Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:Q9UIJ5 (
Rec
)
58,342
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Ecological explanations have been put forward to account for the precocious or delayed development of patency in ducts leading to the vomeronasal organ (VNO) in certain mammals. Perinatal function may be related, in part, to the patency or fusion of the vomeronasal and nasopalatine (
NPD
) ducts. However, few studies have focused on
NPD
development in primates, which generally have a prolonged period of dependence during infancy. In this study we examined 24 prenatal primates and 13 neonatal primates, and a comparative sample of fetal mice and insectivores. In embryonic and early fetal Microcebus murinus, the
NPD
was completely fused, whereas in fetuses of later stages the duct was partially fused or completely patent. M. myoxinus of all stages demonstrated some degree of
NPD
fusion. In all other prenatal primates, the
NPD
was fused to some extent. Four prenatal insectivores (Tenrec ecaudatus) showed some degree of
NPD
fusion. In Mus musculus at 19 days gestation, the
NPD
was patent, although the anatomically separate VNO duct was fused. T. ecaudatus and most of the neonatal primates revealed complete
NPD
patency. An exception was Saguinus geoffroyi, which exhibited fusion of the
NPD
near the VNO opening. These observations may relate to differences in perinatal VNO function. The differences noted in our study suggest that M. murinus and M. myoxinus may differ in perinatal VNO functionality and perhaps in related behavior. Observations of neonatal primates suggest that
NPD
patency may be relatively common at birth and could serve other purposes in addition to being an access route for VNO stimuli.
Anat
Rec
A Discov Mol Cell Evol Biol 2003 Sep
PMID:Ontogeny of the nasopalatine duct in primates. 1292 97
Maternal protein restriction leads to a reduction in the number of cardiomyocytes in the rat heart at birth. However, in rats, cardiomyocytes continue to proliferate until about 2 weeks after birth. Hence, this study aimed to examine the effect of maternal protein restriction, on the number of cardiomyocytes in the young rat heart at a time point when the cardiomyocytes have ceased proliferating and are terminally differentiated. Female Wistar Kyoto rats were fed either a normal protein diet (
NPD
; 20% casein) or a low protein diet (LPD; 8.7% casein) during pregnancy and lactation. Offspring (seven males and seven females per group) were perfusion fixed at 4 weeks of age. Heart volume and total cardiomyocyte number were determined using stereological techniques. At 4 weeks of age, body weights in both male and female LPD offspring were significantly reduced compared with
NPD
controls whereas relative heart volumes were significantly increased in LPD offspring. Total number of cardiomyocytes was not significantly different between groups. In both groups, there was a significant linear correlation between cardiomyocyte number and heart volume. In conclusion, total cardiomyocyte number in the postproliferative rat heart does not appear to be affected by maternal protein restriction per se but is directly related to heart size.
Anat
Rec
(Hoboken) 2010 Mar
PMID:Effect of maternal protein restriction during pregnancy and lactation on the number of cardiomyocytes in the postproliferative weanling rat heart. 2009 84