RESUMEN
Dogs are the primary urban reservoir of Leishmania infantum and play a crucial role in the transmission of this parasite to man via sandflies. The spleen and liver are the main target organs of L. infantum infection, but few studies have evaluated the immune response to this infection in the canine liver. To identify the immunological mediators involved in resistance and/or susceptibility to canine visceral leishmaniosis (CVL), we selected 21 dogs naturally infected by L. infantum and classified as asymptomatic or symptomatic. Immunological parameters were analysed and correlations with clinical signs were determined. Symptomatic dogs showed higher numbers of parasites and less leucocyte infiltration in the liver compared with asymptomatic dogs. The progression of this disease was characterized not only by the down regulation of T helper (Th) 1-related cytokines, such as interferon (IFN)-γ and tumour necrosis factor (TNF)-α, but also by the down regulation of genes encoding interleukin (IL)-17A, inducible nitric oxide synthase (iNOS) and IL-10 in the spleen and liver in symptomatic dogs compared with asymptomatic dogs. Importantly, IL-17A gene transcription level was positively correlated with mRNA expression for iNOS and IFN-γ. Th1- and Th17-related cytokines therefore appear to play a role in restricting parasite growth via iNOS activation and decrease susceptibility of dogs to CVL.
Asunto(s)
Enfermedades de los Perros/inmunología , Interferón gamma/biosíntesis , Interleucina-17/biosíntesis , Leishmaniasis Visceral/veterinaria , Óxido Nítrico Sintasa de Tipo II/biosíntesis , Animales , Citocinas/análisis , Citocinas/biosíntesis , Enfermedades de los Perros/metabolismo , Perros , Ensayo de Inmunoadsorción Enzimática , Leishmaniasis Visceral/inmunología , Leishmaniasis Visceral/metabolismo , Reacción en Cadena en Tiempo Real de la PolimerasaRESUMEN
BACKGROUND: The Quota Law in Brazil determines that the organizations with over 100 workers must hire people with disabilities. OBJECTIVE: The aim of this investigation was to verify the willingness of future professionals to work with people with disabilities. PARTICIPANTS: A survey was conducted with 341 Brazilian university students. METHODS: The following factors were taken into account: the Quota Law favorability (attitude); the conceptions about disability (beliefs); the evaluation of consequences (positive or negative) which the individual attributes to the fact of working with people with disabilities; and the perception of the level of difficulty to insert these people (beliefs about control). RESULTS: Three patterns of willingness have been identified: willingness guided by the focus on the disability; willingness guided by the instrumental focus; and willingness guided towards accessibility. It has also been verified that these forms of willingness were associated to the perception of difficulties in inserting people with disabilities. CONCLUSIONS: These results empirically reinforce the fact that part of the difficulties in inserting people with disabilities is found in the social environment and conditions, suggesting that these aspects need to be taken into account in the studies on attitudes towards people with disabilities.
Asunto(s)
Actitud , Personas con Discapacidad , Empleo , Estudiantes/psicología , Brasil , Personas con Discapacidad/legislación & jurisprudencia , Empleo/legislación & jurisprudencia , Femenino , Humanos , Masculino , Distancia Psicológica , Medio Social , Universidades , Volición , Adulto JovenRESUMEN
When activated, thrombin activatable fibrinolysis inhibitor (TAFI) inhibits fibrinolysis by modifying fibrin, depressing its plasminogen binding potential. Polymorphisms in the TAFI structural gene (CPB2) have been associated with variation in TAFI levels, but the potential occurrence of influential quantitative trait loci (QTLs) located elsewhere in the genome has been explored only in families ascertained in part through probands affected by thrombosis. We report the results of the first genome-wide linkage screen for QTLs that influence TAFI phenotypes. Data are from 635 subjects from 21 randomly ascertained Mexican American families participating in the San Antonio Family Heart Study. Potential QTLs were localized through a genome-wide multipoint linkage scan using 417 highly informative autosomal short tandem repeat markers spaced at approximately 10-cM intervals. We observed a maximum multipoint LOD score of 3.09 on chromosome 13q, the region of the TAFI structural gene. A suggestive linkage signal (LOD = 2.04) also was observed in this region, but may be an artifact. In addition, weak evidence for linkage occurred on chromosomes 17p and 9q. Our results suggest that polymorphisms in the TAFI structural gene or its nearby regulatory elements may contribute strongly to TAFI level variation in the general population, although several genes in other regions of the genome may also influence variation in this phenotype. Our findings support those of the Genetic Analysis of Idiopathic Thrombophilia (GAIT) project, which identified a potential TAFI QTL on chromosome 13q in a genome-wide linkage scan in Spanish thrombophilia families.
Asunto(s)
Carboxipeptidasa B2/genética , Cromosomas Humanos Par 13/genética , Americanos Mexicanos/genética , Sitios de Carácter Cuantitativo/genética , Adulto , Anciano , Anciano de 80 o más Años , Carboxipeptidasa B2/sangre , Carboxipeptidasa B2/fisiología , Femenino , Ligamiento Genético , Genotipo , Humanos , Masculino , Persona de Mediana EdadRESUMEN
Infection with Trypanosoma cruzi causes a strong inflammatory reaction at the inoculation site and, later, in the myocardium. The present study investigates the role of cytokines as modulators of T. cruzi-induced chemokine expression in vivo and in vitro. In macrophage cultures, although the stimulation with interferon (IFN)-gamma increases the expression of IP-10, it blocks KC expression. Tumor necrosis factor (TNF)-alpha, on the other hand, potentiates KC, IP-10, macrophage inflammatory protein-1alpha, and JE/monocyte chemotatic protein-1 expression. Interleukin-10 and transforming growth factor-beta inhibited almost all chemokines tested. The role of IFN-gamma and TNF-alpha in chemokine modulation during infection was investigated in T. cruzi-infected IFN-gamma-deficient (GKO) or TNF-R1/p55-deficient (p55-/-) mice. The expression of chemokines detected in the inoculation site correlated with the infiltrating cell type observed. Although GKO mice had a delayed and intense neutrophilic infiltrate correlating with the expression of KC and macrophage inflammatory protein-2, none of the above was observed in p55-/- mice. The detection of infiltrating T cells, Mig, and IP-10 in the myocardium was observed in wild-type and p55-/-, but not in GKO mice. Together, these results suggest that the regulatory roles of IFN-gamma and TNF-alpha on chemokine expression may play a crucial role in the modulation of the inflammatory response during T. cruzi infection and mediate resistance to infection.
Asunto(s)
Enfermedad de Chagas/metabolismo , Quimiocinas/biosíntesis , Interferón gamma/deficiencia , Peritonitis/parasitología , Receptores del Factor de Necrosis Tumoral/deficiencia , Animales , Antígenos CD , Movimiento Celular , Enfermedad de Chagas/patología , Quimiocina CXCL10 , Quimiocina CXCL9 , Quimiocinas/genética , Quimiocinas CXC/metabolismo , Femenino , Inmunofenotipificación , Interferón gamma/fisiología , Interleucina-10/fisiología , Linfocitos/fisiología , Macrófagos/metabolismo , Ratones , Ratones Endogámicos C3H , Ratones Endogámicos C57BL , Miocardio/metabolismo , ARN Mensajero/metabolismo , Receptores Tipo I de Factores de Necrosis Tumoral , Factor de Crecimiento Transformador beta/fisiología , Factor de Necrosis Tumoral alfa/fisiologíaRESUMEN
To investigate the role of interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) in the resistance to Paracoccidioides brasiliensis (Pb) infection, mice with homologous disruption of the IFN-gamma (GKO) or TNF-alpha receptor p55 (p55KO) were infected with the parasite. GKO and p55KO, but not wild-type (WT) mice, were unable to control the growth of yeast cells and the mice succumbed to infection by days 16 and 90 after infection, respectively. Typical inflammatory granulomas were found only in WT mice. In contrast, knockout mice presented an inflammatory infiltrate composed of a few neutrophils, mononuclear, epithelioid, and multinuclear giant cells forming incipient granulomas in GKO mice and without granuloma formation in p55KO mice. Besides, both groups of knockout mice exhibited elevated numbers of yeast forms in agreement with colony-forming unit counts in organs. Compared with WT, splenocytes from infected GKO mice cultured with the Pb F1 fraction produced lower TNF-alpha levels, whereas leukocytes from infected p55KO mice produced similar amounts of TNF-alpha but higher levels of IFN-gamma. Moreover, splenocytes from infected WT mice produced higher levels of nitric oxide (NO) resulting in a lower T-cell proliferative response to Con A than uninfected WT, or infected p55KO and GKO mice. On the contrary, the addition of IFN-gamma to splenocytes from infected GKO mice resulted in higher NO production and lower T cell proliferation. Taken together, these findings suggests that endogenous TNF-alpha, acting through the p55 receptor, and IFN-gamma mediate resistance to Pb infection and induce NO production that determines marked T cell unresponsiveness.
Asunto(s)
Interferón gamma/fisiología , Paracoccidioidomicosis/patología , Factor de Necrosis Tumoral alfa/fisiología , Animales , Antígenos CD/genética , Antígenos CD/fisiología , Concanavalina A/farmacología , Citocinas/biosíntesis , Susceptibilidad a Enfermedades/microbiología , Femenino , Interferón gamma/genética , Interferón gamma/farmacología , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , Óxido Nítrico/biosíntesis , Paracoccidioides , Paracoccidioidomicosis/inmunología , Paracoccidioidomicosis/prevención & control , Receptores del Factor de Necrosis Tumoral/genética , Receptores del Factor de Necrosis Tumoral/fisiología , Receptores Tipo I de Factores de Necrosis Tumoral , Bazo/citología , Bazo/inmunología , Bazo/metabolismo , Linfocitos T/citología , Linfocitos T/efectos de los fármacos , Linfocitos T/inmunología , Factor de Necrosis Tumoral alfa/genética , omega-N-Metilarginina/farmacologíaRESUMEN
PURPOSE: We tested the hypothesis that early catheter removal may be accomplished safely after radical prostatectomy. MATERIALS AND METHODS: Cystography on postoperative day 4 or 5 in 42 of 67 consecutive patients who underwent radical retropubic prostatectomy revealed no extravasation in 30 and the urethral catheter was removed (group 1). The control group included 25 patients who did not undergo cystography, and the catheter was removed 14 days postoperatively (group 2). RESULTS: Immediate and late continence was achieved in 14 (46.7%) and 25 (83.3%) cases in group 1, and in 8 (32%) and 22 (88%) cases in group 2, respectively (p>0.05). Catheterization was performed easily without any endoscopic or surgical procedure in 2 patients (6.7%) in group 1 who presented in urinary retention after catheter removal. Wound infection and pelvic abscess developed in 1 case (3.3%). There were no late complications. In group 2 urinary retention developed in 1 patient (4%), wound infection in 1 (4%) and hematuria in 1 (4%). Two patients (8%) had late vesical neck contracture at 4 and 10 months, respectively, which required urethrotomy in 1. In 1 patient (4%) a stricture in the anterior urethra was dilated. CONCLUSIONS: Our study shows that early catheter removal may be accomplished safely in most patients after radical retropubic prostatectomy, and was not associated with a higher complication rate.
Asunto(s)
Cuidados Posoperatorios/métodos , Prostatectomía , Cateterismo Urinario , Anciano , Humanos , Masculino , Persona de Mediana Edad , Factores de Tiempo , UretraRESUMEN
In the present study, we describe the ability of Trypanosoma cruzi trypomastigotes to stimulate the synthesis of beta-chemokines by macrophages. In vivo infection with T. cruzi led to MIP-1alpha, RANTES, and JE/MCP1 mRNA expression by cells from peritoneal inflammatory exudate. In addition, in vitro infection with T. cruzi resulted in expression of beta-chemokine MIP-1alpha, MIP-1beta, RANTES, and JE mRNA by macrophages. The expression of the beta-chemokine MIP-1alpha, MIP-1beta, RANTES, and JE proteins by murine macrophages cultured with trypomastigote forms of T. cruzi was confirmed by immunocytochemistry. Interestingly, macrophage infection with T. cruzi also resulted in NO production, which we found to be mediated mainly by beta-chemokines. Hence, treatment with anti-beta-chemokine-specific neutralizing antibodies partially inhibited NO release by macrophages incubated with T. cruzi parasites. Further, the addition of the exogenous beta-chemokines MIP-1alpha, MIP-1beta, RANTES, and JE/MCP-1 induced an increased T. cruzi uptake, leading to enhanced NO production and control of parasite replication in a dose-dependent manner. L-NMMA, a specific inhibitor of the L-arginine-NO pathway, caused a decrease in NO production and parasite killing when added to cultures of macrophages stimulated with beta-chemokines. Among the beta-chemokines tested, JE was more potent in inhibiting parasite growth, although it was much less efficient than gamma interferon (IFN-gamma). Nevertheless, JE potentiates parasite killing by macrophages incubated with low doses of IFN-gamma. Together, these results suggest that in addition to their chemotactic activity, murine beta-chemokines may also contribute to enhancing parasite uptake and promoting control of parasite replication in macrophages and may play a role in resistance to T. cruzi infection.
Asunto(s)
Quimiocina CCL2/biosíntesis , Quimiocina CCL5/biosíntesis , Proteínas Inflamatorias de Macrófagos/biosíntesis , Macrófagos/parasitología , Óxido Nítrico/biosíntesis , Trypanosoma cruzi/inmunología , Animales , Células Cultivadas , Quimiocina CCL2/genética , Quimiocina CCL3 , Quimiocina CCL4 , Quimiocina CCL5/genética , Quimiocinas CC/biosíntesis , Quimiocinas CC/genética , Femenino , Activación de Macrófagos , Proteínas Inflamatorias de Macrófagos/genética , Macrófagos/inmunología , Macrófagos/metabolismo , Ratones , Ratones Endogámicos C3H , Trypanosoma cruzi/crecimiento & desarrolloRESUMEN
Host resistance to Trypanosoma cruzi infection is dependent on both natural and acquired immune responses. During the early acute phase of infection in mice, natural killer (NK) cell-derived IFN-gamma is involved in controlling intracellular parasite replication, mainly through the induction of nitric oxide biosynthesis by activated macrophages. We have shown that IL-12, a powerful inducer of IFN-gamma production by NK cells, is synthesized soon after trypomastigote-macrophage interaction. The role of IL-12 in the control of T. cruzi infection in vivo was determined by treating infected mice with anti-IL-12 monoclonal antibody (mAb) and analyzing both parasitemia and mortality during the acute phase of infection. The anti-IL-12 mAb-treated mice had higher levels of parasitemia and mortality compared to control mice. Also, treatment of infected mice with mAb specific for IFN-gamma or TNF-alpha inhibited the protective effect of exogenous IL-12. On the other hand, TGF-beta and IL-10 produced by infected macrophages inhibited the induction and effects of IL-12. Therefore, while IL-12, TNF-alpha and IFN-gamma correlate with resistance to T. cruzi infection, TGF-beta and IL-10 promote susceptibility. These results provide support for a role of innate immunity in the control of T. cruzi infection. In addition to its protective role, IL-12 may also be involved in the modulation of T. cruzi-induced myocarditis, since treatment of infected mice with IL-12 or anti-IL-12 mAb leads to an enhanced or decreased inflammatory infiltrate in the heart, respectively. Understanding the role of the cytokines produced during the acute phase of T. cruzi infection and their involvement in protection and pathogenesis would be essential to devise new vaccines or therapies.
Asunto(s)
Modelos Animales de Enfermedad , Interleucina-12/fisiología , Trypanosoma cruzi/patogenicidad , Tripanosomiasis/inmunología , Animales , Inmunidad Innata , RatonesRESUMEN
Host resistance to Trypanosoma cruzi infection in dependent on both natural and acquired immune responses. During the early acute phase of infection in mice, natural killer (NK) cell-derived IFN-gamma is involved in controlling intracellular parasite replication, mainly through the induction of nitric oxide biosynthesis by activate macrophages. We have shown that IL-12, a powerful inducer of IFN-gamma production by NK cells, is synthesized soon after trypomastigote-macrophage interaction. The role of IL-12 in the control of T. cruzi infection in vivo was determined by treating infected mice with anti-IL-12 monoclonal antibody (mAb) and analyzing both parasitemia and mortality during the acute phase of infection. The anti-IL-12 mAb-treated mice had higher levels of parasitemia and mortality compared to control mice. Also, treatment of infected mice with mAb spectific for IFN-gamma or TNF-alpha inhibited the protective effect of exogenous IL-12. On the other hand, TGF-beta and IL-10 produced by infected macrophages inhibited the induction and effects of IL-12. Therefore, while IL-12, TNF-alpha and IFN-gamma correlate with resistance to T. cruzi infection, TGF-beta and IL-10 promote susceptibility. These results provide support for a role of innate immunity in the control of T. cruzi infection. In addition to its protective role, IL-12 may also be involved in the modulation of T. cruzi-induced myocarditis, since treatment of infected mice with IL-12 or anti-IL-12 mAb leads to an enhanced or decreased inflammatory infiltrate in the heart, respectively. Understanding the role of the cytokine produced during the acute phase of T. cruzi infection and their involvement in protection and pathogenesis would be essential to devise new vaccines or therapies.
Asunto(s)
Ratones , Animales , Modelos Animales de Enfermedad , Interleucina-12/fisiología , Trypanosoma cruzi/patogenicidad , Tripanosomiasis/inmunología , Tripanosomiasis/fisiopatología , Inmunidad InnataRESUMEN
Penile prosthetic implantation is a successful procedure for the management of male erectile impotence. However, infection remains the most serious complication requiring removal of the device. Later reinsertion can be difficult due to fibrosis and a shortened penis. We present 3 cases of penile infection with Staphylococcus epidermidis in which a new penile prosthesis was placed after 72 hours of continuous irrigation of the corpora cavernosa with rifamycin. The procedure requires judicious selection of patients and a stable clinical status.
Asunto(s)
Prótesis de Pene/efectos adversos , Infecciones Relacionadas con Prótesis/tratamiento farmacológico , Rifamicinas/uso terapéutico , Infecciones Estafilocócicas/tratamiento farmacológico , Anciano , Humanos , Masculino , Persona de Mediana EdadRESUMEN
Estudaram-se 110 casais estereis que procuraram o Setor de Esterilidade da Clinica Ginecologica do Hospital Agamenon Magalhaes (INAMPS - Recife) no periodo de junho de 1980 a julho de 1981. Os casos foram analisados de acordo com a frequencia dos diversos fatores causais, como masculino, tuboperitoneal, ovariano, uterino, imunologico, entre outros. Todos os casais foram submetidos a anamnese, exame fisico e ginecologico completos, seguindo-se os exames especificos: espermograma, biopsia do endometrio, histerossalpingografia, teste de Huhner, pneumopelvigrafia (quando indicada), laparoscopia (quando havia indicacao)