The performance of Santa Inês sheep on three tropical grasses (A. gayanus Kunth. cv. Planaltina, P. maximum Jacq. cv. Aruana and P. maximum Jacq. cv. Tanzânia), and rotational grazing with an occupation period of 14 days and fixed stocking rate of 22 animals/ha, was evaluated in the dry season. The experimental period was 82 days, and the individual performance of 11 lambs on each treatment was measured. With the progression of the dry season, increasing levels of concentrate supplementation was used (300, 400 and 500 g/animal/day for each of the three treatments). Samples of grass leaf blades were taken each 14 days, and bromatological analysis carried out. The weight of animals, measured each 14 days, was used to calculate average dairy gain (GMD), final weight (PF), accumulated gain (GAC) and body condition (CC). The treatments Aruana and Tanzânia showed highest (p<0.05) GMD, respectively with 93.6 and 92.0 g/animal/day, not differing between each other (p>0.05). The animals on Andropogon pasture showed a mean weight gain of 35.6 g/animal/day. For PF, GAC and CC the treatments Aruana and Tanzânia showed the best results (p<0.05), when compared with Andro-pogon. The forage Aruana and Tanzânia, caused better performance in sheep during the dry season compared to Andropogon.

Avaliou-se o desempenho de ovinos da raça Santa Inês, em três gramíneas forrageiras tropicais (A. gayanus Kunth. cv. Planaltina, P. maximum Jacq. cv. Aruana e P. maximum Jacq. cv. Tanzânia), em pastejo rotacionado, com período de ocupação de 14 dias e lotação fixa de 22 animais/ha, no período da seca. O período experimental foi de 82 dias, onde o desempenho de 11 borregos, em cada tratamento, foi acompanhado em um delineamento inteiramente casualizado. Com o avançar da seca foram utilizados níveis crescentes de 300, 400 e 500 g/animal/dia de suplementação concentrada para os três tratamentos. Nas forragens foram colhidas amostras a cada 14 dias para efetuar as análises bromatológicas. Através da verificação do peso dos animais, realizadas a cada 14 dias, foram obtidos o peso vivo, o ganho médio diário (GMD), o peso final (PF), o ganho acumulado (GAC) e a condição corporal (CC). Os ovinos alimentados com Aruana e Tanzânia apresentaram GMD de 93,6 e 92,0 g/animal/dia, respectivamente não diferindo entre si (p>0,05), mas foram superiores aos do Andropogon 35,6 g/animal/dia (p<0,05). Para PF, GAC e CC os tratamentos Aruana e Tanzânia também proporcionaram os melhores resultados (p<0,05), quando comparados aos observados com o tratamento Andropogon. Os tratamentos Aruana e Tanzânia proporcionaram melhores desempenhos dos ovinos durante o período seco em relação ao Andropogon.

Autosomal recessive polycystic kidney disease (ARPKD) is an inherited disease characterized by a malformation complex which includes cystically dilated tubules in the kidneys and ductal plate malformation in the liver. The disorder is observed primarily in infancy and childhood, being responsible for significant pediatric morbidity and mortality. All typical forms of ARPKD are caused by mutations in a single gene, PKHD1 (polycystic kidney and hepatic disease 1). This gene has a minimum of 86 exons, assembled into multiple differentially spliced transcripts and has its highest level of expression in kidney, pancreas and liver. Mutational analyses revealed that all patients with both mutations associated with truncation of the longest open reading frame-encoded protein displayed the severe phenotype. This product, polyductin, is a 4,074-amino acid protein expressed in the cytoplasm, plasma membrane and primary apical cilia, a structure that has been implicated in the pathogenesis of different polycystic kidney diseases. In fact, cholangiocytes isolated from an ARPKD rat model develop shorter and dysmorphic cilia, suggesting polyductin to be important for normal ciliary morphology. Polyductin seems also to participate in tubule morphogenesis and cell mitotic orientation along the tubular axis. The recent advances in the understanding of in vitro and animal models of polycystic kidney diseases have shed light on the molecular and cellular mechanisms of cyst formation and progression, allowing the initiation of therapeutic strategy designing and promising perspectives for ARPKD patients. It is notable that vasopressin V2 receptor antagonists can inhibit/halt the renal cystic disease progression in an orthologous rat model of human ARPKD.