Australian journal of biological sciences最新文献

Two State-wide surveys were carried out in 1978 to detect bluetongue (BLU) virus antibody in cattle and sheep sera in New South Wales (NSW). The first survey showed that BLU group antibody in cattle 18-24 months old was confined to the coastal regions (east of the Great Dividing Range) and the Hunter Valley. However, in the second survey, of cattle more than 5 years old, reactors were much more widely distributed over the north-eastern third of the State and into the western division with prevalences up to 85% in some areas. In contrast, very few reactors were detected in sheep in either survey (less than 1% of the sheep sera tested). In a retrospective study of stored cattle sera, BLU group reactors were detected in the north-east of the State in each year examined since 1968, the earliest year in which samples were available from that region. Areas to the south and west were free of antibody from 1966 until the summer of 1973, but subsequently reactors were common. Examination of selected area for type-specific antibody indicated that infection of cattle with two of the three Australian BLU serotypes which were known at the time, BLU-1 and BLU-21, had occurred in NSW. No antibody to BLU-20, the original Australian isolate, was detected. A close association was observed between strong group antibody reactions and type-specific neutralizing activity against BLU-1 and BLU-21. Both were largely confined to that area of the State in which a high (75% or more) prevalence of group antibody was recognised in the older animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Sentinel cattle at a number of localities in northern and central coastal New South Wales were sampled over the summer and autumn seasons of the years 1979, 1980 and 1981. A total of 118 orbiviruses were isolated; 99 were of the Palyam group, 15 were of the epizootic haemorrhagic disease (EHD) of deer group, and 4 of the bluetongue group. The Palyam group viruses were identified by serotype as 68 Bunyip Creek, 23 CSIRO Village, 7 D'Aguilar and one was not typed. The EHD viruses were identified as 13 type 5 and 2 type 6. All 4 bluetongue viruses were type 21. There was also convincing serological evidence that bluetongue type 1 infection occurred in 1980. Antibody to the bluetongue group, as demonstrated in a gel diffusion precipitin test, was often transient. It appeared to be mostly cross-reactive with, and induced by, other orbivirus infections, particularly those of the EHD group. Viruses of the Palyam group also seemed to be implicated in some circumstances. Where infections by viruses of the bluetongue group were demonstrated, the precipitating antibody responses to a bluetongue group antigen were not noticeably stronger than many which followed EHD virus infection. The results generally confirm previous conclusions, deduced from serological surveys, regarding the frequency of orbivirus infections, the presence of bluetongue viruses, and the transient nature of many bluetongue group antibody reactions.

No significant change occurred in the uptake by the thyroid of male Wistar rats of a standard dose of carrier-free 131I administered intraperitoneally and its retention by the thyroid, as measured by biological and effective half-life, after feeding these rats a powdered pelleted diet containing lithium carbonate (1.1 g per kg of diet) for 7 days. However, continuing this diet for 10 days inhibited thyroid uptake and increased the retention of 131I. Uptake remained suppressed for up to 4 months after lithium treatment and continuing this treatment for 6 months did not result in any significant change in 131I uptake by the thyroid. Lithium treatment for 10 days increased the biological and effective half-life of 131I in the thyroid and this increase continued for the 6 months treatment period. The dose of 131I delivered to the thyroid was significantly lower after 10 days and 1 month of lithium treatment but there was no change in this dose after 2 and 4 months of treatment. However, there was a significant increase after 6 months.

Recent evidence suggests that changes in plasma zinc concentration may play a central role in the development of early lesions of zinc deficiency. The aim of the following work was to better understand events occurring in plasma during the onset of zinc deficiency, and to investigate biochemical mechanisms by which plasma zinc may exert its effects. Fifty male weanling rats of 90 g weight were allocated to five treatment groups of ten rats each. Treatments were: 1, zinc deficient, mixed diet (1-2 mg Zn per kg): 2, zinc deficient, self-select diet; 3, zinc repleted; 4, control, pair fed; 5, control, ad libitum fed. With the exception of treatment 1, which consisted of a 25% casein diet, all rats were offered protein as a separate component of the diet. Control rats received zinc in the drinking water (100 mg l-1). The sequence of events following initiation of zinc deficiency were: reduced plasma zinc concentration (2 days), reduced plasma angiotensin-converting enzyme and alkaline phosphatase activities (3-4 days), reduced feed intake and growth (5-6 days) and reduced percentage protein intake (12 days). Plasma zinc concentration in the deficient rats was inversely correlated with the growth rate of the rat over the previous 24 h. Zinc repletion resulted in marked overshoot in plasma zinc concentration (300%) and converting-enzyme activity (150%) within 24 h, but a return to normal within 72 h. Alkaline phosphatase activity responded likewise, albeit more slowly. Protein self selection had no effect on the manifestations of zinc deficiency, although reduced protein intake was associated with lower plasma zinc concentration. The results provide evidence of a role for plasma zinc in the development of early clinical signs of zinc deficiency, possibly acting biochemically through reduced activity of zinc-dependent peptidases such as angiotensin-converting enzyme.

Lys-beta-urogastrone, an analogue of human beta-urogastrone with an additional N-terminal lysine, was shown to have similar effects in mice and sheep to mouse epidermal growth factor (mEGF). Lys-beta-urogastrone in doses of 0.18-3.24 micrograms g-1 body weight caused both precocious separation of eyelids and eruption of incisors in neonatal mice. In 17 sheep, intravenous infusion of the urogastrone analogue over c. 24 h led, towards the end of infusion, to erythema of the muzzle, caused reductions in voluntary food intake (with doses greater than or equal to 50 micrograms kg-1) and generally easier manual harvesting of the fleece (with infusions greater than or equal to 81 micrograms kg-1), with spontaneous shedding of the fleece (c. 14 days after infusions of greater than or equal to 116 micrograms kg-1). In five sheep infusions of 25, 38, 50, 83 and 118 micrograms kg-1 fleece-free body weight, plasma concentrations of lys-beta-urogastrone were near maximal 20 h after the infusions started and were, respectively, 1.1, 1.7, 5.5, 18 and 79 micrograms l-1 plasma. Plasma concentrations of gastrin, somatostatin and pancreatic polypeptide were determined in these five sheep. Plasma gastrin rose sixfold by the end of infusions of 25 micrograms kg-1 of the urogastrone analogue, and tenfold with the higher doses of infusion. Although plasma somatostatin concentrations were variable, a consistent trend was observed; lower levels were apparent during the lys-beta-urogastrone infusions. There was no discernible trend in pancreatic polypeptide concentrations.

Plasma concentrations of LH, FSH and oestradiol-17 beta were measured in blood samples taken at 15 min intervals for 48 h during the follicular phase of four Merino ewes. The amplitude of pulses of LH and the mean concentration of LH were higher at the beginning of the follicular phase, 36-24 h before the preovulatory surge of LH (amplitude 2.4 ng ml-1, mean concentration 3.9 ng ml-1), than at the end, 24-0 h before the preovulatory surge (amplitude 1.2 +/- 0.1 ng ml-1; mean concentration 1.4 +/- 0.1 ng ml-1). There was no change in the inter-pulse interval during this time (mean 74 +/- 5 min). Over the same period, oestradiol levels increased from 7-8 pg ml-1 to a peak of 10-15 pg ml-1. Mean FSH concentrations declined (36-24 h: 3.6 ng ml-1 vs 24-0 h: 1.8 +/- 0.3 ng ml-1) before rising at the time of the preovulatory surge of LH and again 24 h later. It was concluded that the biphasic response of LH to oestrogen that is seen in ovariectomized ewes may also operate during the follicular phase of the oestrous cycle in entire ewes.

Lipoprotein lipase and hepatic lipase have been shown to be present in the post-heparin plasma of sheep. Intravenous injection of heparin into sheep produced a rapid increase in the free fatty acid concentration and lipolytic enzyme activity of the plasma, both peaking within 5-15 min and then falling to pre-heparin levels within 30-60 min. Lipolytic activity was not detected in plasma before heparin treatment. Two distinct lipolytic activities were separated from the plasma by chromatography on heparin-Sepharose 6B. Lipoprotein lipase was identified on the basis that the lipolytic activity was dependent upon the addition of plasma, inhibited by 1M NaCl, and inhibited by a specific antiserum against lipoprotein lipase. The second lipolytic activity of plasma was identified as hepatic lipase, as it was not dependent upon plasma for activity, nor was it inhibited by 1M NaCl or antiserum against lipoprotein lipase. Its properties were identical to the lipase extracted from the liver of sheep. Lipoprotein-lipase activity, but not hepatic-lipase activity, was dependent upon the nutritional state of the sheep at the time of heparin injection. However, hepatic lipase comprised a significant proportion of the total lipolytic activity.

The adenylate cyclase activity of ram sperm increased on freeze-thawing and the enzyme was stable at 0 degrees C. Its activity was stimulated by Mn2+, Zn2+, Co2+, Mg2+ and Ca2+ in descending order of activity. The enzyme was insensitive to fluoride when Mn2+ concentration was in excess. Mn2+-stimulated enzyme activity was decreased by the simultaneous addition of Co2+, or Cd2+, or Ni2+, and particularly Cu2+. Sulfhydryl compounds (viz. dithiothreitol, glutathione, dithiocarbamate, 2-mercaptoethanol, ergothioneine and cysteine) and chelating agents (viz. D-penicillamine and 8-hydroxyquinoline) were effective, to varying degrees, in overcoming the inhibition by Cu2+. Ca2+ augmented the stimulatory effect of Mg2+, Co2+, Zn2+ and Mn2+ on enzyme activity.

The effects of daily administration of 10 mg of highly purified ovine growth hormone (GH) for a period of 4 weeks on wool growth have been measured in 12 Merino ewes fed either a calculated maintenance energy intake or 1.6 times this amount (six on each ration). Concentrations of hormones, glucose, urea, alpha-amino N and amino acids in the blood were monitored and faeces and urine collected for measurement of nitrogen balance. Wool growth rate decreased by 20% during the 4 weeks of GH treatment in sheep fed the high energy diet, largely because of reduced wool fibre diameter. This was followed by restoration of normal growth and then an increase of up to 20% above control levels, a response which persisted for 12 weeks following cessation of GH administration, and which was due to increases in both fibre length and diameter. GH administration caused marked increases in plasma concentrations of GH, insulin and somatomedin C, glucose and free fatty acids, all of which returned to basal levels following cessation of GH administration. No consistent changes in plasma concentration of T3, T4, cortisol, prolactin or alpha amino N were detected. Plasma urea and methionine levels decreased during GH treatment and returned to, or were raised above, basal levels after the GH treatment period. GH injection also resulted in a net retention of N during treatment, followed by a transient period of net N loss. The GH-induced changes in wool growth may be caused by a change in the partitioning of amino acids between the muscle mass and the skin. No other contributing factor(s) were identified.