Effect of combinations of organic acids in weaned pig diets on microbial species of digestive tract contents and their response on digestibility.

The effect of combinations of organic acids on digestive microbial population and total tract digestibility of piglets was studied. Thirty 19-21 days weaned pigs (5.4 +/- 0.23 kg, six pigs per treatment) were given a mixed feed with 10 ml water/kg (CTL) or 200 mEq/kg of formic acid (FOR), 1:1 formic:fumaric (FOFU), 1:1 formic:lactic (FOLA) or 2:1 formic:lactic (2FOLA). After 6-8 days, animals were slaughtered. In gastric contents, pH was higher (p = 0.01) with FOFU and lactobacilli tended (p = 0.08) to be lower with FOFU than CTL and FOLA, but coliform counts did not differ (p = 0.14). Acetate proportion was lower (p = 0.03), and propionate (p = 0.05) and butyrate (p = 0.01) higher, with FOFU than CTL, FOLA and 2FOLA. Intestinal coliform counts were higher (p = 0.03) with CTL than FOLA and 2FOLA, but there were no differences on lactobacilli. In intestinal contents, acetate tended (p = 0.06) to be lower with FOR than FOLA and 2FOLA, and butyrate was higher (p = 0.001) with FOR. Although not significantly, dry matter digestibility was 0.03-0.05 lower with CTL than with the other treatments. Combinations of organic acids in piglet diets modify gastric and intestinal microflora, the mixtures of formic:lactic appearing as the most interesting.

La actividad transcripcional de NF-kappaB es diferencialmente regulada por dominios específicos del coactivador TIF2 / Different enzymatic activities recruitment by specific domains of TIF2 are involved in NF-kappaB transactivation

We have previously shown that nuclear receptor coactivator overexpression significantly enhanced NF-kappaB activity in a dose response manner. We studied the mechanism by which TIF2 regulates NF-kappaB activity. We determined that: 1) the p38 specific inhibitor reduces 50% NF-kappaB transcriptional activity, even in cells that overexpress distinct TIF2 deletions; 2) there is a physical interaction between TIF2 and p38 and RelA determined through in vitro translated protein binding assays; 3) TIF2 is a p38 substrate; 4) there is a physical interaction between TIF2 and IKK in TNF-alpha 20 ng/ml stimulated or not HEK 293 cell protein extract, and IkappaB only in basal conditions, determined by binding pull down assays. This NF-kappaB complex regulates its activity and targets gene expression in a determined physiologic context depending on the coactivator complex content.

Demonstramos previamente que la sobreeexpresión de coactavadores de receptores nucleares aumenta la actividad NF-kB en forma de dosis depepndiente. Se estudió el mecanismo por el cual el coactavador TIF2 regula la actividad de NF-kB. Determinamos que: 1)el inhibidor específico de p38 disminuye al 50% la actividad transcripcional de NF-kB, aún en células que sobreexpresan distitntas deleciones de TIF2; 2) existe interacción físca directa de TIF2 con p38; y RelA determinada a trav[es de ensayos de unión con proteína traducida in vitro; 3) TIF2 ES SUSTRATO DE P38; 4) mediante ensayos de unión con extractos proteicos de células...

La actividad transcripcional de NF-kappaB es diferencialmente regulada por dominios específicos del coactivador TIF2 / Different enzymatic activities recruitment by specific domains of TIF2 are involved in NF-kappaB transactivation

We have previously shown that nuclear receptor coactivator overexpression significantly enhanced NF-kappaB activity in a dose response manner. We studied the mechanism by which TIF2 regulates NF-kappaB activity. We determined that: 1) the p38 specific inhibitor reduces 50% NF-kappaB transcriptional activity, even in cells that overexpress distinct TIF2 deletions; 2) there is a physical interaction between TIF2 and p38 and RelA determined through in vitro translated protein binding assays; 3) TIF2 is a p38 substrate; 4) there is a physical interaction between TIF2 and IKK in TNF-alpha 20 ng/ml stimulated or not HEK 293 cell protein extract, and IkappaB only in basal conditions, determined by binding pull down assays. This NF-kappaB complex regulates its activity and targets gene expression in a determined physiologic context depending on the coactivator complex content.(AU)

Demonstramos previamente que la sobreeexpresión de coactavadores de receptores nucleares aumenta la actividad NF-kB en forma de dosis depepndiente. Se estudió el mecanismo por el cual el coactavador TIF2 regula la actividad de NF-kB. Determinamos que: 1)el inhibidor específico de p38 disminuye al 50% la actividad transcripcional de NF-kB, aún en células que sobreexpresan distitntas deleciones de TIF2; 2) existe interacción físca directa de TIF2 con p38; y RelA determinada a trav[es de ensayos de unión con proteína traducida in vitro; 3) TIF2 ES SUSTRATO DE P38; 4) mediante ensayos de unión con extractos proteicos de células...(AU)