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J Acoust Soc Am. 2002 May;111(5 Pt 1):2208-12.
Cooperative interaction as the physical basis of the negative stiffness in hair cell stereocilia.

Iwasa KH, Ehrenstein G.

National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland 20892, USA. iwasih.gov

A recent report confirmed that stiffness of the stereocilia can be negative, as predicted by the Howard-Hudspeth model. According to this model, the mechanotransducer channel's gating not only reduces the stereociliary stiffness, but can alter its sign as well. The basic assumptions of this model do not include cooperativity in channel gating. Here we consider two possible explanations for the observed negative stiffness. If the stereocilia have a special structure so that microscopic displacement can be imposed on each channel by controlling the bending of the bundle, negative stiffness can occur without channel cooperativity. If such a microscopic condition cannot be imposed by a macroscopic manipulation, an additional physical process, such as cooperativity in channel gating, is required to explain negative stiffness.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12051440&dopt=Abstract

Environ Res. 2002 May;89(1):1-11.
Neurodevelopmental investigations among methylmercury-exposed children in French Guiana.

Cordier S, Garel M, Mandereau L, Morcel H, Doineau P, Gosme-Seguret S, Josse D, White R, Amiel-Tison C.

Unit 170-Epidemiological and Statistical Research on Environment and Health, National Institute of Health and Medical Research (INSERM), 94807 Villejuif Cedex, France.

French Guiana, like its neighbors, suffers from environmental pollution with methylmercury from gold mining activities, and Amerindian communities are particularly affected. A neurological and a neurospsychological evaluation were carried out in children of three Amerindian communities with various levels of pollution: 156 children from the Upper Maroni (high exposure), 69 from Camopi on the Oyapock river (median exposure), and 153 from Awala on the Atlantic coast (low exposure). Exposure to methylmercury was measured by determination of total mercury in the hair of the children and their mothers (geometric mean, 12.7 microg/g in Upper Maroni). No major neurologic signs were observed in the children examined. After adjustment for potential confounders, we found a dose-dependent association between maternal hair mercury level and increased deep tendon reflexes, poorer coordination of the legs, and decreased performance in the Stanford-Binet Copying score, which measures visuospatial organization. In this last test, the frequency of rotation errors was high in the 5-6 years age group and increased with mercury exposure. These associations depended on the sex of child and were stronger among boys. The interpretation of these results is limited mainly by the cross-sectional design of the study. It identifies specific neurological and neuropsychological deficits, in some cases modulated by sex, which are consistent with known targets of mercury neurotoxicity. 2002 Elsevier Science (USA)

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12051779&dopt=Abstract

Development. 2003 Jan;130(1):221-32.
The zinc finger transcription factor Gfi1, implicated in lymphomagenesis, is required for inner ear hair cell differentiation and survival.

Wallis D, Hamblen M, Zhou Y, Venken KJ, Schumacher A, Grimes HL, Zoghbi HY, Orkin SH, Bellen HJ.

Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.

Gfi1 was first identified as causing interleukin 2-independent growth in T cells and lymphomagenesis in mice. Much work has shown that Gfi1 and Gfi1b, a second mouse homolog, play pivotal roles in blood cell lineage differentiation. However, neither Gfi1 nor Gfi1b has been implicated in nervous system development, even though their invertebrate homologues, senseless in Drosophila and pag-3 in C. elegans are expressed and required in the nervous system. We show that Gfi1 mRNA is expressed in many areas that give rise to neuronal cells during embryonic development in mouse, and that Gfi1 protein has a more restricted expression pattern. By E12.5 Gfi1 mRNA is expressed in both the CNS and PNS as well as in many sensory epithelia including the developing inner ear epithelia. At later developmental stages, Gfi1 expression in the ear is refined to the hair cells and neurons throughout the inner ear. Gfi1 protein is expressed in a more restricted pattern in specialized sensory cells of the PNS, including the eye, presumptive Merkel cells, the lung and hair cells of the inner ear. Gfi1 mutant mice display behavioral defects that are consistent with inner ear anomalies, as they are ataxic, circle, display head tilting behavior and do not respond to noise. They have a unique inner ear phenotype in that the vestibular and cochlear hair cells are differentially affected. Although Gfi1-deficient mice initially specify inner ear hair cells, these hair cells are disorganized in both the vestibule and cochlea. The outer hair cells of the cochlea are improperly innervated and express neuronal markers that are not normally expressed in these cells. Furthermore, Gfi1 mutant mice lose all cochlear hair cells just prior to and soon after birth through apoptosis. Finally, by five months of age there is also a dramatic reduction in the number of cochlear neurons. Hence, Gfi1 is expressed in the developing nervous system, is required for inner ear hair cell differentiation, and its loss causes programmed cell death.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12441305&dopt=Abstract

Audiol Neurootol. 2002 May-Jun;7(3):138-40.
Molecular studies of hair cell development and survival.

Ryan AF.

Otolaryngology and Neurosciences, School of Medicine, University of California, San Diego, La Jolla, CA 92093-0666, USA. aryacsd.edu

The development of hair cells in both the auditory and vestibular sensory epithelia is a complex process that involves the coordinated expression of many regulatory proteins. Among these is the POU-domain transcription factor Brn-3.1. This factor is expressed in hair cell precursors immediately after commitment to the hair cell fate, and continues throughout life. Deletion of this factor in mice leads to failure of hair cell differentiation during development, and to the death of a majority of the undifferentiated cells. Normal expression of Brn-3.1 is required for adult hair cell survival as well, since a mutation in this gene causes dominant, late-onset, inherited hearing loss in humans. The timing of the onset of Brn-3.1 expression suggests that factors regulating its expression may be involved in fate determination of hair cells. Moreover, genes that are themselves directly regulated by Brn-3.1 appear to play critical roles in hair cell development and survival. 2002 S. Karger AG, Basel

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12053133&dopt=Abstract

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