Database : HANSEN
Search on : NECROSE [Subject descriptor]
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Id:19625
Author:Shimizu, Toshiaki; Maw, Win Win; Tomioka, Haruaki.
Title:Roles of tumor necrosis factor-alpha and transforming growth factor-beta in regulating intercellular adhesion molecule-1 expression on murine peritoneal macrophages infected with M. Leprae.
Source:Int. J. Lepr;67(1):36-45, Mar., 1999. tab, graf.
Abstract:Profiles of intercellular adhesion molecule-1 (ICAM-1) expression on murine peritoneal macrophages (M phi s) infected with Mycobacterium leprae during cultivation were examined with special reference to the regulatory effects of tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta (TGF-beta). When M phi s were infected with M. leprae or stimulated with heat-killed M. leprae at day 0, their ICAM-1 expression, measured in terms of the ratio of M phi s positively stained with anti-ICAM-1 antibody (Ab), rapidly increased, peaking during days 1 to 3 and thereafter fell, returning to the normal level by day 7. The addition of TNF-alpha or anti-TGF-beta Ab inhibited the middle phase (day 7) downregulation of M phi ICAM-1 expression, although the late-phase (day 14) downregulation of ICAM-1 was not prevented by them. M. leprae-infected M phi s released small amounts of TNF-alpha and significant amounts of TGF-beta into the culture medium. This may indicate that M. leprae-infected M phi s produced the majority of TNF-alpha in a membrane-bound form. Alternatively, endogenous TNF-alpha might upregulate M phi ICAM-1 expression even at very low concentrations. In any case, these findings indicate the central roles of TNF-alpha and TGF-beta in the early phase upregulation and the middle-to-late phase downregulation, respectively, of ICAM-1 expression by M. leprae-infected M phi s. (AU)^ien.
Descriptors:Fator de Necrose Tumoral alfa/imunol
Fator de Necrose Tumoral alfa/fisiol
Macrófagos/imunol
Macrófagos/microbiol
Mycobacterium leprae/imunol
Mycobacterium leprae/fisiol
Electronic Medium:http://hansen.bvs.ilsl.br/textoc/revistas/intjlepr/1999/pdf/v67n1/v67n1a06.pdf / en
Location:BR191.1


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Id:19552
Author:Aarestrup, Fernando Monteiro; Sampaio, Elizabeth Pereira; Moraes, Milton Ozorio de; Albuquerque, Edson C. A; Castro, Ana Paula V; Sarno, Euzenir Nunes.
Title:Experimental mycobacterium leprae infection in BALB/c Mice: effect of BCG administration on TNF-a production and granuloma development.
Source:Int. J. Lepr;68(2):156-166, Jun., 2000. ilus, graf.
Abstract:In the present study, the experimental model of Mycobacterium leprae infection in the foot pads of BALB/c mice was used to investigate the effects of BCG administration on tumor necrosis factor-alpha (TNF-alpha) production and granuloma development. It was observed that mice intravenously infected with BCG 7 months after M. leprae inoculation into the foot pads presented a more effective mycobacteria clearance, revealed by a significant reduction of BCG-colony forming units in the spleen and by the reduction of acid-fast bacilli (AFB) in the foot pads. BCG infection at the peak of M. leprae infection also modulated the granulomatous response to M. leprae by converting mononuclear granulomas into an epithelioid-cell granuloma. Furthermore, lower TNF-alpha serum levels were detected in M. leprae-infected mice when compared to mice infected with M. leprae + BCG. An analysis of the TNF-alpha gene expression in the spleen by semiquantitative reverse transcription-polymerase chain reactions (RT-PCR) demonstrated that co-infection with BCG induced an earlier expression of TNF-alpha mRNA than in M. leprae-infected mice. The numbers of TNF-alpha-positive cells and apoptotic cells were also enhanced in epithelioid versus non-epithelioid granulomas. As a whole, the data suggest that co-infection of M. leprae-infected mice with BCG modulates TNF-alpha synthesis which, in turn, leads to induction of protective epithelioid granuloma formation in the foot pads and subsequent mycobacterial clearance. Macrophage differentiation into epithelioid cells, in association with the enhancement of TNF-alpha production at the granuloma site, may represent a triggering signal that induced apoptosis in these cells, leading to mycobacterial elimination. Moreover, the rate of apoptosis in epithelioid granulomas may well be related to the extent of immunopathologically mediated tissue damage. (AU)^ien.
Descriptors:Mycobacterium leprae/imunol
Camundongos Endogâmicos BALB C/genet
Camundongos Endogâmicos BALB C/imunol
Vacina BCG/uso terap
Fatores de Necrose Tumoral/genet
Fatores de Necrose Tumoral/imunol
Limits:Animais
Camundongos
Electronic Medium:http://hansen.bvs.ilsl.br/textoc/revistas/intjlepr/2000/pdf/v68n2/v68n2a06.pdf / en
Location:BR191.1


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Id:19482
Author:Santos, Adalberto R; Almeida, Alexandre S; Suffys, Philip N; Moraes, Milton O; S. Filho, Valcemir F; Mattos, Haroldo J; Nery, Jose A. C; Cabello, Pedro H; Sampaio, Elizabeth P; Sarno, Euzenir N.
Title:Tumor necrosis factor promoter polymorphism (TNF2) seems to protect against development of severe forms of leprosy in a pilot study in brazilian patients.
Source:Int. J. Lepr;68(3):325-327, Sept., 2000. tab.
Descriptors:Necrose/compl
Necrose/fisiopatol
Polimorfismo Genético/genet
Polimorfismo Genético/fisiol
Hanseníase/compl
Hanseníase/fisiopatol
Limits:Humanos
Electronic Medium:http://hansen.bvs.ilsl.br/textoc/revistas/intjlepr/2000/pdf/v68n3/v68n3cor03.pdf / en
Location:BR191.1


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Id:19387
Author:Kaur, Inderjeet; Agnihotri, Nalini; Mehta, Manjula; Dogra, Sunil; Ganguly, N. K.
Title:Tumor necrosis factor (TNF) production in leprosy patients.
Source:Int. J. Lepr;69(3):249-250, Sept., 2001. tab.
Descriptors:Fatores de Necrose Tumoral/sint quim
Fatores de Necrose Tumoral/imunol
Hanseníase/imunol
Hanseníase/fisiopatol
Limits:Humanos
Electronic Medium:http://hansen.bvs.ilsl.br/textoc/revistas/intjlepr/2001/pdf/v69n3/v69n3cor02.pdf / en
Location:BR191.1


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Id:19383
Author:Park, Eunkyue; Schuller-Levis, Georgia; Park, Seung Yong; Jia, Jun Hua; Levis, William R.
Title:Pentoxifylline downregulares nitric oxide and tumor necrosis factor-a induced by mycobacterial lipoarabinomannan in a macrophage cell line.
Source:Int. J. Lepr;69(3):225-233, Sept., 2001. ilus, tab, graf.
Abstract:Pentoxifylline (PTX), a phosphodiesterase inhibitor, is known to downregulate tumor necrosis factor-alpha (TNF-alpha) secretion induced by lipopolysacchride (LPS) and gamma interferon (IFN-gamma). We have had limited success in treating leprosy reactions, including erythema nodosum leprosum (ENL), in which TNF-alpha has been identified as a major proinflammatory cytokine. PTX inhibited production of NO (IC50 approximately equal to 1.0 mg/ml) and TNF-alpha (IC50 approximately equal to 0.05 mg/ml) in a dose-dependent fashion. As little as 0.5 mg/ml of PTX decreased NO production and 0.01 mg/ml of PTX inhibited TNF-alpha production. Western blot analyses demonstrated that iNOS was suppressed by PTX. Northern blot analyses showed significant reduction of TNF-alpha mRNA. We conclude that PTX is an effective inhibitor of lipoarabinomannan (LAM)-induced TNF-alpha production at both the product and transcriptional levels in our macrophage cell line. PTX also showed moderate inhibition of NO at the product level as well as translation of iNOS. (AU)^ien.
Descriptors:Pentoxifilina/sint quim
Pentoxifilina/imunol
Fator de Necrose Tumoral alfa/sint quim
Fator de Necrose Tumoral alfa/imunol
Macrófagos/imunol
Electronic Medium:http://hansen.bvs.ilsl.br/textoc/revistas/intjlepr/2001/pdf/v69n3/v69n3a07.pdf / en
Location:BR191.1


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Id:19367
Author:Guerra-Infante, Fernando M; López-Hurtado, Marcela; Flores-Medina, Saúl; Zamora-Ruiz, Angélica; Haro-Cruz, Ma. de Jesús.
Title:Dettection of a tumor necrosis factor-like activity in culture supernatants of armadillo leukocytes.
Source:Int. J. Lepr;69(4):354-357, Dec., 2001. ilus, tab.
Descriptors:Fatores de Necrose Tumoral/fisiol
Fatores de Necrose Tumoral/secr
Fatores de Necrose Tumoral/tox
Leucócitos/imunol
Leucócitos/microbiol
Electronic Medium:http://hansen.bvs.ilsl.br/textoc/revistas/intjlepr/2001/pdf/v69n4/v69n4cor03.pdf / en
Location:BR191.1


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Id:19260
Author:Rojas-Espinosa, Oscar; Wek-Rodríguez, Kendy; Arce-Paredes, Patricia; Aguilar-Torrentera, Fabiola; Truyens, Carine; Carlier, Yves.
Title:Contrary to BCG, MLM fails to induce the production of TNFx and NO by macrophages.
Source:Int. J. Lepr;70(2):111-118, Jun. 2002. ilus, tab, graf.
Abstract:Pathogenic mycobacteria must possess efficient survival mechanisms to resist the harsh conditions of the intraphagosomal milieu. In this sense, Mycobacterium lepraemurium (MLM) is one of the most evolved intracellular parasites of murine macrophages; this microorganism has developed a series of properties that allows it not only to resist, but also to multiply within the inhospitable environment of the phagolysosome. Inside the macrophages, MLM appears surrounded by a thick lipid-envelope that protects the microorganism from the digestive effect of the phagosomal hydrolases and the acid pH. MLM produces a disease in which the loss of specific cell-mediated immunity ensues, thus preventing activation of macrophages. In vitro, and possibly also in vivo, MLM infects macrophages without triggering the oxidative (respiratory burst) response of these cells, thus preventing the production of the toxic reactive oxygen intermediaries (ROI). Supporting the idea that MLM is within the most evolved pathogenic microorganisms, in the present study we found, that contrary to BCG, M. lepraemurium infects macrophages without stimulating these cells to produce meaningful levels of tumor necrosis factor alpha (TNF alpha) or nitric oxide (NO). Thus, the ability of the microorganisms to stimulate in their cellular hosts, the production of ROI and RNI (reactive nitrogen intermediates), seems to be an inverse correlate of their pathogenicity; the lesser their ability, the greater their pathogenicity. (AU)^ien.
Descriptors:Hanseníase/genet
Hanseníase/imunol
Vacina BCG/imunol
Vacina BCG/uso terap
Receptores de Fatores de Necrose Tumoral/imunol
Electronic Medium:http://hansen.bvs.ilsl.br/textoc/revistas/intjlepr/2002/pdf/v70n2/v70n2a03.pdf / en
Location:BR191.1


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Id:18344
Author:Nascimento, Consuelo Maria Santos de Albuquerque; Fleury, Raul Negrão; Barreto, Jaison Antônio.
Title:Reação reversa com vasculites granulomatosas e lesões cutâneas necrosantes e ulcerativas / Reversal reaction with granulomatous vasculities and necrotizing cutaneous lesions
Source:Hansen. int;31(1):[80-95], 2006. ilus.
Abstract:Um indivíduo com 49 anos de idade recebe o diagnóstico de Hanseníase Virchoviana sub-polar. Ele referiu, durante os prévios 11 anos, sintomas, principalmente neurológicos, característicos de hanseníase, mas este diagnóstico não foi definido nos serviços médicos que freqüentou. Após 6 meses de poliquimioterapia passou a apresentar neurites que foram tratadas como reação tipo 2. Em um último episódio apresentou febre, mal estar, mialgias e lesões necróticas e ulcerativas nos membros, nádegas, dorso, pavilhão auricular esquerdo. O aspecto clínico destas lesões era semelhante as lesões observadas no fenômeno de Lúcio e no Eritema nodoso necrosante. As biópsias mostram alterações da microvasculatura superficial, necrose epidérmica e dérmica, similares a estas reações, mas as alterações básicas são vasculites granulomatosas no derma profundo e tecido celular sub-cutâneo. Estes aspectos clínicos e histopatológicos são interpretados e discutidos como reação tipo 1 (reação reversa) com envolvimento vascular predominante.(AU).
Descriptors:VASCULITE/microbiol
VASCULITE/patol
GRANULOMA/genet
GRANULOMA/microbiol
GRANULOMA/patol
ULCERA CUTÂNEA/compl
ULCERA CUTÂNEA/diag
ULCERA CUTÂNEA/microbiol
ULCERA CUTÂNEA/fisiopatol
NECROSE
Limits:RELATO DE CASO
HUMANO
MASCULINO
MEIA-IDADE
Electronic Medium:Internet
Location:BR191.1


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Id:17897
Author:Fleury, Raul Negräo; Somei, Ura; Martelli, Antonio Carlos Ceribelli; Delanina, Wladimir F. Bonilha; Opromolla, Diltor Vladimir Araujo.
Title:Manifestaçäo tardia do eritema nodoso hansênico com arterites necrosantes e exsudativas, arterites cicatriciais, livedo reticular, nódulos e placas reacionais, com focos de necrose / Late menifestation of erythema nodosum leprosum with necrotic and exsudative arteritis, cicatricial arteritis, reticular livedo, reactional nodules and plaques, with foci of necrosis
Source:Hansen. int;26(1):37-42, jan.-jun. 2001. ilus.
Abstract:Os autores descrevem uma paciente portadora de hanseníase virchoviana que apresentava episódios reacionais: por sete anos após alta do tratamento, com placas e nódulos em membros inferiores associado a livedo reticular, ulceraçäo e dor. Várias biópsias foram realizadas e a mais constante alteraçäo observada foi a arterite exsudativa e necrótica na derme profunda e no subcutâneo. Raros focos de infiltrado virchoviano residual estavam presentes e bacilos (granulosos) foram vistos apenas na parede das artérias envolvidas. Arterite exsudativa e cicatricial, flebite cicatricial e alteraçöes dérmicas sugestivas de vasculite livedóide foram observadas em algumas biópsias. Os autores acreditavam que esses episódios podem depender da persistência do antígeno em parede do vaso, provavelmente devido ao intenso parasitismo dos vasos na fase mais alta da hanseníase virchoviana. O aspecto livedóide pode estar relacionado as arterites cicatriciais com obstruçäo vascular que poderia permanecer como sequela. (AU).
Descriptors:ERITEMA NODOSO/compl
ERITEMA NODOSO/diag
ERITEMA NODOSO/patol
HANSENIASE VIRCHOWIANA/compl
HANSENIASE VIRCHOWIANA/patol
HANSENIASE VIRCHOWIANA/fisiopatol
VASCULITE/compl
VASCULITE/diag
VASCULITE/fisiopatol
ARTERITE/compl
 ARTERITE/diag
 ARTERITE/fisiopatol
 DERMATOPATIAS VASCULARES/compl
 DERMATOPATIAS VASCULARES/diag
 DERMATOPATIAS VASCULARES/fisiopatol
 NECROSE
Limits:RELATO DE CASO
HUMANO
FEMININO
ADULTO
Electronic Medium:http://hansen.bvs.ilsl.br/textoc/hansenint/v21aov29/2001/PDF/v26n1/v26n1a05.pdf / pt
Location:BR191.1


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Id:17689
Author:Scollard, D. M; Joyce M. P; Gillis, T. P
Title:Development of leprosy and type 1 leprosy reactions after treatment with infliximab: a report of 2 cases ..-
Source:s.l; s.n; 2006. 4 p. ilus.
Abstract:Humanized monoclonal antibodies to tumor necrosis factor- alpha are valuable for the treatment of rheumatologic conditions, but they have been associated with the development of serious infections. We report the first 2 cases of leprosy developing after treatment with infliximab. After discontinuation of infliximab, both patients developed type 1 ([quot ]reversal[quot ]) leprosy reactions. (AU).
Descriptors:Anticorpos Monoclonais/*AE/IM/TU
Anti-Reumáticos/*AE/IM/TU
Artrite/*DT
Glucocorticóides/TU
Hansenostáticos/TU
Hanseníase Dimorfa/CI/*ET/MI
Fator de Necrose Tumoral alfa/AI
Limits:HUMANO
MASCULINO
FEMININO
MEIA-IDADE
IDOSO
SUPPORT, U.S. GOV'T, NON-P.H.S.
Location:BR191.1; 09363/S


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Id:17562
Author:Kang, Tae Jin; Yeum, Chung Eun; Kim, Byoung Chul; You, Eun-Young; Chae, Gue-Tae
Title:Differential production of interleukin-10 and interleukin-12 in mononuclear cells from leprosy patients with a Toll-like receptor 2 mutation ..-
Source:s.l; s.n; 2004. 7 p. ilus, tab, graf.
Abstract:Toll-like receptor 2 (TLR2) is a key mediator of the immune response to mycobacterial infections, and mutations in TLR2 have been shown to confer susceptibility to infection with mycobacteria. This study investigated the profiles of cytokines, such as interferon (IFN)-gamma, interleukin (IL)-10, IL-12 and tumour necrosis factor (TNF)-alpha in response to Mycobacterium leprae in peripheral blood mononuclear cells (PBMC) with the TLR2 mutation Arg677Trp, a recently reported polymorphism that is associated with lepromatous leprosy. In leprosy patients with the TLR2 mutation, production of IL-2, IL-12, IFN-gamma, and TNF-alpha by M. leprae-stimulated PBMC were significantly decreased compared with that in groups with wild-type TLR2. However, the cells from patients with the TLR2 mutation showed significantly increased production of IL-10. There was no significant difference in IL-4 production between the mutant and wild-type during stimulation. Thus, these results suggest that the TLR2 signal pathway plays a critical role in the alteration of cytokine profiles in PBMC from leprosy patients and the TLR2 mutation Arg677Trp provides a mechanism for the poor cellular immune response associated with lepromatous leprosy. (AU).
Descriptors:Sequência de Bases
Interleucina-10/*BI
Interleucina-12/*BI
Hanseníase/GE/*IM
Leucócitos Mononucleares/IM
Glicoproteínas de Membrana/*GE/ME
Camundongos Nus
Dados de Sequência Molecular
Mutação Puntual/*
Receptores da Superfície Celular/*GE/ME
Receptor 2 Toll-Like
Receptores Toll-Like
Fator de Necrose Tumoral alfa/BI
Limits:Adulto
Idoso
Animais
Feminino
Humanos
Masculino
Camundongos
Research Support, Non-U.S. Gov't
Meia-Idade
Location:BR191.1; 09341/s


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Id:17513
Author:Donner, Robert S; Shively, John A
Title:The "Lucio Phenomenon" in diffuse leprosy ..-
Source:s.l; s.n; 1967. ^f831^l836 p. ilus.
Descriptors:Amputação
Cotos de Amputação
Hipersensibilidade/CO
Perna/SU
Hanseníase
Necrose/ET
Recidiva Local de Neoplasia
Neoplasias de Tecido Muscular/SU
Complicações Pós-Operatórias
Pele/BS
Manifestações Cutâneas/*
Doenças Vasculares/ET/PA
Histiócitos
Limits:RELATO DE CASO
Location:BR191.1; 00874/s


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Id:17305
Author:Leal, Angela M. O; Magalhaes, Patricia K. R; Souza, Cacilda S; Foss, Norma T
Title:Adrenocortical hormones and interleukin patterns in leprosy ..-
Source:s.l; s.n; 2003. 5 p. graf.
Abstract:The functional status of adrenocortical hormones and their relationship to the pattern of inflammatory cytokines in the lepromatous and tuberculoid poles of leprosy were investigated. Interleukin (IL)-1beta, IL-6 and tumour necrosis factor (TNF)-alpha plasma levels, C-reactive protein (CRP) concentrations and erythrocyte sedimentation rates (ESR) were significantly higher in LL/BL (lepromatous) leprosy patients than in control subjects. There was a significant positive correlation between IL-6 and TNF-alpha plasma levels and ESR and CRP concentrations. IL-1beta was positively correlated with ESR but not with CRP. Both baseline and stimulated adrenocorticotropic hormone and cortisol plasma levels were not different between patients and control subjects. In contrast, adrenal androgen dehydroepiandrosterone sulphate (DHEA-S) plasma levels were significantly lower in leprosy patients than in sex-matched control subjects. There was a significant inverse correlation between DHEA-S and IL-6, TNF-alpha, and CRP concentrations. This finding may be of pathogenetic significance in this disease and in other inflammatory states. (AU).
Descriptors:Corticosteróides/*BL
Sedimentação Sanguínea
Proteína C-Reativa/AN
Corticotropina/BL
Sulfato de Desidroepiandrosterona/BL
Hidrocortisona/BL
Interleucina-1/BL
Interleucina-6/BL
Interleucinas/*BL
Hanseníase/*BL/*IM
Hanseníase Dimorfa/BL/IM
Hanseníase Virchowiana/BL/IM
Hanseníase Tuberculóide/BL/IM
Fator de Necrose Tumoral/AN
Limits:Adulto
Estudos de Casos e Controles
Humano
Masculino
Location:BR191.1. 0357/s


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Id:13937
Author:Teles, Rosane M. B; Moraes, Milton O; Geraldo, Natasha T. R; Salles, Ana M; Sarno, Euzenir N; Sampaio, Elizabeth P
Title:Differential TNFalpha mRNA regulation detected in the epidermis of leprosy patients ..-
Source:s.l; s.n; 2002. 8 p. ilus, tab, graf.
Abstract:The epidermis is an important site of the immunoinflammatory response in the skin. In the present study, the expression of cytokine and ICAM-1 (intercellular adhesion molecule-1) genes was evaluated by RT-PCR in the epidermis isolated from biopsies from 25 reactional leprosy patients. TNFalpha and IL-6 mRNAs were detected in all individuals during the reactional state (reversal reaction or erythema nodosum leprosum), IL-8 message was detected in 66.6 per cent and 62.5 per cent of the patients, IL-12 mRNA was present in 91.6 per cent and 62.5 per cent and ICAM-1 in 100 per cent and 71.4 per cent, respectively. In addition, when skin biopsies were obtained from the same patients before and during the reactional episode, an enhancement in cytokine mRNA, but not in ICAM-1 mRNA, was observed. Seven patients were also evaluated at the onset of reaction and during antiinflammatory treatment. In contrast to a preferential decrease in the TNFalpha gene detected in the dermis, during the treatment phase, persistent/enhanced TNFalpha mRNA expression was detected in the epidermis in six out of the seven patients assessed. This peculiar pattern of expression might reflect a differential impact that in vivo antiinflammatory therapy has on the epidermis. The present findings indicate that the epidermis plays an important role in the local inflammatory response in leprosy and that the profile of response detected in the epidermis during the reactions may be regulated differently from that in the dermis. (AU).
Descriptors:CITOCINAS/genet
CITOCINAS/metab
ANTIINFLAMATORIOS ESTERÓIDES/uso terap
DERME/metab
HANSENOSTATICOS/uso terap
EPIDERME/metab
MOLECULA 1 DE ADESAO INTERCELULAR/genet
MOLECULA 1 DE ADESAO INTERCELULAR/metab
HANSENIASE/quimioter
HANSENIASE/metab
PENTOXIFILINA/uso terap
ANTIINFLAMATORIOS/uso terap
RNA MENSAGEIRO/metab
TALIDOMIDA/uso terap
PREDNISONA/uso terap
FATOR DE NECROSE TUMORAL/genet
FATOR DE NECROSE TUMORAL/metab
Limits:HUMANO
MASCULINO
FEMININO
ADULTO
MEIA-IDADE
IDOSO
SUPPORT, NON-U.S. GOV'T
Electronic Medium:http://www.ilsl.br
Location:BR191.1; 09157/s


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Id:13932
Author:Boonpucknavig, Vijitr; Soontornniyomkij, Virawudh
Title:Pathology of renal diseases in the tropics ..-
Source:s.l; s.n; Jan. 2003. 19 p. ilus.
Abstract:Renal diseases unique to the tropics are those that occur in association with infectious diseases including dengue hemorrhagic fever, typhoid fever, shigellosis, leptospirosis, lepromatous leprosy, malaria, opisthorchiasis, and schistosomiasis. These renal complications can be classified on the basis of their clinical and pathologic characteristics into acute transient reversible glomerulonephritis, chronic progressive irreversible glomerulonephritis, amyloidosis, and acute renal failure (ARF) resulting from acute tubular necrosis, acute tubulointerstitial nephritis, and thrombotic microangiopathy. Certain primary glomerular diseases including immunoglobulin (Ig) M nephropathy and focal segmental and global glomerulosclerosis are prevalent in some tropical countries. Renal complications of venomous snakebites also are common in the tropics. This article discusses and summarizes important works in the literature in respect to the clinical syndromes, pathologic features, and pathogenesis of tropical renal diseases both in humans and experimental animal models. (AU).
Descriptors:DOENCAS TRANSMISSIVEIS/compl
DOENCAS TRANSMISSIVEIS/diag
GLOMERULOSCLEROSE FOCAL/etiol
GLOMERULOSCLEROSE FOCAL/patol
IMUNOHISTOQUIMICA
NEFROPATIAS/epidemiol
NEFROPATIAS/etiol
NEFROPATIAS/patol
NECROSE TUBULAR AGUDA/etiol
NECROSE TUBULAR AGUDA/patol
BIOPSIA POR AGULHA
NEFRITE INTERSTICIAL/etiol
NEFRITE INTERSTICIAL/patol
PREVALÊNCIA
PROGNOSTICO
INDICE DE GRAVIDADE DE DOENCA
TAXA DE SOBREVIVÊNCIA
FATORES DE RISCO
CLIMA TROPICAL/ef adv
Limits:HUMANO
MASCULINO
FEMININO
Electronic Medium:http://www.ilsl.br
Location:BR191.1; 09109/s


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Id:13928
Author:Vescovo, Giorgio; Ravara, Barbara; Angelini, Annalisa; Sandri, Marco; Carraro, Ugo; Ceconi, Claudio; Dalla Libera, Luciano
Title:Effect of thalidomide on the skeletal muscle in experimental heart failure ..-
Source:s.l; s.n; 2002. 6 p. ilus, tab.
Abstract:BACKGROUND: Tumour Necrosis Factor alpha (TNFalpha) has been shown to contribute to heart failure (CHF) progression. AIMS: We have tried to antagonise the detrimental effects of TNFalpha on skeletal muscle apoptosis, by using thalidomide, a drug that inhibits its biosynthesis. METHODS: CHF was induced in 20 rats by injecting monocrotaline, which determines right ventricle (RV) failure. After 2 weeks, when CHF developed, 12 rats were treated with thalidomide 3.5.mg/kg per day for 2 weeks. Eight had saline and served as CHF controls. RESULTS: Thalidomide failed to decrease TNFalpha and its second messenger sphingosine (SPH), but was able to prevent the shift toward the fast myosin heavy chains. In the Tibialis Anterior muscle of the thalidomide group, the degree of atrophy, the number of apoptotic nuclei and the levels of caspases, were similar to those of the CHF controls. CONCLUSIONS: Thalidomide, at the doses used in this study, which are the same employed for the treatment of tubercolosis, leprosy, AIDS and cancer in humans, did not lower either TNFalpha or SPH and only marginally influenced the apoptosis-induced muscle atrophy. Since other TNFalpha blockers are under investigation for improving the clinical status of patients with CHF, the present data could be relevant in the design of randomised clinical trials in humans. (AU).
Descriptors:APOPTOSE/ef drogas
INSUFICIÊNCIA CARDIACA CONGESTIVA/ind quim
INSUFICIÊNCIA CARDIACA CONGESTIVA/patol
MONOCROTALINA/tox
MUSCULO ESQUELETICO/ef drogas
MUSCULO ESQUELETICO/patol
ATROFIA MUSCULAR/ind quim
ATROFIA MUSCULAR/patol
CADEIAS PESADAS DE MIOSINA/metab
RATOS SPRAGUE-DAWLEY
ESFINGOSINA/antag
ESFINGOSINA/metab
TALIDOMIDA/farmacol
FATOR DE NECROSE TUMORAL/antag
FATOR DE NECROSE TUMORAL/metab
DISFUNCAO VENTRICULAR DIREITA/ind quim
DISFUNCAO VENTRICULAR DIREITA/patol
Limits:ANIMAL
RATOS
Electronic Medium:http://www.ilsl.br
Location:BR191.1; 09104/s


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Id:13727
Author:Cheadle, Eleanor J; Selby, Peter J; Jackson, Andrew M
Title:Mycobacterium bovis bacillus Calmette-Guérin-infected dendritic cells potently activate autologous T cells via a B7 and interleukin-12-dependent mechanism ..-
Source:s.l; s.n; 2003. 10 p. graf.
Abstract:Mycobacteria are potent adjuvants, can survive intracellularly and have been safely used for many years as vaccines against tuberculosis and leprosy. They are thus important potential vectors for recombinant vaccines. Many of their adjuvant properties are mediated following phagocytosis by dendritic cells (DC), which are in turn critical for priming naïve T cells. Although the maturation of DC in response to mycobacteria, such as Mycobacterium bovis bacillus Calmette-Guérin (BCG), is well described the subsequent responses of autologous T cells to mycobacterium-infected DC remains uncharacterized. In our experiments DC infected with BCG expressed more co-stimulatory molecules than tumour-necrosis factor-alpha (TNF-alpha) -treated DC and stimulated more potent mixed leucocyte reactions. When autologous T cells were co-cultured with BCG-exposed DC they became highly activated, as determined by display of CD25, CD54 and CD71 on both CD4+ and CD8+ cells. In contrast, the response of T cells to TNF-alpha-matured DC was significantly less. Cytokine production from T cells cultured with BCG-exposed DC was enhanced with elevated secretion of interleukin-2 (IL-2), IL-10 and interferon-gamma (IFN-gamma) and was produced by both CD4+ and CD8+ lymphocytes as determined by intracellular staining. In particular, IFN-gamma secretion was increased from 50 pg/ml to 25 000 pg/ml and IL-10 secretion increased from 20 pg/ml to 300 pg/ml in BCG-exposed DC co-cultures. Blocking antibodies to B7.1 and B7.2 or IL-12 significantly reduced the secretion of IFN-gamma and reductions were also seen in the expression of CD25 and CD71 by CD4+ cells. These data demonstrate that mycobacterially infected DC are particularly potent activators of autologous T cells compared to TNF-alpha-exposed DC and that the resultant T cells are functionally superior. (AU).
Descriptors:ANTIGENOS CD/metab
ANTIGENOS CD80/imunol
ANTIGENOS DE DIFERENCIACAO DE LINFOCITOS B/metab
LINFOCITOS T CD4-POSITIVOS/imunol
LINFOCITOS T CD8-POSITIVOS/imunol
CITOCINAS/bios
CELULAS DENDRITICAS/imunol
CELULAS DENDRITICAS/microbiol
MOLECULA 1 DE ADESAO INTERCELULAR
IMUNOFENOTIPAGEM
INTERLEUCINA-12/imunol
TRANSFORMACAO LINFOCITICA/imunol
MYCOBACTERIUM BOVIS/imunol
RECEPTORES DA INTERLEUCINA-2/metab
LINFOCITOS T/imunol
FATOR DE NECROSE TUMORAL/imunol
REGULACAO PARA CIMA/imunol
Limits:HUMANO
SUPPORT, NON-U.S. GOV'T
Electronic Medium:http://www.ilsl.br
Location:BR191.1; 08996/s


  18 / 67 HANSEN  
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Id:13659
Author:Mira, M. T; Alcais, A; Pietrantonio, T. di; Thuc, N. V; Phuong, M. C; Abel, L; Schurr, E
Title:Segregation of HLA/TNF region is linked to leprosy clinical spectrum in families displaying mixed leprosy subtypes ..-
Source:s.l; s.n; 2003. 7 p. ilus, tab, graf.
Abstract:Each year an estimated 600000 new leprosy cases are diagnosed worldwide. The spectrum of the disease varies widely from limited tuberculoid forms to extensive lepromatous forms. A measure of the risk to develop lepromatous forms of leprosy is provided by the extent of skin reactivity to lepromin (Mitsuda reaction). To address a postulated oligogenic control of leprosy pathogenesis, we investigated in the present study linkage of leprosy susceptibility, leprosy clinical subtypes, and extent of the Mitsuda reaction to six chromosomal regions carrying known or suspected leprosy susceptibility loci. The only significant result obtained was linkage of leprosy clinical subtype to the HLA/TNF region on human chromosome 6p21 (P(corrected)=0.00126). In addition, we established that within the same family different HLA/TNF haplotypes segregate into patients with different leprosy subtypes directly demonstrating the importance of this genome region for the control of clinical leprosy presentation. (AU).
Descriptors:CROMOSSOMOS HUMANOS PAR 6/genet
PREDISPOSICAO GENETICA PARA DOENÇA
GENOTIPO
HANSENIASE/clas
HANSENIASE/genet
ANTIGENOS HLA/genet
LIGACAO (GENETICA)/genet
FATOR DE NECROSE TUMORAL/genet
FENOTIPO
 LINHAGEM
Limits:HUMANO
MASCULINO
FEMININO
SUPPORT, NON-U.S. GOV'T
Electronic Medium:http://www.ilsl.br
Location:BR191.1; 09137/s


  19 / 67 HANSEN  
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Id:13650
Author:Hernandez, M. O; Neves Junior, I; Sales, J. S; Carvalho, D. S; Sarno, E. N; Sampaio, E. P
Title:Induction of apoptosis in monocytes by Mycobacterium leprae in vitro: a possible role for tumour necrosis factor-alpha ..-
Source:s.l; s.n; 2003. 9 p. graf.
Abstract:A diverse range of infectious organisms, including mycobacteria, have been reported to induce cell death in vivo and in vitro. Although morphological features of apoptosis have been identified in leprosy lesions, it has not yet been determined whether Mycobacterium leprae modulates programmed cell death. For that purpose, peripheral blood mononuclear cells obtained from leprosy patients were stimulated with different concentrations of this pathogen. Following analysis by flow cytometry on 7AAD/CD14+ cells, it was observed that M. leprae induced apoptosis of monocyte-derived macrophages in a dose-dependent manner in both leprosy patients and healthy individuals, but still with lower efficiency as compared to M. tuberculosis. Expression of tumour necrosis factor-alpha (TNF-alpha), Bax-alpha, Bak mRNA and TNF-alpha protein was also detected in these cultures; in addition, an enhancement in the rate of apoptotic cells (and of TNF-alpha release) was noted when interferon-gamma was added to the wells. On the other hand, incubation of the cells with pentoxifylline impaired mycobacterium-induced cell death, the secretion of TNF-alpha, and gene expression in vitro. In addition, diminished bacterial entry decreased both TNF-alpha levels and the death of CD14+ cells, albeit to a different extent. When investigating leprosy reactions, an enhanced rate of spontaneous apoptosis was detected as compared to the unreactive lepromatous patients. The results demonstrated that M. leprae can lead to apoptosis of macrophages through a mechanism that could be at least partially related to the expression of pro-apoptotic members of the Bcl-2 protein family and of TNF-alpha. Moreover, while phagocytosis may be necessary, it seems not to be crucial to the induction of cell death by the mycobacteria. (AU).
Descriptors:APOPTOSE/ef drogas
APOPTOSE/imunol
CELULAS CULTIVADAS
REGULACAO DA EXPRESSÃO GÊNICA
INTERFERON TIPO II/farmacol
HANSENIASE/imunol
PROTEINAS DE MEMBRANA/genet
MONOCITOS/imunol
MONOCITOS/patol
MYCOBACTERIUM LEPRAE/imunol
PENTOXIFILINA/farmacol
FAGOCITOSE/imunol
PROTEINAS PROTO-ONCOGÊNICAS/genet
FATOR DE NECROSE TUMORAL/imunol
Limits:HUMANO
MASCULINO
FEMININO
ADULTO
MEIA-IDADE
IDOSO
SUPPORT, NON-U.S. GOV'T
Electronic Medium:http://www.ilsl.br
Location:BR191.1; 09128/s


  20 / 67 HANSEN  
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Id:13624
Author:Teo, Steve K; Resztak, Ken E; Scheffler, Michael A; Kook, Karin A; Zeldis, Jerry B; Stirling, David I; Thomas, Steve D
Title:Thalidomide in the treatment of leprosy ..-
Source:s.l; s.n; 2002. 10 p. ilus, tab.
Abstract:Leprosy is a chronic infection of the skin and nerves caused by Mycobacterium leprae. Erythema nodosum leprosum (ENL) is a reactive state in lepromatous leprosy. Thalidomide has been used to treat ENL since the 1960s. One of its mechanisms of action is anti-inflammatory through selective inhibition of the pro-inflammatory cytokine TNF-alpha produced by monocytes. (AU).
Descriptors:QUIMIOTERAPIA COMBINADA
ERITEMA NODOSO/quimioter
ERITEMA NODOSO/patol
INCIDÊNCIA
HANSENOSTATICOS/uso terap
HANSENIASE/quimioter
HANSENIASE/patol
HANSENIASE/transm
HANSENIASE VIRCHOWIANA/quimioter
HANSENIASE VIRCHOWIANA/patol
MODELOS MOLECULARES
MYCOBACTERIUM LEPRAE/patogen
TALIDOMIDA/ef adv
TALIDOMIDA/farmacol
TALIDOMIDA/farmacocin
TALIDOMIDA/uso terap
FATOR DE NECROSE TUMORAL/metab
Limits:HUMANO
Electronic Medium:http://www.ilsl.br
Location:BR191.1; 09014/s



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