Induced liver tumour further support to a genetic marker with its high correlation with chorioallantoic membrane phenotypes in selected layer lines.

The conventional chorioallantoic membrane (CAM) phenotype assay was conducted using 11-day-old embryonatic eggs of white Leghorn strains, each inoculated with 0.2 ml of subgroup A Rous sarcoma virus (RSV) and subgroup C RSV separately containing 10(3)pfu ml(-1). Eggs were further incubated for hatching. Harvesting of CAMs for counting of pocks and monitoring chicks for liver tumour (LT) mortality during 4 weeks of post-hatching period were followed. The conversely associated phenotype (CAP) incidence i.e. CAM(+) LT(-) and CAM(-) LT(+) was observed in all three lines for both subgroup A and C virus infection. The LT deaths of chicks in all strains occurred within 21 days post-hatch irrespective of virus subgroups. The regression analysis of %LT death (transformed data) distributed within pock count range (PCR) basis was performed. The regression coefficients (b(i)'s) were found to be non-significant, indicating that %LT death did not correlate with number of particles that entered the cells because the chicks that had at least 25 pock counts in CAMs died with few exceptions. This study upheld the view that the CAM phenotypes (S and R) under the control of a pair of alleles, a(s) and a(r) at the tva locus and c(s) and c(r) at the tvc locus as reported extensively. Because of a high correlation coefficients between CAM and LT phenotypes [S and LT(+)] in respect of subgroup A (r = 0.72) and subgroup C (r = 0.81) infection, it is obvious that one could postulate a pleiotropic control of the two traits by the tva and tvc genes, respectively. Indeed fitting a 4-allele model in both tva and tvc locus, suggesting that CAPs are the indicator for nullifying the conventional 2-allele model proposed for the induced tumour expression phenotypes by leukosis sarcoma viruses.

Efecto de la hormona liberadora de tirotrofina en la secreción de prolactina de decidua humana / Effect of thyrotropin releasing hormone in the prolactin secretion of human decidua

Para prevenir el síndrome de distress respiratorio (RDS), se ha usado el tratamiento conjunto de betametasona y hormona liberadora de tirotrofina (TRH). La TRH actuaría indirectamente sobre la producción del surfactante pulmonar, estimulando la secreción de hormonas tiroídeas; otra vía para incrementar el surfactante pulmonar es induciendo la secreción de PRL Prolactina (un potente estimulador de la secreción del surfactante pulmonar) desde la hipófisis o de otros tejidos que secreten PRL (como se ha descrito previamente para la decidua). El objetivo de este trabajo fue estudiar el efecto de diferentes dosis de TRH en la secreción de PRL por el tejido corión-decidua y caracterizar las formas bioactivas de PRL secretada por dicho tejido. Veinte placentas de embarazos normales (38-41 semenas), obtenidas por parto normal o cesáreas, fueron recolectadas en el Departamento de Obstetricia y Ginecología del Hospital Clínico de la Universidad de chile. Explantes de tejido corión-decidua secretaron PRL en condiciones basales, con una secreción máxima de la hormona a las 24 horas de incubación. Se encontró un aumento significativo (p<0,05) en la secreción de PRL con 1,5 x 10 elevado 8 M de TRH, el cual fue debido principalmente a un aumento significativo (p<0,05) de la forma little del PRL bioactivo. Estos resultados sugieren que una de las maneras en que TRH acelere la madurez pulmonar fetal podría ser aumentando la secreción de PRL por el tejido decidual; esta hormona podría pasar rápidamente al líquido amniótico para activar la producción del surfactante pulmonar del feto