Database : MEDLINE
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[PMID]: 29510749
[Au] Autor:Sprong H; Azagi T; Hoornstra D; Nijhof AM; Knorr S; Baarsma ME; Hovius JW
[Ad] Address:Centre for Zoonoses & Environmental Microbiology, Centre for Infectious Disease Control, National Institute for Public Health and the Environment, Bilthoven, the Netherlands. hein.sprong@rivm.nl.
[Ti] Title:Control of Lyme borreliosis and other Ixodes ricinus-borne diseases.
[So] Source:Parasit Vectors;11(1):145, 2018 Mar 06.
[Is] ISSN:1756-3305
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Lyme borreliosis (LB) and other Ixodes ricinus-borne diseases (TBDs) are diseases that emerge from interactions of humans and domestic animals with infected ticks in nature. Nature, environmental and health policies at (inter)national and local levels affect the risk, disease burden and costs of TBDs. Knowledge on ticks, their pathogens and the diseases they cause have been increasing, and resulted in the discovery of a diversity of control options, which often are not highly effective on their own. Control strategies involving concerted actions from human and animal health sectors as well as from nature managers have not been formulated, let alone implemented. Control of TBDs asks for a "health in all policies" approach, both at the (inter)national level, but also at local levels. For example, wildlife protection and creating urban green spaces are important for animal and human well-being, but may increase the risk of TBDs. In contrast, culling or fencing out deer decreases the risk for TBDs under specific conditions, but may have adverse effects on biodiversity or may be societally unacceptable. Therefore, in the end, nature and health workers together must carry out tailor-made control options for the control of TBDs for humans and animals, with minimal effects on the environment. In that regard, multidisciplinary approaches in environmental, but also medical settings are needed. To facilitate this, communication and collaboration between experts from different fields, which may include patient representatives, should be promoted.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1186/s13071-018-2744-5

  2 / 68643 MEDLINE  
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[PMID]: 29510721
[Au] Autor:Gill AJ; Garza R; Ambegaokar SS; Gelman BB; Kolson DL
[Ad] Address:Department of Neurology, Perelman School of Medicine, University of Pennsylvania, 415 Curie Boulevard, 280C Clinical Research Building, Philadelphia, PA, 19104, USA.
[Ti] Title:Heme oxygenase-1 promoter region (GT)n polymorphism associates with increased neuroimmune activation and risk for encephalitis in HIV infection.
[So] Source:J Neuroinflammation;15(1):70, 2018 Mar 06.
[Is] ISSN:1742-2094
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Heme oxygenase-1 (HO-1) is a critical cytoprotective enzyme that limits oxidative stress, inflammation, and cellular injury within the central nervous system (CNS) and other tissues. We previously demonstrated that HO-1 protein expression is decreased within the brains of HIV+ subjects and that this HO-1 reduction correlates with CNS immune activation and neurocognitive dysfunction. To define a potential CNS protective role for HO-1 against HIV, we analyzed a well-characterized HIV autopsy cohort for two common HO-1 promoter region polymorphisms that are implicated in regulating HO-1 promoter transcriptional activity, a (GT)n dinucleotide repeat polymorphism and a single nucleotide polymorphism (A(-413)T). Shorter HO-1 (GT)n repeats and the 'A' SNP allele associate with higher HO-1 promoter activity. METHODS: Brain dorsolateral prefrontal cortex tissue samples from an autopsy cohort of HIV-, HIV+, and HIV encephalitis (HIVE) subjects (n = 554) were analyzed as follows: HO-1 (GT)n polymorphism allele lengths were determined by PCR and capillary electrophoresis, A(-413)T SNP alleles were determined by PCR with allele specific probes, and RNA expression of selected neuroimmune markers was analyzed by quantitative PCR. RESULTS: HIV+ subjects with shorter HO-1 (GT)n alleles had a significantly lower risk of HIVE; however, shorter HO-1 (GT)n alleles did not correlate with CNS or peripheral viral loads. In HIV+ subjects without HIVE, shorter HO-1 (GT)n alleles associated significantly with lower expression of brain type I interferon response markers (MX1, ISG15, and IRF1) and T-lymphocyte activation markers (CD38 and GZMB). No significant correlations were found between the HO-1 (GT)n repeat length and brain expression of macrophage markers (CD163, CD68), endothelial markers (PECAM1, VWF), the T-lymphocyte marker CD8A, or the B-lymphocyte maker CD19. Finally, we found no significant associations between the A(-413)T SNP and HIVE diagnosis, HIV viral loads, or any neuroimmune markers. CONCLUSION: Our data suggest that an individual's HO-1 promoter region (GT)n polymorphism allele repeat length exerts unique modifying risk effects on HIV-induced CNS neuroinflammation and associated neuropathogenesis. Shorter HO-1 (GT)n alleles increase HO-1 promoter activity, which could provide neuroprotection through decreased neuroimmune activation. Therapeutic strategies that induce HO-1 expression could decrease HIV-associated CNS neuroinflammation and decrease the risk for development of HIV neurological disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1186/s12974-018-1102-z

  3 / 68643 MEDLINE  
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[PMID]: 29505789
[Au] Autor:Ritchie L; Tate R; Chamberlain LH; Robertson G; Zagnoni M; Sposito T; Wray S; Wright JA; Bryant CE; Gay NJ; Bushell TJ
[Ad] Address:Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow G4 0RE, UK.
[Ti] Title:Toll-like receptor 3 activation impairs excitability and synaptic activity via TRIF signalling in immature rat and human neurons.
[So] Source:Neuropharmacology;135:1-10, 2018 Mar 02.
[Is] ISSN:1873-7064
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Toll like receptor 3 (TLR3) belongs to a family of pattern recognition receptors that recognise molecules found on pathogens referred to as pathogen associated molecular patterns (PAMPs). Its involvement in innate immunity is well known but despite its presence in the central nervous system (CNS), our knowledge of its function is limited. Here, we have investigated whether TLR3 activation modulates synaptic activity in primary hippocampal cultures and induced pluripotent stem cell (iPSC)-derived neurons. Synaptically driven spontaneous action potential (AP) firing was significantly reduced by the TLR3 specific activator, poly I:C, in a concentration-dependent manner following both short (5 min) and long exposures (1h) in rat hippocampal cultures. Notably, the consequence of TLR3 activation on neuronal function was reproduced in iPSC-derived cortical neurons, with poly I:C (25 µg/ml, 1h) significantly inhibiting sAP firing. We examined the mechanisms underlying these effects, with poly I:C significantly reducing peak sodium current, an effect dependent on the MyD88-independent TRIF dependent pathway. Furthermore, poly I:C (25 µg/ml, 1h) resulted in a significant reduction in miniature excitatory postsynaptic potential (mEPSC) frequency and amplitude and significantly reduced surface AMPAR expression. These novel findings reveal that TLR3 activation inhibits neuronal excitability and synaptic activity through multiple mechanisms, with this being observed in both rat and human iPSC-derived neurons. These data might provide further insight into how TLR3 activation may contribute to neurodevelopmental disorders following maternal infection and in patients with increased susceptibility to herpes simplex encephalitis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 68643 MEDLINE  
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[PMID]: 29272336
[Au] Autor:Thompson J; Bi M; Murchison AG; Makuch M; Bien CG; Chu K; Farooque P; Gelfand JM; Geschwind MD; Hirsch LJ; Somerville E; Lang B; Vincent A; Leite MI; Waters P; Irani SR; Faciobrachial Dystonic Seizures Study Group
[Ad] Address:Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, OX3 9DS, UK.
[Ti] Title:The importance of early immunotherapy in patients with faciobrachial dystonic seizures.
[So] Source:Brain;141(2):348-356, 2018 Feb 01.
[Is] ISSN:1460-2156
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Faciobrachial dystonic seizures and limbic encephalitis closely associate with antibodies to leucine-rich glioma-inactivated 1 (LGI1). Here, we describe 103 consecutive patients with faciobrachial dystonic seizures and LGI1 antibodies to understand clinical, therapeutic and serological differences between those with and without cognitive impairment, and to determine whether cessation of faciobrachial dystonic seizures can prevent cognitive impairment. The 22/103 patients without cognitive impairment typically had normal brain MRI, EEGs and serum sodium levels (P < 0.0001). Overall, cessation of faciobrachial dystonic seizures with antiepileptic drugs alone occurred in only 9/89 (10%) patients. By contrast, 51% showed cessation of faciobrachial dystonic seizures 30 days after addition of immunotherapy (P < 0.0001), with earlier cessation in cognitively normal patients (P = 0.038). Indeed, expedited immunotherapy (P = 0.031) and normal cognition (P = 0.0014) also predicted reduced disability at 24 months. Furthermore, of 80 patients with faciobrachial dystonic seizures as their initial feature, 56% developed cognitive impairment after 90 days of active faciobrachial dystonic seizures. Whereas only one patient developed cognitive impairment after cessation of faciobrachial dystonic seizures (P < 0.0001). All patients had IgG4-LGI1 antibodies, but those with cognitive impairment had higher proportions of complement-fixing IgG1 antibodies (P = 0.03). Both subclasses caused LGI1-ADAM22 complex internalization, a potential non-inflammatory epileptogenic mechanism. In summary, faciobrachial dystonic seizures show striking time-sensitive responses to immunotherapy, and their cessation can prevent the development of cognitive impairment.awx323media15681705685001.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1093/brain/awx323

  5 / 68643 MEDLINE  
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[PMID]: 29523913
[Au] Autor:Steiner J; Prüß H; Köhler S; Hasan A; Falkai P
[Ad] Address:Klinik für Psychiatrie und Psychotherapie, Otto-von-Guericke-Universität Magdeburg, Leipziger Str. 44, 39120, Magdeburg, Deutschland. johann.steiner@med.ovgu.de.
[Ti] Title:Autoimmunenzephalitis mit psychotischer Symptomatik : Diagnostik, Warnhinweise und praktisches Vorgehen. [Autoimmune encephalitis with psychotic symptoms : Diagnostics, warning signs and practical approach].
[So] Source:Nervenarzt;, 2018 Mar 09.
[Is] ISSN:1433-0407
[Cp] Country of publication:Germany
[La] Language:ger
[Ab] Abstract:Despite intensive research, a precise cause of schizophrenic and schizoaffective disorders has not yet been identified. Therefore, psychiatric diagnoses are still made based on clinical ICD-10/DSM­5 criteria and not on any objective markers; however, various causes or pathophysiological processes may ultimately lead to similar symptoms. An important task for the future of psychiatry is to identify disease subtypes with a distinct pathophysiology to develop more specific and causally acting therapies. A new diagnostic entity has become established in clinical neurology and psychiatry in recent years: autoimmune encephalitis with psychotic symptoms caused by specific antineuronal antibodies has been identified as a rare but potentially treatable cause of psychotic disorders; however, these inflammatory brain diseases are not reliably detected by routine psychiatric diagnostics. Therefore, this qualitative review is intended to provide structured support for clinical practice, which, guided by clinical warning signals, enables a rapid and reliable diagnosis as well as the initiation of immunotherapy. In the case of psychiatric symptoms, the additional onset of focal neurological signs, disturbances of consciousness and orientation, autonomic instability or epileptic seizures and electroencephalograph (EEG) abnormalities should always be followed by a more specific cerebrospinal fluid analysis with determination of antineuronal autoantibodies. Although the scientific evidence indicates that only a small subgroup of patients is affected, the swift and correct diagnosis is of high therapeutic and prognostic relevance for the affected individuals.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1007/s00115-018-0499-z

  6 / 68643 MEDLINE  
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[PMID]: 29523295
[Au] Autor:Peter-Ross EM
[Ad] Address:Department of Psychiatry and Mental Health, University of Cape Town, Neurogenetic Psychiatric Outpatients Clinic, Groote Schuur Hospital, Main Road, Observatory 7935, Cape Town, South Africa; Life Vincent Pallotti Hospital, Suite 116, Alexandra Road, Pinelands 7405, Cape Town, South Africa. Electronic address: peterem@mweb.co.za.
[Ti] Title:Molecular hypotheses to explain the shared pathways and underlying pathobiological causes in catatonia and in catatonic presentations in neuropsychiatric disorders.
[So] Source:Med Hypotheses;113:54-64, 2018 Apr.
[Is] ISSN:1532-2777
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The pathobiological causes, the shared cellular and molecular pathways in catatonia and in catatonic presentation in neuropsychiatric disorders are yet to be determined. The hypotheses in this paper have been deduced from the latest scientific research findings and clinical observations of patients with genetic disorders, behavioral phenotypes and other family members suffering mental disorders. The first hypothesis postulates that catatonia and the heterogeneity of catatonic signs and symptoms involve nucleolar dysfunction arising from abnormalities of the brain-specific, non-coding micro-RNA, SNORD115 genes (either duplications or deletions) which result in pathobiological dysfunction of various combinations in the downstream pathways (possibly along with other genes in these shared pathways). SNORD115 controls five genes CRHR1, PBRM1, TAF1, DPM2, and RALGPS1 as well as the alternative splicing of serotonin 2C receptor. SNORD115 abnormalities with varying downstream multigene involvement would account for catatonia across the life span within some subtypes of autism spectrum disorders, schizophrenia, bipolar and major depressive disorder, psychosis, genetic disorders, and in immune disorders such as anti-N-methyl-d-aspartate receptor (NMDAR) antibody encephalitis as well as the susceptibility to the neuroleptic malignant syndrome (NMS) if environmentally triggered. Furthermore, SNORD115 genes may underlie a genetic vulnerability when environmental triggers result in excess serotonin producing the serotonin syndrome, a condition similar to NMS in which catatonia may occur. Dysfunction of SNORD115-PBRM1 connecting with SMARCA2 as well as other proven schizophrenia-associated genes might explain why traditionally catatonia has been classified with schizophrenia. SNORD115-TAF1 and SNORD-DPM2 dysfunction introduce possible clues to the parkinsonism and increased creatinine phosphokinase in NMS, while abnormalities of SNORD115-RALGPS1 suggest links to both anti-NMDAR encephalitis and the proven predisposing catatonic SHANK3 gene. The second hypothesis postulates that periodic catatonia (PC) on 15q15 involves abnormalities of vacuolar protein sorting 39 (VPS39), a proven de novo schizophrenic gene in this chromosomal locus and part of the HOPS complex. These will impact the autophagic and endocytic pathways, thereby lowering lysosomal degradation. VPS39 mutations may be considered also to disrupt lysosome-mitochondria tethering and transport of lipids and calcium through membrane contact sites (MCSs). To account for the periodicity in PC it is speculated that the mammalian equivalent of the vacuole and mitochondria patch (vCLAMP) would be altered by VPS39 mutations and subsequently followed by the mammalian equivalent of endoplasmic reticulum mitochondria encounter structure (ERMES) restoring mitochondrial homeostasis. Future precision psychiatry will require accurate pathophysiologically-defined psychiatric diagnoses to accelerate the discovery of specific molecular-targeted medications to improve therapeutic outcomes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process

  7 / 68643 MEDLINE  
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[PMID]: 29522634
[Au] Autor:De Ciervo F; Willimburgh V; Finvarb G
[Ad] Address:Hospital de Niños "Dr. Ricardo Gutiérrez", Ciudad de Buenos Aires. facundo.dc@hotmail.com.
[Ti] Title:Encefalitis por anticuerpos contra el receptor N-metil-D-aspartato: presentación clínica en un adolescente y revisión de la literatura. ¿Cómo manejar los síntomas neuropsiquiátricos? [N-Methyl-D-Aspartate receptor encephalitis: An adolescent case report and literature review. How to manage neuropsychiatric symptoms].
[So] Source:Vertex;XXVIII(132):128-135, 2017 Mar.
[Is] ISSN:0327-6139
[Cp] Country of publication:Argentina
[La] Language:spa
[Ab] Abstract:Anti-N-methyl-D-aspartate receptor encephalitis was described as a clinical entity in 2007. The present case report aims to describe the signs and symptoms, differential diagnosis, treatment and course of a sixteen-year-old boy with this disorder who was hospitalized for almost two months. In addition, we will expose the therapeutic management and the diffculties presented in the handling of neuropsychiatric symptoms, considering the complex context of heterogeneous clinical manifestations caused by this disorder. The authors conducted a PubMed, LILACS and Cochrane search and added supplementary methods to compile the major quantity of evidence to support the clinical decisions. To date no systematic reviews or clinical guidelines about the management of psychiatric symptoms in adolescents with this condition were found. Only case reports and series of cases are available. The quality of evidence is poor as long as there are not analytic studies available. The adolescent presented to the emergency department with confusion, speech disturbances and right brachio-crural hemiparesis. During the course of hospitalization he developed a catatonic syndrome, several episodes of psychomotor agitation, sleep disorders and psychotic symptoms. He received successive immunomodulatory therapy for autoimmune encephalitis and psychiatric medication. He was discharged with recovery almost ad integrum. In conclusion, the diagnosis of anti-rNMDA encephalitis should be suspected in previously healthy adolescents with no psychopathological antecedents who suddenly present psychiatric and neurological symptoms. The evolution and prognosis depend on the early initiation of immunomodulating therapy. Psychiatrists should be aware and suspect this entity rapidly and play an important role as consultants for the management of psychiatric and behavioral disturbances.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  8 / 68643 MEDLINE  
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[PMID]: 29446298
[Au] Autor:Katamanova EV; Dyakovich MP; Kudaeva IV; Shevchenko OI; Eshchina IM; Rukavishnikov VS; Meshchakova NM
[Ti] Title:[Clinical and neurophysiological peculiarities of health disorders in workers in dependence on the vinyl chloride exposure load].
[So] Source:Gig Sanit;95(12):1167-71, 2016.
[Is] ISSN:0016-9900
[Cp] Country of publication:Russia (Federation)
[La] Language:rus
[Ab] Abstract:Results of the clinical and neurophysiological examinations of 42 workers with operating history at the chemical plant exposed to vinyl chloride (VC) are presented. The purpose of research was the identification ofpeculiarities of clinical manifestations and disorders of the functional activity of the brain in workers at the vinyl chloride production, with taking into account the exposure toxic load (ETL). There were made clinical and electroencephalographic examinations with the detection of cognitive evoked potentials (CEP) and statistical analysis of results with the use of the Mann-Whitney U-test, Fisher's F-test, calculation of Spearman's correlation coefficient. The features in clinical picture of the pathology of the nervous system were detected in the form of asthenic disorders with cognitive impairment and autonomic dysfunction syndrome. There was established the increase in the cognitive impairment rate (p = 0.03), the decline in a-EEG activity (p = 0.01) and the worsening of indices of the amplitude (p = 0.011) and latency (p = 0,05) of CEP in extremely high level of ETL in comparison with same indices in the group with moderately high ETL. In the first group there was revealed a statistically significant exceedance of the frequency of hypertension - by 1.6 times, skin diseases - by 9 times, chronic subatrophic rhino-pharyngitis by 1.4 times in comparison with cases from the second group. In the group with moderately high level of ETL there was established the statistically significant inverse correlationship between the ETL and the index of P300 amplitude from the left side (r = -0.38, p = 0.019) and in the group with extremely high level ETL - between ETL and index of the ß2 - rhythm (r = - 0.73, p = 0.0008).
[Mh] MeSH terms primary: Air Pollutants, Occupational
Manufacturing Industry
Neurotoxicity Syndromes
Vinyl Chloride
[Mh] MeSH terms secundary: Air Pollutants, Occupational/analysis
Air Pollutants, Occupational/toxicity
Electroencephalography/methods
Humans
Male
Manufacturing Industry/methods
Manufacturing Industry/standards
Middle Aged
Neurotoxicity Syndromes/diagnosis
Neurotoxicity Syndromes/epidemiology
Neurotoxicity Syndromes/etiology
Neurotoxicity Syndromes/physiopathology
Occupational Exposure/adverse effects
Occupational Exposure/analysis
Occupational Exposure/prevention & control
Risk Assessment/methods
Risk Assessment/statistics & numerical data
Risk Factors
Siberia/epidemiology
Time Factors
Vinyl Chloride/analysis
Vinyl Chloride/toxicity
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Air Pollutants, Occupational); WD06X94M2D (Vinyl Chloride)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180216
[St] Status:MEDLINE

  9 / 68643 MEDLINE  
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[PMID]: 29521254
[Au] Autor:Stolyarova E; Beduleva L; Menshikov I; Snigiryev A; Khramova T
[Ad] Address:Department of Immunology and Cell Biology, Institute of Natural Sciences, Udmurt State University. Russian Federation.
[Ti] Title:Mechanism by which regulatory rheumatoid factor prevents experimental autoimmune encephalomyelitis.
[So] Source:Endocr Metab Immune Disord Drug Targets;, 2018 Mar 08.
[Is] ISSN:2212-3873
[Cp] Country of publication:United Arab Emirates
[La] Language:eng
[Ab] Abstract:BACKGROUND: One mechanism that underlies protection from autoimmunity and avoidance of uncontrolled inflammation is the controlled contraction of lymphocyte expansion during the immune response. We identified regulatory rheumatoid factor (regRF), the production of which is associated with resistance to and remission of experimental autoimmune diseases. RegRF is anti-idiotypic antibodies to lymphocyte receptors against autoimmune disease-inducing antigens; at the same time, it is specific to epitopes in the hinge Fc fragments of IgG. OBJECTIVE: The aim of this study is to test the hypothesis that regRF prevents autoimmunity by limiting the expansion of lymphocytes. METHODS: To test this hypothesis, we used a model of experimental autoimmune encephalitis. RESULTS: We found that in the lymph nodes that drain the injection site in rats producing regRF in response to immunization with myelin basic protein (MBP) the proportion of CD4+lymphocytes was lower than in rats in which MBP-immunization did not induce higher regRF levels. RegRF-containing plasma obtained from MBP-immunized rats induces complement-dependent killing of MBP-activated lymphocytes. Activated MBP-specific lymphocytes are not sensitive to the regRF-containing plasma of intact rats. CONCLUSION: The regRF produced during the immune response is a specific control factor for the expansion of antigen-activated CD4+lymphocytes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.2174/1871530318666180308123350

  10 / 68643 MEDLINE  
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[PMID]: 29521099
[Au] Autor:Al-Obaidi MMJ; Bahadoran A; Wang SM; Manikam R; Raju CS; Sekaran SD
[Ti] Title:Disruption of the blood brain barrier is vital property of neurotropic viral infection of the central nervous system.
[So] Source:Acta Virol;62(1):16-27, 2018.
[Is] ISSN:0001-723X
[Cp] Country of publication:Slovakia
[La] Language:eng
[Ab] Abstract:The blood brain barrier consisting of astrocytes, pericytes and brain microvascular endothelial cells plays a vital role in the pathogenesis of neurotropic viruses by controlling the access of circulating molecules, immune cells or viruses into the central nervous system (CNS). However, this barrier is not impenetrable and neuroviruses have evolved to disrupt and evade it. This review aims to describe the underlying entry mechanisms of several neuroviruses such as (Japanese encephalitis virus (JEV), West Nile virus (WNV), Zika virus (ZIKV), Nipah virus (NiV), Rabies virus (RABV), Herpes simplex virus (HSV) and Human immunodeficiency virus (HIV)) into the CNS through BBB disruption. The mechanisms, through which neurotropic viruses enter the BBB, are being studied and are becoming clearer, however, some aspects still remain unknown. Some of these viruses are able to invade the brain parenchyma by a 'Trojan horse' mechanism, through diapedesis of infected immune cells that either cross the BBB paracellularly or transcellularly. Important mechanisms of BBB disruption associated with paracellular entry of viruses include alterations in expression or phosphorylation of tight junction proteins, disruption of the basal lamina and disruption of the actin cytoskeleton. In the absence of such mechanisms, indirect effects of viruses on the immune system are likely causes of barrier disruption.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.4149/av_2018_102


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