Hidden Hearing Loss: Causes, Current Knowledge, and Future Directions

Introduction: Hidden hearing loss (HHL) is a type of auditory disorder that affects the auditory neural processing and hearing sensitivity in subjects with normal hearing thresholds. Unlike central auditory processing disorders, HHL happens when the cochlea (the peripheral auditory organ) is affected. There are several known risk factors to HHL which includes noise exposure, ototoxic drugs, and peripheral neuropathies, and age. Recent studies have shed light on this type of hearing loss, its etiology, prevalence, and how it can affect the auditory acuity in humans. Methods: This paper covers the current research regarding HHL, its causes, the different mechanisms involved in this disorder, and the diagnosis and potential treatments related to it. We will delve deeply into different researches concerning HHL. 4 articles from 285 were selected focusing on normal hearing individuals with bad speech intelligibility were discussed in this paper. In addition, articles discussing the effects of noise exposure on hearing impaired individuals were not considered as this study solely aims to focus on normal hearing sensitivity individuals with HHL, resulting in 4 articles from 285. Results: Numerous literatures over the decades have suggested that HHL is due to the degeneration of cochlear ribbon synapses, or hair cells synapses without hair cell damage. Their association with HHL was noted several times through this study, whether we were studying the effect of noise exposure, of age, or of ototoxicity. In all cases, no significant hair cell damage was observed, and normal thresholds were recovered. However, a decline in the amplitude of Auditory Brainstem Response (ABR) peak I from auditory nerve (AN) responses in noise exposed subjects and a decline in compound action potential (CAP) was measured when certain drugs were applied to the round window of Guinea pigs. Conclusion: Most studies, have proven that cochlear synaptophysin is the major contributor to noise induced, age, and ototoxic related HHL. There are several audiometric tests that were used to help identify HHL including Puretone audiometry in background noise, ABR, CAP, Distortion Product Otoacoustic Emission (DPOAE).

Chemical screening reveals Ronidazole is a superior prodrug to Metronidazole for nitroreductase-induced cell ablation system in zebrafish larvae

The Metronidazole(MTZ)/nitroreductase(NTR)-mediated cell ablation system is the most commonly used chemical-genetic cell ablation method in zebrafish. This system can specifically ablate target cells under spatial and temporal control. The MTZ/NTR system has become a widely used cell ablation system in biological, developmental, and functional studies. However, the inadequate cell-ablation ability of some cell types and the side effects of high concentration MTZ impede extensive applications of the MTZ/NTR system. In the present study, the US drug collection library was searched to extend the NTR system. Six MTZ analogs were found, and the cell-ablation ability of these analogs was tested in zebrafish larvae. The results revealed that two of the NTR substrates, Furazolidone and Ronidazole, ablated target cells more efficiently than MTZ at lower concentrations. Furthermore, the working concentration of Ronidazole, but not Furazolidone and MTZ, did not affect axonal bridge formation during spinal cord regeneration. Our results,taken together, indicate that Ronidazole is a superior prodrug to MTZ for the NTR system, especially for the study of neuron regeneration in zebrafish larvae.

No Intestinal Stem Cell Regeneration after Complete Progenitor Ablation in Drosophila Adult Midgut

Adult stem cells or progenitors are essential for maintaining the normal structure and function of adult tissues （i.e., ho- meostasis）. One of the best examples is the adult intestinal epithelium which is constantly renewed by the progeny of intestinal stem cells （ISCs）. The proliferation and differentiation of adult stem cells must be tightly controlled in order to maintain resident tissue homeostasis. Mis-regulation of stem cell proliferation and differentiation leads to depletion or excessive proliferation of stem cells, eventually resulting in severe diseases such as cancer （Radtke and Clevers, 2005; Morrison and Spradling, 2008）. Understanding the detailed regulatory mechanisms of stem cell proliferation and differ- entiation will shed insights into the causes of related human diseases.