The effect of cooking methods on the lipid composition of potatoes

The effect of boiling and baking in either a convential or microwave oven on the lipid content of potatoes was investigated. The crude lipid content of potatoes was lowered significantly by all methods of cooking. The loss was highest in potatoes cooked in a microwave oven, least in boiled tubers, and intermediate in tubers baked in a conventional oven. Similar trends were observed for both cortex and pith tissues. Generally, the phospholipid content followed the same trend as the crude lipid, the exception being the cortex tissue of tubers baked in the conventional oven, in which the greatest loss of phospholipid occurred. Cooking did not significantly alter the fatty acid composition of tubers. A possible relationship between the degree of cell rupturing, known to be influenced by different mechanisms of heat transfer, and the amounts of tuber lipid associated with different cooking methods was discussed.     

Inheritance of genes coding for gliadin proteins and glume colour introgressed into Triticum aestivum from a synthetic wheat

A synthetic hexaploid, Triticum timofeevii×T. tauschii, was used to transfer disease resistance genes to the commercial cultivar Saratovskaya 29 (S29) by backcrossing. After five backcrosses the resulting derivatives still showed some traits of the synthetic, namely brown spike glumes and several gliadin components. Genetic analysis showed that the derived forms had inherited the Gli-D1 allele of the synthetic, which was found to be tightly linked to a gene for glume colour. Recombination percentages between these genes was estimated to be 2.5 ± 1.7%. The development of the derivatives was also accompanied by a rearrangement within the Gli-B1 locus, resulting in the formation of a new variant of the allele in S29.     

Recording of the reticular motility in cattle with experimental and spontaneous traumatic reticuloperitonitis

Using the method described in a previous publication for recording the reticulum action in normal cows the authors have investigated three cows with experimentally produced reticuloperitonitis as well as a group of cows with spontaneous peritonitis under treatment at the stationary clinic. The experimental animals were provided with permanent rumen fistulas.In the three cows with experimentally produced peritonitis the pointed object worked loose spontaneously during the first 24 hrs. The symptoms were mild after the first perforation and became aggravated after further perforations.An abnormally prolonged reticulum interval was recorded immediately after the perforation and continued to be clearly distinguishable for two to three days. In the cows with spontaneous peritonitis, this change was observed only in the acute stage.Prolongation of the second phase of the reticulum was the most pronounced finding from the recordings of the reticular movements, both in the cows with experimental peritonitis and in those in the spontaneous group. The change was at its height after two to seven days, and then subsided gradually in the experimental animals in which repeated recordings had been made.The pressure elevation in reticulum during the contractions was lower both in the animals with experimental peritonitis and in the spontaneous group than in the healthy animals.The cows with reticuloperitonitis also displayed impaired ability to pass the recording catheter from the atrium ruminis to the reticulum.     

Factors involved in the early pathogenesis of bovine Staphylococcus aureus mastitis with emphasis on bacterial adhesion and invasion. A review

Staphylococcus aureus is the most important and prevalent contagious mammary pathogen; it causes clinical and subclinical intramammary infection with serious economic loss and herd management problems in dairy cows. In vitro studies have shown that Staphylococcus aureus adheres to mammary epithelial cells and extracellular matrix components and invades into mammary epithelial as well as other mammary cells. Staphylococcus aureus strains from intramammary infection produce several cell surface-associated and extracellular secretory products. The exact pathogenic roles of most of the products and their effects on adhesion and invasion are not well evaluated. It is also known that mammary epithelial cell-associated molecules and extracellular matrix components interact with S. aureus during the pathogenesis of mastitis, but their roles on adhesion and invasion have not been characterized. The adhesion of S. aureus to epithelial cells may involve non-specific physicochemical interactions and/or specific interactions between bacterial cell-associated ligands and host cell surface receptors. In vitro adhesion depends on the S. aureus strain, the growth phase of the bacteria, the growth medium and the origin of the epithelial cells. Adhesion is hypothesized to be a prerequisite and crucial early step for mammary gland infection. Staphylococcus aureus invades mammary epithelial cells. It also invades other cells such as endothelial cells and fibroblasts. Bacteria are found enclosed in membrane bound vacuoles in the cytoplasm of mammary epithelial cells. Recent observations indicate that S. aureus escapes from the phagosome into the cytoplasm and induces apoptosis. The invasion into mammary epithelial cells may occur through an endocytic process that requires involvement of elements of the cytoskeleton or by direct binding of bacteria to epithelial cells through a process mediated by specific receptors that needs de novo protein synthesis by both cells. Thus, the recurrent subclinical infection may result from this intracellular existence of bacteria that are protected from host defenses and effects of antibiotics. This review emphasizes on recent findings on S. aureus adhesion to mammary epithelial cells and extracellular matrix components and invasion into mammary epithelial cells.