A expressão de Smads e de membros da família AP1/ jun-fos podem refletir alterações da via de TGFb, uma via importante para o câncer epidermóide de cabeça e pescoço (HNSCC). Encontramos expressão aumentada dos mRNAs das Smads1-8 em HNSCC em comparação com tecido normal adjacente, por RPA. Além disso, as curvas de sobrevida de Kaplan Meier e a análise multivariada mostraram que a Smad6+ parece ser um fator determinante de bom prognóstico em HNSCC. Quanto a família AP-1, mensurado por Northern blot, somente Fra-1 mostrou-se aumentado no tumor e associado à presença de linfonodos comprometidos. Nossos dados sugerem que a positividade de Smad6 possa ser marcador de bom prognóstico em HNSCC / Smad and AP1 messenger RNA expression may underlie disruptions affecting TGFb signaling in head and neck squamous cell carcinoma (HNSCC). Analysis of Smads1-8 mRNA expression by RPA has shown Smad expression is globally increased in tumor as compared to adjacent normal tissue. Kaplan Meier survival curves and multivariate analysis revealed that Smad6 positivity in tumor was an independent good prognostic factor in HNSCC. In relation to AP-1, as measured by Northern blot, only Fra-1 was overexpressed in tumor and directly related to the presence of lymph node involvement. Our data suggest that Smad6 may be a marker of good prognosis in HNSCC

O objetivo deste estudo foi avaliar a contribuição de linfoproliferação (1 parâmetro) em associação a provas sorológicas de alto desempenho (4 parâmetros), estudo epidemiológico (1) e parasitológico (1) em indivíduos com sorologia convencional inconclusiva para a doença de Chagas. Mostramos que o diagnóstico de doença de Chagas é provável quando 3 ou mais desses parâmetros são positivos em 7 (15/73). A combinação: TESA-blot e linfoproliferação positivos revelou-se útil diante de antecedentes epidemiológicos positivos / This study aims to evaluate the contribution of lymphoproliferation (1 parameter) in association with high performance serological tests (4), epidemiological data (1) and parasitological tests (1) for Chagas disease in patients with inconclusive conventional serological tests. We showed that this diagnosis is probable in individuals presenting > three positive of these 7 parameters (15 of 73 individuals). The combination of TESA-blot, lymphoproliferation was useful when epidemiological data were positive

A doença de Pompe (GSDII), autossômica recessiva, é causada pela deficiência da enzima lisossomal que degrada o glicogênio, -glucosidase ácida (GAA). O quadro clínico varia de acordo com a idade de início da doença, grau de progressão e envolvimento dos tecidos: predominantemente cardíaco e muscular esquelético na forma de início-precoce (FIP) e mais restrito no músculo esquelético na forma de início-tardio (FIT). A sobrevida média na FIP é de 9-12 meses. Com avanço dos métodos histológicos, histoquímicos e imunoistoquímicos intensificou-se a análise estrutural e funcional dos tipos de fibras musculares. O estudo da vascularização também é de importância pelo aporte nutricional e funcional das fibras. O objetivo do presente trabalho é analisar a correlação da distribuição do tipo de fibras com a forma de apresentação clínica da doença de Pompe, seu genótipo correspondente e a quantidade residual da enzima GAA. Analisou-se 10 biópsias musculares de pacientes FIP e 09 de FIT comparados com o grupo controle, pareados por idade e gênero. Os pacientes foram selecionados segundo dados clínicos e laboratoriais, sendo feito o seqüenciamento de toda parte codificante do gene e Western Blotting (WB) com anticorpo monoclonal 15362-157, cedido pela Genzyme (primário 1:200 e secundário 1:10.000). A confirmação do diagnóstico foi feita através da medida da atividade residual de GAA em papel filtro, da presença de miopatia vacuolar com grânulos PAS e fosfatase ácida positivos em biópsia muscular e pela presença de mutação no gene GAA. A reação de imunoistoquímica foi realizada para fibras tipo I (lenta), tipo II (rápida) e densidade capilar (ulex), utilizando anticorpos monoclonais, respectivamente: antimiosina lenta (1:80), anti-miosina rápida (1:40) da Novocastra e ulex da Vector (1:800). A contagem das fibras foi realizada por 2 observadores em todo fragmento do corte transversal da biópsia com auxílio de um programa semi-automatizado. Observou-se predomínio de fibras tipo II em ambos os gêneros na FIP e predomínio de fibras tipo I em mulheres e tipo II em homens, na FIT. Aumento da densidade capilar, em comparação com os controles, foi notada em ambas as formas IP e IT. Verificou-se em média 90% de fibras vacuoladas nos casos FIP com completa distorção da arquitetura, enquanto na FIT, a porcentagem de fibras vacuoladas foi variável (0-88%). Como alguns genes constitutivos influenciam na distribuição das fibras musculares, como o gene ACE, o polimorfismo deste gene foi analisado quanto aos genótipos I/I, D/D e I/D. Observou-se ausência de concordância entre o genótipo do ACE e a distribuição de fibras em 60% dos casos da FIP e FIT, atribuindo-se o resultado da distribuição do tipo de fibras como parte da patologia da doença de Pompe. A gravidade da doença variou inversamente com a quantidade de enzima residual, sendo compatível com o quadro clínico do paciente. A presença de mutação deletéria em ambos os alelos foi observada em 3/10 casos de IP, sendo que todos os 3 casos apresentaram ausência total de enzima no WB. Há maior envolvimento de fibras tipo II em GSDII, sem depleção da microcirculação muscular. Estudos demonstram que a remoção do depósito de glicogênio ocorre diferencialmente nos tipos de fibra, sendo menos eficiente nas fibras tipo II. O achado do presente estudo poderá ter implicações na resposta à recente terapêutica proposta por reposição enzimática. / The glycogen storage disease type II (GSDII), autosomal recessive disorder, is caused by the deficiency of GAA (acid -glucosidase) a lysossomal enzyme that degrades the glycogen. The clinical findings are in accordance to great variability of age onset, degree of disease progression and extent of tissue involvement: predominantly cardiac and skeletal muscle in the infantile form (I) and more restricted to the skeletal muscle in the late-onset form (LO). The average survival time of the infantile form is 9-12 months. With advances of the histological, histochemical and imunohistochemical methods structural and functional analysis of muscle fiber types were intensified. The study of the capillary density is also important for nutritional and functional aspects. The objective of the present work is to analyze the correlations of the fiber type distribution to clinical presentation, genotype and residual GAA enzymatic activity. We analyzed 10 muscle biopsies of infantile and 09 of late-onset patients and compared to age and gender matched controls. The patients were selected according to clinical and laboratorial data, molecular diagnosis by full gene sequencing, and Western Blotting (WB) with monoclonal antibody 15362-157, courtesy Genzyme Science Group (primary 1:200 and secondary 1:10.000). Diagnostic confirmation was made by GAA enzymatic measurement in DBS, presence of vacuolar myopathy in muscle biopsy, and presence of mutation in GAA gene. The imunohistochemical study was carried out by detection of type I (slow), type II (fast) fibers and capillaries, using monoclonal antibodies, respectively: anti-slow myosin (1:80), anti-fast myosin (1:40) (Novocastra) and ulex (1:800) (Vector). Morphometry was performed by 2 observers using a half-automatized program. Type II fiber predominance was observed in both gender in the infantile form, type I fiber predominance in women and type II predominance in men with LO. Increase of the capillary density, in comparison to controls was noticed in both forms. 90% of vacuolated fibers with complete distortion of fiber architecture were demonstrated in I cases, while in LO, the percentage of vacuolated fibers ranged from 0 to 88%. As some constitutive gene, like ACE, influence muscle fiber distribution, its polymorphisms I/I, D/D and I/D gene were analyzed. Absence of agreement was observed between ACE genotype and fiber type distribution in 60% of I and LO cases, which was attributed as consequence of Pompe disease pathology itself. The disease severity varied inversely to the amount of residual GAA enzymatic activity, being compatible with the patient clinical findings. The presence of deleterious mutation in both alleles was observed in 3/10 infantile cases, and all 3 presented total enzyme absence at WB. A greater fiber type II involvement was observed in GSDII, without decrease in muscle capillary density. Recent studies demonstrated that glycogen deposit removal occurs distinctively in different fiber types, being less efficient in type II fibers. The present findings might have implications in the reply to the recent proposed enzyme replacement therapy.

Humans have two plasminogen activators (PAs), tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA), which generate plasmin to breakdown fibrin and other barriers to cell migration. Both PAs are used as pharmaceuticals but their efficacies are limited by their rapid clearance from the circulation, predominantly by parenchymal cells of the liver. At the commencement of the work presented here, the hepatic receptors responsible for mediating the catabolism of the PAs were little understood. tPA degradation by hepatic cell lines was known to depend on the formation of binary complexes with the major PA inhibitor, plasminogen activator inhibitor type-1 (PAI-1). Initial studies presented here established that uPA was catabolised in a fashion similar to tPA by the hepatoma cell line, HepG2. Other laboratories around this time found that the major receptor mediating the binding and endocytosis of the PAs is Low Density Lipoprotein Receptor-related Protein (LRP1). LRP1 is a giant 600 kDa protein that binds a range of structurally and functionally diverse ligands including, activated α2 macroglobulin, apolipoproteins, β amyloid precursor protein, and a number of serpin-enzymes complexes, including PA??PAI-1 complexes. Further studies for the work presented here centred on this receptor. By using radiolabelled binding assays, ligand blots, and Western blots on cultured cells, the major findings are that: (1) basal LRP1 expression on HepG2 is low compared to a clone termed, HepG2a16, but appears to increase in long term culture; (2) a soluble form of LRP1, which retains ligand-binding capacity, is present in human circulation; (3) soluble LRP1 is also present in cerebral spinal fluid where its role in neurological disorders such as Alzheimer??s disease is a developing area of interest; and (4) the release of LRP1 is a mechanism conserved in evolution, possibly as distantly as molluscs. The discovery, identification, and characterisation of soluble LRP1 introduces this protein in the human circulation, and presents a possible further level of regulation for its associated receptor system.

O objetivo deste estudo foi avaliar a contribuição de linfoproliferação (1 parâmetro) em associação a provas sorológicas de alto desempenho (4 parâmetros), estudo epidemiológico (1) e parasitológico (1) em indivíduos com sorologia convencional inconclusiva para a doença de Chagas. Mostramos que o diagnóstico de doença de Chagas é provável quando 3 ou mais desses parâmetros são positivos em 7 (15/73). A combinação: TESA-blot e linfoproliferação positivos revelou-se útil diante de antecedentes epidemiológicos positivos / This study aims to evaluate the contribution of lymphoproliferation (1 parameter) in association with high performance serological tests (4), epidemiological data (1) and parasitological tests (1) for Chagas disease in patients with inconclusive conventional serological tests. We showed that this diagnosis is probable in individuals presenting > three positive of these 7 parameters (15 of 73 individuals). The combination of TESA-blot, lymphoproliferation was useful when epidemiological data were positive

A doença de Pompe (GSDII), autossômica recessiva, é causada pela deficiência da enzima lisossomal que degrada o glicogênio, -glucosidase ácida (GAA). O quadro clínico varia de acordo com a idade de início da doença, grau de progressão e envolvimento dos tecidos: predominantemente cardíaco e muscular esquelético na forma de início-precoce (FIP) e mais restrito no músculo esquelético na forma de início-tardio (FIT). A sobrevida média na FIP é de 9-12 meses. Com avanço dos métodos histológicos, histoquímicos e imunoistoquímicos intensificou-se a análise estrutural e funcional dos tipos de fibras musculares. O estudo da vascularização também é de importância pelo aporte nutricional e funcional das fibras. O objetivo do presente trabalho é analisar a correlação da distribuição do tipo de fibras com a forma de apresentação clínica da doença de Pompe, seu genótipo correspondente e a quantidade residual da enzima GAA. Analisou-se 10 biópsias musculares de pacientes FIP e 09 de FIT comparados com o grupo controle, pareados por idade e gênero. Os pacientes foram selecionados segundo dados clínicos e laboratoriais, sendo feito o seqüenciamento de toda parte codificante do gene e Western Blotting (WB) com anticorpo monoclonal 15362-157, cedido pela Genzyme (primário 1:200 e secundário 1:10.000). A confirmação do diagnóstico foi feita através da medida da atividade residual de GAA em papel filtro, da presença de miopatia vacuolar com grânulos PAS e fosfatase ácida positivos em biópsia muscular e pela presença de mutação no gene GAA. A reação de imunoistoquímica foi realizada para fibras tipo I (lenta), tipo II (rápida) e densidade capilar (ulex), utilizando anticorpos monoclonais, respectivamente: antimiosina lenta (1:80), anti-miosina rápida (1:40) da Novocastra e ulex da Vector (1:800). A contagem das fibras foi realizada por 2 observadores em todo fragmento do corte transversal da biópsia com auxílio de um programa semi-automatizado. Observou-se predomínio de fibras tipo II em ambos os gêneros na FIP e predomínio de fibras tipo I em mulheres e tipo II em homens, na FIT. Aumento da densidade capilar, em comparação com os controles, foi notada em ambas as formas IP e IT. Verificou-se em média 90% de fibras vacuoladas nos casos FIP com completa distorção da arquitetura, enquanto na FIT, a porcentagem de fibras vacuoladas foi variável (0-88%). Como alguns genes constitutivos influenciam na distribuição das fibras musculares, como o gene ACE, o polimorfismo deste gene foi analisado quanto aos genótipos I/I, D/D e I/D. Observou-se ausência de concordância entre o genótipo do ACE e a distribuição de fibras em 60% dos casos da FIP e FIT, atribuindo-se o resultado da distribuição do tipo de fibras como parte da patologia da doença de Pompe. A gravidade da doença variou inversamente com a quantidade de enzima residual, sendo compatível com o quadro clínico do paciente. A presença de mutação deletéria em ambos os alelos foi observada em 3/10 casos de IP, sendo que todos os 3 casos apresentaram ausência total de enzima no WB. Há maior envolvimento de fibras tipo II em GSDII, sem depleção da microcirculação muscular. Estudos demonstram que a remoção do depósito de glicogênio ocorre diferencialmente nos tipos de fibra, sendo menos eficiente nas fibras tipo II. O achado do presente estudo poderá ter implicações na resposta à recente terapêutica proposta por reposição enzimática. / The glycogen storage disease type II (GSDII), autosomal recessive disorder, is caused by the deficiency of GAA (acid -glucosidase) a lysossomal enzyme that degrades the glycogen. The clinical findings are in accordance to great variability of age onset, degree of disease progression and extent of tissue involvement: predominantly cardiac and skeletal muscle in the infantile form (I) and more restricted to the skeletal muscle in the late-onset form (LO). The average survival time of the infantile form is 9-12 months. With advances of the histological, histochemical and imunohistochemical methods structural and functional analysis of muscle fiber types were intensified. The study of the capillary density is also important for nutritional and functional aspects. The objective of the present work is to analyze the correlations of the fiber type distribution to clinical presentation, genotype and residual GAA enzymatic activity. We analyzed 10 muscle biopsies of infantile and 09 of late-onset patients and compared to age and gender matched controls. The patients were selected according to clinical and laboratorial data, molecular diagnosis by full gene sequencing, and Western Blotting (WB) with monoclonal antibody 15362-157, courtesy Genzyme Science Group (primary 1:200 and secondary 1:10.000). Diagnostic confirmation was made by GAA enzymatic measurement in DBS, presence of vacuolar myopathy in muscle biopsy, and presence of mutation in GAA gene. The imunohistochemical study was carried out by detection of type I (slow), type II (fast) fibers and capillaries, using monoclonal antibodies, respectively: anti-slow myosin (1:80), anti-fast myosin (1:40) (Novocastra) and ulex (1:800) (Vector). Morphometry was performed by 2 observers using a half-automatized program. Type II fiber predominance was observed in both gender in the infantile form, type I fiber predominance in women and type II predominance in men with LO. Increase of the capillary density, in comparison to controls was noticed in both forms. 90% of vacuolated fibers with complete distortion of fiber architecture were demonstrated in I cases, while in LO, the percentage of vacuolated fibers ranged from 0 to 88%. As some constitutive gene, like ACE, influence muscle fiber distribution, its polymorphisms I/I, D/D and I/D gene were analyzed. Absence of agreement was observed between ACE genotype and fiber type distribution in 60% of I and LO cases, which was attributed as consequence of Pompe disease pathology itself. The disease severity varied inversely to the amount of residual GAA enzymatic activity, being compatible with the patient clinical findings. The presence of deleterious mutation in both alleles was observed in 3/10 infantile cases, and all 3 presented total enzyme absence at WB. A greater fiber type II involvement was observed in GSDII, without decrease in muscle capillary density. Recent studies demonstrated that glycogen deposit removal occurs distinctively in different fiber types, being less efficient in type II fibers. The present findings might have implications in the reply to the recent proposed enzyme replacement therapy.

A expressão de Smads e de membros da família AP1/ jun-fos podem refletir alterações da via de TGFb, uma via importante para o câncer epidermóide de cabeça e pescoço (HNSCC). Encontramos expressão aumentada dos mRNAs das Smads1-8 em HNSCC em comparação com tecido normal adjacente, por RPA. Além disso, as curvas de sobrevida de Kaplan Meier e a análise multivariada mostraram que a Smad6+ parece ser um fator determinante de bom prognóstico em HNSCC. Quanto a família AP-1, mensurado por Northern blot, somente Fra-1 mostrou-se aumentado no tumor e associado à presença de linfonodos comprometidos. Nossos dados sugerem que a positividade de Smad6 possa ser marcador de bom prognóstico em HNSCC / Smad and AP1 messenger RNA expression may underlie disruptions affecting TGFb signaling in head and neck squamous cell carcinoma (HNSCC). Analysis of Smads1-8 mRNA expression by RPA has shown Smad expression is globally increased in tumor as compared to adjacent normal tissue. Kaplan Meier survival curves and multivariate analysis revealed that Smad6 positivity in tumor was an independent good prognostic factor in HNSCC. In relation to AP-1, as measured by Northern blot, only Fra-1 was overexpressed in tumor and directly related to the presence of lymph node involvement. Our data suggest that Smad6 may be a marker of good prognosis in HNSCC

Saccharomyces cerevisiae ist ein bekanntester Modellorganismen in der Systembiologie, der häufig zur Untersuchung des mitotischen Zellzyklus eukaryotischer Zellen verwendet wird. Des Zellzyklus wird durch Cycline, Cyclin-abhängige Kinasen (CDK) und CDK-Inhibitoren (CKI) reguliert. Der wichtigste Kontrollpunkt innerhalb des Zellzyklus reguliert den Übergang von der G1 in die S Phase und wird START genannt. Im dieser Arbeit verwenden wir einen stochastischen Modellierungsansatz, um die Auswirkungen verschiedener Synchronisationsmethoden auf den Zellzyklus zu untersuchen. Um Modellparameter zu schätzen, kombinieren wir Phasen aufgelöste mRNA-Verteilungen unsynchronisierter Einzelzellen und Protein-Zeitreihen synchronisierter Zellpopulationen. Somit können wir mRNA-Dynamiken für ausgewählte Synchronisationsmethoden vorhersagen. In einem zweistufigen Optimierungsansatz unterscheiden wir zwischen mRNA- und Protein-Ebene. Die Parameterschätzung basiert auf der Maximum-Likelihood-Methode. Die Phasen aufgelösten mRNA-Verteilungen wurden mithilfe der smFISH-Technik für SIC1, CLN2 und CLB5 gemessen. Die Protein-Zeitreihen wurden mithilfe von Western Blots für entsprechenden Proteine gemessen. Die gemessenen Moleküle sind die Hauptregulatoren des G1-S Phasenübergangs, welche die Komponenten unseres Zellzyklusmodells darstellen. Durch die erfolgreiche Integration von qualitativ unterschiedlichen Datentypen in der Parameterschätzung konnten wir eine systematische Analyse von Synchronisationseffekten auf den Zellzyklus durchführen. Der zeitlicher Ablauf des Zellzyklus ist dabei maßgeblich beeinflusst. Die stärksten zeitlichen Veränderungen weist die Synchronisation mit alpha-Faktor auf. Elutrierte Zellen sind den unsynchronisierten Zellen trotz verlängerter G1 Phase am ähnlichsten. Wir zeigen in dieser Arbeit, dass synchronisierte Zellpopulationen unzureichend sind, um Rückschlüsse auf den Zellzyklus unsynchronisierter Zellen zu ziehen. / cell cycle, G1/S transition, stochastic modeling, parameter estimation, smFISH, singel cells, Western blotting, cell populations Saccharomyces cerevisiae is a famous model organism in systems biology to study the mitotic cell cycle in eukaryotic cells. The cell cycle is a highly controlled process which is regulated by cyclins, cycline-dependent kinases (CDK) and cyclin-dependent kinase inhibitors (CKI). The main kinase involved in cell cycle regulation is Cdc28. START is the most important check point and controls the G1 to S phase transition. At this point, cells decide if they enter a new cell division cycle or not. In this study, we analyze influences of different synchronization methods on the cell cycle and differences between unsynchronized and synchronized cells by using a stochastic modeling approach. We combine phase-resolved mRNA distributions of unsynchronized single cells and protein time courses of synchronized cell populations to estimate model parameters and to predict synchronization specific mRNA dynamics. Parameter estimation is based on a maximum likelihood approach and performed in a 2-step-optimization in which we differentiate between mRNA and protein level. We measured phase-resolved mRNA distributions of mRNA species SIC1, CLN2 and CLB5 by smFISH and protein time courses of protein species Sic1, Cln2 and Clb5 by Western blotting. These molecules are key regulators of the G1 to S phase transition and represent components of our cell cycle model. By integrating qualitatively different data types in parameter estimation, we come up with a systematic analysis of synchronization effects on the cell cycle. Cell cycle timing is mainly responsible for differences between unsynchronized and synchronized cells and is mostly affected in alpha-factor synchronized cells. Ignoring the prolongation of the G1 phase, elutriated cells are most similar to unsynchronized cells. We show that synchronized cell populations are insufficient to derive general cell cycle behavior of unsynchronized cells.

BACKGROUND: Scythe/BAT3 is a member of the BAG protein family whose role in apoptosis has been extensively studied. However, since the developmental defects observed in Bat3-null mouse embryos cannot be explained solely by defects in apoptosis, we investigated whether BAT3 is also involved in cell-cycle progression. METHODS/PRINCIPAL FINDINGS: Using a stable-inducible Bat3-knockdown cellular system, we demonstrated that reduced BAT3 protein level causes a delay in both G1/S transition and G2/M progression. Concurrent with these changes in cell-cycle progression, we observed a reduction in the turnover and phosphorylation of the CDK inhibitor p21, which is best known as an inhibitor of DNA replication; however, phosphorylated p21 has also been shown to promote G2/M progression. Our findings indicate that in Bat3-knockdown cells, p21 continues to be synthesized during cell-cycle phases that do not normally require p21, resulting in p21 protein accumulation and a subsequent delay in cell-cycle progression. Finally, we showed that BAT3 co-localizes with p21 during the cell cycle and is required for the translocation of p21 from the cytoplasm to the nucleus during the G1/S transition and G2/M progression. CONCLUSION: Our study reveals a novel, non-apoptotic role for BAT3 in cell-cycle regulation. By maintaining a low p21 protein level during the G1/S transition, BAT3 counteracts the inhibitory effect of p21 on DNA replication and thus enables the cells to progress from G1 to S phase. Conversely, during G2/M progression, BAT3 facilitates p21 phosphorylation by cyclin A/Cdk2, an event required for G2/M progression. BAT3 modulates these pro- and anti-proliferative roles of p21 at least in part by regulating cyclin A abundance, as well as p21 translocation between the cytoplasm and the nucleus to ensure that it functions in the appropriate intracellular compartment during each phase of the cell cycle. / Dissertation

Made available in DSpace on 2015-06-08T13:58:11Z (GMT). No. of bitstreams: 2 16.pdf: 27181026 bytes, checksum: 6dd85c661271ca63e8ec1eaa11f96d9b (MD5) license.txt: 1748 bytes, checksum: 8a4605be74aa9ea9d79846c1fba20a33 (MD5) Previous issue date: 2014 / Fundação Oswaldo Cruz. Centro de Pesquisas Aggeu Magalhães. Recife, PE, Brasil / A leishmaniose visceral canina (LVC) e uma doença parasitária causada por protozoários do gênero Leishmania, principalmente por Leishmania infantum. A epidemiologia da doença varia de região para região e o entendimento dos fatores associados à infecção em cães pode ajudar na elaboração de medidas de controle mais específicas. O diagnóstico sorológico da infecção sofreu mudanças importantes nos últimos anos com a introdução do TR-DPP® e do estabelecimento de novos critérios de diagnóstico (TR-DPP® + EIE-LVC) pelo Ministério da Saúde. Dentro desse contexto, no presente estudo objetivou-se estudar a epidemiologia da LVC no município de Goiana, estado de Pernambuco, nordeste do Brasil. Para tal, realizaram-se testes sorológicos (TR-DPP® e EIE-LVC) e análise clínico-epidemiológica em 360 cães semi e domiciliados, de ambos os sexos, raças e idades variadas, nos distritos de Atapuz, Tejucupapo e Pontas de Pedra no referido município. No TR-DPP®47 (13,1 por cento) animais foram reagentes, onde se observou associação significativa dos resultados com os seguintes sinais clínicos: alopecia, lesões na pele paresia e linfonodomegalia. Já no EIE-LVC 21 (5,8 por cento) animais foram reagentes, havendo associação significativa entre a classificação clínica dos animais, condição corporal, alopecia, lesões na pele, secreção ocular, paresia e linfonodomegalia. Já de acordo com o critério do Ministério da Saúde do Brasil, apenas 15 (4,2 por cento) animais foram classificados como positivos. De fato, verificou-se uma fraca concordância (Kappa = 0,39) entre os dois testes sorológicos. Conclui-se que a LVC encontra-se estabelecida em Goiana e que o uso do TR-DPP® como teste de triagem e do EIE-LVC como teste confirmatório pode levar a perda de cães infectados, uma vez que cães positivos do TR-DPP® são negativos no EIE-LVC e vice-versa