Egg laying performance and economics of production of japanese quails fed diets containing peeled and cooked sweet potato meal

Japanese quails are small in size, early maturing, come to egg production between 5th and 6th week of life, hardy and prolific but requires local feeds for sustainability. Thus, a feeding trial which lasted for six months was carried out to investigate the effect of feeding peeled and cooked sweet potato tuber on hen-day egg production and economics of production of Japanese quails. Five isonitrogenous (20%CP) diets were compounded. The control diet (A) had zero sweet potato tuber meal. In the other four diets, 25, 50, 75 and 100% of maize was replaced with peeled and cooked sweet potato tuber meal. Three hundred point-of-lay female Japanese quail birds were randomly allotted to the diets in a completely randomized design. Feed and water were provided ad libitum for six months. Each diet was allocated to 60 quail chicks, which were further divided into three replicates of 20 birds each to determine the performance characteristics of the quails. Feed intake, body weight change, age at first eggs, age at 50% egg production, age at 75% egg production, hen-day egg production, hen-housed egg production and feed per dozen eggs were similar (p? 0.05) across the diets. Water intake by birds on diet A was significantly (p? 0.05) lower than the birds on the sweet potato diets. Water intake was significantly (p? 0.05) higher by birds on diet D (51.93ml/bird/day) than those on diets A (42.60) and C (46.68mL/bird/day). Total cost of production did not differ significantly across the diets. Gross margin was significantly higher on diet C (N67, 227.64) than on the other diets except for diet D (N65, 795.52). Results showed that peeled and cooked sweet potato can completely replace maize in the diet of laying quails without adverse effects on performance or on economics of production

Abnormal secretion and function of recombinant human factor VII as the result of modification to a calcium binding site caused by a 15 base pair insertion in the factor VII gene

A case of a novel mutation in the F7 gene that results in factor VII coagulant activity (VII:c) of less than 1% and VII antigen (VII:Ag) levels of 10% is presented. DNA analysis revealed a homozygous 15-base pair (bp) in-frame insertion-type mutation at nucleotide 10554, This insertion consisted of a duplication of residues leucine (L)213 to aspartic acid (D)217 (leucine, serine, glutamic acid, histidine, and aspartic acid), probably arising by slipped mispairing between 2 copies of a direct repeat (GCGAGCACGAC) separated by 4 bp, Molecular graphic analyses showed that the insertion is located at the surface of the catalytic domain in an exposed loop stabilized by extensive salt-bridge and hydrogen bond formation at which the calcium binding site is located. The mutation probably interferes with protein folding during VII biosynthesis and/or diminishes functional activity through the loss of calcium binding, In vitro expression studies demonstrated that the levels of VII:Ag in lysates of cells transfected with wild type VII (VIIWT) were equivalent to those with mutant type VII (VIIMT), but the level of secreted VIIMT was 5% to 10% that of VIIWT. Pulse chase studies demonstrated that VIIMT did not accumulate intracellularly, and studies with inhibitors of protein degradation showed that recombinant VIIMT was partially degraded in the pre-Golgi compartment, Accordingly, only small amounts of VIIMT with undetectable procoagulant activity were secreted into conditioned media. These results demonstrate that a combination of secretion and functional defects is the mechanism whereby this insertion causes VII deficiency. (C) 2001 by The American Society of Hematology