RESUMEN
The aim of this paper was to highlight the importance of a multidisciplinary and multiprofessional management of SIDS for a complete approach to this tragic event. Both biomedical and psychosocial aspects are evaluated, focusing on the impact of SIDS diagnosis on the family. The paper describes the organization of our team, composed of a network of specialists involved in both prevention and management of SIDS. A protocol is proposed to improve SIDS diagnosis and management. In our team, the clinical pediatrician is the coordinator of specialists and the mediator between the family and the other specialists, thanks to his direct relationship with parents.
Asunto(s)
Grupo de Atención al Paciente/organización & administración , Relaciones Profesional-Familia , Muerte Súbita del Lactante/diagnóstico , Humanos , Lactante , Recién Nacido , Padres/psicología , Especialización , Muerte Súbita del Lactante/prevención & controlRESUMEN
Antigen decay in archival formalin-fixed paraffin-embedded (FFPE) tissue sections for immunohistochemistry is a well-known phenomenon which may have repercussions on translational and research studies and length of storage time appears fundamental. The aim of this study was to evaluate all possible factors which may lead to antigen decay on a prospective standardized collection of human tissues with a panel of 14 routinely used antibodies. Serial slide sections from FFPE control tissues were stored using different methods (routine storage at room temperature, Parafilm(®) protected, paraffin coated and cold stored at 4 °C) and for different time periods: 1, 6, 9, 12, 24 and 36 months. Immunohistochemistry was performed at each time cutoff simultaneously on stored sections and on freshly cut sections using a panel of 14 antibodies. Immunoreactivity was compared with immunoreactions performed at time zero. Reduction in immunostaining was observed for a subset of antibodies (CD3, CD 31, CD117, estrogen and progesterone receptors, Ki67, p53, TTF-1, vimentin) while for others (smooth muscle actin, keratins 7, 20, AE1/AE3, 34ßE12), no antigen decay was observed. Loss of antigenicity was proportional to tissue section age and was dependent on mode of storage with cold storage slides being the least affected. All antigens with reductions in immunosignal were nuclear or membranous, and they all required heat pre-treatment for antigen retrieval. In contrast to results from other studies, when pre-analytical factors are strictly controlled and standardized, antigen decay seems to be restricted to nuclear or membrane antigens which require heat antigen retrieval.
Asunto(s)
Inmunohistoquímica/métodos , Adhesión en Parafina , Manejo de Especímenes , Fijación del Tejido , Anticuerpos , Antígenos , Fijadores , Formaldehído , HumanosAsunto(s)
Anticuerpos/inmunología , Activación de Complemento , Rechazo de Injerto , Antígenos HLA/inmunología , Enfermedades Renales/inmunología , Adolescente , Femenino , Antígenos HLA/química , Humanos , Enfermedades Renales/cirugía , Trasplante de Riñón , Periodo Posparto , Embarazo , Complicaciones del Embarazo , Factores de Riesgo , Sensibilidad y Especificidad , Donantes de Tejidos , Adulto JovenRESUMEN
Mycosis fungoides (MF) is a cutaneous T-cell lymphoma that can undergo local progression with possible systemic dissemination. We report a case of a patient affected by MF with a pancreatic mass that was a diagnostic challenge between primitive tumor and pancreatic metastasis from MF. Clinical setting findings and imaging studies raised the suspicion of a pancreatic primary neoplasm. A diagnostic clue was provided by the combined histomorphologic/immunohistochemical study of pancreatic and cutaneous biopsies, which revealed a pancreatic localization of MF. Considering the rarity of metastatic localization of MF to the pancreas, we next investigated whether chemokine-chemokine receptor interactions could be involved in the phenomenon to provide new insight into the possible mechanisms underlying metastatic localization of MF to the pancreas. Histological analyses of archival pancreatic tissue demonstrated that glucagon-secreting cells of the pancreatic islets expressed the CCL27 chemokine, which may have attracted in our case metastatic MF cells expressing the complementary receptor CCR10.