RESUMEN
OBJECTIVE: Recurrent infection in Down syndrome (DS) has been previously documented; the potential role of platelets and neutrophil-platelet interaction has not been addressed in previous studies. PATIENTS AND METHODS: Using flow cytometry, we evaluated CD40 and CD18 expression as activation markers for neutrophils and CD62p as an activation marker for platelets, before and after lipopolysaccharide (LPS) stimulation, in 34 patients with DS and 39 control patients. RESULTS: Markers were evaluated as percentage of positivity, mean fluorescent intensity (MFI), and activation index (MFI after stimulation/MFI before stimulation). Patients showed a significantly lower CD40 MFI (Pâ =â .019) after LPS stimulation, a lower CD62p percentage before and after LPS stimulation (Pâ =â .013 and Pâ =â .029), and a higher CD62p MFI (Pâ =â .011) after LPS stimulation. Patients showed a lower activation index for CD40 and CD18 (Pâ ≤ .001) but not for CD62p (Pâ =â .338). Dysfunctional efficiency in neutrophils and in the neutrophil-platelet interaction could not be correlated to infection. CONCLUSION: A consensus on a scoring system for infection is needed for an objective evaluation of correlation to infection.
Asunto(s)
Síndrome de Down , Neutrófilos , Plaquetas , Síndrome de Down/complicaciones , Síndrome de Down/metabolismo , Citometría de Flujo , Humanos , Lipopolisacáridos/metabolismo , Activación PlaquetariaRESUMEN
The presence of non-progressive cognitive impairment is recognized as a common feature in a substantial proportion of patients with Duchenne muscular dystrophy (DMD). Concurrently, the amyloid beta peptide (Aß42) protein has been associated with changes in memory and cognitive functions. Also, it has been shown that different subtypes of neural stem/progenitor cells (CD 34, CD 45, nestin) are involved in the innate repair of plasticity mechanisms by the injured brain, in which Nerve Growth Factor (NGF) acts as chemotactic agents to recruit such cells. Accordingly, the present study investigated levels of CD 34, CD 45, nestin and NGF in an attempt to investigate makers of neural regeneration in DMD. Neural damage was assayed in terms of Aß42. Results showed that Aß42 (21.9 ± 6.7 vs. 12.13 ± 4.5) was significantly increased among DMD patients compared to controls. NGF (165.8 ± 72 vs. 89.8 ± 35.9) and mononuclear cells expressing nestin (18.9 ± 6 vs. 9 ± 4), CD 45 (64 ± 5.4 vs. 53.3 ± 5.2) and CD34 (75 ± 6.2 vs. 60 ± 4.8) were significantly increased among DMD patients compared to controls. In conclusion cognitive function decline in DMD patients is associated with increased levels of Aß42, which is suggested to be the cause of brain damage in such patients. The significant increase plasma NFG and in the number of mononuclear cells bearing CD34, CD45 and nestin indicates that regeneration is an ongoing process in these patients. However, this regeneration cannot counterbalance the damage induced by dystrophine mutation and increased Aß42.
Asunto(s)
Antígenos CD34/metabolismo , Trastornos del Conocimiento/metabolismo , Trastornos del Conocimiento/fisiopatología , Antígenos Comunes de Leucocito/metabolismo , Distrofia Muscular de Duchenne/metabolismo , Distrofia Muscular de Duchenne/fisiopatología , Factor de Crecimiento Nervioso/metabolismo , Nestina/metabolismo , Estudios de Casos y Controles , Niño , Ensayo de Inmunoadsorción Enzimática , Humanos , MasculinoRESUMEN
The purpose of this study was to evaluate the feasibility of the use oral ibuprofen suspension (OIS) in the treatment of patent ductus arteriosus (PDA) in premature infants. Premature infants (