PubMed · 11633797
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F Secret. 1971. [Not Available].. https://pubmed.ncbi.nlm.nih.gov/11633797/
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The stria vascularis (SV) is an essential component of the inner ear that regulates the ionic environment required for hearing. SV degeneration disrupts cochlear homeostasis, leading to irreversible hearing loss, yet a comprehensive understanding of the SV, and consequently therapeutic availability for SV degeneration, is lacking. We developed a whole-tissue explant model from neonatal and mature mice to create a platform for advancing SV research. We validated our model by demonstrating that the proliferative behavior of the SV in vitro mimics SV in vivo. We also provided evidence for pharmacological experimentation by investigating the role of Wnt/β-catenin signaling in SV proliferation. Finally, we performed single-cell RNA sequencing from in vivo neonatal and mature mouse SV and surrounding tissue and revealed key genes and pathways that may play a role in SV proliferation and maintenance. Together, our results contribute new insights into investigating biological solutions for SV-associated hearing loss.
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The mechanism of divalent Ca2+ cation induction of Escherichia coli competence is still not fully understood, though it is a common method for introducing recombinant DNA into bacterial cells in gene engineering. Quantum dots (QDs), as a new fluorescent probe of being applied in biology research, have aroused great interest. In this paper, we explored the mechanism of E. coli competence development using QDs for the first time. Results showed that water-soluble QDs of diameter 3-4 nm could go into competent cells, but could not enter noncompetent cells. This result was further confirmed using atomic force microscopy and DNA transforming experiments, suggesting that nonphysiological, high concentrations of Ca2+ enhanced the penetrability of cell membranes so that QDs, which cannot enter cells normally due to their greater diameter (3-4 nm), can do so easily into competent cells. Therefore, we believe that, at least for E. coli, the mechanism of Ca2+-induced competence development is mediated physicochemically rather than physiologically.