scholarly journals Penggunaan Tetes Telinga Serum Autologous dengan Amnion untuk Penutupan Perforasi Membran Timpani

2012 ◽  
Vol 1 (1) ◽  
Author(s):  
Hidayatul Fitria ◽  
Yan Edward
Keyword(s):  
Growth Factor ◽  
Tympanic Membrane ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Tympanic Membrane Perforation ◽  
Autologous Serum ◽  
Membrane Perforation ◽  
Epidermal Growth ◽  
Tgf Β1

Abstrak Latar Belakang: Gangguan pendengaran atau ketulian mempunyai dampak yang merugikan bagi penderita , keluarga, masyarakat maupun negara. Salah satu penyebab ketulian yang sering dijumpai adalah radang telinga tengah, terutama yang disertai perforasi membran timpani yang menetap. Penutupan perforasi membran timpani dapat dilakukan dengan operatif dan konservatif. Secara konservatif sudah banyak cara yang dilakukan. Salah satunya dengan mengkaustik tepi perforasi dengan menggunakan silver nitrat untuk membuat luka baru, kemudian digunakan amnion sebagai jembatan (bridge) dan faktor regulasi yang terdapat pada tetes telinga serum autologous. Tujuan: Untuk menjelaskan gambaran penggunaan amnion sebagai jembatan dan tetes telinga serum autologous sebagai faktor regulasi. Tinjauan pustaka: Penutupan perforasi membran timpani dapat dilakukan secara konservatif salah satunya dengan menggunakan tetes telinga serum autologous sebagai faktor regulator, amnion sebagai jembatan dan penggunaan silver nitrat pada tepi perforasi untuk membuat luka baru. Serum autologous memiliki asselerator pertumbuhan yaitu epidermal growth factor (EGF) , transforming growth factor β1 (TGF- β1) dan fibronektin. Asselerator pertumbuhan ini dapat kita temukan pada penyembuhan membran timpani normal. Sedangkan membran amnion adalah jaringan semi transparan tipis yang membentuk lapisan terdalam membran fetus dengan susunan membran basalis yang tebal dan jaringan stroma avaskuler. Membran amnion mempercepat pembentukan epitel normal dengan menekan pembentukan jaringan fibrosis. Sel epitel amnion memproduksi faktor pertumbuhan seperti fibroblast growth factor dan transforming growth factor beta. Faktor pertumbuhan akan membantu komunikasi antara epitel dan sel fibroblast stroma untuk menekan proliferasi dan diferensiasi jaringan fibrosis. Kesimpulan: Diperlukan tiga elemen pada penutupan perforasi membran timpani yaitu faktor regulasi, jembatan (bridge) dan membuat luka baru pada tepi perforasi. Kata kunci: tetes telinga serum autologous, membran amnion, perforasi membran timpani Abstract Background: Hearing loss or deafness have an adverse impact on patients, families, communities and the country. One cause of deafness that often met is middle ear inflammation, especially those with persistent tympanic membrane perforation. Closure of tympanic membrane perforation can be performed with operative and conservative. The conservatives have done with a lot of ways. One of them is cauterize edge of perforation by using silver nitrate to make a new wound, then used the amnion as a bridge and regulatory factors present in autologous serum eardrops. Objective: To describe the use of amnion as a bridge and autologous serum eardrops as a regulatory factor. Literature review: Closure of tympanic membrane perforation conservatively can be done either by using the autologous serum eardrops as a factor regulator, amnion as a bridge and the use of silver nitrate on the edge of the perforation to create a new wound. Autologous serum have asselator growth of Epidermal Growth Factor (EGF), Transforming Growth Factor β1 (TGF-β1) and fibronectin. Asselerator growth factor can be found on normal tympanic membrane healing. While the amniotic membrane is semi-transparant thin tissue that forms the deepest layer of fetal membranes with formation of a thick basement membrane and tissue stroma avaskuler. Amniotic membrane accelerate the formation of normal epithelial tissue by pressing the formation of fibrosis. Amniotic epithelial cells produce growth factors such as fibroblast growth factor and transforming growth factor beta. Growth factors will help the communication between epithelial and stromal fibroblast cells to suppress proliferation and differentiation of tissue fibrosis. Conclusion: It takes three elements on the closure of tympanic membrane perforation factor regulation, bridge and make new cuts on the edge of the perforation. Keywords: autologous serum eardrops, amnion membrane, tympanic membrane perforation

Topical Application of Epidermal Growth Factor (EGF) to Changes in Tympanic Membrane Perforation Diameter

2018 ◽  
Vol 18 (4) ◽  
pp. 186-191 ◽  
Author(s):  
Riskiana Djamin ◽  
Raihanah Aziza ◽  
Sutji Pratiwi Rahardjo ◽  
Eka Savitri ◽  
Abdul Qadar Punagi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Tympanic Membrane ◽  
Topical Application ◽  
Tympanic Membrane Perforation ◽  
Membrane Perforation ◽  
Epidermal Growth

The proliferative responses of porcine thyroid follicular cells to epidermal growth factor and thyrotrophin reflect the autocrine production of transforming growth factor-β1

1996 ◽  
Vol 148 (1) ◽  
pp. 87-94 ◽  
Author(s):  
A J Cowin ◽  
E L Heaton ◽  
S H Cheshire ◽  
S P Bidey
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Transforming Growth Factor ◽  
Thymidine Incorporation ◽  
Transforming Growth Factor Β1 ◽  
Follicular Cells ◽  
Stimulatory Action ◽  
Thyroid Follicular Cells ◽  
Epidermal Growth ◽  
Tgf Β1

Abstract The present study has investigated an involvement of autocrine transforming growth factor-β1 (TGF-β1) in regulating the proliferative response of porcine thyroid follicular cells (TFCs) to epidermal growth factor (EGF) and TSH. Primary monolayer TFC cultures exposed to EGF over the range 0–0·4 nmol/l showed a dose-dependent increase in [methyl-3H]thymidine incorporation, whereas higher EGF doses were associated with a reduction in the level of [methyl-3 H]thymidine incorporation. TGF-β immunoneutralisation had little effect on the stimulatory action of low EGF doses, but led to an increase in [methyl-3H]thymidine incorporation at higher EGF levels. In TFC cultures exposed to TSH, the level of [methyl-3H]thymidine incorporation attained at a dose of 1 U TSH/1 was enhanced in the presence of TGF-β1 antiserum, although the similar stimulatory effect of 8-bromo cAMP was unaffected. Treatment of TFCs with phorbol 12-myristate 13-acetate (8 nmol/l) to activate protein kinase C (PKC) led to an enhanced incorporation of [methyl-3H]thymidine which was increased further after neutralisation of endogenous TGF-β1. While confirming, therefore, a role for autocrine TGF-β1 in maintaining control of TFC DNA synthesis in vitro, these findings provide evidence that an increase in the availability of autocrine TGF-β1 effected by EGF and TSH may play an instrumental role in limiting the cellular hyperplasia induced by these factors within the thyroid follicular microenvironment. Moreover, the present data also suggest that the availability of active autocrine TGF-β1 to TFCs under such conditions may be dependent upon a PKC-mediated mechanism. Journal of Endocrinology (1996) 148, 87–94

scholarly journals Transforming growth factor-β1 and activin A generate antiproliferative signaling in thyroid cancer cells

2006 ◽  
Vol 190 (1) ◽  
pp. 141-150 ◽  
Author(s):  
Sílvia Emiko Matsuo ◽  
Suzana Garcia Leoni ◽  
Alison Colquhoun ◽  
Edna Teruko Kimura
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Intracellular Signaling ◽  
Target Genes ◽  
Transforming Growth Factor ◽  
Carcinoma Cell ◽  
Transforming Growth Factor Β1 ◽  
Activin A ◽  
Antiproliferative Signaling ◽  
Tgf Β1

Transforming growth factor-beta 1 (TGF-β1) and activin A (ActA) induce similar intracellular signaling mediated by the mothers against decapentaplegic homolog (SMAD) proteins. TGF-β1 is a potent antimitogenic factor for thyroid follicular cells, while the role of ActA is not clear. In our study, the proliferation of TPC-1, the papillary thyroid carcinoma cell line, was reduced by both recombinant ActA and TGF-β1. Due to the concomitant expression of TGF-β1 and ActA in thyroid tumors, we investigated the effects of either TGF-β1 or ActA gene silencing by RNA interference in TPC-1 cells in order to distinguish the specific participation of each in proliferation and intracellular signaling. An increased proliferation and reduced SMAD2, SMAD3, and SMAD4 mRNA expression were observed in both TGF-β1 and ActA knockdown cells. Recombinant TGF-β1 and ActA increased the expression of inhibitory SMAD7, whereas they reduced c-MYC. Accordingly, we detected a reduction in SMAD7 expression in knockdown cells while, unexpectedly, c-MYC was reduced. Our data indicate that both TGF-β1 and ActA generate SMADs signaling with each regulating the expression of their target genes, SMAD7 and c-MYC. Furthermore, TGF-β1 and ActA have an antiproliferative effect on thyroid papillary carcinoma cell, exerting an important role in the control of thyroid tumorigenesis.

scholarly journals HUBUNGAN ANTARA KADAR TGF-Β1 DENGAN KADAR ALBUMIN DALAM URIN PASIEN DM TIPE-2 DENGAN NEFROPATI DIABETIK

2019 ◽  
Vol 7 (1) ◽  
pp. 73-81
Author(s):  
Elfiani Elfiani ◽  
Rita Halim ◽  
M Haldian Hakir
Keyword(s):  
Diabetic Nephropathy ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Albumin Level ◽  
Cross Sectional ◽  
Integrin Linked Kinase ◽  
Tgf Β1

ABSTRACT Background: Diabetic nephropathy (DN) is a complication of diabetes in the kidney that frequently causes terminal kidney disease. This kidney disease caused by diabetes is a syndrome characterized by albumin in urine (albuminuria). Growth factor-β1 (TGF- β1) is a multifunctional cytokine that controls many biological processes, including immunity, differentiation, tumor suppression, tumor metastasis, aging, migration, wound healing, apoptosis, adipogenesis, and osteogenesis. Previous studies had showed that TGF-β1 plays a role in albuminuria, where TGF-β1 expression in the kidney increases in diabetes patients. Elevation of cytokine level, especially transforming growth factor beta-1 (TGF-β1) that induces the increase of several extra cellular matrices (ECM), i.e. fibronectin, integrin-linked kinase (ILK) and type IV collagen. This TGF-β1 activity causes the accumulation of ECM, which leads to thickened glomerular basement membrane (GBM). Thickening of GBM and changes in kidney structure in the form of hypertrophy and reduced glomerular podocytes caused by apoptosis and attachment in GBM causes protein components to exit through urine (albuminuria). This study aimed to prove the correlation between transforming growth factor-β1 and albumin level in urine of diabetic nephropathy. Metode : This study a observasional with desain Cross-sectional  comparative study. Results: Mean TGF-β1 level in type 2 DM patients with diabetic nephropathy in this study was 47.30 ± 14.70 ng/ml, with similar value between men and women with 43.1 ng/ml and 44.7 ng/ml, respectively. Out of 60 type 2 DM participants with ND, the mean albuminuria level according to ACR was 722.53 ± 1854.96 mg/g. The result of male participants was lower compared to female participants, with 667.8 mg/mg and 777.2 mg/g, respectively. Conclusion: There was insignificant correlation between TGF-β1 in diabetic nephropathy (DN) and albumin level in urine measured using albumin and urine creatinine ratio (ACR) (p = 0.066). Keywords: Diabetic Nephropathy, Albuminuria, TGF-β1   ABSTRAK Latar Belakang : Nefropati diabetik (ND) merupakan komplikasi diabetes pada ginjal yang paling sering menyebabkan terjadinya penyakit ginjal terminal. Penyakit ginjal akibat diabetes ini merupakan sindroma dengan karakteristik terdapatnya albumin dalam urine (albuminuria). Faktor pertumbuhan-β1 (TGF-β1) adalah sebuah sitokin multifungsi yang mengendalikan banyak proses biologis termasuk kekebalan, diferensiasi, tumor supresi, tumor metastasis, penuaan, migrasi, penyembuhan luka, apoptosis, adipogenesis, dan osteogenesis. Sejumlah penelitian sebelumnya menunjukkan bahwa TGF-β1 berperan terhadap terjadinya albuminuria, dimana pasien diabetes didapatkan ekspresi TGF-β1 di ginjal meningkat. Peningkatan kadar cytokine terutama Transforming Growth Factor Beta-1 (TGF-β1) yang menginduksi peningkatan beberapa Extra Cellular Matrix (ECM) antara lain fibronectin, integrin-linked kinase (ILK) dan collagen tipe-IV. Aktifitas TGF-β1 ini menyebabkan akumulasi ECM sehingga terjadi penebalan Glomerular Basement Membrane (GBM). Penebalan dari GBM dan terjadinya perubahan struktur ginjal berupa hipertrofi dan berkurangnya sel-sel podocyte glomerulus akibat kerusakan (apoptosis) dan perlengketan di GBM menyebabkan komponen protein keluar melalui urin (albuminuria). Tujuan penelitian ini untuk membuktikan hubungan antara kadar transforming growth  factor-β1 dengan kadar albumin dalam urin pada Nefropati Diabetik. Metode : Penelitian ini merupakan penelitian Observasional dengan desain Cross-sectional   comparative study. Hasil : Kadar rata-rata TGF-β1 pasien DM tipe-2 dengan Nefropati Diabetik pada penelitian ini adalah 47,30 ± 14,70 ng/ml, tidak jauh berbeda antara laki-laki yaitu 43,1 ng/ml dengan perempuan 44,7 ng/ml. Dari 60 orang responden DM tipe-2 dengan ND pada penelitian ini didapatkan kadar albuminuria rata-rata berdasarkan ACR adalah 722,53 ± 1854,96 mg/g. Responden laki-laki lebih rendah dibanding perempuan yaitu 667,8 mg/g berbanding 777,2 mg/g. Kesimpulan : Tidak terdapat hubungan yang bermakna antara TGF-β1 pada Nefropati Diabetik (ND) dengan kadar albumin dalam urin yang dihitung berdasarkan rasio albumin dan creatinin urin (ACR) (p=0,066). Kata Kunci : Nefropati Diabetik, Albuminuria, TGF-β1

TGF-β1-mediated hypertrophy involves inhibiting pRB phosphorylation by blocking activation of cyclin E kinase

1999 ◽  
Vol 277 (2) ◽  
pp. F186-F194 ◽  
Author(s):  
Baolian Liu ◽  
Patricia Preisig
Keyword(s):  
Growth Factor ◽  
Cell Cycle Progression ◽  
Growth Response ◽  
Transforming Growth Factor ◽  
Cyclin E ◽  
Transforming Growth Factor Β1 ◽  
Cycle Progression ◽  
Hypertrophic Growth ◽  
Epidermal Growth ◽  
Tgf Β1

When renal epithelial cells are exposed to epidermal growth factor-transforming growth factor-β1 (EGF-TGF-β1) the typical EGF-mediated hyperplastic growth response is converted to a hypertrophic growth response. Hypertrophy in this setting involves cell entrance into G1, but arrest of cell cycle progression at the G1/S interface. Late G1 arrest is mediated by retaining retinoblastoma protein (pRB) in its active, hypophosphorylated state. The present studies examine the mechanism by which pRB is retained in its active state. The results demonstrate that TGF-β1-mediated conversion of hyperplasia to hypertrophy involves preventing activation of cdk2/cyclin E kinase but has no effect on cdk4(6)/cyclin D kinase activity. Preventing activation of cyclin E kinase is associated with 1) decreased abundance of cdk2/cyclin E complexes and 2) retention of p57Kip2 in formed cdk2/cyclin E complexes. The development of hypertrophy does not involve regulation of either cdk2, cyclin E, or cdc25A protein abundances, or the abundance of p27Kip1 or p21 in formed complexes.

scholarly journals Transforming Growth Factor β1 and Tropoelastin Expression in Uterine Prolapse

2016 ◽  
pp. 70
Author(s):  
Alvilusia Alvilusia ◽  
Amir Fauzi ◽  
Azhari Azhari ◽  
Wresnindyatsih Wresnindyatsih ◽  
Irsan Saleh
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Uterine Prolapse ◽  
Transforming Growth Factor Β1 ◽  
Moderate Correlation ◽  
Cross Sectional ◽  
Positive Correlation ◽  
Growth Factor Beta ◽  
Tgf Β1

Objective: To know the correlation of the expression of transforming growth factor beta (TGF-β1) and tropoelastin in uterine prolapse. Method: A cross-sectional study of 30 subjects suffered from uterine prolapse in the Department of Obstetrics and Gynecology Dr. Mohammad Hoesin hospital Palembang. The study was conducted since December 1st, 2014 until July 31st, 2015. The sample was from the sacrouterine ligament and immunohistochemical examination was conducted to see the expression of TGF-β1 and tropoelastin. Result: Of the 30 subjects obtained, the expression of TGF-β1 was on 30 subjects consisting of 18 (60%) for weak expression and 12 (40%) for strong expression. Meanwhile, the strong tropoelastin expression was on 18 subjects (60%) and weak tropoelastin expression on 12 subjects (40%). There was a positive correlation between TGF-β1 and tropoelastin expression with moderate correlation (p=0.014; r=0.44). Conclusion: There is a positive correlation between the TGF-β1 and tropoelastin expression of sacrouterine ligament in uterine prolapse with moderate correlation. [Indones J Obstet Gynecol 2016; 4-2: 70-74] Keywords: transforming Growth Factor Beta 1, tropoelastin, uterine prolapse

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