(BMC physiology[TA])
254 results
  • Claudin expression during early postnatal development of the murine cochlea. [Journal Article]
    BMC Physiol. 2018 Jan 25; 18(1):1.Kudo T, Wangemann P, Marcus DCBP
  • CONCLUSIONS: We demonstrated developmental patterns of claudin isoform transcript expression in the murine cochlea. Most of the claudins were associated with stria vascularis and organ of Corti, tissue fractions rich in tight junctions. However, this study suggests a novel function of Cldn-13 in the cochlea, which may be linked to cochlear bone marrow maturation.
  • Endothelial dysfunction in the pathogenesis of pre-eclampsia in Ghanaian women. [Journal Article]
    BMC Physiol. 2017 Mar 29; 17(1):5.Adu-Bonsaffoh K, Antwi DA, … Obed SABP
  • CONCLUSIONS: Endothelial dysfunction contributes significantly to the pathogenesis of pre-eclampsia as demonstrated by profound decrease in maternal serum VEGF levels in PE compared to normotensive pregnancy and non-pregnancy state. The pathophysiology of early-onset pre-eclampsia may be partly explained by marked reduction in free serum VEGF levels with resultant severe endothelial dysfunction.
  • The gastric H,K-ATPase in stria vascularis contributes to pH regulation of cochlear endolymph but not to K secretion. [Journal Article]
    BMC Physiol. 2016 Aug 11; 17(1):1.Miyazaki H, Wangemann P, Marcus DCBP
  • CONCLUSIONS: These observations suggest that stria vascularis may be an important site of control of cochlear acid-base balance and demonstrate a functional role of several acid-base transporters in stria vascularis, including basolateral H,K-ATPase and apical Na,H-exchange. Previous suggestions that H secretion is mediated by an apical vH-ATPase and that basolateral H,K-ATPase contributes importantly to K secretion in stria vascularis are not supported. These results advance our understanding of inner ear acid-base balance and provide a stronger basis to interpret the etiology of genetic and pharmacologic cochlear dysfunctions that are influenced by endolymphatic pH.