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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Up-regulation of mesotocin receptors in the tammar wallaby myometrium is pregnancy-specific and independent of estrogen.

The oxytocin-like peptide of most Australian marsupials is mesotocin, which stimulates uterine contractions and is important for normal birth in the tammar wallaby. Female marsupials have two uteri and, in monovular species such as the tammar, one uterus is gravid with a single fetus, whereas the contralateral uterus is nongravid. A significant increase in myometrial mesotocin receptor concentrations occurs only in the gravid uterus on Day 23 of the 26-day gestation. This study examined whether or not mesotocin receptors are present in the myometrium and are up-regulated at the equivalent stage of the luteal phase in unmated tammars. In contrast to the marked increase in mesotocin receptor mRNA and protein concentrations in the myometrium of the gravid uterus during pregnancy, receptors did not increase in the unmated animals. There were also no significant differences between the two uteri, except on Day 27. Plasma profiles of peripheral estradiol-17beta and progesterone did not differ significantly between pregnant and nonpregnant cycles. However, progesterone concentrations were significantly lower on Day 1 postpartum compared with Day 27 of the nonpregnant cycle. In pregnant tammars, the molar ratio of circulating estradiol-17beta to progesterone increased significantly between Day 25 of gestation and 1 day postpartum, but was not correlated with an increase in mesotocin receptor concentrations in either uterus. The data confirm that a local fetal influence is more important than systemic factors, such as estrogen, in the regulation of uterine mesotocin receptors in the tammar wallaby.[1]

References

  1. Up-regulation of mesotocin receptors in the tammar wallaby myometrium is pregnancy-specific and independent of estrogen. Siebel, A.L., Gehring, H.M., Nave, C.D., Bathgate, R.A., Borchers, C.E., Parry, L.J. Biol. Reprod. (2002) [Pubmed]
 
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