Browsing by Subject "Scanning electron microscope"

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    Characterization of the early pathology of cochlear stereocilia in four inbred mouse strains with progressive hearing loss
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2019) Liu, Xiang; Xie, Yi; Huang, Shanshan; Xu, Ang; Zhao, Mengmeng; Kang, Xiaoxia; Yan, Aiwei; Li, Ping; Jin, Changzhu; Han, Fengchan
    Objective. Inbred strains of mice offer promising models for understanding the genetic basis of age-related hearing loss (AHL). NOD/LtJ, A/J, DBA/2J and C57BL/6J mice are classical models of age-related hearing loss and exhibit early onset of pathology of AHL. This study was carried out to characterize the early pathology of cochlear stereocilia in the four mouse strains with age-related hearing loss. Methods. The structural features of stereocilia in NOD/LtJ, A/J, DBA/2J and C57BL/6J mice were observed by scanning electron microscopy (SEM) at age of 2, 4, 6 or 8, and 10 or 12 weeks. Meanwhile, auditoryevoked brainstem response (ABR) and distortion product otoacoustic emission (DPOAE) amplitudes of the mice were measured at various intervals (3, 4, 6, 8, 10 and 12 weeks of age). Results. The ABR thresholds in NOD/LtJ, A/J and DBA/2J mice increased with age from 3 to 12 weeks. DPOAE amplitudes in NOD/LtJ, A/J, DBA/2J mice were very low at 4 weeks and became negative at 8 weeks at f2 frequency of 17 672 Hz. In addition to the progressive hearing loss, the four mouse strains displayed early onset (at 2 weeks of age) and progressive degeneration of stereocilia in hair cells. Conclusion. Early degeneration of stereocilia contributes to the functional impairment of hair cells and hearing loss in NOD/LtJ, A/J, DBA/2J and C57BL/6J mice.
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    Ultrastructural evidence of the evolutional process in malakoplakia
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Jung, Yeon Seung; Chung, Dong Yong; Kim, Eun Jin; Cho, Nam Hoon
    Context. Malakoplakia can be caused by incomplete digestion of Escherichia coli by lysosomes, leading to recurrent urinary tract infections and consequential mass-forming events that mimic tumors. Objectives. By using ultrastructural findings, we aimed to specify the process of phagolysosome to evoke malakoplakia. Design. We observed a series of processes to form a peculiar Michaelis-Gutmann (MG) body in three patients with malakoplakia and compared with xanthogranulomatous pyelonephritis. Results. The ultrastructural findings were realigned according to the sequence of events as pre-phagosomal, phagosomal, and post-phagosomal stages. For the mature MG body, numerous lysosomal aggregates targeting pathogens and subsequent incomplete digestion are prerequisite factors for the pre-phagosomal stage. Scattered lamellated residue is late evidence of the pre- phagosomal stage. Phagosomes can be formed by the fusion of multiple pathogens and multiple lysosomes. We utilized transmission and scanning electron microscopy to speculate on the process of phagolysosomal formation. Conclusion. The recognition of E. coli captured by phagosomes or partially damaged by lysosomal attack within the cell was recorded for the first time. Furthermore, SEM observation was performed on human tissue