The nucleotide sequence of chicken Mx cDNA was reported earlier using the White Leghorn breed in Germany, but it showed no enhanced resistance to viruses. In this study, the nucleotide sequences of chicken Mx cDNA were determined in many breeds. A total of 25 nucleotide substitutions, of which 14 were deduced to cause amino acid exchanges, were detected, suggesting that the chicken Mx gene is very polymorphic. Transfected cell clones expressing chicken Mx mRNA were established after the Mx cDNA was constructed with an expression vector and introduced into mouse 3T3 cells, and the Mx genes from some breeds were demonstrated to confer positive antiviral responses to influenza virus and vesicular stomatitis virus. On the basis of the comparison among the antiviral activities associated with many Mx variations, a specific amino acid substitution at position 631 (Ser to Asn) was considered to determine the antivirally positive or negative Mx gene. Thus, a single amino acid substitution influences the antiviral activity of Mx in domesticated chickens
Gonadal germ cells (GGC) were collected from the gonads of 7‐ or 9‐day‐old White Leghorn chick embryos and suspended in freezing medium containing 10% dimethylsulfoxide (DMSO). The cell suspension was frozen at −1°C/min. until the temperature reached −80°C. Then, the cells were immersed in liquid nitrogen at −196°C and stored for 3–4 months. Approximately 50 frozen/thawed GGC were injected into the dorsal aorta of each 2‐day‐old Rhode Island Red (RIR) embryo, from which blood was drawn before germ‐cell injection. The injected embryos were incubated until they hatched and the chicks were raised until sexually mature. On reaching sexual maturity, a progeny test was performed by mating recipient chicks with normal RIR of the opposite sex. Progenies were obtained from male germ cell recipients that were injected with germ cells collected from 7‐ and 9‐day‐old embryos. The results demonstrated that frozen/thawed GGC collected from 7‐ or 9‐day‐old fertilized eggs can be used to produce male germ‐line chimeras.
The possible involvement of pituitary endorphins in the pathophysiology of shock was evaluated by measuring cardiorespiratory variables after naloxone injection in conscious hypophysectomized and sham-hypophysectomized rats subjected to controlled hemorrhage. Additionally, the role of the central nervous system (CNS) in mediating the cardiodepressant effects of endorphins in shock was studied. After the induction of hypovolemic shock (20 min at below 40 mmHg), hypophysectomized and sham-hypophysectomized rats received intraventricular (ivt) injections of naloxone HCl (10 micrograms) or an equivalent volume of saline (20 microliters over 20 s). In sham-hypophysectomized rats, both injections significantly elevated mean arterial pressure and pulse pressure; however, the increase produced by naloxone was significantly greater than that produced by saline. By contrast, hypophysectomized rats showed no response to naloxone or saline. Intravenous (iv) administration of naloxone HCl (3 mg/kg) or saline to these same hypophysectomized rats 15 min after ivt administration had no additional cardiovascular effects; as before, only animals with intact pituitaries responded to naloxone. Heart rate and respiration rate were unaffected by ivt or iv naloxone. From these data we suggest that pituitary endorphins contribute to the pathophysiology of hypovolemic shock, at least in part through actions within the CNS.
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