Brenda M. Ryals

Bio: Brenda M. Ryals is an academic researcher from James Madison University. The author has contributed to research in topics: Hair cell & Cochlea. The author has an hindex of 21, co-authored 36 publications receiving 1883 citations. Previous affiliations of Brenda M. Ryals include University of Virginia & United States Department of Veterans Affairs.

Hair cell regeneration after acoustic trauma in adult Coturnix quail.

Abstract: Recovery of hair cells was studied at various times after acoustic trauma in adult quail. An initial loss of hair cells recovered to within 5 percent of the original number of cells. Tritium-labeled thymidine was injected after this acoustic trauma to determine if mitosis played a role in recovery of hair cells. Within 10 days of acoustic trauma, incorporation of [3H]thymidine was seen over the nuclei of hair cells and supporting cells in the region of initial hair cell loss. Thus, hair cell regeneration can occur after embryonic terminal mitosis.

Development of the place principle: acoustic trauma

Abstract: Developmental changes in the site of receptor damage following pure-tone acoustic overstimulation were examined in the basilar papillae of embryonic and hatchling chickens. During development, a systematic shift in the position of damage toward the apex of the cochlea was produced by each of three frequencies, suggesting that the transduction properties of the sensory epithelium systematically shift with age. These results imply that neurons in the central nervous system may be maximally stimulated by different sounds during development.

Patterns of Hair Cell Loss in Chick Basilar Papilla After Intense Auditory Stimulation1:Frequency Organization

Abstract: Ten-day-old chicks were continuously exposed to pure tones (500, 1500, or 3 000 Hz) at 125 dB SPL for 12 hours and sacrificed 10 days after exposure. The basilar papillae were embedded in plastic, sectioned and hair cells were counted at 100-mum intervals throughout the length of the papilla. The position of hair cell loss along the basilar membrane varied systematically as a log-linear function with the frequency of stimulation. This systematic relationship was used to predict the frequency organization of the chick basilar papilla. It is concluded that although the avian basilar papilla differs greatly in morphological detail from the mammalian cochlea, its response to intense acoustic stimulation is quite similar.Es wurde festgestellt, dasz sich die Partes basilares der Vougel, obwoohl morphologisch bei Sauugetieren gaunzlich andersartig, bei intensiven akustischen Anregungen auhnlich verhalten.

Patterns of Hair Cell Loss in Chick Basilar Papilla After Intense Auditory Stimulation: Exposure duration and survival time

Abstract: Ten-day-old chicks were exposed to a pure tone (1.5 kHz) or white noise at 125 dB SPL avg. RMS for 4 to 24 hours, and were sacrificed either 10, 30 or 60 days after exposure. The basilar papillae were embedded in plastic, sectioned, and hair cells were counted at 100-mum intervals throughout the length of the papilla. As sound exposure duration increased, both the maximum number of hair cells lost, and the extent of the damaged area along the basilar membrane increased. Short hair cells situated on the free area of the basilar papilla were more susceptible to damage than were tall hair cells. The location of hair cell loss varied as a function of frequency band of exposure; the pure tone produced a well localized basal lesion, while wide-band noise produced a more general lesion which extending toward the apex. Degeneration continued with increased survival time up to 30 days. It is concluded that avians respond to acoustic overstimulation in a manner very similar to mammals. The convenience of this prepa...

Increased cell division as a cause of human cancer

Abstract: Carcinogenesis research is increasingly focused on chemicals that are not genotoxic and yet, at high doses, can induce cancer, apparently by increasing cell proliferation. We hypothesize that increased cell division per se stimulated by external or internal factors is also associated with the development of many human cancers. Although this hypothesis is well substantiated in the experimental literature, it has not been generalized as an important mechanism for carcinogenesis in human populations. Under this increased cell division model, the pathogenesis of cancer may result from molecular genetic errors induced during the process of cell division and from altered growth control of malignant or premalignant cells. Molecular genetic analysis of human cancers has shown that tumor cells contain multiple genetic defects including mutations, translocations, and amplifications of oncogenes and are reduced to homozygosity for putative tumor suppressor genes; these phenomena all require cell division for their occurrence and fixation. Increased cell division increases the risk of such events occurring. An accumulation of a combination of such genetic errors leads to a neoplastic phenotype. Examples are discussed of human cancers in which increased cell division, which drives the accumulation of genetic errors and can lead to neoplastic transformation, is caused by hormones, drugs, infectious agents, chemicals, physical or mechanical trauma, and other chronic irritation.

Overexpression of Math1 induces robust production of extra hair cells in postnatal rat inner ears.

Abstract: For mammalian cochlear hair cells, fate determination is normally completed by birth. We report here that overexpression of Math1, a mouse homolog of the Drosophila gene atonal, in postnatal rat cochlear explant cultures resulted in extra hair cells. Surprisingly, we found that the source of the ectopic hair cells was columnar epithelial cells located outside the sensory epithelium in the greater epithelial ridge, which normally give rise to inner sulcus cells. Moreover, Math1 expression also facilitated conversion of postnatal utricular supporting cells into hair cells. Thus Math1 was sufficient for the production of hair cells in the ear, and immature postnatal mammalian inner ears retained the competence to generate new hair cells.

Regeneration of Sensory Hair Cells after Acoustic Trauma

Abstract: Any loss of cochlear hair cells has been presumed to result in a permanent hearing deficit because the production of these cells normally ceases before birth. However, after acoustic trauma, injured sensory cells in the mature cochlea of the chicken are replaced. New cells appear to be produced by mitosis of supporting cells that survive at the lesion site and do not divide in the absence of trauma. This trauma-induced division of normally postmitotic cells may lead to recovery from profound hearing loss.

How the ear's works work

Abstract: The senses of hearing and equilibrium depend on sensory receptors called hair cells which can detect motions of atomic dimensions and respond more than 100,000 times a second. Biophysical studies suggest that mechanical forces control the opening and closing of transduction channels by acting through elastic components in each hair cell's mechanoreceptive hair bundle. Other ion channels, as well as the mechanical and hydrodynamic properties of hair bundles, tune individual hair cells to particular frequencies of stimulation.

Hair cell regeneration after acoustic trauma in adult Coturnix quail.

Abstract: Recovery of hair cells was studied at various times after acoustic trauma in adult quail. An initial loss of hair cells recovered to within 5 percent of the original number of cells. Tritium-labeled thymidine was injected after this acoustic trauma to determine if mitosis played a role in recovery of hair cells. Within 10 days of acoustic trauma, incorporation of [3H]thymidine was seen over the nuclei of hair cells and supporting cells in the region of initial hair cell loss. Thus, hair cell regeneration can occur after embryonic terminal mitosis.