR and HGMV (: -1.0, P = 0.03) and UACR and normalized TWMLV (: -0.2, P = 0.03). Kidney function and albuminuria did not correlate with cognitive testing. CONCLUSIONS: In EAs with mild CKD enriched for T2D, brain structure and cognitive performance were generally not impacted. Longitudinal studies are necessary to determine when cerebral structural changes and cognitive dysfunction develop with progressive CKD in EAs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150725
[Lr] Last revision date:150725
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1093/ndt/gfv030

  4 / 264667 MEDLINE  
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[PMID]: 25963901
[Au] Autor:Graham DL; Buendia MA; Chapman MA; Durai HH; Stanwood GD
[Ad] Address:Department of Biomedical Sciences, Florida State University College of Medicine, Tallahassee, Florida, 32303....
[Ti] Title:Deletion of Gαq in the telencephalon alters specific neurobehavioral outcomes.
[So] Source:Synapse;69(9):434-45, 2015 Sep.
[Is] ISSN:1098-2396
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Gαq -coupled receptors are ubiquitously expressed throughout the brain and body, and it has been shown that these receptors and associated signaling cascades are involved in a number of functional outputs, including motor function and learning and memory. Genetic alterations to Gαq have been implicated in neurodevelopmental disorders such as Sturge-Weber syndrome. Some of these associated disease outcomes have been modeled in laboratory animals, but as Gαq is expressed in all cell types, it is difficult to differentiate the underlying circuitry or causative neuronal population. To begin to address neuronal cell type diversity in Gαq function, we utilized a conditional knockout mouse whereby Gαq was eliminated from telencephalic glutamatergic neurons. Unlike the global Gαq knockout mouse, we found that these conditional knockout mice were not physically different from control mice, nor did they exhibit any gross motor abnormalities. However, similarly to the constitutive knockout animal, Gαq conditional knockout mice demonstrated apparent deficits in spatial working memory. Loss of Gαq from glutamatergic neurons also produced enhanced sensitivity to cocaine-induced locomotion, suggesting that cortical Gαq signaling may limit behavioral responses to psychostimulants. Screening for a variety of markers of forebrain neuronal architecture revealed no obvious differences in the conditional knockouts, suggesting that the loss of Gαq in telencephalic excitatory neurons does not result in major alterations in brain structure or neuronal differentiation. Taken together, our results define specific modulation of spatial working memory and psychostimulant responses through disruptions in Gαq signaling within cerebral cortical glutamatergic neurons. Synapse 69:434-445, 2015. 2015 Wiley Periodicals, Inc.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150725
[Lr] Last revision date:150725
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1002/syn.21830

  5 / 264667 MEDLINE  
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[PMID]: 25791036
[Au] Autor:Smith AL; Alexander M; Chrobak JJ; Rosenkrantz TS; Fitch RH
[Ad] Address:Department of Psychology, Behavioral Neuroscience Division, University of Connecticut, Storrs, Conn., USA.
[Ti] Title:Dissociation in the Effects of Induced Neonatal Hypoxia-Ischemia on Rapid Auditory Processing and Spatial Working Memory in Male Rats.
[So] Source:Dev Neurosci;37(4-5):440-52, 2015.
[Is] ISSN:1421-9859
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Infants born prematurely are at risk for cardiovascular events causing hypoxia-ischemia (HI; reduced blood and oxygen to the brain). HI in turn can cause neuropathology, though patterns of damage are sometimes diffuse and often highly variable (with clinical heterogeneity further magnified by rapid development). As a result, though HI injury is associated with long-term behavioral and cognitive impairments in general, pathology indices for specific infants can provide only limited insight into individual prognosis. The current paper addresses this important clinical issue using a rat model that simulates unilateral HI in a late preterm infant coupled with long-term behavioral evaluation in two processing domains - auditory discrimination and spatial learning/memory. We examined the following: (1) whether deficits on one task would predict deficits on the other (suggesting that subjects with more severe injury perform worse across all cognitive domains) or (2) whether domain-specific outcomes among HI-injured subjects would be uncorrelated (suggesting differential damage to orthogonal neural systems). All animals (sham and HI) received initial auditory testing and were assigned to additional auditory testing (group A) or spatial maze testing (group B). This allowed within-task (group A) and between-task (group B) correlation. Anatomic measures of cortical, hippocampal and ventricular volume (indexing HI damage) were also obtained and correlated against behavioral measures. Results showed that auditory discrimination in the juvenile period was not correlated with spatial working memory in adulthood (group B) in either sham or HI rats. Conversely, early auditory processing performance for group A HI animals significantly predicted auditory deficits in adulthood (p = 0.05; no correlation in shams). Anatomic data also revealed significant relationships between the volumes of different brain areas within both HI and shams, but anatomic measures did not correlate with any behavioral measure in the HI group (though we saw a hippocampal/spatial correlation in shams, in the expected direction). Overall, current data provide an impetus to enhance tools for characterizing individual HI-related pathology in neonates, which could provide more accurate individual prognoses within specific cognitive/behavioral domains and thus improved patient-specific early interventions. 2015 S. Karger AG, Basel.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150725
[Lr] Last revision date:150725
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1159/000375487

  6 / 264667 MEDLINE  
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[PMID]: 26193280
[Au] Autor:Jin S; Cui W; Jin Z; Wang Y
[Ad] Address:School of Electronic Information Engineering, Tianjin University, Tianjin 300072, China. Shanye2006@163.com....
[Ti] Title:AF-DHNN: Fuzzy Clustering and Inference-Based Node Fault Diagnosis Method for Fire Detection.
[So] Source:Sensors (Basel);15(7):17366-96, 2015.
[Is] ISSN:1424-8220
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Wireless Sensor Networks (WSNs) have been utilized for node fault diagnosis in the fire detection field since the 1990s. However, the traditional methods have some problems, including complicated system structures, intensive computation needs, unsteady data detection and local minimum values. In this paper, a new diagnosis mechanism for WSN nodes is proposed, which is based on fuzzy theory and an Adaptive Fuzzy Discrete Hopfield Neural Network (AF-DHNN). First, the original status of each sensor over time is obtained with two features. One is the root mean square of the filtered signal (FRMS), the other is the normalized summation of the positive amplitudes of the difference spectrum between the measured signal and the healthy one (NSDS). Secondly, distributed fuzzy inference is introduced. The evident abnormal nodes' status is pre-alarmed to save time. Thirdly, according to the dimensions of the diagnostic data, an adaptive diagnostic status system is established with a Fuzzy C-Means Algorithm (FCMA) and Sorting and Classification Algorithm to reducing the complexity of the fault determination. Fourthly, a Discrete Hopfield Neural Network (DHNN) with iterations is improved with the optimization of the sensors' detected status information and standard diagnostic levels, with which the associative memory is achieved, and the search efficiency is improved. The experimental results show that the AF-DHNN method can diagnose abnormal WSN node faults promptly and effectively, which improves the WSN reliability.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.3390/s150717366

  7 / 264667 MEDLINE  
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[PMID]: 26194093
[Au] Autor:Chang L; Cui W; Yang Y; Xu S; Zhou W; Fu H; Hu S; Mak S; Hu J; Wang Q; Pui-Yan Ma V; Chung-Lit Choi T; Dik-Lung Ma E; Tao L; Pang Y; Rowan MJ; Anwyl R; Han Y; Wang Q
[Ad] Address:Department of Physiology, Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University. Ningbo 315211, China....
[Ti] Title:Protection against -amyloid-induced synaptic and memory impairments via altering -amyloid assembly by bis(heptyl)-cognitin.
[So] Source:Sci Rep;5:10256, 2015.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:-amyloid (A) oligomers have been closely implicated in the pathogenesis of Alzheimer's disease (AD). We found, for the first time, that bis(heptyl)-cognitin, a novel dimeric acetylcholinesterase (AChE) inhibitor derived from tacrine, prevented A oligomers-induced inhibition of long-term potentiation (LTP) at concentrations that did not interfere with normal LTP. Bis(heptyl)-cognitin also prevented A oligomers-induced synaptotoxicity in primary hippocampal neurons. In contrast, tacrine and donepezil, typical AChE inhibitors, could not prevent synaptic impairments in these models, indicating that the modification of A oligomers toxicity by bis(heptyl)-cognitin might be attributed to a mechanism other than AChE inhibition. Studies by using dot blotting, immunoblotting, circular dichroism spectroscopy, and transmission electron microscopy have shown that bis(heptyl)-cognitin altered A assembly via directly inhibiting A oligomers formation and reducing the amount of preformed A oligomers. Molecular docking analysis further suggested that bis(heptyl)-cognitin presumably interacted with the hydrophobic pockets of A, which confers stabilizing powers and assembly alteration effects on A. Most importantly, bis(heptyl)-cognitin significantly reduced cognitive impairments induced by intra-hippocampal infusion of A oligomers in mice. These results clearly demonstrated how dimeric agents prevent A oligomers-induced synaptic and memory impairments, and offered a strong support for the beneficial therapeutic effects of bis(heptyl)-cognitin in the treatment of AD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/srep10256

  8 / 264667 MEDLINE  
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[PMID]: 26191658
[Au] Autor:Plumlee CR; Obar JJ; Colpitts SL; Jellison ER; Haining WN; Lefrancois L; Khanna KM
[Ad] Address:Dept. of Immunology, University of Connecticut Health Center, Farmington, CT....
[Ti] Title:Early Effector CD8 T Cells Display Plasticity in Populating the Short-Lived Effector and Memory-Precursor Pools Following Bacterial or Viral Infection.
[So] Source:Sci Rep;5:12264, 2015.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Nave antigen-specific CD8 T cells expand in response to infection and can be phenotypically separated into distinct effector populations, which include memory precursor effector cells (MPECs) and short-lived effector cells (SLECs). In the days before the peak of the T cell response, a third population called early effector cells (EECs) predominate the antigen-specific response. However, the contribution of the EEC population to the CD8 T cell differentiation program during an antimicrobial immune response is not well understood. To test if EEC populations were pre-committed to either an MPEC or SLEC fate, we purified EECs from mice infected with Listeria monocytogenes (LM) or vesicular stomatitis virus (VSV), where the relative frequency of each population is known to be different at the peak of the response. Sorted EECs transferred into uninfected hosts revealed that EECs were pre-programmed to differentiate based on early signals received from the distinct infectious environments. Surprisingly, when these same EECs were transferred early into mismatched infected hosts, the transferred EECs could be diverted from their original fate. These results delineate a model of differentiation where EECs are programmed to form MPECs or SLECs, but remain susceptible to additional inflammatory stimuli that can alter their fate.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/srep12264

  9 / 264667 MEDLINE  
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[PMID]: 26193112
[Au] Autor:Lench AM; Robson E; Jones RS
[Ad] Address:Department of Pharmacy and Pharmacology, University of Bath, Bath, United Kingdom.
[Ti] Title:Differential Effects of D-Cycloserine and ACBC at NMDA Receptors in the Rat Entorhinal Cortex Are Related to Efficacy at the Co-Agonist Binding Site.
[So] Source:PLoS One;10(7):e0133548, 2015.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Partial agonists at the NMDA receptor co-agonist binding site may have potential therapeutic efficacy in a number of cognitive and neurological conditions. The entorhinal cortex is a key brain area in spatial memory and cognitive processing. At synapses in the entorhinal cortex, NMDA receptors not only mediate postsynaptic excitation but are expressed in presynaptic terminals where they tonically facilitate glutamate release. In a previous study we showed that the co-agonist binding site of the presynaptic NMDA receptor is endogenously and tonically activated by D-serine released from astrocytes. In this study we determined the effects of two co-agonist site partial agonists on both presynaptic and postsynaptic NMDA receptors in layer II of the entorhinal cortex. The high efficacy partial agonist, D-cycloserine, decreased the decay time of postsynaptic NMDA receptor mediated currents evoked by electrical stimulation, but had no effect on amplitude or other kinetic parameters. In contrast, a lower efficacy partial agonist, 1-aminocyclobutane-1-carboxylic acid, decreased decay time to a greater extent than D-cycloserine, and also reduced the peak amplitude of the evoked NMDA receptor mediated postsynaptic responses. Presynaptic NMDA receptors, (monitored indirectly by effects on the frequency of AMPA receptor mediated spontaneous excitatory currents) were unaffected by D-cycloserine, but were reduced in effectiveness by 1-aminocyclobutane-1-carboxylic acid. We discuss these results in the context of the effect of endogenous regulation of the NMDA receptor co-agonist site on receptor gating and the potential therapeutic implications for cognitive disorders.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1371/journal.pone.0133548

  10 / 264667 MEDLINE  
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[PMID]: 26191794
[Au] Autor:Fuery A; Richmond PC; Currie AJ
[Ad] Address:School of Paediatrics and Child Health, The University of Western Australia, 35 Stirling Highway, Perth, WA 6009, Australia; Wesfarmers Centre for Vaccines and Infectious Diseases, Telethon Kids Institute, The University of Western Australia, 100 Roberts Road, Perth, WA 6008, Australia.
[Ti] Title:Human Infant Memory B Cell and CD4+ T Cell Responses to HibMenCY-TT Glyco-Conjugate Vaccine.
[So] Source:PLoS One;10(7):e0133126, 2015.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:UNLABELLED: Carrier-specific T cell and polysaccharide-specific B cell memory responses are not well characterised in infants following glyco-conjugate vaccination. We aimed to determine if the number of Meningococcal (Men) C- and Y- specific memory B cells and; number and quality of Tetanus Toxoid (TT) carrier-specific memory CD4+ T cells are associated with polysaccharide-specific IgG post HibMenCY-TT vaccination. Healthy infants received HibMenCY-TT vaccine at 2, 4 and 6 months with a booster at 12 months. Peripheral blood mononuclear cells were isolated and polysaccharide-specific memory B cells enumerated using ELISpot. TT-specific memory CD4+ T cells were detected and phenotyped based on CD154 expression and intracellular TNF-α, IL-2 and IFN-γ expression following stimulation. Functional polysaccharide-specific IgG titres were measured using the serum bactericidal activity (SBA) assay. Polysaccharide-specific Men C- but not Men Y- specific memory B cell frequencies pre-boost (12 months) were significantly associated with post-boost (13 months) SBA titres. Regression analysis showed no association between memory B cell frequencies post-priming (at 6 or 7 months) and SBA at 12 months or 13 months. TT-specific CD4+ T cells were detected at frequencies between 0.001 and 0.112 as a percentage of CD3+ T cells, but their numbers were not associated with SBA titres. There were significant negative associations between SBA titres at M13 and cytokine expression at M7 and M12. CONCLUSION: Induction of persistent polysaccharide-specific memory B cells prior to boosting is an important determinant of secondary IgG responses in infants. However, polysaccharide-specific functional IgG responses appear to be independent of the number and quality of circulating carrier-specific CD4+ T cells after priming.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0133126


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