Monahan Risager (grounddead02)

AVP-sensitive currents showed inward rectification with a reversal potential close to the K+ reversal potential, suggesting the involvement of inwardly rectifying K+ channels. AVP-induced currents were sensitive to the micromolar concentration of Ba2+ and tertiapin-Q, whereas application of ML 133, a selective Kir2 channel blocker had no effects, suggesting that AVP excited CA1 pyramidal neurons by depressing G protein-gated inwardly rectifying K+ channels. Activation of V1a receptors in the CA1 region facilitated glutamatergic transmission onto subicular pyramidal neurons, suggesting that AVP modulates network activity in the brain. Our results may provide one of the cellular and molecular mechanisms to explain the in vivo physiological functions of AVP.Individual differences in the effects of a chronic neuropathic injury on social behaviours characterize both the human experience and pre-clinical animal models. The impacts of these changes to the well-being of the individual are often underappreciated. Earlier work from our laboratory using GeneChip® microarrays identified increased cholecystokinin (CCK) gene expression in the periaqueductal gray (PAG) of rats that showed persistent changes in social interactions during a Resident-Intruder encounter following sciatic nerve chronic constriction injury (CCI). In this study, we confirmed these gene regulation patterns using RT-PCR and identified the anatomical location of the CCK-mRNA as well as the translated CCK peptides in the midbrains of rats with a CCI. We found that rats with persistent CCI-induced changes in social behaviours had increased CCK-mRNA in neurons of the ventrolateral PAG and dorsal raphe nuclei, as well as increased CCK-8 peptide expression in terminal boutons located in the lateral and ventrolateral PAG. The functional significance of these changes was explored by microinjecting small volumes of CCK-8 into the PAG of uninjured rats and observing their Resident-Intruder social interactions. Disturbances to social interactions identical to those observed in CCI rats were evoked when injection sites were located in the rostral lateral and ventrolateral PAG. We suggest that CCI-induced changes in CCK expression in these PAG regions contributes to the disruptions to social behaviours experienced by a subset of individuals with neuropathic injury.Retraction "Long noncoding RNA HOTAIR knockdown inhibits autophagy and epithelial-mesenchymal transition through the Wnt signaling pathway in radioresistant human cervical cancer HeLa cells," by Xinggang Guo, Hongqi Xiao, Sihong Guo, Jing Li, Yuxia Wang, Jie Chen, Ge Lou, J Cell Physiol. 2019; 3478-3489 The above article, published online on 26 October 2018 in Wiley Online Library (https//onlinelibrary.wiley.com/doi/full/10.1002/jcp.26828), has been retracted by agreement between the journal's Editor in Chief, Prof. Dr. Gregg Fields, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. As several flaws and inconsistencies between results presented and experimental methods described were found, the editors consider the conclusions of this article to be invalid.Retraction "MicroRNA-150 contributes to ischemic stroke through its effect on cerebral cortical neuron survival and function by inhibiting ERK1/2 axis via Mal," by Hui Lv, Jie Li, Yu-Qin Che, J Cell Physiol. 2019; 1477-1490 The above article, published online on 24 August 2018 in Wiley Online Library (https//onlinelibrary.wiley.com/doi/10.1002/jcp.26960) has been retracted by agreement between the journal's Editor in Chief, Prof. Dr. Gregg Fields, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. A detailed investigation revealed that several image elements of the experimental data were published elsewhere in a different scientific context. Thus, the editors consider the conclusions of this article to be in