Please use this identifier to cite or link to this item:
https://ptsldigital.ukm.my/jspui/handle/123456789/457965Full metadata record
| DC Field | Value | Language |
|---|---|---|
| dc.contributor.advisor | Goh Bee See, Prof. Dr | - |
| dc.contributor.author | Mohamad Fikeri Bin Ishak (P 45021) | - |
| dc.date.accessioned | 2023-09-13T01:48:54Z | - |
| dc.date.available | 2023-09-13T01:48:54Z | - |
| dc.date.issued | 2014-07-17 | - |
| dc.identifier.other | ukmvital:80484 | - |
| dc.identifier.uri | https://ptsldigital.ukm.my/jspui/handle/123456789/457965 | - |
| dc.description | Mikrotia adalah kecacatan kongenital yang mengakibatkan pembentukan telinga yang tidak sempurna. Keadaan ini boleh terjadi secara unilateral atau bilateral. Etiologinya tidak diketahui dengan jelas. Rawatan terkini termasuklah pembentukan telinga luar dengan menggunakan rawan rangka rusuk yang sekaligus meningkatkan morbiditi. Justeru, alternatif sumber sel atau rawan yang lain perlu dikaji. Malangnya, tidak banyak kajian yang telah dilakukan berkaitan kondrosit dari tisu mikrotia. Maka, kajian ini dijalankan untuk mencirikan sel yang diisolasi dari telinga mikrotia berbanding tisu normal dan menilai potensinya untuk digunakan sebagai sumber sel alternatif dalam pembentukan cuping telinga. Kajian ini melibatkan kajian in vitro dan in vivo. Kondrosit diisolasi dari tisu rawan normal dan mikrotik dan dikembangbiak sehingga pasaj 4. Seterusnya, kondrosit dari setiap pasaj (P1,P2,P3 dan P4) dianalisis. Tidak terdapat perbezaan yang signifikan dalam profil pertumbuhan, analisis kitaran sel dan analisis aliran sitometri bagi kedua-dua kumpulan. Analisis gen secara RT-PCR menunjukkan tidak terdapat perbezaan yang signifikan dalam pengekspresan gen kondrogenik, tetapi terdapat perbezaan yang signifikan dalam pengekspresan gen sel stem di antara kedua-dua kumpulan (sox 2, nestin, BST-1 and OCT-4). Penemuan ini menunjukkan bahawa penurunan dalam paras pengekspresan gen sel stem mungkin menjadi penyebab kepada pertumbuhan telinga yang terencat sekaligus menyebabkan mikrotia. Kajian in vivo melibatkan implantasi konstruk pada tikus atimik selama 8 minggu. Analisis post-implantasi menunjukkan pembentukan tisu seperti rawan. Pewarnaan histologi menunjukkan taburan sel yang sekata. Pewarnaan H & E menunjukkan tisu terdiri daripada lakuna yang bulat didalam matriks basofilik. Pewarnaan Safranin O pula menunjukkan pewarnaan positif jingga kemerahan, menandakan kehadiran proteoglikan. Analisis imunohistokimia menggunakan antibodi kolagen jenis II menunjukkan pewarnaan positif yang kuat, menandakan kehadiran kolagen jenis II yang banyak. Tisu itu juga menunjukkan pewarnaan yang pudar dengan antibodi kolagen jenis I dalam kedua-dua kumpulan. Analisis RT-PCR menunjukkan tidak terdapat perbezaan yang signifikan dalam pengekspresan gen kondrogenik di antara kedua-dua kumpulan (kolagen jenis I, kolagen jenis II, elastin, agrekan, sox 9). Kesimpulannya, kajian ini menunjukkan kekurangan dalam ciri-ciri sel stem diperingkat gen mungkin telah mengakibatkan mikrotia terjadi, namun kondrosit yang diisolasi dari pesakit mikrotia mempunyai potensi untuk digunakan sebagai sumber alternatif dalam pembentukan telinga.,Microtia is a congenital deformity that causes the ear to form incompletely. This condition can exist unilaterally or bilaterally. Little is known about the etiology of this condition. Current treatment involved the reconstruction of the ear using rib cartilage that increases morbidity. Thus, alternative cell source is needed urgently. Unfortunately, there are not much documented studies on chondrocytes of microtic origin. Thus, this study was conducted to characterize cells isolated from microtic auricular cartilage as compared to normal tissue and evaluating its potential as an alternative cell source for ear pinna reconstruction. The study involves in vitro and in vivo work. Chondrocytes were isolated from normal and microtic human auricular cartilage and culture expanded until passage 4. Upon confluent, cultured chondrocytes at each passage (P1, P2, P3 and P4) were harvested and subjected to analyses. There were no significant differences in the growth profile, cell cycle analysis and flowcytometry analysis between both groups. RT-PCR showed no significant differences in the expression of chondrogenic genes, but there are significantly lower in the expression of stem cell genes tested between both groups (sox 2, nestin, BST-1 and OCT-4). This finding suggests that the reduction in stem cell properties at the gene level might be the possible cause for the under developed ear that caused microtia. In vivo study involved construct implantation in the nude mice for 8 weeks. Post implantation analysis showed formation of cartilage-like tissue. Histological staining showed normal cell distribution. H&E staining demonstrated the tissue composed of round to oval lacunae cells embedded in a basophilic matrix. Safranin O stain showed positive orange-red staining, denoting abundant proteoglycans production. Immunohistochemistry analysis using collagen type II antibody was strongly positive, marking the tissue were rich with type II collagen. The tissue also stained faintly with type I collagen antibody. RT-PCR analysis showed no significant differences in the expression of chondrogenic genes (collagen type I, collagen type II, elastin, agreccan core protein, sox 9) between both groups. In conclusion, this study showed that lack of stem cell properties at the gene level could have caused microtia but chondrocytes isolated from microtia patients still have the potential to be used as a cell source in ear reconstruction.,Master | - |
| dc.language.iso | may | - |
| dc.publisher | UKM, Kuala Lumpur | - |
| dc.relation | Faculty of Medicine / Fakulti Perubatan | - |
| dc.rights | UKM | - |
| dc.subject | Rawan aurikular | - |
| dc.subject | Mikrotia | - |
| dc.subject | Cartilage aurikular | - |
| dc.subject | Microtia | - |
| dc.subject | Dissertations, Academic -- Malaysia | - |
| dc.title | Pencirian dan potensi regenerasi rawan aurikular manusia dari tisu mikrotik | - |
| dc.type | theses | - |
| dc.format.pages | 94 | - |
| Appears in Collections: | Faculty of Medicine / Fakulti Perubatan | |
Files in This Item:
| File | Description | Size | Format | |
|---|---|---|---|---|
| ukmvital_80484+SOURCE1+SOURCE1.0.PDF Restricted Access | 5.59 MB | Adobe PDF |  View/Open |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.