PubMed · 11635863
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P Zambelli. 1987. [Not Available].. https://pubmed.ncbi.nlm.nih.gov/11635863/
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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.
Past discoveries usually become aggrandized in retrospect, especially at jubilee celebrations, and the double helix is no exception. The historical record reveals a muted response by the scientific community to the proposal of this structure in 1953. Indeed, it was only when the outlines appeared of a mechanism for DNA's involvement in protein synthesis that the biochemical community began to take a serious interest in the structure.
Some of us who were born in the middle of Europe between World Wars I and II had to face quite a few unusual challenges that we all met in different ways. I was born and raised in Prague, Czechoslovakia, a country at the time of my birth that was governed by a Western style of democracy, which was later destroyed by the occupation by Nazi Germany and subsequently by the takeover by the equally cruel Communists. Life required special means of adaptation to the changing living conditions and a great deal of luck to survive. After graduating from the School of Technology, I started working in the Department of Medicine at Charles University in Prague as a clinical chemist in endocrinology. This work was followed with training in basic biochemistry and the study of metabolic changes in stress. This rather diversified research, due to my changing of workplaces, led to the findings that diet can change enzymatic activity of liver tryptophan oxygenase. For a short time I worked on the metabolism of cyclic AMP in Escherichia coli, and at the age of 41, I made a risky move and succeeded in escaping with my family from the "paradise of communism." The reasons for this decision will become clear. After settling in the United States, I worked on the mechanism of activation of liver tryptophan oxygenase by cyclic AMP and eventually moved to the Vanderbilt University School of Medicine. There I initially worked on the mechanism of action of steroid hormones and finally on the molecular mechanism of action of retinoids, retinol, and retinoic acid. Also in cooperation with neonatologists, I initiated studies on prematurely born human neonates which led to successful supplementation of these patients with vitamin A. The work from my laboratory and my coworkers eventually became recognized.