Physiological effects of arginine vasotocin and mesotocin in cockerels

1. The effects of continuous infusion of 0.1, 1.0 and 10.0 mU/min/kg body weight of arginine vasotocin (AVT) or mesotocin (MT) on cardiovascular and thermoregulatory responses, on plasma osmolality and ionic composition and on plasma concentrations of AVT, MT, prolactin and aldosterone, were investigated in conscious White Leghorn cockerels.

2. Neither of the peptides, at any dose, affected cardiovascular functions, plasma ions and osmolality. Infusion of MT at the rate of 10 mU/min/kg body weight increased respiratory rate. Both peptides at doses of 1 and 10 mU/min/kg reduced the temperatures of the comb and shank but had no effect on the skin and cloaca.

3. Doses of 0.1 and 1.0 mU MT/mu/kg reduced plasma aldosterone and at 10 mU/min/kg increased plasma AVT. At any given dose MT had no effect on plasma prolactin. AVT at 0.1 and 1.0 mU/min/kg of AVT reduced plasma MT. AVT at 1.0 mU/min/kg increased plasma prolactin and at 10 mU/min/kg reduced plasma aldosterone.

4. During saline infusion, plasma MT was positively correlated with plasma AVT and negatively correlated with respiratory rate and cloacal temperature. Plasma AVT showed a positive correlation with plasma MT and aldosterone and a negative correlation with respiratory rate and skin temperature.

5. During saline infusion, there was no significant correlation between cardiovascular functions, or plasma osmolality and ionic composition and plasma MT or AVT.

6. The present study suggests that interrelationships between circulating concentrations of AVT and MT do exist and that AVT affects     

Parainfluenza-3 virus: difference in capacity of neuraminidase-weak and strong strains to infect young calves and to elicit cellular immune response.

Calves less than four weeks old could not be infected with a neuraminidase-weak strain of parainfluenza-3 virus (Pi3) but were successfully infected with either of two neuraminidase-strong strains. The criteria for infection were virus excretion, cell-mediated and antibody-mediated immune responses. In the lymphocyte stimulation test, calves infected with the neuraminidase-strong Pi3 strain Tüb-E6 responded more strongly to antigen prepared from this strain than to antigen from the heterologous Pi3 strain Um-23. The non-immunoglobulin haemagglutination inhibition activity of the liquid phase of nasal secretions of newborn calves decreased after treatment with Vibrio cholerae neuraminidase. For virus-bound neuraminidase the liquid phase from newborn calves was a richer substrate than the liquid phase from older animals.     

Nonabsorbable dietary fat enhances disposal of 2,2',4,4'-tetrabromodiphenyl ether in rats through interruption of enterohepatic circulation

Polybrominated diphenyl ethers are lipophilic persistent organic pollutants (POPs), which accumulate in the environment, leading to human exposure. The compounds exert a negative impact on human health. Strategies to prevent or diminish their accumulation in humans are required. We investigated in rats whether the disposal rate of 14C-labeled tetrabromodiphenyl ether (BDE-47) could be enhanced by increasing fecal fat excretion through dietary treatment with nonabsorbable fat (sucrose polyester, SPE). As compared to control rats, SPE treatment increased fecal excretion rates of fat (+188%, p < 0.05) and 14C-BDE-47 (+291%, p < 0.05). On the basis of biliary secretion and fecal excretion rates of 14C-BDE-47, SPE effectively inhibited the enterohepatic circulation of 14C-BDE-47. In conclusion, dietary supplementation of nonabsorbable fat can enhance excretion of hydrophobic POPs by interruption of their enterohepatic circulation. Our data indicate that this strategy could decrease concentrations of hydrophobic POPs in the human body and thereby their impact on human health.     

CD46 in meningococcal disease

The human-specific bacterial pathogen Neisseria meningitidis is a major cause of sepsis and/or meningitis. The pili of N. meningitidis interact with CD46, a human cell-surface protein involved in regulation of complement activation. Transgenic mice expressing human CD46 were susceptible to meningococcal disease, because bacteria crossed the blood-brain barrier in these mice. Development of disease was more efficient with piliated bacteria after intranasal, but not intraperitoneal, challenge of CD46 transgenic mice, suggesting that human CD46 facilitates pilus-dependent interactions at the epithelial mucosa. Hence, the human CD46 transgenic mice model is a potentially useful tool for studying pathogenesis and for vaccine development against meningococcal disease.     

Phage sensitivity in relation to pathogenicity and virulence of the cotton bacterial blight pathogen of Sudan

At least two pathotypes of Xanthomonas campestris pv. malvacearum are now known to exist in Sudan. The pre-Barakat (race 1) and post-Barakat (race 2) pathogens have been shown to exhibit different host specificity. The former is pathogenic and highly aggressive on only cultivars with no resistance genes or with the B₂ and/or B₃ resistance factors, while the latter can infect the B₆ cultivars also. Race 2 in Sudan, which was previously reported to infect all the standard differentials, produced milder angular leaf spot symptoms and occasionally restricted vein infection. Moreover, it exhibited reduced growth in planta compared with race 1.
Bacteriophage studies revealed that the two races are quite distinct in their phage sensitivity. Race 1 can be lysed by only three, or rarely four, of the six phages used for typing, while race 2 is sensitive to all of them. The present study suggests that phage 7 may be the type-determining phage for race 2. Race 2 strain mutants resistant to phage 3 or 4 were found to be sensitive to phage 7 and pathogenic to both Acala and Barakat, although showing marked attenuation of virulence. However, mutants resistant to phage 2 or 7 were insensitive to all the phages and although they retained their pathogenicity to Acala, they either lost the ability to infect Barakat or produced a hypersensitive reaction. The resistance of all mutants was found to be due to failure to adsorb the homologous phage, indicating a change in the cell wall. The association of this with the attenuation of virulence suggests that bacterial wall components may function as virulence determinants in Xanthomonas campestris pv. malvacearum.