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    <title>DSpace community: 附設醫院耳鼻喉部</title>
    <link>http://ntur.lib.ntu.edu.tw/handle/246246/48106</link>
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      <title>Semaphorin Signaling Facilitates Cleft Formation in the Developing Salivary Gland</title>
      <link>http://ntur.lib.ntu.edu.tw/handle/246246/170962</link>
      <description>title: Semaphorin Signaling Facilitates Cleft Formation in the Developing Salivary Gland abstract: Semaphorin signaling plays integral roles in multiple developmental processes. Branching morphogenesis is one such role that has not been thoroughly explored. Here, we show in mice that functional blockage of neuropilin 1 (Npn1) inhibits cleft formation in the developing submandibular gland (SMG) cultured ex vivo. This Npn1-dependent morphogenesis is mediated by Sema3A and Sema3C in an additive manner, and can be abolished by decreasing the expression of plexin A2 or plexin D1. VEGF, another known Npn1 ligand, has no apparent effects on SMG development. FGF signaling, which also mediates SMG branching morphogenesis, acts in parallel with semaphorin signaling. Finally, in contrast to the effect of FGF signaling, we find that semaphorins do not stimulate the proliferation of SMG epithelial cells. Instead, the semaphorin signals act locally on the epithelial cells to facilitate SMG cleft formation.
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      <pubDate>Wed, 14 Oct 2009 11:51:17 GMT</pubDate>
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    <item>
      <title>Potentiation of Noise-Induced Hearing Loss by Amikacin in Guinea Pigs</title>
      <link>http://ntur.lib.ntu.edu.tw/handle/246246/170956</link>
      <description>title: Potentiation of Noise-Induced Hearing Loss by Amikacin in Guinea Pigs abstract: Noise and aminoglycosides initially attack cochlear outer hair cells ( OHCs). Distortion product otoacoustic emissions( DPOAEs) are used for the early diagnosis of damage to OHCs. The effects of sub-damaging doses of amikacin, an aminoglycoside antibiotic agent, on noise-induced hearing loss (NIHL) were examined in guinea pigs. Animals were grouped by gender and exposed to broadband noise at 105 dB SPL for 12 It and/or injected i.m . with either amikacin (100 mg/kg/day) or saline for 10 days. Auditory brainstem response (ABR) thresholds, along with DPOAE amplitudes, were measured serially before and after noise exposure. DPOAE amplitudes decreased and ABR thresholds elevated immediately after noise exposure and then gradually recovered. At all frequencies, the emission amplitudes recovered completely to pre-exposure baseline values by 4 days after noise exposure . There was no effect of amikacin on either the ABR threshold or DPOAE amplitudes, in animals treated with amikacin only. However, amikacin significantly prolonged the effect of noise exposure on DPOAE amplitude but not on the noise-induced temporary threshold shift (TTS) of the ABR. In animals treated with a combination of noise and amikacin, significant changes in DPOAE amplitudes were still observed at 4 weeks after cessation of noise exposure. No gender difference in the responses to noise and/or amikacin could be demonstrated. The present findings indicate that even sub -damaging dosages of amikacin might impair recovery from NIHL in guinea pigs. (C) 2001 Elsevier Science B.V. All rights reserved.
&lt;br&gt;</description>
      <pubDate>Wed, 14 Oct 2009 11:47:42 GMT</pubDate>
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    <item>
      <title>Effect of Radiation on the Cochlear Blood Flow in Guinea Pigs</title>
      <link>http://ntur.lib.ntu.edu.tw/handle/246246/170952</link>
      <description>title: Effect of Radiation on the Cochlear Blood Flow in Guinea Pigs abstract: 　　Radiation for malignant head and neck tumors often affects the end organs of the fearing apparatus. The effect of radiation-induced vascular change may play an important role in the post-radiotherapy hearing loss. To evaluate the effect of irradiation on the cochlear blood flow, 12 fuinea pigs were irradiated in fractionatdion with a otal dosage of 5000 cGy of Co-60. Irradiation was given in 5 days per week, the daily dose being 200 cGy. The guinea pigs were sacrificed 10-12 months after the completion of irradiation. The cochlear blood flow was neasured with non- radioactive microspheres organ perfusion method. In comparison with similar age-matched non-irradiated guinea pigs, the cochlear blood flow of the irradiated group was significantly lower than the non-irradiated group.#0127#
&lt;br&gt;</description>
      <pubDate>Wed, 14 Oct 2009 11:43:26 GMT</pubDate>
    </item>
    <item>
      <title>Effects of Gentamicin and Ph on Ca+ in Apical and Basal Outer Hair Cells from Guinea Pigs</title>
      <link>http://ntur.lib.ntu.edu.tw/handle/246246/170948</link>
      <description>title: Effects of Gentamicin and Ph on Ca+ in Apical and Basal Outer Hair Cells from Guinea Pigs abstract: Abstract Aminoglycosides are widely used antibiotics and frequently produce acute ototoxicity. In this study we attempted to comparatively investigate the effects of gentamicin on Ca 2+ influx of apical and basal outer hair cells (OHCS) isolated from guinea- pig cochlea. Since the solution of gentamicin sulfate salt is acidic (pH 3.1 3.3), we also explored the effect of external acidification on Ca 2 1influx. By means of fura-2 microspectrofluorimetry, we measured the intracellular calcium concentration ([Ca&amp;quot;]i) of OHCs bathed in Hanks' balanced salt solution (pH 7.40) during either a resting state or high K+-induced depolarization. Our results show that at the resting state, the baseline [Ca 2, ], in apical OHCs (94 ± 2.0 nM) was slightly lower than that in basal OHCs (IO ].I ±2.4 nM). By contrast, the increase in [Ca 2-+ ]i evoked by high K' depolarization in apical OHCs was about two-fold greater than that in basal OHCS. Nifedipine (30 pM) abolished the increased [Ca 2+ ], in both types of OHCS, suggesting that Ca 2-, influx was mainly through L-type Ca 2+ channels of OHCS. While gentamicin and extracellular acidification (pH7 . 14) can separately attenuate this increase in [Ca 2 in both types of OHCS, their suppressive effects are additive in basal OHCS, but not in apical OHCS. The implications of these findings are that: (1) apical and basal OHCs behave differently in response to depolarization-increased [Ca&amp;quot; ]i, and (2) basal OHCs are more vulnerable to the impairment of Ca 2+ entry during depolarization by a combination of gentamicin and extracellular acidification, which is correlated with the clinical observation that ototoxicity of aminoglycosides at the basal coil of OHCs is more severe than that at the apical coils. Moreover, the possibility that extracellular acidification may enhance the acute ototoxic effects of aminoglycosides should be considered especially in topical applications. 2001 Elsevier Science B. V. All rights reserved.
&lt;br&gt;</description>
      <pubDate>Wed, 14 Oct 2009 11:40:53 GMT</pubDate>
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