The Effect of Post Milking Teat Dip and Suckling on Teat Skin Condition,Bacterial Colonisation,and Udder Health

The teat skin of cows was scored (1: smooth as silk; 2: smooth; 3: slightly rough; 4: rough; 5: cracked; and 6: sores) by trained technicians who moved their fingers down the barrel of the teat with a light touch. Technicians ranked the same population of teats in the same rank order, but their mean values differed by half a score which probably could be related to the skin condition of their own fingers. Half udder experiments were carried out for 6 months at 4 farms with 35 to 52 cows each. A postmilking teat spray with 10% glycerol improved teat skin condition (p<0.10) compared with no teat spray. A postmilking teat spray with 120 ppm chlorine dioxide did not influence teat skin condition compared with no teat spray. No differences in udder health could be proven between treatments. Control studies revealed that 10% glycerol as an emollient of a postmilking teat spray improved teat skin condition within 3 weeks from being slightly rough to being smooth for lactating cows (p<0.05) but not for dry cows having smooth teat skin. Neither glycerol nor chlorine dioxide influenced absolute number of bacteria on teat skin after a challenge with Streptococcus uberis and Staphylococcus aureus but half life of S. aureus on unsprayed teats was longest (p = 0.05). Suckling made teat skin more rough than machine milking. Nevertheless, suckling lowered the number of esculin positive bacteria on the teat skin. We concluded that the condition of healthy teat skin (scores 1–4) has no influence on bacterial colonisation in the absence of cracks and sores (scores 5–6).     

Calmodulin is required for cell-cycle progression during G1 and mitosis.

In order to examine the consequences of a transient increase or decrease in intracellular calmodulin (CaM) levels, two bovine-papilloma-virus (BPV)-based expression vectors capable of inducibly synthesizing CaM sense (BPV-MCM) or anti-sense (BPV-CaMAS) RNA have been constructed and used to stably transform mouse C127 cells. Upon addition of Zn2+, cells containing the BPV-MCM vector have transiently increased CaM mRNA and protein levels. Cells carrying the BPV-CaMAS vector transiently produce CaM anti-sense RNA resulting in a significant decrease in intracellular CaM concentration. Increased CaM caused a transient acceleration of proliferation, while the anti-sense RNA induced decrease in CaM caused a transient cell cycle arrest. Flow cytometric analysis showed that progression through G1 and mitosis was affected by changes in CaM levels. These data indicate that CaM levels may limit the rate of cell-cycle progression under normal conditions of growth.     

Biosynthesis of lipid A. Enzymatic incorporation of 3-deoxy-D-mannooctulosonate into a precursor of lipid A in Salmonella typhimurium.

The cell envelope fraction of Salmonella typhimurium contains an enzyme system which catalyzes transfer of 3-deoxyoctulosonate (KDO) from CMP-KDO to an incomplete, KDO-deficient precursor of lipid A. The enzyme system is firmly membrane-bound, but has been solubilized by treatment with nonionic detergent at alkaline pH and partially purified. Both the particulate and partially purified fractions catalyzed formation of a single reaction product containing 2 residues of KDO. Periodate oxidation of the purified product permitted tentative identification of the KDO disaccharide structure as KDO2-4KDO.     

Stimulation by glucagon of the incorporation of U-14 C-labeled substrates into glucose by isolated hepatocytes from fed rats

The effect of glucagon on the incorporation of U-¹⁴ C-labeled lactate, pyruvate or alanine into glucose has been studied using isolated hepatocytes from livers of fed rats. Rates of incorporation into glucose were about the same as observed in perfused liver preparations provided precautions were taken to avoid depletion of certain metabolities by the preparative procedures. With each substrate, stimulation of the incorporation into glucose by a maximally effective concentration of glucagon (10 nM) was associated with about a 75% reduction in the substrate concentration required for a half-maximal rate and with about a 30% increase in maximum rate. Consequently, the hormone caused a substantial (2–4-fold) stimulation when any one of the above substrates was present at a near physiological concentration, but brought about only a relatively small stimulation (1.4-fold) when very high substrate concentrations were used. Provision of cytoplasmic reducing equivalents (by ethanol addition), or of precursor for acetyl-coenzyme A formation (by acetate addition)-stimulated incorporation of labeled alanine into glucose and their effects were additive with that of glucagon. This suggested that provision of either of these intermediates was not a means by which the hormone increased the incorporation of labeled substrate into glucose. NH₄⁺ stimulated the incorporation of 20 mM [U-¹⁴ C] lactate into glucose 2-fold, probably by promoting glutamate synthesis and thus enhancing the transamination of oxaloacetate to aspartate. Evidence was obtained to support the view that glucagon also increases glutamate production (presumably from endogenous protein). However, the stimulation of incorporatio into glucose from 20 mM [U-¹⁴ C] lactate by NH₄⁺ plus glucagon was synergistic. This suggested that glucagon also stimulates the incorporation of labeled substrate into glucose by additional means. Stimulation of the incorporation of [U-¹⁴ C] alanine into glucose by β-hydroxybutyrate plus glucagon was also synergistic. This suggested that another action of glucagon may be to provide more intramitochondrial reducing potential.     

Studies on the biochemical basis of oxygen toxicity

The toxic effects of high pressure oxygen on the isolated toad urinary bladder have been studied. Sodium transport in this system is reversibly inhibited by high pressure O₂. This inhibition is potentiated by adrenal steroid hormones, and occurs despite both increased glycolytic and Kreb's cycle flux and tissue ATP content. High pressure O₂ leads to increased pyruvate/lactate and pyruvate/malate redox couples, as well as to a decrease in the weight percentage of phospholipid long-chain unsaturated fatty acids and [2-¹⁴C]pyruvate incorporation into tissue lipid. During recovery from high pressure O₂ treatment, [2-¹⁴C]Pyruvate incorporation into lipid is increased and the weight percentage of long-chain unsaturated fatty acids increases. These data indicate that high pressure O₂ poisoning in this tissue does not result from an inhibition of carbohydrate metabolism, but may result from the formation of toxic lipid peroxides.