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Ruffner User Guide
No full textThe User Guide for the Library of Appalachian Preaching is a Google Sheet that can be searched, sorted, and downloaded for offline use.
At the moment, Ruffner has only one address in the Library; it has a Guide of its own so the records will be complete. It includes the title, date and place it was delivered, and so on. This information is available in the master list of sermons as well.https://mds.marshall.edu/ruffner_henry/1001/thumbnail.jp
Astrocyte-Derived Thrombospondin Induces Cortical Synaptogenesis in a Sex-Specific Manner
Get PDFThe regulation of synaptic connectivity in the brain is vital to proper functioning and development of the CNS. Formation of neural networks in the CNS has been shown to be heavily influenced by astrocytes, which secrete factors, including thrombospondin (TSP) family proteins, that promote synaptogenesis. However, whether this process is different between males and females has not been thoroughly investigated. In this study, we found that cortical neurons purified from newborn male rats showed a significantly more robust synaptogenic response compared with female-derived cells when exposed to factors secreted from astrocytes. This difference was driven largely by the neuronal response to TSP2, which increased synapses in male neurons while showing no effect on female neurons. Blockade of endogenous 17b -estradiol (E2) production with letrozole normalized the TSP response between male and female cells, indicating a level of regulation by estrogen signaling. Our results suggest that male and female neurons show a divergent response to TSP synaptogenic signaling, contributing to sex differences in astrocyte-mediated synaptic connectivity
Artificial Intelligence Aided Receiver Design for Wireless Communication Systems
Get PDFPhysical layer (PHY) design in the wireless communication field realizes gratifying achievements in the past few decades, especially in the emerging cellular communication systems starting from the first generation to the fifth generation (5G). With the gradual increase in technical requirements of large data processing and end-to-end system optimization, introducing artificial intelligence (AI) in PHY design has cautiously become a trend. A deep neural network (DNN), one of the population techniques of AI, enables the utilization of its ‘learnable’ feature to handle big data and establish a global system model. In this thesis, we exploited this characteristic of DNN as powerful assistance to implement two receiver designs in two different use-cases. We considered a DNN-based joint baseband demodulator and channel decoder (DeModCoder), and a DNN-based joint equalizer, baseband demodulator, and channel decoder (DeTecModCoder) in two single operational blocks, respectively. The multi-label classification (MLC) scheme was equipped to the output of conducted DNN model and hence yielded lower computational complexity than the multiple output classification (MOC) manner. The functional DNN model can be trained offline over a wide range of SNR values under different types of noises, channel fading, etc., and deployed in the real-time application; therefore, the demands of estimation of noise variance and statistical information of underlying noise can be avoided. The simulation performances indicated that compared to the corresponding conventional receiver signal processing schemes, the proposed AI-aided receiver designs have achieved the same bit error rate (BER) with around 3 dB lower SNR
Role of Na/K-ATPase Non-enzymatic Signaling in Renal Proximal Tubule Sodium Transport
Get PDFThe renal proximal tubule (RPT) is the center stage for renal handling of Na+ , a potent determinant of systemic Na+ and volume homeostasis in health and disease. In the RPT, through its classic ion-pumping function, Na + /K+ -ATPase (NKA) generates the Na+ gradient that drives apical Na+ absorption, mostly through Na+ /H+ exchanger (NHE3). In contrast, pharmacological evidence suggests that the activation of the NKA non-enzymatic signaling function, through Src and other signaling partners, triggers a cellular redistribution of NKA and NHE3 that decreases transcellular Na+ flux in cultured RPT cells. However, the physiological relevance of the nonenzymatic function of NKA compared to its enzymatic function in the regulation of RPT Na+ transport has not been directly studied. Thus, to address this, we developed a genetic approach in RPT cells and mice. Loss of NKA α1 in RPT cells in vitro and in vivo resulted in a prominent increase in transepithelial Na+ transport coupled to an increased membrane abundance of apical NHE3 and basolateral Na/HCO3 - cotransporter-1A (NBCe1A). Consistently, the hyperabsorptive phenotype observed in RPT-specific hypomorphic NKA α1 mice was rescued upon crossing with RPT-specific hypomorphic NHE3 mice, confirming the importance of NKA/NHE3 coupling. Consistent with previous pharmacological studies reported a role for Src in the natriuretic regulation by NKA receptor, rescue of RPT cells with wild-type but not Src-binding null NKA α1 restored NHE3 and NBCe1A to basal levels, indicative of a role for NKA/Src receptor function in the tonic inhibition of Na+ transporters in vitro. In vivo, while female mice expressing Src-binding mutant NKA α1 in RPT exhibit increased NHE3 and RPT Na+ transport, male mice exhibit no change. These observations are compatible with a sexual dimorphism in the NKA/Src mechanism of regulation of NHE3 and Na+ transport in the RPT. Hence, NKA nonenzymatic signaling is a potent natriuretic mechanism of tonic inhibition of RPT Na+ transport by regulating key apical and basolateral Na+ transporters. Remarkably, the natriuretic NKA signaling is also functionally dominant over its classically recognized anti-natriuretic ion-pumping role. NKA signaling therefore provides a long sought-after mechanism for the natriuretic action of endogenous NKA ligands such as cardiotonic steroids
