ABSTRACT
PURPOSE: To assess p53 gene expression in pterygia with and without recurrence. The pathogenesis of pterygium has not yet been determined. The most widely recognized etiologic factor is ultraviolet radiation, which leads to degeneration of the conjunctiva. However, pterygium was recently found to have several tumor-like characteristics. The p53 gene is a common marker for neoplasia, and is known to control cell cycle, cell differentiation and apoptosis. In this study we examined the expression of the p53 gene in primary pterygia with and without recurrence, searching for the pathogenesis of this very common lesion and for a prognostic factor for recurrence. METHODS: Immunohistochemical staining using a monoclonal antibody to human p53 (DO-7) was performed on 13 consecutive patients with primary pterygia, four pterygia without recurrence and nine pterygia which recurred during a 12-month follow-up. As a control we used two specimens of normal conjunctiva. RESULTS: Seven of the 13 pterygia specimens (54%) were positive for abnormal p53 expression. There was no difference between the groups with and without recurrence. Two out of four pterygia (50%) without recurrence and five out of nine (55.5%) pterygia with recurrence were positive. No pathological staining was observed in the control specimens. CONCLUSIONS: In this study, abnormal p53 expression was found in pterygial epithelium, suggesting that pterygium could be a result of uncontrolled cell proliferation, and not as a degenerative lesion. There seems to be no connection between abnormal p53 expression and recurrence.
Subject(s)
Genes, p53 , Pterygium/metabolism , Tumor Suppressor Protein p53/metabolism , Antibodies, Monoclonal/immunology , Biomarkers/analysis , Cell Division , Follow-Up Studies , Humans , Immunoenzyme Techniques , Prognosis , Recurrence , Tumor Suppressor Protein p53/immunologyABSTRACT
This study was designed to measure acetaminophen (paracetamol) levels in tears, and to compare it to serum levels. Paracetamol levels were measured in 20 paired tears and serum samples from 10 healthy volunteers, 1 and 2 hours after ingesting 1.5 g paracetamol. Tears were collected using glass microcapillary tubes while stimulating the conjunctiva with a small sponge placed in the lower fornix. Blood samples were taken simultaneously. The samples were analyzed for paracetamol levels using homogeneous enzyme immunoassay. Tears and serum paracetamol levels 1 hour after ingestion were 16.3 microg/mL +/- 7.2 (mean +/- SD), and 21.4 microg/mL +/- 7.7 (mean +/- SD) respectively. Tears and serum levels 2 hours after ingestion were 14.4 microg/mL +/- 7.8 (mean +/- SD), and 17 microg/mL +/- 7.6 (mean +/- SD) respectively. Tears and serum paracetamol levels of all the 20 paired samples (1 h and 2 h after ingestion) were 15.35 microg/mL +/- 7.4, and 19.25 microg/mL +/- 7.8, respectively (mean +/- SD). There was a strong and highly significant correlation between paracetamol levels in serum and in tears 1 and 2 hours after ingestion (r = 0.8, p = 0.005, r = 0.85, p = 0.002 respectively). Mean +/- SD ratio of tears/serum paracetamol levels 1 hour and 2 hours after ingestion were 0.77 +/- 0.21 and 0.81 +/- 0.25 respectively. Delta tears (difference in mean levels at 1 and 2 hours) paracetamol levels is significantly correlated with delta serum levels (r = 0.7, p = 0.025). A reliable, convenient, and feasible noninvasive method is described for measuring paracetamol in tears. There is no information in the literature about tears paracetamol secretion, and little information of tears drugs concentration.
Subject(s)
Acetaminophen/blood , Tears/chemistry , Administration, Oral , Adult , Humans , Immunoenzyme Techniques , Middle Aged , Time FactorsABSTRACT
Las células Natural Killer (cél NK), linfocitos efectores de actividad citolítica natural, son críticas en la defensa antiinfecciosa. En la infección por VIH-I se ha descrito una disminución de la actividad citolítica NK; sin embargo, se desconocen los mecanismos involucrados, por lo que el objetivo de este trabajo fue estudiar la ACNK y la acción in vitro de inmunomoduladores para intentar explicar esta deficiencia. Se analizaron 20 individuos infectados por VIH-I (10 asintomáticos y 10 con SIDA) y 30 individuos seronegativos como controles. La ACNK se determinó utilizando cél K-562 radiomarcadas con 51-Cr (cromato de sodio) como cél blanco y cél mononucleares periféricas como cél efectoras, expresándose los resultados como por ciento de Lisis específica. En cultivos in vitro, se analizó el efecto de inmunomoduladores sobre la ACNK: interleuquina-2 (IL-2, 25 U/mL), interferon-alfa (IFN-a, 500 U/mL) y la acción conjunta de ionófor de calcio A23187 (lo, 10.0 uM) más un éster de forbol (TPA, 250 ng/mL)(Io+TPA). El análisis fenotípico, CD 16+/56+ se efectuó por citometría de flujo con Ac monoclonales fluorescentes (Becton Dickinson)