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[PMID]:29406049
[Au] Autor:Salim SA; Yousuf T; Patel A; Fülöp T; Agarwal M
[Ad] Endereço:Department of Internal Medicine, University of Mississippi Medical Center, Jackson, Mississippi.
[Ti] Título:Hypocomplementemic Urticarial Vasculitis Syndrome With Crescentic Glomerulonephritis.
[So] Source:Am J Med Sci;355(2):195-200, 2018 Feb.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hypocomplementemic urticarial vasculitis syndrome (HUVS) is a rare autoimmune disease characterized by multiple organ system involvement, including renal disease, with low complement levels. We report the case of a 31-year-old woman who presented with nonspecific symptoms including fatigue, diarrhea, macular rash and abdominal pain with acute renal failure leading to end-stage kidney disease. Laboratory results showed hematuria, nephrotic range proteinuria, worsening creatinine and low C1q levels. Left kidney biopsy showed proliferative glomerulonephritis with crescent formation. She was treated with 6 months of intravenous cyclophosphamide, followed by 2 doses of intravenous rituximab (1g each), thereafter maintained on mycophenolate mofetil and glucocorticoid-based therapy. She experienced a full recovery of renal function after 12 months of dialysis dependence. Hypocomplementemic urticarial vasculitis syndrome with crescentic glomerulonephritis is a rare disease with only 5 other reported cases in literature. In our case, we document a delayed but excellent renal recovery during a 2-year follow-up.
[Mh] Termos MeSH primário: Ciclofosfamida/administração & dosagem
Glomerulonefrite Membranoproliferativa
Ácido Micofenólico/administração & dosagem
Rituximab/administração & dosagem
Urticária
Vasculite
[Mh] Termos MeSH secundário: Adulto
Complemento C1q/metabolismo
Feminino
Glomerulonefrite Membranoproliferativa/complicações
Glomerulonefrite Membranoproliferativa/tratamento farmacológico
Glomerulonefrite Membranoproliferativa/metabolismo
Glomerulonefrite Membranoproliferativa/patologia
Hematúria/complicações
Hematúria/tratamento farmacológico
Hematúria/metabolismo
Hematúria/patologia
Seres Humanos
Falência Renal Crônica/complicações
Falência Renal Crônica/tratamento farmacológico
Falência Renal Crônica/metabolismo
Falência Renal Crônica/patologia
Proteinúria/complicações
Proteinúria/tratamento farmacológico
Proteinúria/metabolismo
Proteinúria/patologia
Síndrome
Urticária/complicações
Urticária/tratamento farmacológico
Urticária/metabolismo
Urticária/patologia
Vasculite/complicações
Vasculite/tratamento farmacológico
Vasculite/metabolismo
Vasculite/patologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
4F4X42SYQ6 (Rituximab); 80295-33-6 (Complement C1q); 8N3DW7272P (Cyclophosphamide); HU9DX48N0T (Mycophenolic Acid)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


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[PMID]:29236760
[Au] Autor:Liu D; Liu J; Wang J; Guo L; Liu C; Jiang Y; Wang H; Yang S
[Ad] Endereço:Department of Pediatric Rheumatology and Allergy, The First Hospital, Jilin University, Changchun, China.
[Ti] Título:Distribution of circulating T follicular helper cell subsets is altered in immunoglobulin A vasculitis in children.
[So] Source:PLoS One;12(12):e0189133, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Immunoglobulin A vasculitis (IgAV) is the most common vasculitis in children. Previously, we demonstrated that patients with IgAV show abnormal proliferation of cluster of differentiation (CD)4+C-X-C chemokine receptor type (CXCR)5+ follicular helper T (Tfh) cells. Here, we explored the status of Tfh cell subsets and plasma cytokine levels in patients with IgAV. METHODS: CD4+CXCR5+CD45RA-, CD45RA-CXCR3+CCR6-, CD45RA-CXCR3-CCR6-, CD45RA-CXCR3-CCR6+, and CD45RA-CXCR3+CCR6+ Tfh cell fractions and plasma concentrations of interferon-γ, interleukin (IL)-4, and IL-17A were evaluated by flow cytometry and a flow cytometric bead array, respectively, in 30 patients with IgAV and 15 healthy controls (HCs). RESULTS: Tfh2 and Tfh17 cell fractions were larger and the Tfh2+Tfh17/Tfh1 ratio and plasmaIL-4 and -17A levels were higher in patients with IgAV than in the HCs. Only Tfh1 cell counts were reduced in the abdominal subtype. The elevations in Tfh2 and Tfh17 cell counts and plasma IL-4 levels were abrogated by treatment. Tfh2 cell number was positively correlated with serum IgA and plasma IL-4 levels, but negatively correlated with the serum C4 concentration, while Tfh17 cell number was positively correlated with the serum IgA level and Tfh2 cell counts. CONCLUSIONS: Abnormally high numbers of Tfh2 and Tfh17 cells are linked to the occurrence and development of IgAV, but are not specific to the abdominal type. Only Tfh1 cells play a critical role in abdominal-type IgAV.
[Mh] Termos MeSH primário: Imunoglobulina A/imunologia
Vasculite/imunologia
[Mh] Termos MeSH secundário: Criança
Seres Humanos
Subpopulações de Linfócitos T
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulin A)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189133


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[PMID]:29236702
[Au] Autor:Liu C; Zhou MS; Li Y; Wang A; Chadipiralla K; Tian R; Raij L
[Ad] Endereço:Department of Endocrinology, First Affiliated Hospital, Jinzhou Medical University, Jinzhou, P.R. of China.
[Ti] Título:Oral nicotine aggravates endothelial dysfunction and vascular inflammation in diet-induced obese rats: Role of macrophage TNFα.
[So] Source:PLoS One;12(12):e0188439, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Obesity and cigarette smoke are major cardiovascular (CV) risk factors and, when coexisting in the same individuals, have additive/synergistic effects upon CVD. We studied the mechanisms involved in nicotine enhancement of CVD in Sprague Dawley rats with diet-induced obesity. The rats were fed either a high fat (HFD) or normal rat chow diet with or without nicotine (100 mg/L in drinking water) for 20 weeks. HFD rats developed central obesity, increased systolic blood pressure (SBP), aortic superoxide (O2-) production, and impaired endothelial nitric oxide synthase (eNOS) and endothelium-dependent relaxation to acetylcholine (EDR). Nicotine further increased SBP, O2- and impaired eNOS and EDR in obese rats. In the peritoneal macrophages from obese rats, tumor necrosis factor (TNF) α, interleukin 1ß and CD36 were increased, and were further increased in nicotine-treated obese rats. Using PCR array we found that 3 of 84 target proinflammatory genes were increased by 2-4 fold in the aorta of obese rats, 11 of the target genes were further increased in nicotine-treated obese rats. HUVECs, incubated with conditioned medium from the peritoneal macrophages of nicotine treated-obese rats, exhibited reduced eNOS and increased NADPH oxidase subunits gp91phox and p22phox expression. Those effects were partially prevented by adding anti-TNFα antibody to the conditioned medium. Our results suggest that nicotine aggravates the CV effects of diet-induced obesity including the oxidative stress, vascular inflammation and endothelial dysfunction. The underlying mechanisms may involve in targeting endothelium by enhancement of macrophage-derived TNFα.
[Mh] Termos MeSH primário: Cotinina/sangue
Dieta Hiperlipídica/efeitos adversos
Endotélio Vascular/efeitos dos fármacos
Macrófagos Peritoneais/metabolismo
Nicotina/farmacologia
Obesidade/fisiopatologia
Fator de Necrose Tumoral alfa/fisiologia
Vasculite/fisiopatologia
[Mh] Termos MeSH secundário: Administração Oral
Animais
Pressão Sanguínea/efeitos dos fármacos
Peso Corporal/efeitos dos fármacos
Proteína C-Reativa/metabolismo
Endotélio Vascular/enzimologia
Endotélio Vascular/metabolismo
Endotélio Vascular/fisiopatologia
Masculino
Nicotina/administração & dosagem
Obesidade/complicações
Obesidade/etiologia
Ratos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Vasculite/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 0 (Tumor Necrosis Factor-alpha); 6M3C89ZY6R (Nicotine); 9007-41-4 (C-Reactive Protein); K5161X06LL (Cotinine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188439


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[PMID]:29228031
[Au] Autor:Comstock E; Kim CW; Murphy A; Emmanuel B; Zhang X; Sneller M; Poonia B; Kottilil S
[Ad] Endereço:Division of Clinical Care and Research, Institute of Human Virology, University of Maryland School of Medicine, Baltimore, MD, United States of America.
[Ti] Título:Transcriptional profiling of PBMCs unravels B cell mediated immunopathogenic imprints of HCV vasculitis.
[So] Source:PLoS One;12(12):e0188314, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:B cell depletion therapy using rituximab has been shown to be effective in achieving remission in patients with HCV-mixed cryoglobulinemic (MC) vasculitis. Previously, we have demonstrated abnormalities in peripheral immune cells involving neutrophils, chemotaxis, and innate immune activation among patients with HCV-MC vasculitis when compared to HCV patients without vasculitis. In this study, we evaluated the effect of B cell depletion therapy on transcriptional profiles of peripheral blood mononuclear cells before and after riruximab therapy, in order to unravel the pathogenic mechanism involved in HCV-MC vasculitis induced by abnormal B cell proliferation. DNA microarray analysis was performed using RNA from PBMCs from seven patients with HCV-MC vasculitis and seven normal volunteers. DNA was hybridized to Affymetrix U133A chips. After normalization, differentially expressed gene list with treatment was generated using partitional clustering. RT-PCR, flow cytometry, and enzyme immunoassay (EIA) was used to validate DNA microarray findings. Differentially expressed genes included B cells and non-B cell genes. Validation of genes using purified cell subsets demonstrated distinct effect of B cell depletion therapy on non-B cells, such as monocytes, T cells, and NK cells. Notably, B lymphocyte stimulator (BLyS) levels were persistently elevated in patients who subsequently relapsed. In conclusion, pathogenesis of HCV-MC vasculitis is mediated by abnormal proliferation of B cells, driven by BLyS, leading to significant effects on non-B cells in mediating symptomatology. Future therapeutics using a combination approach of B cell depletion and proliferation may be desired to achieve long-term remission.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Perfilação da Expressão Gênica
Hepacivirus/patogenicidade
Hepatite C/imunologia
Transcrição Genética
Vasculite/imunologia
[Mh] Termos MeSH secundário: Adulto
Ensaio de Imunoadsorção Enzimática
Feminino
Citometria de Fluxo
Hepatite C/complicações
Seres Humanos
Depleção Linfocítica
Masculino
Meia-Idade
Análise de Sequência com Séries de Oligonucleotídeos
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Vasculite/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188314


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[PMID]:29109302
[Au] Autor:Herman AB; Autieri MV
[Ad] Endereço:Department of Physiology, Independence Blue Cross Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, U.S.A.
[Ti] Título:Inflammation-regulated mRNA stability and the progression of vascular inflammatory diseases.
[So] Source:Clin Sci (Lond);131(22):2687-2699, 2017 Nov 15.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cardiovascular disease remains a major medical and socioeconomic burden in developed and developing societies, and will increase with an aging and increasingly sedentary society. Vascular disease and atherosclerotic vascular syndromes are essentially inflammatory disorders, and transcriptional and post-transcriptional processes play essential roles in the ability of resident vascular and inflammatory cells to adapt to environmental stimuli. The regulation of mRNA translocation, stability, and translation are key processes of post-transcriptional regulation that permit these cells to rapidly respond to inflammatory stimuli. For the most part, these processes are controlled by elements in the 3'-UTR of labile, proinflammatory transcripts. Since proinflammatory transcripts almost exclusively contain AU-rich elements (AREs), this represents a tightly regulated and specific mechanism for initiation and maintenance of the proinflammatory phenotype. RNA-binding proteins (RBPs) recognize cis elements in 3'-UTR, and regulate each of these processes, but there is little literature exploring the concept that RBPs themselves can be directly regulated by inflammatory stimuli. Conceptually, inflammation-responsive RBPs represent an attractive target of rational therapies to combat vascular inflammatory syndromes. Herein we briefly describe the cellular and molecular etiology of atherosclerosis, and summarize our current understanding of RBPs and their specific roles in regulation of inflammatory mRNA stability. We also detail RBPs as targets of current anti-inflammatory modalities and how this may translate into better treatment for vascular inflammatory diseases.
[Mh] Termos MeSH primário: Citocinas/genética
Mediadores da Inflamação
Inflamação/genética
Estabilidade de RNA
RNA Mensageiro/genética
Vasculite/genética
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Citocinas/imunologia
Citocinas/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Inflamação/imunologia
Inflamação/metabolismo
Mediadores da Inflamação/imunologia
Mediadores da Inflamação/metabolismo
RNA Mensageiro/metabolismo
Proteínas de Ligação a RNA/genética
Proteínas de Ligação a RNA/metabolismo
Transdução de Sinais
Vasculite/imunologia
Vasculite/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Cytokines); 0 (Inflammation Mediators); 0 (RNA, Messenger); 0 (RNA-Binding Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171108
[St] Status:MEDLINE
[do] DOI:10.1042/CS20171373


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[PMID]:29028793
[Au] Autor:Negera E; Walker SL; Girma S; Doni SN; Tsegaye D; Lambert SM; Idriss MH; Tsegay Y; Dockrell HM; Aseffa A; Lockwood DN
[Ad] Endereço:London School of Hygiene and Tropical Medicine (LSHTM), London, United Kingdom.
[Ti] Título:Clinico-pathological features of erythema nodosum leprosum: A case-control study at ALERT hospital, Ethiopia.
[So] Source:PLoS Negl Trop Dis;11(10):e0006011, 2017 Oct.
[Is] ISSN:1935-2735
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Leprosy reactions are a significant cause of morbidity in leprosy population. Erythema nodosum leprosum (ENL) is an immunological complication affecting approximately 50% of patients with lepromatous leprosy (LL) and 10% of borderline lepromatous (BL) leprosy. ENL is associated with clinical features such as skin lesions, neuritis, arthritis, dactylitis, eye inflammation, osteitis, orchitis, lymphadenitis and nephritis. ENL is treated mainly with corticosteroids and corticosteroids are often required for extended periods of time which may lead to serious adverse effects. High mortality rate and increased morbidity associated with corticosteroid treatment of ENL has been reported. For improved and evidence-based treatment of ENL, documenting the systems affected by ENL is important. We report here the clinical features of ENL in a cohort of patients with acute ENL who were recruited for a clinico-pathological study before and after prednisolone treatment. MATERIALS AND METHODS: A case-control study was performed at ALERT hospital, Ethiopia. Forty-six LL patients with ENL and 31 non-reactional LL matched controls were enrolled to the study and followed for 28 weeks. Clinical features were systematically documented at three visits (before, during and after predinsolone treatment of ENL cases) using a specifically designed form. Skin biopsy samples were obtained from each patient before and after treatment and used for histopathological investigations to supplement the clinical data. RESULTS: Pain was the most common symptom reported (98%) by patients with ENL. Eighty percent of them had reported skin pain and more than 70% had nerve and joint pain at enrolment. About 40% of the patients developed chronic ENL. Most individuals 95.7% had nodular skin lesions. Over half of patients with ENL had old nerve function impairment (NFI) while 13% had new NFI at enrolment. Facial and limb oedema were present in 60% patients. Regarding pathological findings before treatment, dermal neutrophilic infiltration was noted in 58.8% of patients with ENL compared to 14.3% in LL controls. Only 14.7% patients with ENL had evidence of vasculitis at enrolment. CONCLUSION: In our study, painful nodular skin lesions were present in all ENL patients. Only 58% patients had dermal polymorphonuclear cell infiltration showing that not all clinically confirmed ENL cases have neutrophilic infiltration in lesions. Very few patients had histological evidence of vasculitis. Many patients developed chronic ENL and these patients require inpatient corticosteroid treatment for extended periods which challenges the health service facility in resource poor settings, as well as the patient's quality of life.
[Mh] Termos MeSH primário: Eritema Nodoso/patologia
Eritema Nodoso/fisiopatologia
Hanseníase Virchowiana/patologia
Hanseníase Virchowiana/fisiopatologia
Pele/patologia
[Mh] Termos MeSH secundário: Adolescente
Corticosteroides/efeitos adversos
Corticosteroides/uso terapêutico
Adulto
Biópsia
Estudos de Casos e Controles
Edema/etiologia
Eritema Nodoso/tratamento farmacológico
Etiópia/epidemiologia
Extremidades
Feminino
Hospitais
Seres Humanos
Hanseníase Dimorfa/complicações
Hanseníase Virchowiana/complicações
Hanseníase Virchowiana/microbiologia
Masculino
Meia-Idade
Infiltração de Neutrófilos
Dor
Qualidade de Vida
Pele/efeitos dos fármacos
Pele/imunologia
Pele/microbiologia
Vasculite/etiologia
Vasculite/patologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenal Cortex Hormones)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pntd.0006011


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[PMID]:29016683
[Au] Autor:de Jong RCM; Ewing MM; de Vries MR; Karper JC; Bastiaansen AJNM; Peters HAB; Baghana F; van den Elsen PJ; Gongora C; Jukema JW; Quax PHA
[Ad] Endereço:Department of Surgery, Leiden University Medical Center (LUMC), Leiden, The Netherlands.
[Ti] Título:The epigenetic factor PCAF regulates vascular inflammation and is essential for intimal hyperplasia development.
[So] Source:PLoS One;12(10):e0185820, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Genetic P300/CBP-associated factor (PCAF) variation affects restenosis-risk in patients. PCAF has lysine acetyltransferase activity and promotes nuclear factor kappa-beta (NFκB)-mediated inflammation, which drives post-interventional intimal hyperplasia development. We studied the contributing role of PCAF in post-interventional intimal hyperplasia. METHODS AND RESULTS: PCAF contribution to inflammation and intimal hyperplasia was assessed in leukocytes, macrophages and vascular smooth muscle cells (vSMCs) in vitro and in a mouse model for intimal hyperplasia, in which a cuff is placed around the femoral artery. PCAF deficiency downregulate CCL2, IL-6 and TNF-alpha expression, as demonstrated on cultured vSMCs, leukocytes and macrophages. PCAF KO mice showed a 71.8% reduction of vSMC-rich intimal hyperplasia, a 73.4% reduction of intima/media ratio and a 63.7% reduction of luminal stenosis after femoral artery cuff placement compared to wild type (WT) mice. The association of PCAF and vascular inflammation was further investigated using the potent natural PCAF inhibitor garcinol. Garcinol treatment reduced CCL2 and TNF-alpha expression, as demonstrated on cultured vSMCs and leukocytes. To assess the effect of garcinol treatment on vascular inflammation we used hypercholesterolemic ApoE*3-Leiden mice. After cuff placement, garcinol treatment resulted in reduced arterial leukocyte and macrophage adherence and infiltration after three days compared to untreated animals. CONCLUSIONS: These results identify a vital role for the lysine acetyltransferase PCAF in the regulation of local inflammation after arterial injury and likely the subsequent vSMC proliferation, responsible for intimal hyperplasia.
[Mh] Termos MeSH primário: Epigênese Genética
Hiperplasia/prevenção & controle
Terpenos/farmacologia
Vasculite/prevenção & controle
Fatores de Transcrição de p300-CBP/genética
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas E/genética
Apolipoproteínas E/metabolismo
Adesão Celular/efeitos dos fármacos
Quimiocina CCL2/genética
Quimiocina CCL2/metabolismo
Modelos Animais de Doenças
Artéria Femoral/efeitos dos fármacos
Artéria Femoral/metabolismo
Artéria Femoral/patologia
Seres Humanos
Hiperplasia/genética
Hiperplasia/metabolismo
Hiperplasia/patologia
Interleucina-6/genética
Interleucina-6/metabolismo
Leucócitos/efeitos dos fármacos
Leucócitos/metabolismo
Leucócitos/patologia
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Macrófagos/patologia
Masculino
Camundongos
Camundongos Knockout
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/metabolismo
Miócitos de Músculo Liso/patologia
NF-kappa B/genética
NF-kappa B/metabolismo
Cultura Primária de Células
Transdução de Sinais
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
Túnica Íntima/efeitos dos fármacos
Túnica Íntima/metabolismo
Túnica Íntima/patologia
Vasculite/genética
Vasculite/metabolismo
Vasculite/patologia
Fatores de Transcrição de p300-CBP/antagonistas & inibidores
Fatores de Transcrição de p300-CBP/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Ccl2 protein, mouse); 0 (Chemokine CCL2); 0 (Interleukin-6); 0 (NF-kappa B); 0 (Terpenes); 0 (Tumor Necrosis Factor-alpha); 0 (interleukin-6, mouse); EC 2.3.1.48 (p300-CBP Transcription Factors); EC 2.3.1.48 (p300-CBP-associated factor); TR1VR1V71B (garcinol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171011
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185820


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[PMID]:28954096
[Au] Autor:AlGhamdi KM; Kumar A; Ashour AE; Al-Rikabi AC; AlOmrani AH; Ahamed SS
[Ad] Endereço:Dermatology Department, College of Medicine, King Saud University - Riyadh, Saudi Arabia.
[Ti] Título:Vascular sclerosing effects of bleomycin on cutaneous veins: a pharmacopathologic study on experimental animals.
[So] Source:An Bras Dermatol;92(4):484-491, 2017 Jul-Aug.
[Is] ISSN:1806-4841
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Background:: Varicose veins and the complications of venous disease are common disorders in humans. Objective:: To study the effects of bleomycin as a potential new sclerosing agent and its adverse events in treating varicose veins. Methods:: Bleomycin-loaded liposomes 0.1ml was injected in the dorsal ear veins of white New Zealand rabbits. Sodium tetradecyl sulfate was used as a positive control. Normal saline was used as negative control. The blood vessels of the treated ears were photographed before and at one hour and two, eight and 45 days after treatment. Biopsies from the treated areas were obtained for histological examination. Blood samples were collected to determine any possible toxicity. Results:: Bleomycin by itself was ineffective; therefore, liposomes were used as a vector to deliver bleomycin to the vein lumen. Subsequently, bleomycin started showing its sclerosing effects. Toxicity monitoring showed no apparent hematologic, pulmonary, hepatic or renal toxicities. This study revealed that bleomycin induced vasculitis, which led to vascular occlusion, which was observed on day 1 and day 8. No bleomycin-related injury was noted by histopathological examination of lung sections. The calculation of the lung/body weight coefficient indicated that edema was present in the experimental groups compared with the negative and positive controls. Study limitations:: Relatively small number of experimental animals used. Conclusions:: This study showed that bleomycin-loaded liposomes were able to induce vasculitis and vascular occlusion without any toxicity or complications. It might be useful, hence, to treat patients suffering from Varicose veins and other ectatic vascular diseases with this agent.
[Mh] Termos MeSH primário: Antibióticos Antineoplásicos/administração & dosagem
Bleomicina/farmacologia
Soluções Esclerosantes/farmacologia
Escleroterapia/métodos
Tetradecilsulfato de Sódio/administração & dosagem
Varizes/terapia
[Mh] Termos MeSH secundário: Animais
Bleomicina/administração & dosagem
Modelos Animais de Doenças
Avaliação Pré-Clínica de Medicamentos
Injeções Intravenosas
Lipossomos
Coelhos
Soluções Esclerosantes/administração & dosagem
Soluções Esclerosantes/efeitos adversos
Vasculite/induzido quimicamente
Vasculite/tratamento farmacológico
Veias/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibiotics, Antineoplastic); 0 (Liposomes); 0 (Sclerosing Solutions); 11056-06-7 (Bleomycin); Q1SUG5KBD6 (Sodium Tetradecyl Sulfate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE


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[PMID]:28931222
[Au] Autor:Benjamin LA; Allain TJ; Mzinganjira H; Connor MD; Smith C; Lucas S; Joekes E; Kampondeni S; Chetcuti K; Turnbull I; Hopkins M; Kamiza S; Corbett EL; Heyderman RS; Solomon T
[Ad] Endereço:Malawi-Liverpool-Wellcome Trust Clinical Research Programme, University of Malawi College of Medicine, Blantyre.
[Ti] Título:The Role of Human Immunodeficiency Virus-Associated Vasculopathy in the Etiology of Stroke.
[So] Source:J Infect Dis;216(5):545-553, 2017 Sep 01.
[Is] ISSN:1537-6613
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Human immunodeficiency virus (HIV) infection is a recognized risk factor for stroke among young populations, but the exact mechanisms are poorly understood. We studied the clinical, radiologic, and histologic features of HIV-related ischemic stroke to gain insight into the disease mechanisms. Methods: We conducted a prospective, in-depth analysis of adult ischemic stroke patients presenting to Queen Elizabeth Central Hospital, Blantyre, Malawi, in 2011. Results: We recruited 64 HIV-infected and 107 HIV-uninfected patients. Those with HIV were significantly younger (P < .001) and less likely to have established vascular risk factors. Patients with HIV were more likely to have large artery disease (21% vs 10%; P < .001). The commonest etiology was HIV-associated vasculopathy (24 [38%]), followed by opportunistic infections (16 [25%]). Sixteen of 64 (25%) had a stroke soon after starting antiretroviral therapy (ART), suggesting an immune reconstitution-like syndrome. In this group, CD4+ T-lymphocyte count was low, despite a significantly lower HIV viral load in those recently started on treatment (P < .001). Conclusions: HIV-associated vasculopathy and opportunistic infections are common causes of HIV-related ischemic stroke. Furthermore, subtypes of HIV-associated vasculopathy may manifest as a result of an immune reconstitution-like syndrome after starting ART. A better understanding of this mechanism may point toward new treatments.
[Mh] Termos MeSH primário: Infecções por HIV/complicações
Acidente Vascular Cerebral/virologia
Vasculite/complicações
[Mh] Termos MeSH secundário: Adulto
Idoso
Fármacos Anti-HIV/uso terapêutico
Terapia Antirretroviral de Alta Atividade
Contagem de Linfócito CD4
Estudos de Casos e Controles
Feminino
HIV
Infecções por HIV/tratamento farmacológico
Seres Humanos
Síndrome Inflamatória da Reconstituição Imune/etiologia
Síndrome Inflamatória da Reconstituição Imune/virologia
Malaui
Masculino
Meia-Idade
Estudos Prospectivos
Fatores de Risco
Acidente Vascular Cerebral/diagnóstico por imagem
Acidente Vascular Cerebral/etiologia
Vasculite/diagnóstico
Vasculite/virologia
Carga Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-HIV Agents)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1093/infdis/jix340


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[PMID]:28882238
[Au] Autor:Teague HL; Ahlman MA; Alavi A; Wagner DD; Lichtman AH; Nahrendorf M; Swirski FK; Nestle F; Gelfand JM; Kaplan MJ; Grinspoon S; Ridker PM; Newby DE; Tawakol A; Fayad ZA; Mehta NN
[Ad] Endereço:National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.
[Ti] Título:Unraveling Vascular Inflammation: From Immunology to Imaging.
[So] Source:J Am Coll Cardiol;70(11):1403-1412, 2017 Sep 12.
[Is] ISSN:1558-3597
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammation is a critical factor in early atherosclerosis and its progression to myocardial infarction. The search for valid surrogate markers of arterial vascular inflammation led to the increasing use of positron emission tomography/computed tomography. Indeed, vascular inflammation is associated with future risk for myocardial infarction and can be modulated with short-term therapies, such as statins, that mitigate cardiovascular risk. However, to better understand vascular inflammation and its mechanisms, a panel was recently convened of world experts in immunology, human translational research, and positron emission tomographic vascular imaging. This contemporary review first strives to understand the diverse roles of immune cells implicated in atherogenesis. Next, the authors describe human chronic inflammatory disease models that can help elucidate the pathophysiology of vascular inflammation. Finally, the authors review positron emission tomography-based imaging techniques to characterize the vessel wall in vivo.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/diagnóstico
Diagnóstico por Imagem
Imunidade Inata
Inflamação/diagnóstico
[Mh] Termos MeSH secundário: Doenças Cardiovasculares/imunologia
Seres Humanos
Inflamação/imunologia
Fatores de Risco
Vasculite/diagnóstico
Vasculite/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171028
[Lr] Data última revisão:
171028
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE



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