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[PMID]:28412068
[Au] Autor:Venkatesh P; Selvan H; Singh SB; Gupta D; Kashyap S; Temkar S; Gogia V; Tripathy K; Chawla R; Vohra R
[Ad] Endereço:Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India.
[Ti] Título:Vitreous Amyloidosis: Ocular, Systemic, and Genetic Insights.
[So] Source:Ophthalmology;124(7):1014-1022, 2017 Jul.
[Is] ISSN:1549-4713
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To report the unique clinical and surgical characteristics encountered in eyes with vitreous amyloidosis. Systemic evaluation and visual outcome after vitrectomy are discussed. A novel mutation in the transthyretin gene (TTR) in Indian patients with familial amyloid polyneuropathy (FAP) is described. DESIGN: Retrospective, observational study. PARTICIPANTS: Ten eyes of 5 patients from 2 pedigrees with a diagnosis of vitreous amyloidosis. METHODS: Detailed history, pedigree charting, systemic and ocular examination of 10 eyes (5 patients from 2 pedigrees) were carried out. Tests were performed to rule out vitreitis, retinal vasculitis, vitreous hemorrhage, and systemic amyloidosis. Genetic analysis to identify the mutation was performed in 1 patient. Vitreous biopsy, followed by 25-gauge pars plana vitrectomy, was performed in the same sitting in all cases. Samples were sent for Congo red staining and polarized microscopy. Patients were followed up on days 1, 7, and 28 and then every 2 months. Visual acuity assessment, intraocular pressure measurement, and fundus examination were performed each time. MAIN OUTCOME MEASURES: Mutations in TTR and postoperative visual acuity. RESULTS: Mean age at presentation was 32 years, with a 3:2 male-to-female distribution. Family history was positive in all patients. Nine eyes had pseudopodia lentis, whereas all 10 had glass wool-like vitreous. Glaucoma developed in 1 patient (2 eyes). Waxy paper-like vitreous with firm vitreous adhesions beyond major arcades and along retinal vessels was noted during surgery in all eyes. Congo red staining and apple green birefringence demonstrated vitreous amyloidosis. The mean preoperative best-corrected visual acuity (BCVA) was 1.39±0.64 logarithm of the minimum angle of resolution (logMAR), whereas the postoperative BCVA improved to 0.17±0.07 logMAR (P = 0.004). Gene sequencing revealed a phenylalanine→isoleucine mutation in the 33rd position of exon 2 of TTR in 1 patient of 1 pedigree, confirming the diagnosis of FAP. Two patients subsequently were found to have sensorimotor autonomic neuropathy, whereas 2 others had subclinical autonomic dysfunction. CONCLUSIONS: The clinical clues, management strategy, surgical characteristics, vitrectomy outcomes, and significance of systemic evaluation in vitreous amyloidosis are highlighted. A novel single mutation (Phe33Ile) in a case of FAP with vitreous amyloidosis from India is reported.
[Mh] Termos MeSH primário: Neuropatias Amiloides Familiares/diagnóstico
DNA/genética
Mutação
Receptores de Albumina/genética
Acuidade Visual
Corpo Vítreo/patologia
[Mh] Termos MeSH secundário: Adulto
Neuropatias Amiloides Familiares/genética
Análise Mutacional de DNA
Éxons
Feminino
Seguimentos
Seres Humanos
Masculino
Linhagem
Pré-Albumina
Receptores de Albumina/metabolismo
Estudos Retrospectivos
Tomografia de Coerência Óptica
Vitrectomia/métodos
Corpo Vítreo/cirurgia
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Prealbumin); 0 (Receptors, Albumin); 0 (transthyretin receptor); 9007-49-2 (DNA)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170721
[Lr] Data última revisão:
170721
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170417
[St] Status:MEDLINE


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[PMID]:27903888
[Au] Autor:Elkayam E; Parmar R; Brown CR; Willoughby JL; Theile CS; Manoharan M; Joshua-Tor L
[Ad] Endereço:Keck Structural Biology Lab, Cold Spring Harbor, NY 11724, USA.
[Ti] Título:siRNA carrying an (E)-vinylphosphonate moiety at the 5΄ end of the guide strand augments gene silencing by enhanced binding to human Argonaute-2.
[So] Source:Nucleic Acids Res;45(6):3528-3536, 2017 Apr 07.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Efficient gene silencing by RNA interference (RNAi) in vivo requires the recognition and binding of the 5΄- phosphate of the guide strand of an siRNA by the Argonaute protein. However, for exogenous siRNAs it is limited by the rapid removal of the 5΄- phosphate of the guide strand by metabolic enzymes. Here, we have determined the crystal structure of human Argonaute-2 in complex with the metabolically stable 5΄-(E)-vinylphosphonate (5΄-E-VP) guide RNA at 2.5-Šresolution. The structure demonstrates how the 5΄ binding site in the Mid domain of human Argonaute-2 is able to adjust the key residues in the 5΄-nucleotide binding pocket to compensate for the change introduced by the modified nucleotide. This observation also explains improved binding affinity of the 5΄-E-VP -modified siRNA to human Argonaute-2 in-vitro, as well as the enhanced silencing in the context of the trivalent N-acetylgalactosamine (GalNAc)-conjugated siRNA in mice relative to the un-modified siRNA.
[Mh] Termos MeSH primário: Proteínas Argonauta/química
Proteínas Argonauta/metabolismo
Organofosfonatos/química
Interferência de RNA
RNA Interferente Pequeno/química
RNA Interferente Pequeno/metabolismo
Compostos de Vinila/química
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Seres Humanos
Camundongos
Modelos Moleculares
RNA Guia/química
RNA Guia/metabolismo
Receptores de Albumina/genética
Receptores de Albumina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Argonaute Proteins); 0 (EIF2C2 protein, human); 0 (Organophosphonates); 0 (RNA, Guide); 0 (RNA, Small Interfering); 0 (Receptors, Albumin); 0 (Vinyl Compounds); 0 (transthyretin receptor); 1746-03-8 (vinylphosphonic acid)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161202
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkw1171


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[PMID]:26800456
[Au] Autor:Adams D; Cauquil C; Labeyrie C; Beaudonnet G; Algalarrondo V; Théaudin M
[Ad] Endereço:a Neurology , CHU Bicêtre, APHP , Le Kremlin Bicêtre , France.
[Ti] Título:TTR kinetic stabilizers and TTR gene silencing: a new era in therapy for familial amyloidotic polyneuropathies.
[So] Source:Expert Opin Pharmacother;17(6):791-802, 2016.
[Is] ISSN:1744-7666
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Transthyretin Familial Amyloid Polyneuropathy (TTR-FAP) is a rare disease with autosomal dominant transmission due to a point mutation of the TTR gene. By removing the main source of systemic mutant TTR, liver transplantation (LT) has become the reference therapy of this severe and fatal polyneuropathy of adult-onset, stopping disease progression in subgroup of patients. Recently, new therapeutic strategies have emerged, which intend to stabilize TTR or to silence the TTR gene. Amongst them, the TTR kinetic stabilizer tafamidis is the first drug approved in the EU. AREAS COVERED: We shall review the natural history of TTR-FAP and the best indications for LT. Data on the efficacy, safety and tolerability of the TTR kinetic stabilizers, tafamidis and diflunisal, have been reviewed, from the pivotal Phase III clinical trials published in PubMed medical journals or presented at international meetings. We will review the ongoing phase III clinical trials of TTR gene silencing with RNAi therapeutics and ASO published in clinicaltrialgov. EXPERT OPINION: Due to the data on efficacy, tolerability, safety, tafamidis and diflunisal became the first line anti-amyloid treatment in stage 1 TTR-FAP. Both drugs slow progression of the disease. Only tafamidis got marketing authorization. We are waiting for results of the 2 phase III clinical trials of TTR gene silencing in varied stages of the disease.
[Mh] Termos MeSH primário: Neuropatias Amiloides Familiares/tratamento farmacológico
Benzoxazóis/uso terapêutico
Diflunisal/uso terapêutico
Pré-Albumina/metabolismo
Receptores de Albumina/metabolismo
[Mh] Termos MeSH secundário: Ensaios Clínicos Fase III como Assunto
Progressão da Doença
Inativação Gênica
Seres Humanos
Transplante de Fígado
Receptores de Albumina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Benzoxazoles); 0 (Prealbumin); 0 (Receptors, Albumin); 0 (transthyretin receptor); 7C546U4DEN (Diflunisal); 8FG9H9D31J (tafamidis)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:160331
[Lr] Data última revisão:
160331
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160123
[St] Status:MEDLINE
[do] DOI:10.1517/14656566.2016.1145664


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[PMID]:26740554
[Au] Autor:Peters SL; Déry MA; LeBlanc AC
[Ad] Endereço:Bloomfield Center for Research in Aging, Lady Davis Institute for Medical Research, Jewish General Hospital, 3755 Ch. Cote Ste-Catherine, Montreal, QC H3T 1E2, Canada and Department of Neurology and Neurosurgery, McGill University, 3775 University Street, Montreal, QC H2A 2B4, Canada.
[Ti] Título:Familial prion protein mutants inhibit Hrd1-mediated retrotranslocation of misfolded proteins by depleting misfolded protein sensor BiP.
[So] Source:Hum Mol Genet;25(5):976-88, 2016 Mar 01.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Similar to many proteins trafficking through the secretory pathway, cellular prion protein (PrP) partly retrotranslocates from the endoplasmic reticulum to the cytosol through the endoplasmic reticulum-associated degradation (ERAD) pathway in an attempt to alleviate accumulation of cellular misfolded PrP. Surprisingly, familial PrP mutants fail to retrotranslocate and simultaneously block normal cellular PrP retrotranslocation. That impairments in retrotranslocation of misfolded proteins could lead to global disruptions in cellular homeostasis prompted further investigations into PrP mutant retrotranslocation defects. A gain- and loss-of-function approach identified human E3 ubiquitin ligase, Hrd1, as a critical regulator of PrP retrotranslocation in mammalian cells. Expression of familial human PrP mutants, V210I(129V) and M232R(129V), not only abolished PrP retrotranslocation, but also that of Hrd1-dependent ERAD substrates, transthyretin TTR(D18G) and α1-anti-trypsin A1AT(NHK). Mutant PrP expression decreased binding immunoglobulin protein (BiP) levels by 50% and attenuated ER stress-induced BiP by increasing BiP turnover 6-fold. Overexpression of BiP with PrP mutants rescued retrotranslocation of PrP, TTR(D18G) and A1AT(NHK). PrP mutants-induced cell death was also rescued by co-expression of BiP. These results show that PrP mutants highjack the Hrd1-dependent ERAD pathway, an action that would result in misfolded protein accumulation especially in terminally differentiated neurons. This could explain the age-dependent neuronal degeneration in familial prion diseases.
[Mh] Termos MeSH primário: Degradação Associada com o Retículo Endoplasmático/genética
Proteínas de Choque Térmico/genética
Neurônios/metabolismo
Príons/metabolismo
Ubiquitina-Proteína Ligases/genética
[Mh] Termos MeSH secundário: Animais
Morte Celular
Linhagem Celular Tumoral
Retículo Endoplasmático/genética
Retículo Endoplasmático/metabolismo
Regulação da Expressão Gênica
Proteínas de Choque Térmico/metabolismo
Seres Humanos
Mutação
Neuroglia/metabolismo
Neuroglia/patologia
Neurônios/patologia
Príons/genética
Dobramento de Proteína
Transporte Proteico
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Receptores de Albumina/genética
Receptores de Albumina/metabolismo
Transdução de Sinais
Ubiquitina-Proteína Ligases/antagonistas & inibidores
Ubiquitina-Proteína Ligases/metabolismo
alfa 1-Antitripsina/genética
alfa 1-Antitripsina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Heat-Shock Proteins); 0 (Prions); 0 (RNA, Small Interfering); 0 (Receptors, Albumin); 0 (alpha 1-Antitrypsin); 0 (molecular chaperone GRP78); 0 (transthyretin receptor); EC 2.3.2.27 (SYVN1 protein, human); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170301
[Lr] Data última revisão:
170301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160108
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddv630


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[PMID]:25646614
[Au] Autor:Leung A; Murphy GJ
[Ad] Endereço:School of Medicine and the Center for Regenerative Medicine (CReM), Boston University, Boston, MA, USA.
[Ti] Título:Multisystemic Disease Modeling of Liver-Derived Protein Folding Disorders Using Induced Pluripotent Stem Cells (iPSCs).
[So] Source:Methods Mol Biol;1353:261-70, 2016.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Familial transthyretin amyloidosis (ATTR) is an autosomal dominant protein-folding disorder caused by over 100 distinct mutations in the transthyretin (TTR) gene. In ATTR, protein secreted from the liver aggregates and forms fibrils in target organs, chiefly the heart and peripheral nervous system, highlighting the need for a model capable of recapitulating the multisystem complexity of this clinically variable disease. Here, we describe detailed methodologies for the directed differentiation of protein folding disease-specific iPSCs into hepatocytes that produce mutant protein, and neural-lineage cells often targeted in disease. Methodologies are also described for the construction of multisystem models and drug screening using iPSCs.
[Mh] Termos MeSH primário: Neuropatias Amiloides Familiares/patologia
Técnicas de Cultura de Células
Reprogramação Celular
Hepatócitos/citologia
Células-Tronco Pluripotentes Induzidas/citologia
Neurônios/citologia
[Mh] Termos MeSH secundário: Ativinas/farmacologia
Neuropatias Amiloides Familiares/genética
Neuropatias Amiloides Familiares/metabolismo
Fator Neurotrófico Derivado do Encéfalo/farmacologia
Diferenciação Celular/efeitos dos fármacos
Sobrevivência Celular
Colágeno/química
Combinação de Medicamentos
Expressão Gênica
Fator Neurotrófico Derivado de Linhagem de Célula Glial/farmacologia
Hepatócitos/efeitos dos fármacos
Hepatócitos/metabolismo
Seres Humanos
Células-Tronco Pluripotentes Induzidas/efeitos dos fármacos
Células-Tronco Pluripotentes Induzidas/metabolismo
Laminina/química
Modelos Biológicos
Mutação
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Cultura Primária de Células
Dobramento de Proteína
Proteoglicanas/química
Receptores de Albumina/genética
Receptores de Albumina/metabolismo
Tretinoína/farmacologia
Proteína Wnt3/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor); 0 (Drug Combinations); 0 (GDNF protein, human); 0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (Laminin); 0 (Proteoglycans); 0 (Receptors, Albumin); 0 (WNT3 protein, human); 0 (Wnt3 Protein); 0 (activin A); 0 (brain-derived neurotrophic factor, human); 0 (transthyretin receptor); 104625-48-1 (Activins); 119978-18-6 (matrigel); 5688UTC01R (Tretinoin); 9007-34-5 (Collagen)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150204
[St] Status:MEDLINE
[do] DOI:10.1007/7651_2014_194


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[PMID]:26055641
[Au] Autor:Bern M; Sand KM; Nilsen J; Sandlie I; Andersen JT
[Ad] Endereço:Centre for Immune Regulation (CIR) and Department of Biosciences, University of Oslo, N-0316 Oslo, Norway; CIR and Department of Immunology, Oslo University Hospital Rikshospitalet, Norway, PO Box 4950, N-0424 Oslo, Norway.
[Ti] Título:The role of albumin receptors in regulation of albumin homeostasis: Implications for drug delivery.
[So] Source:J Control Release;211:144-62, 2015 Aug 10.
[Is] ISSN:1873-4995
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Albumin is the most abundant protein in blood and acts as a molecular taxi for a plethora of small insoluble substances such as nutrients, hormones, metals and toxins. In addition, it binds a range of medical drugs. It has an unusually long serum half-life of almost 3weeks, and although the structure and function of albumin has been studied for decades, a biological explanation for the long half-life has been lacking. Now, recent research has unravelled that albumin-binding cellular receptors play key roles in the homeostatic regulation of albumin. Here, we review our current understanding of albumin homeostasis with a particular focus on the impact of the cellular receptors, namely the neonatal Fc receptor (FcRn) and the cubilin-megalin complex, and we discuss their importance on uses of albumin in drug delivery.
[Mh] Termos MeSH primário: Sistemas de Liberação de Medicamentos/métodos
Homeostase/fisiologia
Receptores de Albumina/fisiologia
Albumina Sérica/fisiologia
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação/fisiologia
Seres Humanos
Estrutura Secundária de Proteína
Receptores de Albumina/química
Albumina Sérica/administração & dosagem
Albumina Sérica/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Receptors, Albumin); 0 (Serum Albumin)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:150701
[Lr] Data última revisão:
150701
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150610
[St] Status:MEDLINE


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[PMID]:25526974
[Au] Autor:Kollmer J; Hund E; Hornung B; Hegenbart U; Schönland SO; Kimmich C; Kristen AV; Purrucker J; Röcken C; Heiland S; Bendszus M; Pham M
[Ad] Endereço:1 Department of Neuroradiology, University of Heidelberg, Heidelberg, Germany 2 Amyloidosis Centre Heidelberg, University of Heidelberg, Heidelberg, Germany jennifer.kollmer@med.uni-heidelberg.de.
[Ti] Título:In vivo detection of nerve injury in familial amyloid polyneuropathy by magnetic resonance neurography.
[So] Source:Brain;138(Pt 3):549-62, 2015 Mar.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Transthyretin familial amyloid polyneuropathy is a rare, autosomal-dominant inherited multisystem disorder usually manifesting with a rapidly progressive, axonal, distally-symmetric polyneuropathy. The detection of nerve injury by nerve conduction studies is limited, due to preferential involvement of small-fibres in early stages. We investigated whether lower limb nerve-injury can be detected, localized and quantified in vivo by high-resolution magnetic resonance neurography. We prospectively included 20 patients (12 male and eight female patients, mean age 47.9 years, range 26-66) with confirmed mutation in the transthyretin gene: 13 with symptomatic polyneuropathy and seven asymptomatic gene carriers. A large age- and sex-matched cohort of healthy volunteers served as controls (20 male and 20 female, mean age 48.1 years, range 30-73). All patients received detailed neurological and electrophysiological examinations and were scored using the Neuropathy Impairment Score-Lower Limbs, Neuropathy Deficit and Neuropathy Symptom Score. Magnetic resonance neurography (3 T) was performed with large longitudinal coverage from proximal thigh to ankle-level and separately for each leg (140 axial slices/leg) by using axial T2-weighted (repetition time/echo time = 5970/55 ms) and dual echo (repetition time 5210 ms, echo times 12 and 73 ms) turbo spin echo 2D sequences with spectral fat saturation. A 3D T2-weighted inversion-recovery sequence (repetition time/echo time 3000/202 ms) was acquired for imaging of the spinal nerves and lumbar plexus (50 axial slice reformations). Precise manual segmentation of the spinal/sciatic/tibial/common peroneal nerves was performed on each slice. Histogram-based normalization of nerve-voxel signal intensities was performed using the age- and sex-matched control group as normative reference. Nerve-voxels were subsequently classified as lesion-voxels if a threshold of >1.2 (normalized signal-intensity) was exceeded. At distal thigh level, where a predominant nerve-lesion-voxel burden was observed, signal quantification was performed by calculating proton spin density and T2-relaxation time as microstructural markers of nerve tissue integrity. The total number of nerve-lesion voxels (cumulated from proximal-to-distal) was significantly higher in symptomatic patients (20 405 ± 1586) versus asymptomatic gene carriers (12 294 ± 3199; P = 0.036) and versus controls (6536 ± 467; P < 0.0001). It was also higher in asymptomatic carriers compared to controls (P = 0.043). The number of nerve-lesion voxels was significantly higher at thigh level compared to more distal levels (lower leg/ankle) of the lower extremities (f-value = 279.22, P < 0.0001). Further signal-quantification at this proximal site (thigh level) revealed a significant increase of proton-density (P < 0.0001) and T2-relaxation-time (P = 0.0011) in symptomatic patients, whereas asymptomatic gene-carriers presented with a significant increase of proton-density only. Lower limb nerve injury could be detected and quantified in vivo on microstructural level by magnetic resonance neurography in symptomatic familial amyloid polyneuropathy, and also in yet asymptomatic gene carriers, in whom imaging detection precedes clinical and electrophysiological manifestation. Although symptoms start and prevail distally, the focus of predominant nerve injury and injury progression was found proximally at thigh level with strong and unambiguous lesion-contrast. Imaging of proximal nerve lesions, which are difficult to detect by nerve conduction studies, may have future implications also for other distally-symmetric polyneuropathies.
[Mh] Termos MeSH primário: Neuropatias Amiloides Familiares/diagnóstico por imagem
Angiografia por Ressonância Magnética
Traumatismos dos Nervos Periféricos/diagnóstico por imagem
[Mh] Termos MeSH secundário: Adulto
Idoso
Amiloide/metabolismo
Neuropatias Amiloides Familiares/genética
Neuropatias Amiloides Familiares/fisiopatologia
Biópsia
Estudos de Casos e Controles
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Mutação/genética
Condução Nervosa/fisiologia
Traumatismos dos Nervos Periféricos/etiologia
Estudos Prospectivos
Radiografia
Receptores de Albumina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amyloid); 0 (Receptors, Albumin); 0 (transthyretin receptor)
[Em] Mês de entrada:1504
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:141221
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awu344


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[PMID]:24586698
[Au] Autor:Kraiklang R; Pairojkul C; Khuntikeo N; Imtawil K; Wongkham S; Wongkham C
[Ad] Endereço:Department of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand ; Liver Fluke and Cholangiocarcinoma Research Center, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
[Ti] Título:A novel predictive equation for potential diagnosis of cholangiocarcinoma.
[So] Source:PLoS One;9(2):e89337, 2014.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cholangiocarcinoma (CCA) is the second most common-primary liver cancer. The difficulties in diagnosis limit successful treatment of CCA. At present, histological investigation is the standard diagnosis for CCA. However, there are some poor-defined tumor tissues which cannot be definitively diagnosed by general histopathology. As molecular signatures can define molecular phenotypes related to diagnosis, prognosis, or treatment outcome, and CCA is the second most common cancer found after hepatocellularcarcinoma (HCC), the aim of this study was to develop a predictive model which differentiates CCA from HCC and normal liver tissues. An in-house PCR array containing 176 putative CCA marker genes was tested with the training set tissues of 20 CCA and 10 HCC cases. The molecular signature of CCA revealed the prominent expression of genes involved in cell adhesion and cell movement, whereas HCC showed elevated expression of genes related to cell proliferation/differentiation and metabolisms. A total of 69 genes differentially expressed in CCA and HCC were optimized statistically to formulate a diagnostic equation which distinguished CCA cases from HCC cases. Finally, a four-gene diagnostic equation (CLDN4, HOXB7, TMSB4 and TTR) was formulated and then successfully validated using real-time PCR in an independent testing set of 68 CCA samples and 77 non-CCA controls. Discrimination analysis showed that a combination of these genes could be used as a diagnostic marker for CCA with better diagnostic parameters with high sensitivity and specificity than using a single gene marker or the usual serum markers (CA19-9 and CEA). This new combination marker may help physicians to identify CCA in liver tissues when the histopathology is uncertain.
[Mh] Termos MeSH primário: Colangiocarcinoma/genética
[Mh] Termos MeSH secundário: Diferenciação Celular/fisiologia
Proliferação Celular
Claudina-4/genética
Proteínas de Homeodomínio/genética
Seres Humanos
Reação em Cadeia da Polimerase em Tempo Real
Receptores de Albumina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CLDN4 protein, human); 0 (Claudin-4); 0 (HOXB7 protein, human); 0 (Homeodomain Proteins); 0 (Receptors, Albumin); 0 (transthyretin receptor)
[Em] Mês de entrada:1411
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140304
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0089337


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[PMID]:24422404
[Au] Autor:Feng YJ; Wang YJ; Zhang FC; Zhou C; Quan QZ
[Ad] Endereço:Department of Gastroenterology, Jinan Military General Hospital of PLA, Jinan 250031, China.
[Ti] Título:[Effect of Hanfangji compound on proliferation of hepatic stellate cells and expressions of TTR, ITIH1 and SERPINF2].
[So] Source:Zhongguo Zhong Yao Za Zhi;38(19):3338-42, 2013 Oct.
[Is] ISSN:1001-5302
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To observe and compare the effects of Hanfangji Compound and IFN-gamma on expressions of transthyretin (TTR) , inter-alpha inhibitor H1 (ITIH1) and serpin peptidase inhibitor clade F member 2 (SERPINF2) of hepatic stellate cells (HSC-T6). METHOD: Hanfangji Compound and IFN-gammaof different concentrations were used in hepatic stellate cell-T6 (HSC-T6) for 48 h. Flow cytometer was used to detect the effects of Hanfangji Compound and IFN-gamma on HSC proliferation. RT-PCR method was adopted to detect mRNA expressions of TFR, ITIH1 and SERPINF2. TTR, ITIH1 and SERPINF2 secretions were detected by ELISA. The protein localizations of TTR, ITIH1 and SERPINF2 were examined by immune fluorescence. The protein expression of TfR and ITIHI were determined by Western blot. RESULT: After Hanfangji Compound and IFN-gamma were adopted in HSC-T6, compared with the control group, the cell proliferation was inhibited obviously (P < 0. 05) , protein expressions of TTR, ITIH1 and SERPINF2 and mRNA expression increased significantly, with certain correlation with concentrations of Hanfangji Compound. The 2. 5 g L-I Hanfangji Compound group was superior to the IFN-gamma group (P <0. 05). CONCLUSION: Hanfangji Compound can inhibit HSC proliferation, upregulated TTR, ITIH1 and SERPINF2 proteins and mRNA expression, which may be one of mechanisms of anti-hepatic fibrosis of Hanfangji Compound.
[Mh] Termos MeSH primário: alfa-Globulinas/metabolismo
Medicamentos de Ervas Chinesas/farmacologia
Células Estreladas do Fígado/citologia
Células Estreladas do Fígado/metabolismo
Receptores de Albumina/metabolismo
alfa 2-Antiplasmina/metabolismo
[Mh] Termos MeSH secundário: alfa-Globulinas/genética
Western Blotting
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Ensaio de Imunoadsorção Enzimática
Células Estreladas do Fígado/efeitos dos fármacos
Seres Humanos
Receptores de Albumina/genética
alfa 2-Antiplasmina/genética
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alpha-Globulins); 0 (Drugs, Chinese Herbal); 0 (Receptors, Albumin); 0 (SERPINF2 protein, human); 0 (alpha-2-Antiplasmin); 0 (transthyretin receptor); 39346-44-6 (inter-alpha-inhibitor)
[Em] Mês de entrada:1403
[Cu] Atualização por classe:140115
[Lr] Data última revisão:
140115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140116
[St] Status:MEDLINE


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[PMID]:22974092
[Au] Autor:Byström P; Berglund Å; Nygren P; Wernroth L; Johansson B; Larsson A; Glimelius B
[Ad] Endereço:Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden. per.bystrom@akademiska.se
[Ti] Título:Evaluation of predictive markers for patients with advanced colorectal cancer.
[So] Source:Acta Oncol;51(7):849-59, 2012 Sep.
[Is] ISSN:1651-226X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: To evaluate the predictive and prognostic value of serum and plasma tumor markers, in comparison with clinical and biomedical parameters for response rate (RR), progression-free survival (PFS) and overall survival (OS) among patients with metastatic colorectal cancer (mCRC) treated with combination chemotherapy. MATERIAL AND METHODS: One-hundred and six patients with mCRC from three centers, part of a multicenter study, received irinotecan with the Nordic bolus 5-fluorouracil (5-FU) and folinic acid schedule (FLIRI) or the de Gramont schedule (Lv5FU2-IRI). Blood samples for CEA, CA19-9, TPA, TIMP-1, SAA, transthyretin and CRP were taken at baseline and after two, four and eight weeks of treatment. Tumor marker levels at baseline and longitudinally were compared with responses evaluated (CT/MRI) after two and four months of treatment. The correlations to RR, PFS and OS were evaluated with regression analyses. RESULTS: A significant correlation to OS was seen for baseline levels of all markers. In multivariate analyses with clinical parameters, TPA, CRP, SAA and TIMP-1 provided independent information. The baseline values of CEA, TPA and TIMP-1 were also significantly correlated to PFS and TPA to RR. Changes during treatment, i.e. the slope gave with the exception of CA19-9 for OS less information about outcomes. The best correlation to response was seen for CEA, CA19-9 and TPA with AUC values of 0.78, 0.83 and 0.79, respectively, using a combined model based upon an interaction between the slope and the baseline value. CONCLUSIONS: Baseline tumor markers together with clinical parameters provide prognostic information about survival in patients with mCRC. The ability of the individual tumor markers to predict treatment response and PFS is limited. Changes in marker levels during the first two months of treatment are less informative of outcome.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Biomarcadores Tumorais/sangue
Neoplasias Colorretais/sangue
Neoplasias Colorretais/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Área Sob a Curva
Proteína C-Reativa/metabolismo
Antígeno CA-19-9/sangue
Camptotecina/administração & dosagem
Camptotecina/análogos & derivados
Antígeno Carcinoembrionário/sangue
Neoplasias Colorretais/mortalidade
Neoplasias Colorretais/patologia
Intervalo Livre de Doença
Esquema de Medicação
Estudos de Avaliação como Assunto
Feminino
Fluoruracila/administração & dosagem
Seres Humanos
Leucovorina/administração & dosagem
Modelos Lineares
Masculino
Meia-Idade
Análise Multivariada
Estadiamento de Neoplasias
Pré-Albumina/metabolismo
Valor Preditivo dos Testes
Prognóstico
Receptores de Albumina/sangue
Sensibilidade e Especificidade
Proteína Amiloide A Sérica/metabolismo
Suécia
Inibidor Tecidual de Metaloproteinase-1/sangue
Antígeno Polipeptídico Tecidual/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CA-19-9 Antigen); 0 (Carcinoembryonic Antigen); 0 (Prealbumin); 0 (Receptors, Albumin); 0 (Serum Amyloid A Protein); 0 (Tissue Inhibitor of Metalloproteinase-1); 0 (Tissue Polypeptide Antigen); 0 (transthyretin receptor); 7673326042 (irinotecan); 9007-41-4 (C-Reactive Protein); Q573I9DVLP (Leucovorin); U3P01618RT (Fluorouracil); XT3Z54Z28A (Camptothecin)
[Em] Mês de entrada:1301
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120915
[St] Status:MEDLINE
[do] DOI:10.3109/0284186X.2012.705020



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