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1.
Persoonia ; 39: 254-269, 2017 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-29503477

RESUMO

Ganodermataceae is a remarkable group of polypore fungi, mainly characterized by particular double-walled basidiospores with a coloured endosporium ornamented with columns or crests, and a hyaline smooth exosporium. In order to establish an integrative morphological and molecular phylogenetic approach to clarify relationship of Neotropical Amauroderma s.lat. within the Ganodermataceae family, morphological analyses, including scanning electron microscopy, as well as a molecular phylogenetic approach based on one (ITS) and four loci (ITS-5.8S, LSU, TEF-1α and RPB1), were carried out. Ultrastructural analyses raised up a new character for Ganodermataceae systematics, i.e., the presence of perforation in the exosporium with holes that are connected with hollow columns of the endosporium. This character is considered as a synapomorphy in Foraminispora, a new genus proposed here to accommodate Porothelium rugosum (≡ Amauroderma sprucei). Furtadoa is proposed to accommodate species with monomitic context: F. biseptata, F. brasiliensis and F. corneri. Molecular phylogenetic analyses confirm that both genera grouped as strongly supported distinct lineages out of the Amauroderma s.str. clade.

2.
Biol Trace Elem Res ; 120(1-3): 133-40, 2007.
Artigo em Inglês | MEDLINE | ID: mdl-17916965

RESUMO

Most zinc studies show its benefits or changes that coincide with its deficiency, but some have reported damages by supplements. In this work, the effects of zinc in different cell lines (U-937, human monocytes, and murine bone marrow cells) were analyzed. The cells were put in their specific culture medium either alone or with a stimulant [1-phorbol 12-myristate 13-acetate (PMA) for U-937 and monocytes, granulocyte macrophage colony stimulating factor (GM-CSF) for bone marrow cells]. These preparations, with or without zinc (0.05 to 1.0 mM), were incubated and microscopically analyzed on days 3, 9, and 11. The viability of all cells cultivated with 0.05 and 0.1 mM of zinc was similar to that of the controls without zinc (90%). With 1.0 mM of zinc, the viability diminished (p < 0.005) to 80% in U-937 and to 50% in monocytes and bone marrow cells; the number of cells increased in the three lines, but there was no differentiation. We conclude that the effects observed with different doses of zinc vary not only among the different species but also according to the time the cells were exposed to the metal. The same doses of zinc can have either a stimulatory or an inhibitory effect.


Assuntos
Diferenciação Celular/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Zinco/farmacologia , Animais , Células da Medula Óssea/efeitos dos fármacos , Humanos , Camundongos , Monócitos/efeitos dos fármacos , Células U937
3.
Rheumatology (Oxford) ; 46(3): 431-4, 2007 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-17003171

RESUMO

OBJECTIVE: The aim of this study was to assess the potential contribution of HLA-class I MICA and HLA-B gene polymorphisms towards the pathogenesis of giant cell arteritis (GCA). METHODS: Ninety-eight biopsy-proven GCA patients and 225 ethnically matched controls from Lugo, Northwest Spain, were genotyped for the MICA-TM microsatellite polymorphism using a polymerase chain reaction (PCR)-based method. Genotyping of HLA-B was performed using PCR and detection with a reverse sequence-specific oligonucleotide (SSO) probes system. RESULTS: A significant difference in the distribution of the alleles of MICA between patient and control groups (P = 0.005) was found. This was due to an increased frequency of the MICA A5 allele in GCA patients compared with controls (26 vs 13.6%; P = 0.0001; P(C) = 0.0005; OR 2.2, 95% CI 1.4-3.4). In addition, the HLA-B*15 allele showed a higher frequency in GCA patients compared with controls (P = 0.004; P(C) = 0.04; OR 2.7, 95% CI 1.3-5.7). Interestingly, the association observed with the MICA A5 allele seems to be independent of linkage disequilibrium with HLA-B, as well as independent of that previously described with HLA-DRB1*04. Remarkably, simultaneous presence of MICA A5 and HLA-B*15 or HLA-DRB1*04 genetic markers leads to an increase in the OR obtained for each individual genetic marker (MICA A5 + B*15 OR 3.2; MICA A5 + DRB1*04 OR 5.8). CONCLUSIONS: Our results provide the first evidence that the MICA and HLA-B genes are independently associated with the genetic susceptibility to GCA, and suggest that several genes within the MHC might have independent effects in the susceptibility to this systemic vasculitis.


Assuntos
Genes MHC Classe I , Predisposição Genética para Doença , Arterite de Células Gigantes/genética , Idoso , Idoso de 80 Anos ou mais , Feminino , Frequência do Gene , Genótipo , Antígenos HLA-B/genética , Antígeno HLA-B15 , Antígenos HLA-DR/genética , Cadeias HLA-DRB1 , Antígenos de Histocompatibilidade Classe I/genética , Humanos , Masculino , Repetições de Microssatélites/genética , Pessoa de Meia-Idade
4.
Cell Death Differ ; 13(11): 1857-65, 2006 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-16485030

RESUMO

Breast cancer cells often show increased activity of the mitogen-activated protein kinase (MAPK) pathway. We report here that this pathway reduces their sensitivity to death ligand tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and present the underlying mechanism. Activation of protein kinase C (PKC) inhibited TRAIL-induced apoptosis in a protein synthesis-independent manner. Deliberate activation of MAPK was also inhibitory. In digitonin-permeabilized cells, PKC activation interfered with the capacity of recombinant truncated (t)Bid to release cytochrome c from mitochondria. MAPK activation did not affect TRAIL or tumor necrosis factor (TNF)alpha-induced Bid cleavage. However, it did inhibit translocation of (t)Bid to mitochondria as determined both by subcellular fractionation analysis and confocal microscopy. Steady state tBid mitochondrial localization was prohibited by activation of the MAPK pathway, also when the Bcl-2 homology domain 3 (BH3) domain of tBid was disrupted. We conclude that the MAPK pathway inhibits TRAIL-induced apoptosis in MCF-7 cells by prohibiting anchoring of tBid to the mitochondrial membrane. This anchoring is independent of its interaction with resident Bcl-2 family members.


Assuntos
Apoptose/efeitos dos fármacos , Proteína Agonista de Morte Celular de Domínio Interatuante com BH3/metabolismo , Sistema de Sinalização das MAP Quinases , Mitocôndrias/metabolismo , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Ligante Indutor de Apoptose Relacionado a TNF/farmacologia , Neoplasias da Mama/patologia , Caspases/metabolismo , Ativação Enzimática/efeitos dos fármacos , Humanos , Membranas Mitocondriais/metabolismo , Permeabilidade/efeitos dos fármacos , Ligação Proteica , Biossíntese de Proteínas/efeitos dos fármacos , Proteína Quinase C/metabolismo , Transporte Proteico/efeitos dos fármacos , Receptores do Fator de Necrose Tumoral/metabolismo , Proteínas Recombinantes de Fusão/metabolismo , Acetato de Tetradecanoilforbol/farmacologia , Fator de Necrose Tumoral alfa/farmacologia
5.
Appl Microbiol Biotechnol ; 62(5-6): 484-8, 2003 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-12827317

RESUMO

A mixed culture formed by Bacillus sp. and Geotrichum sp. produced tobacco aroma compounds from the carotenoid lutein through the formation of the intermediate beta-ionone. Both microorganisms can grow independently in a medium supplemented with lutein, but only Geotrichum produces beta-ionone. This intermediate was incorporated by the bacilli, converted to aroma and this product excreted to the culture medium. Bacillus sp. did not utilize beta-ionone for growth but modified it. We conclude that, in the bioconversion of lutein to products with tobacco aroma, Geotrichum sp. is involved in carotenoid oxidation to produce beta-ionone and Bacillus sp. is responsible for the norisoprenoid reduction to produce 7,8-dihydro-beta-ionone and 7,8-dihydro-beta-ionol.


Assuntos
Bacillus/metabolismo , Geotrichum/metabolismo , Luteína/metabolismo , Nicotiana , Norisoprenoides/metabolismo , Odorantes , Bacillus/crescimento & desenvolvimento , Geotrichum/crescimento & desenvolvimento , Proteínas/análise
6.
Oncogene ; 20(48): 7128-33, 2001 Oct 25.
Artigo em Inglês | MEDLINE | ID: mdl-11704839

RESUMO

Bc1-2 protein is a potent anti-apoptotic protein that inhibits a mitochondria-operated pathway of apoptosis in many cells. DNA damaging agents and death receptor ligands can activate this mitochondrial apoptotic mechanism. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been suggested to escape from the inhibitory action of Bc1-2 protein. We show that in human breast tumor MCF-7 cells, TRAIL induced a mitochondrial pathway of apoptosis that involved cytochrome c release from mitochondria and activation of caspase 9. The DNA damaging drug doxorubicin also activated this mitochondria-regulated mechanism of apoptosis, which was inhibited in Bc1-2-overexpressing cells. We also demonstrate that in MCF-7 cells Bc1-2 might confer resistance to TRAIL-induced apoptosis, depending on the expression levels of the anti-apoptotic protein. These results indicate that enhanced expression of Bc1-2 in tumor cells can render these cells less sensitive not only to chemotherapeutic drugs but also to TRAIL.


Assuntos
Adenocarcinoma/patologia , Antibióticos Antineoplásicos/farmacologia , Antineoplásicos/farmacologia , Apoptose/efeitos dos fármacos , Neoplasias da Mama/patologia , Doxorrubicina/farmacologia , Resistencia a Medicamentos Antineoplásicos/fisiologia , Glicoproteínas de Membrana/farmacologia , Proteínas de Neoplasias/fisiologia , Proteínas Proto-Oncogênicas c-bcl-2/fisiologia , Fator de Necrose Tumoral alfa/farmacologia , Adenocarcinoma/genética , Adenocarcinoma/metabolismo , Proteínas Reguladoras de Apoptose , Neoplasias da Mama/genética , Neoplasias da Mama/metabolismo , Caspase 9 , Caspases/metabolismo , Grupo dos Citocromos c/metabolismo , Dano ao DNA , DNA de Neoplasias/efeitos dos fármacos , DNA de Neoplasias/genética , Ativação Enzimática/efeitos dos fármacos , Feminino , Humanos , Mitocôndrias/efeitos dos fármacos , Proteínas de Neoplasias/análise , Transporte Proteico/efeitos dos fármacos , Proteínas Proto-Oncogênicas/metabolismo , Ligante Indutor de Apoptose Relacionado a TNF , Tubulina (Proteína)/análise , Células Tumorais Cultivadas/efeitos dos fármacos , Células Tumorais Cultivadas/patologia , Proteína X Associada a bcl-2
7.
Rev. méd. Hosp. Gen. Méx ; 64(2): 91-96, abr.-jun. 2001. CD-ROM
Artigo em Espanhol | LILACS | ID: lil-303062

RESUMO

Las enfermedades pulmonares crónicas son una causa frecuente de hipertensión pulmonar y cor pulmonale crónico, su existencia implica una menor supervivencia y por lo tanto mal pronóstico. Esta revisión analiza los probables factores fisiopatológicos que participan en la génesis de la hipertensión pulmonar de nuestros tres primeros grupos de trabajo (enfermedad pulmonar obstructiva crónica, neumopatía intersticial y apnea obstructiva del sueño). En general, la hipertensión pulmonar de este grupo de pacientes es el resultado de uno o varios factores: factores vasoactivos (hipoxia, acidosis, etcétera), factores pasivos (hiperflujo, hipertensión venocapilar y daño vascular); este último factor a su vez puede ser mediado por la patología de base (fibrosis, inflamación, obstrucción, etcétera) o bien ser secundario a remodelación de la circulación pulmonar por hipoxia crónica e hiperflujo. Otros factores de origen funcional descritos han sido la disminución del volumen pulmonar propia de las patologías intersticiales; así como el aumento en la resistencia de la vía aérea y la eritrocitosis secundaria, hallazgos que caracterizan a la enfermedad pulmonar obstructiva crónica. El adecuado conocimiento en la fisiopatología de estas enfermedades, así como la magnitud de la hipertensión pulmonar requiere del estudio de la circulación pulmonar a través del cateterismo cardiaco derecho por lo que se justifica la existencia de un servicio de hemodinamia en todo hospital dedicado a la enseñanza de la neumología.


Assuntos
Doença Cardiopulmonar , Hemodinâmica/fisiologia , Hipertensão Pulmonar/etiologia , Pneumopatias Obstrutivas/complicações , Vasodilatadores , Cateterismo Cardíaco/métodos
8.
J Biol Chem ; 276(21): 17779-87, 2001 May 25.
Artigo em Inglês | MEDLINE | ID: mdl-11279136

RESUMO

The role of interferon (IFN)-gamma as a sensitizing agent in apoptosis induced by ligation of death receptors has been evaluated in human myeloid leukemia cells. Incubation of U937 cells with IFN-gamma sensitized these cells to apoptosis induced by tumor necrosis factor-alpha, agonistic CD95 antibody, and tumor necrosis factor-related apoptosis-inducing ligand. Other human myeloid leukemic cells were also sensitized by IFN-gamma to death receptor-mediated apoptosis. Treatment of U937 cells with IFN-gamma up-regulated the expression of caspase-8 and potently synergized with death receptor ligation in the processing of caspase-8 and BID cleavage. Concomitantly, a marked down-regulation of BCL-2 protein was also observed in cells incubated with IFN-gamma. Furthermore, the caspase-dependent generation of a 23-kDa fragment of BCL-2 protein, the release of cytochrome c from mitochondria and the activation of caspase-9 were also enhanced upon death receptor ligation in IFN-gamma-treated cells. Ectopically expressed Bcl-2 protein inhibited IFN-gamma-induced sensitization to apoptosis. In summary, these results indicate that IFN-gamma sensitizes human myeloid leukemic cells to a death receptor-induced, mitochondria-mediated pathway of apoptosis.


Assuntos
Antineoplásicos/farmacologia , Apoptose/efeitos dos fármacos , Apoptose/fisiologia , Interferon gama/farmacologia , Receptores do Fator de Necrose Tumoral/fisiologia , Caspase 8 , Caspase 9 , Caspases/fisiologia , Humanos , Leucemia Mieloide/patologia , Proteínas Proto-Oncogênicas c-bcl-2/fisiologia , Transdução de Sinais/efeitos dos fármacos , Células U937
9.
J Immunol ; 163(9): 4737-46, 1999 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-10528172

RESUMO

We have recently reported that activation of protein kinase C (PKC) plays a negative role in CD95-mediated apoptosis in human T cell lines. Here we present data indicating that although the PKC-induced mitogen-activated protein kinase pathway could be partially implicated in the abrogation of CD95-mediated apoptosis by phorbol esters in Jurkat T cells, the major inhibitory effect is exerted through a PKC-dependent, mitogen-activated protein kinase-independent signaling pathway. Furthermore, we demonstrate that activation of PKC diminishes CD95 receptor aggregation elicited by agonistic CD95 Abs. On the other hand, it has been reported that UV radiation-induced apoptosis is mediated at least in part by the induction of CD95 oligomerization at the cell surface. Here we show that activation of PKC also inhibits UVB light-induced CD95 aggregation and apoptosis in Jurkat T cells. These results reveal a novel mechanism by which T cells may restrain their sensitivity to CD95-induced cell death through PKC-mediated regulation of CD95 receptor oligomerization at the cell membrane.


Assuntos
Apoptose/imunologia , Proteína Quinase C/fisiologia , Proteínas Serina-Treonina Quinases , Linfócitos T/enzimologia , Linfócitos T/imunologia , Receptor fas/fisiologia , Animais , Anticorpos Monoclonais/farmacologia , Apoptose/efeitos da radiação , Ativação Enzimática/efeitos dos fármacos , Ativação Enzimática/imunologia , Ativação Enzimática/efeitos da radiação , Inibidores Enzimáticos/farmacologia , Proteína Ligante Fas , Flavonoides/farmacologia , Humanos , Células Jurkat , Ligantes , MAP Quinase Quinase 1 , Glicoproteínas de Membrana/biossíntese , Glicoproteínas de Membrana/efeitos da radiação , Quinases de Proteína Quinase Ativadas por Mitógeno/antagonistas & inibidores , Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo , Proteína Quinase C/metabolismo , Ratos , Agregação de Receptores/imunologia , Agregação de Receptores/efeitos da radiação , Linfócitos T/fisiologia , Linfócitos T/efeitos da radiação , Raios Ultravioleta , Receptor fas/imunologia , Receptor fas/metabolismo
10.
Actas Urol Esp ; 13(4): 264-7, 1989.
Artigo em Espanhol | MEDLINE | ID: mdl-2801272

RESUMO

We present six cases of psoas abscess, three primary and three secondary. The etiologic, pathogenic and therapeutic considerations are outlined. Staphylococcal infections prevail in the primary abscesses. The diagnostic difficulties are considerable but nowadays are facilitated by echography and TAC. In the secondary ones, the psoas abscess is an epiphenomenon of a more easily recognised clinical syndrome. It is surprising how these septic processes are increasingly placed in the hands of urologists in recognition of their mastery of retroperitoneal surgery.


Assuntos
Abscesso/cirurgia , Doenças Musculares/cirurgia , Espaço Retroperitoneal , Abscesso/diagnóstico por imagem , Adulto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Doenças Musculares/diagnóstico por imagem , Encaminhamento e Consulta , Tomografia Computadorizada por Raios X
11.
Bol. méd. Hosp. Infant. Méx ; 46(2): 106-12, feb. 1989. ilus, tab
Artigo em Espanhol | LILACS | ID: lil-72094

RESUMO

Se presenta la correlación en 40 neonatos y lactantes a los cuales se les practicó estudio por ultrasonido del cerebro y tomografía computada del mismo. Las indicaciones para dichos estudios fueron: dismorfias 15 casos; presencia de signos neurológicos 16 y neonatos de pretérmino con peso inferior a 1,500 g nueve casos. El resultado de esta correlación fue: imágenes semejantes en ambos estudios 24 casos (60%), mejor resolución de las imágenes por ultrasonido 14 casos (35%), mejor resolución por la tomografía un caso (2.5%) e imágenes no coincidentes un caso (2.5%). Se concluye que en el campo de la neonatología el estudio por ultrasonido tiene más ventajas. Ultrasonografía del cerebro; tomografía computada del cerebro


Assuntos
Recém-Nascido , Lactente , Humanos , Cérebro , Tomografia Computadorizada por Raios X , Ultrassonografia , México
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