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Interferon research abs 1 || Hemoglobin research abs || Stem cell research abs || Nucleic acid research abs || Herpes research abs || Bronchitis research abs || Schizophrenia research abs || Tuberculosis research abs || Pneumonia research abs || Constipation research abs || Laxative research abs || hair research abs || hair related research references

Neurobiol Dis. 2001 Feb;8(1):69-77.
Origin of vestibular dysfunction in Usher syndrome type 1B.

Sun JC, van Alphen AM, Wagenaar M, Huygen P, Hoogenraad CC, Hasson T, Koekkoek SK, Bohne BA, De Zeeuw CI.

Department of Anatomy, Erasmus University Rotterdam, Rotterdam, 3000DR, The Netherlands.

It is still debated to what extent the vestibular deficits in Usher patients are due to either central vestibulocerebellar or peripheral vestibular problems. Here, we determined the origin of the vestibular symptoms in Usher 1B patients by subjecting them to compensatory eye movement tests and by investigating the shaker-1 mouse model, which is known to have the same mutation in the myosin-VIIa gene as Usher 1B patients. We show that myosin-VIIa is not expressed in the human or mouse cerebellum and that the vestibulocerebellum of both Usher 1B patients and shaker-1 mice is functionally intact in that the gain and phase values of their optokinetic reflex are normal. In addition, Usher 1B patients and shaker-1 mice do not show an angular vestibuloocular reflex even though eye movement responses evoked by electrical stimulation of the vestibular nerve appear intact. Finally, we show histological abnormalities in the vestibular hair cells of shaker-1 mice at the ultrastructural level, while the distribution of the primary vestibular afferents and the vestibular brainstem circuitries are unaffected. We conclude that the vestibular dysfunction of Usher 1B patients and shaker-1 mice is peripheral in origin. 2001 Academic Press.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11162241&dopt=Abstract

Exp Cell Res. 1999 Mar 15;247(2):484-94.
Different types of ROS-scavenging enzymes are expressed during cutaneous wound repair.

Steiling H, Munz B, Werner S, Brauchle M.

Max-Planck-Institut fur Biochemie, Am Klopferspitz 18a, Martinsried, D-82152, Germany.

Injury to the skin initiates a series of events including inflammation, new tissue formation, and matrix remodeling. During the early inflammatory phase, polymorphonuclear leukocytes and macrophages infiltrate the wounded tissue. Once activated, they produce large amounts of reactive oxygen species (ROS) as part of their defense mechanism. Although this process is beneficial, increased levels of ROS can inhibit cell migration and proliferation and can even cause severe tissue damage. Therefore, cells must develop strategies for the detoxification of these molecules. To gain insight into the mechanisms which underlie this process, we analyzed the temporal and spatial expression pattern of various ROS-scavenging enzymes during the healing process of full-thickness excisional wounds in mice. Here we demonstrate a strong mRNA expression of two types of superoxide dismutase (SOD), as well as of catalase, and the selenoenzymes glutathione peroxidase (SeGPx) and phospholipid hydroperoxide glutathione peroxidase in normal and wounded skin. Most importantly, mRNA levels of the SODs and of SeGPx increased strongly after skin injury. In situ hybridization and immunofluorescence studies revealed the presence of these transcripts at multiple places in the wound, whereby particularly high expression levels were detected in the hyperproliferative epithelium and the hair follicles at the wound edge. These data suggest an important role of ROS-scavenging enzymes in the detoxification of ROS during cutaneous wound repair. 1999 Academic Press.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10066376&dopt=Abstract

Hum Gene Ther. 1999 Mar 20;10(5):813-23.
Hair cell protection from aminoglycoside ototoxicity by adenovirus-mediated overexpression of glial cell line-derived neurotrophic factor.

Yagi M, Magal E, Sheng Z, Ang KA, Raphael Y.

Kresge Hearing Research Institute, The University of Michigan, Ann Arbor 48109-0648, USA.

Aminoglycosides are commonly used antimicrobial drugs that often have ototoxic side effects. The ototoxicity often involves permanent loss of cochlear hair cells (HCs). Neurotrophic factors have been shown to protect a variety of tissues, including HCs, from toxic trauma. To determine if glial cell line-derived neurotrophic factor (GDNF) can protect cochlear HCs from trauma, we inoculated an adenoviral vector encoding the human GDNF gene into guinea pig cochleae via the round window membrane 4 days prior to injection of aminoglycosides. Control groups showed little or no negative influence of the viral inoculation on cochlear structure and function. In contrast, ears that were inoculated with the GDNF vector had better hearing and fewer missing HCs after exposure to the ototoxins, as compared with controls. Our results demonstrate the feasibility of gene therapy for cochlear application and suggest that virus-mediated overexpression of GDNF may be developed as a valuable prevention against trauma-induced HC death.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10210148&dopt=Abstract

Zhonghua Er Bi Yan Hou Ke Za Zhi. 1999 Aug;34(4):221-3.
[Protective effect of poly DL-aspartic acid on ototoxicity of gentamicin]

[Article in Chinese]

Guo Y, Li Z, Hu M.

Department of Otolaryngology, PLA General Hospital, Beijing 100853.

OBJECTIVE: To observe the protective effect of poly DL-aspartic acid (PAA) on ototoxicity of gentamicin (GM). METHODS: Fifty F-344 rats were divided into four groups, GM only PAA + GM, PAA only and saline control. ABR thresholds at different frequencies were measured at different times and hair cell losses were numerated. Two-dimensional diffusion assays in the culture medium were performed to evaluate the effect of PAA on the antimicrobial activity. RESULTS: Eighteen days after the treatment, ABR thresholds at 10 kHz and 8 kHz as well as hair cell losses in the GM-treated group showed significant differences as compared with other three groups (P < 0.01). CONCLUSION: PAA had the protective effect against the cochlear ototoxicity of GM without decreasing its antimicrobial activity.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12764776&dopt=Abstract [PubMed - in process]

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