RESUMEN
Conjoined twins are a rare congenital anomaly of unknown aetiology. We report the successful anaesthetic management of separation of ischiopagus tetrapus conjoined twins. The importance of a multidisciplinary approach, thorough pre-operative evaluation and planning, vigilant monitoring and anticipation of complications such as massive blood and fluid loss, haemodynamic instability, hypothermia and intensive, post-operative care are emphasised.
RESUMEN
Idiopathic pulmonary fibrosis (IPF) is characterised by myofibroblast proliferation leading to architectural destruction. Neither the origin nor the continued proliferation of myofibroblasts is well understood. Explanted human IPF lungs were stained by immunohistochemistry for calretinin, a marker of pleural mesothelial cells (PMCs). Chronic obstructive pulmonary disease (COPD) and cystic fibrosis (CF) lungs acted as controls. The number of PMCs per 100 nucleated cells and per photomicrograph was estimated along with the Ashcroft score of fibrosis. Mouse PMCs expressing green fluorescent protein (GFP) or labelled with nanoparticles were injected into the pleural space of mice given intranasal transforming growth factor (TGF)-ß1. Mouse lungs were lavaged and examined for the presence of GFP, smooth muscle α-actin (α-SMA) and calretinin. Calretinin-positive PMCs were found throughout IPF lungs, but not in COPD or CF lungs. The number of PMCs correlated with the Ashcroft score. In mice, nanoparticle-laden PMCs were recoverable by bronchoalveolar lavage, depending on the TGF-ß1 dose. Fluorescent staining showed α-SMA expression in GFP-expressing PMCs, with co-localisation of GFP and α-SMA. PMCs can traffic through the lung and show myofibroblast phenotypic markers. PMCs are present in IPF lungs, and their number correlates with IPF severity. Since IPF presumably begins subpleurally, PMCs could play a pathogenetic role via mesothelial-mesenchymal transition.
Asunto(s)
Epitelio/patología , Fibrosis Pulmonar Idiopática/fisiopatología , Pulmón/metabolismo , Proteína G de Unión al Calcio S100/sangre , Adolescente , Adulto , Anciano , Animales , Calbindina 2 , Núcleo Celular/metabolismo , Niño , Fibrosis Quística/metabolismo , Transición Epitelial-Mesenquimal , Femenino , Proteínas Ligadas a GPI/sangre , Humanos , Inmunohistoquímica/métodos , Masculino , Mesotelina , Ratones , Ratones Endogámicos C57BL , Persona de Mediana Edad , Miofibroblastos/citología , Pleura/metabolismo , Enfermedad Pulmonar Obstructiva Crónica/metabolismoRESUMEN
Pneumocystis carinii causes severe pneumonia in immunocompromised patients. Recent studies indicate that P. carinii uses a Cdc2 cyclin-dependent kinase to control its proliferation. To further study the regulation of the life cycle of P. carinii, we characterized the P. carinii B-type cyclin termed Cdc13, whose binding to Cdc2 is necessary for kinase activity. Antibodies to B-type cyclins (Cdc13) specifically immunoprecipitated Cdc2/ Cdc13 complexes with associated kinase activity from P. carinii extracts. To clone P. carinii cdc13, degenerate polymerase chain reaction was undertaken using primers generated from amino-acid motifs conserved in fungal Cdc13 proteins. This amplicon was used to obtain full-length genomic and complementary DNA (cDNA) clones. A specific synthetic peptide antibody generated to P. carinii Cdc13 further demonstrated differential Cdc2/Cdc13 activity over the life cycle of P. carinii, with greater activity in cysts compared with trophic forms of the organism. Finally, P. carinii cdc13 cDNA was used to rescue mutant Schizosaccharomyces pombe strains containing temperature-sensitive deficiencies of endogenous Cdc13 activity, thus verifying function of the P. carinii Cdc13 protein. Therefore, P. carinii contains a Cdc13 cyclin, which is variably active over its life cycle and which promotes fungal proliferation.
Asunto(s)
Ciclina B/genética , Ciclina B/metabolismo , Pneumocystis/crecimiento & desarrollo , Neumonía por Pneumocystis/metabolismo , Secuencia de Aminoácidos , Animales , Anticuerpos Antifúngicos , Secuencia de Bases , División Celular/fisiología , Ciclina B/inmunología , ADN Complementario , Regulación de la Expresión Génica/fisiología , Genes Fúngicos/fisiología , Huésped Inmunocomprometido , Datos de Secuencia Molecular , Mutación , Pneumocystis/citología , Pneumocystis/enzimología , Proteínas Quinasas/metabolismo , Ratas , Ratas Sprague-Dawley , Proteínas Recombinantes/genética , Proteínas Recombinantes/inmunología , Schizosaccharomyces , TemperaturaRESUMEN
Pulmonary tuberculosis is characterized by granulomatous inflammation with an extensive infiltration of mononuclear phagocytes, but the mechanisms of phagocyte recruitment to the pleural space is unknown. In this study, pleural fluid from patients with tuberculosis contained significantly (P<.001) more biologically active MIP-1alpha and MCP-1 (C-C cytokines) than did effusions from patients with congestive heart failure. Antigenic MIP-1alpha and MCP-1 was detected by immunocytochemistry in pleural biopsy sections of patients with tuberculous pleurisy. In vitro, pleural mesothelial cells stimulated with bacille Calmette-Guérin (BCG) or interferon (IFN)-gamma produced MIP-1alpha and MCP-1. Reverse transcription-polymerase chain reaction studies confirmed that both BCG and IFN-gamma induced MIP-1alpha and MCP-1 expression in mesothelial cells, demonstrating that mesothelial cell-derived C-C chemokines play a biologically important role in the recruitment of mononuclear cells to the pleural space.