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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

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Quinine is a suitable model substance for the study of otoacoustic emissions (OAEs) as it reversibly affects the outer hair cells, thus reducing sensitivity, frequency-selectivity and various forms of OAEs. The aim of this experiment was to study quinine-induced changes in the input/output (I/O) function of 2f1 - f2 distortion product OAE (DPOAE; f2/f1 = 1.22; 750-6,000 Hz). Six volunteers with normal hearing (26-39 years old) were intravenously infused to achieve pseudostable quinine plasma concentrations (approximately12 microM) inducing an average pure-tone threshold (PTT; 750-6,000 Hz) shift of 18 dB (5-30 dB) (frequency-independent and reversible). The mean quinine-induced DPOAE shift increased continuously with decreasing equal-level primary tones, e.g. from 1.0 dB at 70 dB sound pressure level (SPL) (n = 42) to 10.5 dB (n = 22) at 40 dB SPL (pooled data, no frequency dependence). According to recruitment, the mean slope of the DPOAE I/O function (at 30-60 dB SPL) increased from 0.86 to 1.35 dB/dB. The lack of correlation between shifts in DPOAE and PTT is in stark contrast to the excellent correlation reported between shifts in transient evoked OAE detection threshold and its corresponding psychoacoustic threshold. The highly vulnerable spontaneous OAEs, in combination with the less vulnerable DPOAEs, fit into a recently proposed taxonomic classification for OAEs.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11039869&dopt=Abstract

Genetics. 2002 Jul;161(3):1029-42.
The Saccharomyces cerevisiae RNase mitochondrial RNA processing is critical for cell cycle progression at the end of mitosis.

Cai T, Aulds J, Gill T, Cerio M, Schmitt ME.

Department of Biochemistry and Molecular Biology, State University of New York Upstate Medical University, 50 E Adams Street, Syracuse, NY 13210, USA.

We have identified a cell cycle delay in Saccharomyces cerevisiae RNase MRP mutants. Mutants delay with large budded cells, dumbbell-shaped nuclei, and extended spindles characteristic of "exit from mitosis" mutants. In accord with this, a RNase MRP mutation can be suppressed by overexpressing the polo-like kinase CDC5 or by deleting the B-type cyclin CLB1, without restoring the MRP-dependent rRNA-processing step. In addition, we identified a series of genetic interactions between RNase MRP mutations and mutations in CDC5, CDC14, CDC15, CLB2, and CLB5. As in most "exit from mitosis" mutants, levels of the Clb2 cyclin were increased. The buildup of Clb2 protein is not the result of a defect in the release of the Cdc14 phosphatase from the nucleolus, but rather the result of an increase in CLB2 mRNA levels. These results indicate a clear role of RNase MRP in cell cycle progression at the end of mitosis. Conservation of this function in humans may explain many of the pleiotropic phenotypes of cartilage hair hypoplasia.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12136008&dopt=Abstract

Mol Cell Biol. 2002 Dec;22(24):8592-600.
Deletion of the GATA domain of TRPS1 causes an absence of facial hair and provides new insights into the bone disorder in inherited tricho-rhino-phalangeal syndromes.

Malik TH, Von Stechow D, Bronson RT, Shivdasani RA.

Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.

GATA transcription factors mediate cell differentiation in diverse tissues, and their dysfunction is associated with certain congenital human disorders. The six classical vertebrate GATA proteins, GATA-1 to GATA-6, are highly homologous, bear two tandem zinc fingers of the C(4) (GATA) type, and activate transcription. TRPS1, the only other vertebrate protein with the GATA motif, is a large, multitype zinc finger protein that harbors a single DNA-binding GATA domain and represses transcription. Monoallelic TRPS1 mutations cause two dominantly inherited human developmental disorders of the hair, face, and digits, tricho-rhino-phalangeal syndrome (TRPS) types I (MIM 190350) and III (MIM 190351); missense GATA domain mutations account for the more severe type III form. Here we report that heterozygous mice with deletions of the TRPS1 GATA domain (TRPS1(+/Deltagt)) display facial anomalies that overlap with findings for TRPS, whereas TRPS1(Deltagt/Deltagt) mice additionally reveal a complete absence of vibrissae. Unexpectedly, TRPS1(Deltagt/Deltagt) mice die of neonatal respiratory failure resulting from abnormalities of the thoracic spine and ribs. Heterozygotes also develop thoracic kyphoscoliosis with age and reveal structural deficits in cortical and trabecular bones. These findings directly implicate the GATA type zinc finger of TRPS1 in regulation of bone and hair development and suggest that skeletal abnormalities emphasized in descriptions of TRPS are only the extreme manifestations of a generalized bone dysplasia.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12446778&dopt=Abstract

Genes Cells. 2002 Sep;7(9):923-31.
Targeted elimination of the follicular label-retaining cells by photo-induced cell killing caused a defect on follicular renewal on mice.

Kameda T, Hatakeyama S, Ma YZ, Kawarada Y, Kawamata M, Terada K, Sugiyama T.

Department of Biochemistry, Akita University School of Medicine 1-1-1 Hondo, Akita 010-8543, Japan. tkameded.akita-u.ac.jp

BACKGROUND: One of the most well-known ways to identify stem cells is to search for the slow-cycling cells (label-retaining cells; LRCs), by labelling their DNA. The bulge of hair follicle is assumed to identify the location of the follicular stem cells. While this assumption was supported by previous analyses of cell tracing, it is still not clear whether the LRCs are critical for follicular renewal. RESULTS: To solve this problem, we tried to selectively eliminate the bromodeoxyuridine (BrdU)-labelled follicular LRCs by a photo-induced cell killing method, in combination with Hoechst 33258 treatment. We labelled the slow-cycling cells in the follicular bulge by repeated administration of the BrdU, followed by a chase period. When the labelled mice skin was irradiated at the telogen phase after the Hoechst 33258 treatment, we observed apoptotic cells in the bulge area 18 h after the irradiation and a defect on the follicular renewal at the next anagen phase. The time course of appearance of hair defect suggests that only the late telogen follicle is sensitive to irradiation. CONCLUSIONS: This finding suggests that the LRCs contribute to the renewal of the hair follicle, and they might proliferate at a restricted point in the hair cycle to supply hair germinative cells as previously predicted.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12296823&dopt=Abstract

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