استقرار مدل موش ناک اوت
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استقرار مدل موش ناک اوت

عنوان فارسی مقاله: استقرار مدل موش ناک اوت ژن آنتی ژن ۶ مرتبط با اسپرم و مکانیسم آن در ناشنوایی
عنوان انگلیسی مقاله: Establishment of sperm associated antigen 6 gene knockout mouse model and its mechanism of deafness
مجله/کنفرانس: مجله علوم زیست شناسی عربستان – Saudi Journal of Biological Sciences
رشته های تحصیلی مرتبط: پزشکی
گرایش های تحصیلی مرتبط: ژنتیک پزشکی، پزشکی گوش و حلق و بینی
کلمات کلیدی فارسی: ژن های Spag6، موشهای ناک اوت، اختلال شنوایی، ژنهای Prestin، ژنهای Pgrn، عفونت گوش میانی
کلمات کلیدی انگلیسی: Spag6 genes، Knockout mice، Hearing impairment، Prestin genes، Pgrn genes، Otitis media
نوع نگارش مقاله: مقاله پژوهشی (Research Article)
نمایه: Scopus – Master Journals List – JCR
شناسه دیجیتال (DOI): https://doi.org/10.1016/j.sjbs.2020.03.017
دانشگاه: Department of Otolaryngology, First Affiliated Hospital of Wenzhou Medical University, Wenzhou city 325000, China
ناشر: الزویر - Elsevier
نوع ارائه مقاله: ژورنال
نوع مقاله: ISI
سال انتشار مقاله: 2020
ایمپکت فاکتور: 2.868 در سال 2019
شاخص H_index: 33 در سال 2020
شاخص SJR: 0.703 در سال 2019
شناسه ISSN: 1319-562X
شاخص Quartile (چارک): Q1 در سال 2019
فرمت مقاله انگلیسی: PDF
تعداد صفحات مقاله انگلیسی: 7
وضعیت ترجمه: ترجمه نشده است
قیمت مقاله انگلیسی: رایگان
آیا این مقاله بیس است: خیر
آیا این مقاله مدل مفهومی دارد: ندارد
آیا این مقاله پرسشنامه دارد: ندارد
آیا این مقاله متغیر دارد: ندارد
کد محصول: E14954
رفرنس: دارای رفرنس در داخل متن و انتهای مقاله
فهرست انگلیسی مطالب

Abstract


۱٫ Introduction


۲٫ Materials and methods


۳٫ Results


۴٫ Discussion


Acknowledgement


References

نمونه متن انگلیسی مقاله

Abstract


To investigate the effects of knocking out the Sperm associated antigen6 (Spag6) gene on the auditory system of mice, the heterozygous type Spag6 knockout mouse model built in the previous period was used for mating and breeding, and homozygous type Spag6 gene knockout mouse (Spag/), heterozygous type Spag6 gene knockout mouse (Spag+/) and wild type mouse (Spag+/+) were obtained. PCR technology was used to verify mouse models with different genotypes. After verification, the hearing threshold responses of Spag+/+ and Spag/ genotype mice were detected. The localization of Spag6 gene in the basal membrane of the cochlea of the inner ear was detected by immunofluorescence staining. The changes of middle ear tissues were observed by H.E. staining sections. The relative expression of Prestin gene and Pgrn gene in different age mice was detected by fluorescence quantitative PCR. The relative expression of Prestin gene was detected by western blot. The results showed that Spag/ mice had hearing impairment compared with Spag+/+ mice. And Spag6 protein is distributed in different genotypes of mouse hair cells; Spag/ mice showed otitis media. The expression of Prestin mRNA and protein in Spag/ mice was significantly higher than that in Spag+/+ mice (P < 0.01). The expression of Pgrn gene in Spag+/+ mice was significantly higher than that in Spag/ mice (P < 0.05). It indicates that the loss of Spag6 gene would lead to the decline of hearing sense in mice. It is likely that the Spag6 gene could affect hearing by regulating the expression of Prestin gene. And the absence of the Spag6 gene causes otitis media in mice. The results of this study can lay a theoretical foundation for the follow-up studies of Spag6 gene in deafness diseases.


Introduction


Deafness has the highest incidence of diseases with sensory or functional defects in humans, and there are many factors causing deafness, and the causes are also very complex (Godinho et al., 2017). Otitis media is a disease that occurs frequently in children. Severe otitis media can lead to permanent neurological deafness. But overall, deafness is caused by both genetic and environmental factors, with genetic factors accounting for the main cause. At present, hundreds of genes have been found to be closely related to the occurrence and development of deafness (Hoberman et al., 2017). In mammals, the perception of sound is that the external sound enters the inner ear after passing through the external auditory canal and middle ear canal. The vibration of hair bundles on the surface of hair cells and the basement membrane transforms the sound signal into electrical signal, and finally transmits it to the brain for sound perception. Hair cells are very important auditory related cells, which can quickly regulate their own morphology and respond to sound stimulation, and this response mechanism originates from a gene specifically expressed in the lateral wall of outer hair cells (Guevar et al., 2018).

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