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[PMID]:29390429
[Au] Autor:Feng H; Zhou H
[Ad] Endereço:Department of Neurology, West China Hospital, Sichuan University, Chengdu, China.
[Ti] Título:New compound heterozygous variants of the cholinergic receptor nicotinic delta subunit gene in a Chinese male with congenital myasthenic syndrome: A case report.
[So] Source:Medicine (Baltimore);96(51):e8981, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Congenital myasthenic syndromes (CMS) are a group of genetic disorders that stem mostly from molecular defects in nicotinic acetylcholine receptors (AChRs). Defects in the cholinergic receptor nicotinic delta subunit (CHRND) gene can cause a series of myasthenic syndromes. Here, we report 2 new compound heterozygous variants of the CHRND gene in a Chinese male with CMS. CASE PRESENTATION: A 43-year-old Chinese male presented with progressive muscle weakness, difficulty chewing, and an inability to lift his head from the time he was 8 years old. He was treated with pyridostigmine, which was partially effective. Two weeks prior, he was hospitalized for dyspnea. Upon examination, he was unable to drum his cheeks and exhibited fatigable muscle weakness and facial muscle atrophy. Sequencing of his exome revealed 2 previously unreported mutations in CHRND, c.59G>A (exon2) and c.423G>C (exon5). CONCLUSIONS: We identified a new mutational site that contributes to the onset of CMS.
[Mh] Termos MeSH primário: Síndromes Miastênicas Congênitas/diagnóstico
Receptores Colinérgicos/genética
[Mh] Termos MeSH secundário: Adulto
Grupo com Ancestrais do Continente Asiático
Diagnóstico Diferencial
Seres Humanos
Masculino
Debilidade Muscular/etiologia
Síndromes Miastênicas Congênitas/complicações
Síndromes Miastênicas Congênitas/genética
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CHRND protein, human); 0 (Receptors, Cholinergic)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008981


  2 / 13162 MEDLINE  
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[PMID]:28470860
[Au] Autor:Hong Y; Zisimopoulou P; Trakas N; Karagiorgou K; Stergiou C; Skeie GO; Hao HJ; Gao X; Owe JF; Zhang X; Yue YX; Romi F; Wang Q; Li HF; Gilhus NE; Tzartos SJ
[Ad] Endereço:Department of Clinical Medicine, University of Bergen, Bergen, Norway.
[Ti] Título:Multiple antibody detection in 'seronegative' myasthenia gravis patients.
[So] Source:Eur J Neurol;24(6):844-850, 2017 Jun.
[Is] ISSN:1468-1331
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Myasthenia gravis (MG) is an autoimmune disease caused by antibody mediated impairment in the neuromuscular junction. Seronegative MG (SNMG) without antibodies against acetylcholine receptor (AChR) and muscle-specific kinase (MuSK) by routine assays accounts for about 20% of all MG patients. METHODS: Plasma from 81 Chinese MG patients previously found to be seronegative was tested by routine assays for AChR and MuSK antibodies. These samples were screened by (i) a novel, highly sensitive radioimmunoassay for AChR antibodies; (ii) cell-based assays for clustered AChR, MuSK and lipoprotein receptor-related protein 4 (LRP4) antibodies; (iii) a radioimmunoassay for titin antibodies. RESULTS: Antibodies to AChR, MuSK, LRP4 and titin were found in 25% (20/81), 4% (3/81), 7% (6/81) and 6% (5/78) of SNMG patients, respectively. In total, 37% of SNMG patients were found to be positive for at least one of the tested antibodies. AChR antibody positive patients had more severe disease (P = 0.008) and a trend towards fewer remissions/minimal manifestations than AChR antibody negative patients. The four patients with coexistence of antibodies had more severe disease, whilst the seronegative patients had milder MG (P = 0.015). CONCLUSIONS: Detection of multiple muscle antibodies by more sensitive assays provides additional information in diagnosing and subgrouping of MG and may guide MG treatment.
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Conectina/imunologia
Proteínas Relacionadas a Receptor de LDL/imunologia
Miastenia Gravis/imunologia
Receptores Proteína Tirosina Quinases/imunologia
Receptores Colinérgicos/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Feminino
Seres Humanos
Masculino
Meia-Idade
Miastenia Gravis/sangue
Radioimunoensaio
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Connectin); 0 (LDL-Receptor Related Proteins); 0 (LRP4 protein, human); 0 (Receptors, Cholinergic); 0 (TTN protein, human); EC 2.7.10.1 (MUSK protein, human); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1111/ene.13300


  3 / 13162 MEDLINE  
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[PMID]:29238017
[Au] Autor:Nakane S; Mukaino A; Ando Y
[Ad] Endereço:Department of Neurology, Graduate School of Medical Sciences, Kumamoto University.
[Ti] Título:[The interface between the immune system and autonomic nervous system].
[So] Source:Nihon Rinsho Meneki Gakkai Kaishi;40(5):352-360, 2017.
[Is] ISSN:1349-7413
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:  The nervous system and the immune system are two major systems in human body. Although it was revealed these two systems correlated, the control of immune cell dynamics by the nervous system has come to draw a lot of attention at the present time. Recent advances in basic and preclinical science reveal that reflex neural circuits inhibit the production of cytokines and inflammation in several animal models. One well-characterized cytokine-inhibiting mechanism, termed the "inflammatory reflex", is dependent upon vagus nerve stimulation that inhibits cytokine production and attenuates the inflammation. And the mechanism for controlling lymphocyte trafficking becomes clear, and molecular basis of immune regulation by the nervous system was reported. On the other hand, the nervous system is protected from the invasion of harmful agents by the barrier. However, there are neuroimmunological disorders, which is associated with autoimmunity, tumor immunity, and infection immunity. Autoimmune autonomic ganglionopathy (AAG) is an acquired immune-mediated disorder that leads to widespread autonomic manifestations, in which autoantibodies to ganglionic nicotinic acetylcholine receptors play a central role. Previously, we elucidated the prevalence of extra-autonomic manifestations in patients with AAG. It is necessary to establish the new systems for the detection of autoantibodies to other subunits of acetylcholine receptor.
[Mh] Termos MeSH primário: Sistema Nervoso Autônomo/imunologia
Sistema Imunitário/imunologia
Inflamação/imunologia
[Mh] Termos MeSH secundário: Animais
Autoanticorpos/imunologia
Autoimunidade/imunologia
Citocinas/imunologia
Citocinas/metabolismo
Gânglios Autônomos/imunologia
Seres Humanos
Neuroimunomodulação/imunologia
Receptores Colinérgicos/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Cytokines); 0 (Receptors, Cholinergic)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.2177/jsci.40.352


  4 / 13162 MEDLINE  
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[PMID]:28912035
[Au] Autor:Lazaridis K; Dalianoudis I; Baltatzidi V; Tzartos SJ
[Ad] Endereço:Hellenic Pasteur Institute, Athens, Greece. Electronic address: klazaridis@pasteur.gr.
[Ti] Título:Specific removal of autoantibodies by extracorporeal immunoadsorption ameliorates experimental autoimmune myasthenia gravis.
[So] Source:J Neuroimmunol;312:24-30, 2017 Nov 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Myasthenia gravis (MG) is caused by autoantibodies, the majority of which target the muscle acetylcholine receptor (AChR). Plasmapheresis and IgG-immunoadsorption are useful therapy options, but are highly non-specific. Antigen-specific immunoadsorption would remove only the pathogenic autoantibodies, reducing the possibility of side effects while maximizing the benefit. We have extensively characterized such adsorbents, but in vivo studies are missing. We used rats with experimental autoimmune MG to perform antigen-specific immunoadsorptions over three weeks, regularly monitoring symptoms and autoantibody titers. Immunoadsorption was effective, resulting in a marked autoantibody titer decrease while the immunoadsorbed, but not the mock-treated, animals showed a dramatic symptom improvement. Overall, the procedure was found to be efficient, suggesting the subsequent initiation of clinical trials.
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Remoção de Componentes Sanguíneos/métodos
Imunoadsorventes/uso terapêutico
Miastenia Gravis Autoimune Experimental/imunologia
Miastenia Gravis Autoimune Experimental/terapia
[Mh] Termos MeSH secundário: Animais
Peso Corporal
Modelos Animais de Doenças
Eletromiografia
Feminino
Miastenia Gravis Autoimune Experimental/metabolismo
Miastenia Gravis Autoimune Experimental/fisiopatologia
Ratos
Ratos Endogâmicos Lew
Receptores Colinérgicos/imunologia
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Immunosorbents); 0 (Receptors, Cholinergic)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE


  5 / 13162 MEDLINE  
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[PMID]:28830630
[Au] Autor:Sundar K; Venkatasubramanian S; Shanmugam S; Arthur P; Subbaraya R; Hazeena P
[Ad] Endereço:Department of Neurology, Sri Ramachandra University, India. Electronic address: drkaushiksundar@rediffmail.com.
[Ti] Título:False positive immunoassay for acetyl choline receptor antibody (AChR Ab) in patients exposed to polyvalent antisnake venom.
[So] Source:J Neuroimmunol;311:68-70, 2017 Oct 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Acute flaccid paralysis is a neuromuscular emergency characterized by rapidly worsening weakness that evolves quickly to cause diaphragmatic failure. The challenge for the treating physician is to stabilize the patient, generate the differential diagnosis and determine the management; all in quick time. Neurotoxic snake bites have inadequate signs of inflammation and are easily missed. Myasthenic crisis, on the other hand, could be the first sign of myasthenia gravis in up to 20% of patients. Both present with acute respiratory failure and inadequate history. Two of our patients presented with similar clinical picture, and received polyvalent anti-snake venom obtained from hyperimmunised horses (Equus caballus). Both tested positive for anti-acetyl choline receptor antibody. After recovery, both patients narrated a history suggestive of neurotoxic envenomation. We later discovered that patients, who are exposed to polyvalent anti-snake venom (Equus caballus) prior to radioimmunoassay, demonstrate high titers of Anti-AChR Ab in their serum erroneously.
[Mh] Termos MeSH primário: Antivenenos/uso terapêutico
Autoanticorpos/sangue
Receptores Colinérgicos/imunologia
Insuficiência Respiratória/tratamento farmacológico
Mordeduras de Serpentes/tratamento farmacológico
Peçonhas/imunologia
[Mh] Termos MeSH secundário: Adulto
Seres Humanos
Masculino
Radioimunoensaio
Insuficiência Respiratória/etiologia
Mordeduras de Serpentes/complicações
Mordeduras de Serpentes/imunologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antivenins); 0 (Autoantibodies); 0 (Receptors, Cholinergic); 0 (Venoms)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE


  6 / 13162 MEDLINE  
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[PMID]:28825343
[Au] Autor:Ohno K; Ohkawara B; Ito M
[Ad] Endereço:a Division of Neurogenetics , Nagoya University Graduate School of Medicine , Nagoya , Japan.
[Ti] Título:Agrin-LRP4-MuSK signaling as a therapeutic target for myasthenia gravis and other neuromuscular disorders.
[So] Source:Expert Opin Ther Targets;21(10):949-958, 2017 Oct.
[Is] ISSN:1744-7631
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Signal transduction at the neuromuscular junction (NMJ) is compromised in a diverse array of diseases including myasthenia gravis, Lambert-Eaton myasthenic syndrome, Isaacs' syndrome, congenital myasthenic syndromes, Fukuyama-type congenital muscular dystrophy, amyotrophic lateral sclerosis, and sarcopenia. Except for sarcopenia, all are orphan diseases. In addition, the NMJ signal transduction is impaired by tetanus, botulinum, curare, α-bungarotoxin, conotoxins, organophosphate, sarin, VX, and soman to name a few. Areas covered: This review covers the agrin-LRP4-MuSK signaling pathway, which drives clustering of acetylcholine receptors (AChRs) and ensures efficient signal transduction at the NMJ. We also address diseases caused by autoantibodies against the NMJ molecules and by germline mutations in genes encoding the NMJ molecules. Expert opinion: Representative small compounds to treat the defective NMJ signal transduction are cholinesterase inhibitors, which exert their effects by increasing the amount of acetylcholine at the synaptic space. Another possible therapeutic strategy to enhance the NMJ signal transduction is to increase the number of AChRs, but no currently available drug has this functionality.
[Mh] Termos MeSH primário: Terapia de Alvo Molecular
Miastenia Gravis/tratamento farmacológico
Doenças Neuromusculares/tratamento farmacológico
[Mh] Termos MeSH secundário: Agrina/metabolismo
Animais
Inibidores da Colinesterase/farmacologia
Desenho de Drogas
Mutação em Linhagem Germinativa
Seres Humanos
Proteínas Relacionadas a Receptor de LDL/metabolismo
Miastenia Gravis/genética
Miastenia Gravis/fisiopatologia
Doenças Neuromusculares/genética
Doenças Neuromusculares/fisiopatologia
Junção Neuromuscular/efeitos dos fármacos
Junção Neuromuscular/metabolismo
Receptores Proteína Tirosina Quinases/metabolismo
Receptores Colinérgicos/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Agrin); 0 (Cholinesterase Inhibitors); 0 (LDL-Receptor Related Proteins); 0 (LRP4 protein, human); 0 (Receptors, Cholinergic); EC 2.7.10.1 (MUSK protein, human); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170822
[St] Status:MEDLINE
[do] DOI:10.1080/14728222.2017.1369960


  7 / 13162 MEDLINE  
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[PMID]:28801338
[Au] Autor:Hehir MK; Hobson-Webb LD; Benatar M; Barnett C; Silvestri NJ; Howard JF; Howard D; Visser A; Crum BA; Nowak R; Beekman R; Kumar A; Ruzhansky K; Chen IA; Pulley MT; LaBoy SM; Fellman MA; Greene SM; Pasnoor M; Burns TM
[Ad] Endereço:From the Larner College of Medicine at the University of Vermont (M.K.H., D.H., S.M.G.), Burlington; Duke University School of Medicine (L.D.H.-W.), Durham, NC; University of Miami Health System (M.B., M.A.F.), FL; University of Toronto School of Medicine (C.B.), Canada; SUNY Buffalo Jacobs School o
[Ti] Título:Rituximab as treatment for anti-MuSK myasthenia gravis: Multicenter blinded prospective review.
[So] Source:Neurology;89(10):1069-1077, 2017 Sep 05.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To evaluate the efficacy of rituximab in treatment of anti-muscle-specific kinase (MuSK) myasthenia gravis (MG). METHODS: This was a multicenter, blinded, prospective review, comparing anti-MuSK-positive patients with MG treated with rituximab to those not treated with rituximab. The primary clinical endpoint was the Myasthenia Gravis Status and Treatment Intensity (MGSTI), a novel outcome that combines the Myasthenia Gravis Foundation of America (MGFA) postintervention status (PIS) and the number and dosages of other immunosuppressant therapies used. A priori, an MGSTI of level ≤2 was used to define a favorable outcome. Secondary outcomes included modified MGFA PIS of minimal manifestations or better, mean/median prednisone dose, and mean/median doses of other immunosuppressant drugs. RESULTS: Seventy-seven of 119 patients with anti-MuSK MG evaluated between January 1, 2005, and January 1, 2015, at 10 neuromuscular centers were selected for analysis after review of limited clinical data by a blinded expert panel. An additional 22 patients were excluded due to insufficient follow-up. Baseline characteristics were similar between the rituximab-treated patients (n = 24) and the controls (n = 31). Median follow-up duration was >3.5 years. At last visit, 58% (14/24) of rituximab-treated patients reached the primary outcome compared to 16% (5/31) of controls ( = 0.002). Number needed to treat for the primary outcome is 2.4. At last visit, 29% of rituximab-treated patients were taking prednisone (mean dose 4.5 mg/day) compared to 74% of controls (mean dose 13 mg/day) ( 0.001 and = 0.005). CLASSIFICATION OF EVIDENCE: This study provides Class IV evidence that for patients with anti-MuSK MG, rituximab increased the probability of a favorable outcome.
[Mh] Termos MeSH primário: Autoanticorpos/metabolismo
Fatores Imunológicos/uso terapêutico
Miastenia Gravis/tratamento farmacológico
Miastenia Gravis/imunologia
Receptores Proteína Tirosina Quinases/imunologia
Receptores Colinérgicos/imunologia
Rituximab/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Anti-Inflamatórios/uso terapêutico
Feminino
Seguimentos
Seres Humanos
Masculino
Meia-Idade
Prednisona/uso terapêutico
Estudos Prospectivos
Índice de Gravidade de Doença
Método Simples-Cego
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Autoantibodies); 0 (Immunologic Factors); 0 (Receptors, Cholinergic); 4F4X42SYQ6 (Rituximab); EC 2.7.10.1 (MUSK protein, human); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); VB0R961HZT (Prednisone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170813
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000004341


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[PMID]:28789841
[Au] Autor:Jing S; Song Y; Song J; Pang S; Quan C; Zhou L; Huang Y; Lu J; Xi J; Zhao C
[Ad] Endereço:Department of Neurology, Jing'an District Centre Hospital of Shanghai, China; Department of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, China.
[Ti] Título:Responsiveness to low-dose rituximab in refractory generalized myasthenia gravis.
[So] Source:J Neuroimmunol;311:14-21, 2017 Oct 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We aim to investigate the effect of a low dose of rituximab (RTX) in improving the clinical symptoms of refractory generalized myasthenia gravis (MG). Eight patients with refractory generalized MG were treated with a low dose of 600mg RTX. Patients were evaluated by serial clinical scales, flow cytometry of peripheral blood B, T and NK cells, immunoglobulin, complement levels and antibody titer. The quantitative MG score (QMGS), manual muscle testing (MMT), MG-related activities of daily living (MG-ADL) and MG-specific quality-of-life (QOL) were recorded at baseline as well as 1, 3, and 6months after RTX infusion. The initial improvement was recorded at 1month after treatment. QMGS, MMT and MG-ADL were significantly improved and the average steroid dosage reduction was 43% (p=0.018) at 6months. 600mg RTX was sufficient to deplete B cells and maintain low B-cell counts until 6months after infusion. Treatment with RTX did not result in a significant change in the percentage of CD , CD T-cells while an average increase in the percentage of NK cells. Our study found successful B cell depletion was parallel to symptoms remission and change in serum C3 and C4 levels. Serum AChR antibody levels were independent of clinical response and not influenced by RTX. Therefore, low dose of 600mg RTX may be sufficient in depleting B cells, maintaining low B-cell counts and improving the clinical symptoms of MG in 6months.
[Mh] Termos MeSH primário: Fatores Imunológicos/uso terapêutico
Miastenia Gravis/tratamento farmacológico
Rituximab/uso terapêutico
Resultado do Tratamento
[Mh] Termos MeSH secundário: Adulto
Anti-Inflamatórios/farmacologia
Anti-Inflamatórios/uso terapêutico
Antígenos CD/metabolismo
Autoanticorpos/sangue
Relação Dose-Resposta a Droga
Feminino
Seguimentos
Seres Humanos
Imunoglobulinas Intravenosas/efeitos adversos
Fatores Imunológicos/farmacologia
Masculino
Meia-Idade
Miastenia Gravis/imunologia
Miastenia Gravis/patologia
Troca Plasmática/efeitos adversos
Prednisona/farmacologia
Prednisona/uso terapêutico
Receptores Colinérgicos/imunologia
Estudos Retrospectivos
Rituximab/farmacologia
Linfócitos T/efeitos dos fármacos
Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antigens, CD); 0 (Autoantibodies); 0 (Immunoglobulins, Intravenous); 0 (Immunologic Factors); 0 (Receptors, Cholinergic); 4F4X42SYQ6 (Rituximab); VB0R961HZT (Prednisone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE


  9 / 13162 MEDLINE  
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[PMID]:28738696
[Au] Autor:Ruzieh M; Batizy L; Dasa O; Oostra C; Grubb B
[Ad] Endereço:a Department of Internal Medicine , University of Toledo , Toledo , OH , USA.
[Ti] Título:The role of autoantibodies in the syndromes of orthostatic intolerance: a systematic review.
[So] Source:Scand Cardiovasc J;51(5):243-247, 2017 Oct.
[Is] ISSN:1651-2006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Orthostatic intolerance is defined as the provocation of symptoms upon standing, commonly caused by neurogenic orthostatic hypotension (OH) and postural tachycardia syndrome (POTS), the etiology for which has not been fully uncovered yet. Many reports have described the occurrence of dysautonomia, orthostatic intolerance and POTS following febrile illness, presumably viral and post-vaccine. Furthermore, patients with dysautonomia have higher rates of autoimmune disorders such as Hashimoto thyroiditis and SLE. Recent evidence has shown the presence of adrenergic and cholinergic receptor antibodies in patients with POTS and orthostatic hypotension. In patients with cholinergic receptor antibodies, higher titers correlate with the disease severity. Few reports have shown that immunomodulation therapy resulted in significant improvement in symptoms. In this article, we review the available literature correlating autoimmunity with orthostatic intolerance syndromes. Future studies are warranted to evaluate the prevalence of such antibodies and examine different treatment modalities in this sub group of patients.
[Mh] Termos MeSH primário: Autoanticorpos/imunologia
Autoimunidade
Pressão Sanguínea
Intolerância Ortostática/imunologia
Postura
Receptores Adrenérgicos/imunologia
Receptores Colinérgicos/imunologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Intolerância Ortostática/fisiopatologia
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Receptors, Adrenergic); 0 (Receptors, Cholinergic)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1080/14017431.2017.1355068


  10 / 13162 MEDLINE  
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[PMID]:28672694
[Au] Autor:Ribeiro H; Ramos S; Homem V; Santos L
[Ad] Endereço:LEPABE - Laboratory for Process Engineering, Environment, Biotechnology and Energy, Faculty of Engineering, University of Porto, Rua Dr. Roberto Frias, 4200-465 Porto, Portugal.
[Ti] Título:Can coastline plant species be used as biosamplers of emerging contaminants? - UV-filters and synthetic musks as case studies.
[So] Source:Chemosphere;184:1134-1140, 2017 Oct.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Personal care products, an important class of emerging contaminants, have been frequently detected in different environmental matrices. Included in this category are synthetic musks compounds (SMCs) and UV-filters. Their occurrence in the coastal environment has been poorly studied. Therefore, this work aimed to verify whether five coastline plant species (Carpobrotus edulis, Cakile maritima, Medicago marina, Elymus farctus borealis-atlanticus and Euphorbia paralias) have the ability to accumulate 11 SMCs (cashmeran, celestolide, phantolide, galaxolide, tonalide, exaltolide, musk moskene, tibetene, ambrette, xylene and ketone) and 2 organic UVB filters (3-(4'-methylbenzylidene) camphor and octocrylene), functioning as biosamplers. To accomplish this task, a QuEChERS technique ("Quick, Easy, Cheap, Effective, Rugged, and Safe") was employed to extract the target compounds from the plant material collected in 15 beaches of Matosinhos and Vila Nova de Gaia (Portugal). The resulting extracts were analysed by gas chromatography-mass spectrometry. Limits of detection ranged from 0.02 ng g for celestolide and tonalide to 1.32 ng g for musk ambrette. The obtained recoveries were around 93% and relative standard deviation was generally less than 15%. SMCs were detected at levels ranging from 1.56 to 350 ng g dw and UV-filters from 2.9 to 264 ng g dw. Galaxolide and 3-(4'-methylbenzylidene) camphor were the synthetic musk and UV-filter detected in higher concentrations, respectively. Plants with higher water content accumulate better SMCs (hottentot-fig), while those with higher lipid content retain better the UV-filters (sea spurge).
[Mh] Termos MeSH primário: Monitoramento Ambiental
Ácidos Graxos Monoinsaturados/análise
Água do Mar/química
Protetores Solares/análise
Poluentes Químicos da Água/análise
[Mh] Termos MeSH secundário: Benzopiranos
Dinitrobenzenos
Cromatografia Gasosa-Espectrometria de Massas/métodos
Indanos
Portugal
Receptores Proteína Tirosina Quinases
Receptores Colinérgicos
Tetra-Hidronaftalenos
Xilenos/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzopyrans); 0 (Dinitrobenzenes); 0 (Fatty Acids, Monounsaturated); 0 (Indans); 0 (Receptors, Cholinergic); 0 (Sunscreening Agents); 0 (Tetrahydronaphthalenes); 0 (Water Pollutants, Chemical); 0 (Xylenes); 095I377U8F (musk); 14170060AT (galaxolide); 1Q49IC9FAW (moskene); 21145-77-7 (acetyl methyl tetramethyl tetralin); 83-66-9 (musk ambrette (artificial)); BZR4438MY4 (6,7-dihydro-1,1,2,3,3-pentamethyl-4-(5H)indanone); EC 2.7.10.1 (MUSK protein, human); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE



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