Effects of dietary free fatty acid content and degree of fat saturation on tibia bone properties of laying hens.

Acid oils and fatty acid distillates are fat by-products of the refining process of edible oils and are characterized by their high proportion of free fatty acids (FFA). While lipids are essential in poultry diets, their chemical structure may interfere with calcium absorption. Therefore, this study investigated the effects of dietary FFA content and the degree of fat saturation on bone metabolism in commercial layers. For 15-wk, a total of 144 laying hens (19-wk-old) were randomly assigned to 8 treatments (6 replicates with 3 birds each), which were obtained by gradually replacing crude soybean oil (rich in unsaturated fatty acids [UFA]) with soybean acid oil (rich in UFA and FFA), or crude palm oil (rich in saturated fatty acids [SFA]) with palm fatty acid distillate (rich in SFA and FFA). Following a 2 × 4 factorial design, 4 UFA-rich and 4 SFA-rich diets were created with varying FFA content: 10, 20, 30, and 45%. Tibiae (6 birds/treatment) were collected at the end of the trial for the assessment of mineral composition, morphological properties, and mechanical characteristics. The data were analyzed using a 2-way ANOVA with the GLM procedure. Orthogonal polynomial contrasts were employed to determine the linear effect of increasing %FFA, with statistical significance set at P < 0.05. The degree of saturation was found to negatively impact on calcium and phosphorus bone content, with higher levels found in soybean-based diets (P < 0.001). A significant interaction was observed for medullary bone mineral content, showing a linear decrease as the dietary %FFA increased (P < 0.05) in palm diets. In contrast, morphological and mechanical bone traits, total ash content, and cortical bone mineral composition remained unaffected (P > 0.05). These results suggest that the degree of fat saturation exerts a greater impact than FFA content on bone mineral metabolism, supporting the commercial use of fat by-products rich in FFA in laying hen diets, at least during the early stages of the laying cycle.

Practical diagnosis of red cell disorders in southern Spain.

BACKGROUND: Hereditary red cell disorders are associated with a protective effect against malaria, which results in an increased prevalence in malaria-endemic areas. Migratory flows from these areas are resulting in a marked increase in such abnormalities in Southern Spain. METHODS: All hemoglobin disorders diagnosed between 1997 and 2010 have been recorded. Since 2008, we have performed systematic screening for hemoglobinopathies on African patients. A high-pressure liquid chromatography system was used as screening method for structural hemoglobinopathies and for separation of hemoglobin (Hb) F and A(2). RESULTS: We detected 666 cases in patients of foreign origin and 308 in native Spanish patients. Thalassemias (thal) are the most frequent disorders amongst the local population: ß-thal minor, 57.1% (176/308); α-thal, 18.2% (56/308), and δß-thal, 7.8% (24/308). In ethnic minorities, there is a huge variety of hemoglobinopathies: heterozygous Hb S, 45% (300/666); heterozygous Hb C, 15% (100/666); ß-thal minor, 13.7% (91/666); α-thal, 10.2% (68/666); Hb SS in 14 patients, and Hb CC in 9 patients. Of the native patients, 14 were found to have Hb AS and 9 Hb AC. CONCLUSION: Given the modern migratory flows, greater knowledge of these disorders is needed by all medical staff, and new practical and cost/time-effective diagnostic approaches have to be devised.

Hipercoagulabilidad debida a resistencia adquirida a la proteína C activada: ¿primer signo de neoplasia de colon? / Hypercoagulable state due to acquired protein C resistance. Harbinger of colonic neoplasm?

La resistencia a la proteína C activada (RPCa) hereditaria se ha identificado como un importante factor de riesgo para sucesos tromboembólicos, y consiste en una mutación del factor V que lo hace irreconocible para la inhibición por la proteína C activada (Factor V Leiden, FVL). Sin embargo, la RPCa también se describe en pacientes sin FVL (RPCa adquirida) asociada a la presencia de anticoagulante lúpico, embarazo y neoplasias. Describimos un caso de TVP en una mujer de 54 años, sin síntomas digestivos y con marcadores tumorales negativos, que presentaba RPCa y fue diagnosticada un año después de adenocarcinoma de colon. Una vez consiguió remisión completa, se normalizó la RPCa y se descartó que presentara FVL. En el estudio de trombofilia, el hallazgo de RPCa puede verse influida por reactantes de fase aguda o por un proceso neoplásico, por lo que requiere una valoración evolutiva y un rastreo genético del FVL

Hereditary activated protein C resistance (aPCR) has been indentified as an important risk factor for the occurrence of thromboembolic events. It is most frequently hereditary, and caused by a point mutation in factor V, named Factor V Leiden (FVL), which renders it resistant to the anticoagulant action of circulating protein C. However, aPCR can also be found in absence of FVL (acquired aPCR), associated to lupus anticoagulant, pregnancy or neoplasms. We report a case of deep venous thrombosis (DVT) in a 54 year-old woman, with no digestive symptoms and negative screening for biochemical tumor markers, who presented with DVT from FVL-negative aPCR, one year before being diagnosed of colonic adenocarcinoma. Once complete remission of the carcinoma was reached, aPCR returned to normal values. In thrombophilia screening studies, the finding of aPCR may be caused by acute-phase reactants or neoplastic processes, and therefore require evolutive evaluation and genetic search for FVL

[Hypercoagulable state due to acquired protein C resistance, harbinger of colonic neoplasm?]. / Hipercoagulabilidad debida a resistencia adquirida a la proteína C activada: primer signo de neoplasia de colon?

Hereditary activated protein C resistance (aPCR) has been identified as an important risk factor for the occurrence of thromboembolic events. It is most frequently hereditary, and caused by a point mutation in factor V, named Factor V Leiden (FVL), which renders it resistant to the anticoagulant action of circulating protein C. However, aPCR can also be found in absence of FVL (acquired aPCR), associated to lupus anticoagulant, pregnancy or neoplasms. We report a case of deep venous thrombosis (DVT) in a 54 year-old woman, with no digestive symptoms and negative screening for biochemical tumor markers, who presented with DVT from FVL-negative aPCR, one year before being diagnosed of colonic adenocarcinoma. Once complete remission of the carcinoma was reached, aPCR returned to normal values. In thrombophilia screening studies, the finding of aPCR may be caused by acute-phase reactants or neoplastic processes, and therefore require evolutive evaluation and genetic search for FVL.