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Abstrak :
Selama oogenesis, oosit tumbuh dalam ukuran dan memperoleh kompetensi pematangannya. Kompetensi pematangan oosit sangat diperlukan untuk mendukung terjadinya fertilisasi dan perkembangan embrio berkualitas baik. Ketidakmampuan untuk menentukan oosit yang berpotensi menghasilkan embrio yang viable masih menjadi kendala utama pada proses Fertilisasi In Vitro (FIV). Penelitian ini bertujuan mengetahui apakah ukuran diameter oosit bisa menjadi prediktor kualitas oosit dan embrio. Penelitian ini menggunakan desain penelitian prospektif cohort. Metode penelitian untuk pengukuran diameter oosit menggunakan aplikasi Image J, setiap oosit dan sel granulosa dikelompokkan sesuai ukuran diameter oosit, oosit dilakukan fertilisasi dengan teknik ICSI/IMSI kemudian diikuti perkembangan embrio sampai hari ke-5. Pemeriksaan ELISA dipakai untuk mengkonfirmasi kualitas oosit dengan melihat kadar protein Akt dan total Akt pada sel granulosa kumulus oosit, sedangkan untuk mengkonfirmasi kualitas embrio adalah dengan melihat parameter morfokinetik embrio, pencapaian blastokista dan frekuensi abnormalitas pembelahan. Hasil penelitian menunjukkan tidak ada perbedaan signifikan (P>0,05) pada kadar protein p-Akt dan total Akt sel granulosa kumulus antara ketiga kelompok. Selain itu pengamatan morfokinetik embrio menunjukkan tidak ada perbedaan signifikan (P>0.05) kecuali parameter S2, begitu pula dengan pencapaian blastokista serta frekuensi abnormalitas pembelahan kecuali parameter reverse cleavage (RC). Kesimpulan yang didapat dari penelitian ini adalah ukuran diameter oosit tidak mempengaruhi kualitas oosit dan embrio. Ukuran diameter oosit tidak bisa menjadi prediktor kualitas oosit dan embrio, karena tidak ada perbedaan signifikan pada kualitas oosit dan embrio ketiga kelompok. Oosit dengan ukuran diameter kecil memiliki potensi untuk menjadi embrio dengan kualitas baik. ......During oogenesis, oocytes grow in size and acquire maturation competence. Oocyte maturation competence is necessary to support fertilization and the development of good quality embryos. The inability to determine which oocytes have the potential to produce viable embryos remains a major obstacle in the In Vitro Fertilization (IVF). This study aims to determine whether oocyte diameter can be a predictor of oocyte and embryo quality. This study used a prospective cohort research design. The method used for measuring oocyte diameter using Image J application. Each oocyte and cumulus granulosa cells is grouped according to the size of oocyte diameter, oocyte are fertilized with ICSI/IMSI techniques and then followed by embryo development until day 5. ELISA examination is used to confirm oocyte quality by looking at p-Akt and Akt total protein levels in oocyte cumulus granulosa cells, while to confirm embryo quality by looking at the morphokinetic embryo, blastocyst achievement and frequency of cleavage abnormalities. The results showed no significant difference (P>0.05) in p-Akt and Akt total protein levels in cumulus granulosa cells between the three groups. In addition, morphokinetic observation of embryos showed no significant difference (P>0.05) except S2 parameter, as well as the achievement of blastocyst and the frequency of cleavage abnormalities except the reverse cleavage (RC) parameter. The conclusion obtained from this study is that the size of the oocyte diameter does not affect the quality of oocytes and embryos. Oocytes diameter size can not be a predictor of oocyte and embryo quality, because there is no significant difference in the quality of oocytes and embryos of the three groups. Oocytes with a small diameter size have the potential to become embryos with good quality.

Abstrak :
Mukopolisakaridosis tipe II (MPS II) merupakan penyakit kelainan lisosomal langka yang disebabkan oleh mutasi pada gen iduronat 2-sulfatase (IDS) dapat menyebabkan disfungsi dari enzim I2S yang dihasilkan sehingga molekul heparan sulfat (HS) dan dermatan sulfat (DS) terakumulasi pada jaringan. Penelitian ini dilakukan untuk mengetahui dan menganalisis hubungan kadar HS dan DS urin dengan jenis mutasi gen IDS pada penderita MPS II di Indonesia. Data susunan nukleotida gen IDS dari tujuh pasien MPS II dianalisis untuk melihat jenis mutasi dan dibuat model 3D proteinnya. Analisis 3D protein akan dikorelasikan dengan kadar HS dan DS urin pasien tersebut yang diukur menggunakan metode Enzyme-Linked Immunosorbent Assay (ELISA). Hasil analisis mutasi ditemukan beberapa jenis mutasi, seperti mutasi nonsense (1/7), delesi (2/7), insersi (1/7), dan missense (3/7). Dari ketujuh pasien tersebut, tiga diantaranya (P2, P6, P7) telah menjalani terapi ERT. Kadar HS urin dari ketujuh pasien menunjukkan peningkatan yang beragam dibandingkan dengan kadar HS normal. Berbeda dengan HS, kadar DS urin sampel pasien ada yang mengalami sedikit peningkatan (P1, P2, P7) dan ada pula yang tetap berada pada rentang kadar DS normal (P3, P4, P5, P6). Keragaman kadar HS dan DS sampel pasien tersebut sangat dipengaruhi oleh letak mutasi, jenis mutasi, diagnosis dan prognosis yang ditegakkan sedini mungkin, terapi ERT yang telah dilakukan pasie, durasi ERT, dan respon masing-masing pasien terhadap pengobatan yang telah diberikan. ......Mucopolysaccharidosis type II (MPS II) is a rare lysosomal disorder caused by mutations in the iduronat 2-sulfatase (IDS) gene that can cause dysfunction of I2S enzyme so that the heparan sulfate (HS) and dermatan sulfate (DS) molecules accumulate in the tissue. This study was conducted to determine and analyze the relationship of urinary HS and DS levels with the type of IDS gene mutation in MPS II patients in Indonesia. The nucleotide of IDS genes sequences from seven MPS II patients were analyzed to see the type of mutation and the 3D protein model was made. 3D protein analysis will be correlated with urinary HS and DS levels of the patients measured by using the Enzyme-Linked Immunosorbent Assay (ELISA) method. Results of mutation analysis results found several types of mutations, such as nonsense mutations (1/7), deletions (2/7), insertions (1/7), and missense (3/7). From the seven patients, three of them (P2, P6, P7) had undergone ERT therapy. The urine HS level of the seven patients showed a varied increase compared to normal HS levels. In contrast to HS, the urine DS level of the sample of patients had a slight increase (P1, P2, P7) and some remained in the normal DS level range (P3, P4, P5, P6). The diversity of HS and DS levels of the patient's samples is strongly influenced by the location of the mutation, type of mutation, diagnosis and prognosis that is enforced as early as possible, ERT therapy has been carried out, ERT duration, and each patient's response to the treatment given.

Abstrak :
ABSTRAK
LATAR BELAKANG: Proses remodelling tulang ditentukan oleh keseimbangan antara proses pembentukan oleh osteoblast dan resorpsi sel tulang oleh osteoklas. Osteprotegerin (OPG) memiliki peran penting dalam menghambat proses resorpsi tulang oleh osteoklas. Pada wanita menopause, proses resorpsi lebih tinggi daripada proses pembentukan tulang, sehingga dapat mengakibatkan terjadinya osteoporosis. Pada penelitian ini, single nucleotide polymorphisms (SNPs) pada daerah promoter gen OPG diteliti untuk mengetahui hubungannya dengan risiko osteoporosis pada wanita menopause.

BAHAN dan CARA KERJA: Penelitian ini melibatkan 285 wanita Indonesia menopause yang terdiri dari 81 wanita normal, 143 wanita dengan osteopenia dan 61 wanita dengan osteoporosis. Angka T-score diperoleh dengan pengukuran menggunakan Ultrasound Densitometry. Analisis genetik dilakukan menggunakan teknik PCR-RFLP. Analisis statistik menggunakan uji chi-square dengan asumsi kemaknaan p<0,05.

HASIL: Hasil penelitian memperlihatkan bahwa frekuensi genotip (TT, TC dan CC) pada semua kelompok (normal, osteopenia dan osteoporosis) tidak berbeda bermakna (p>0,05). Frekuensi alotip (alel T dan C) pada semua kelompok juga tidak berbeda bermakna (p>0,05). Hasil perhitungan odd ratio dengan menggunakan genotip TT sebagai pembanding memperlihatkan bahwa genotip CC memiliki kemungkinan mengalami gangguan kelainan tulang (osteopenia dan osteoporosis) 0,29 kali (22%) dan TC 0,88 kali (46%) lebih besar dibandingkan dengan genotip TT. Dari hasil penelitian ini, dapat disimpulkan bahwa SNP T950C tidak memiliki peranan dalam kejadian osteoporosis pada wanita menopause di Indonesia.

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ABSTRACT
INTRODUCTION: Bone remodelling process is determined by the balance between the bone formation and resorption. Osteoprotegerin (OPG) has an important role to inhibit bone resorption by osteoclast. In menopausal women, the rate of bone resorption is higher than its formation, thereby inducing osteoporosis. In this study, single nucleotide polymorphism (SNPs) in promoter region of gene OPG is studied regarding to the association to the risk of the osteoporosis in menopausal Indonesian women.

MATERIAL and METHODS: The study samples consist of 285 menopausal Indonesian women, of which 81 are classified as normal (healthy), 143 are with osteopenia and 61 are with osteoporosis. T-score is obtained from the measurement using Ultrasound Densitometry, and genetic polymorphism analysis was performed by PCR RFLP. The statistical analysis uses chi-square with significance assumption at p<0.05.

RESULT: This study shows the frequency of genotypes (TT, TC and CC) to all groups (normal, osteopenia and osteoporosis), but it does not demonstrate any significant differences (p>0.05). The frequency of allotypes (T and C) to all groups also does not show the significance (p>0.05). Odd ratio calculations demonstrate that the possibility of developing bone disorders (osteopenia and osteoporosis) for both CC genotype and TC genotype is higher than TT genotype, as much as 0.29 times higher (22%) and 0.88 times higher (46%), respectively.

Abstrak :
Ameloblastoma merupakan tumor jinak yang berkembang lambat, bersifat invasif secara lokal dan sering terjadi rekurensi. Ameloblastoma tipe multikistik/padat merupakan tipe yang paling sering ditemukan. Cell adhesion molecules (CAMs) mempunyai peranan penting dalam proses morfogenesis jaringan pada saat perkembangan dan mempertahankan diferensiasi jaringan pada organisme dewasa. Faktor adhesi seluler dan motility merupakan mekanisme yang bertanggung jawab terhadap inisiasi dan perkembangan tumor. E-cadherin adalah molekul adhesi antar sel paling berpengaruh dalam adherens junction yang menjaga sel epitel melekat satu sama lain. Hilangnya fungsi protein E-cadherin sebagai tumor suppresor berhubungan dengan meningkatnya sifat invasif dan metastasis tumor. Tujuan penelitian ini adalah untuk menganalisis ekspresi Ecadherin pada ameloblastoma multikistik/padat pola folikuler, pola pleksiformis, dan pola campuran. Metode penelitian : 52 kasus ameloblastoma multikistik/padat dilakukan pemeriksaan ekspresi E-cadherin secara imunohistokimia. Hasil penelitian dievaluasi secara semikuantitatif, dengan melihat persentase sel tumor yang terpulas dan intensitas pulasan. Hasil : sampel penelitian berjumlah 52 (18 pola folikuler, 14 pola pleksiformis, dan 20 pola campuran). Secara imunohistokimia E-cadherin terekspresi pada lebih dari 50% sel tumor. Analisis secara statistik menunjukkan tidak terdapat perbedaan yang bermakna antara ketiga pola ameloblastoma multikistik/padat (p>0,05). Kesimpulan : pada hasil penelitian tampak bahwa ekspresi E-cadherin antara ketiga pola ameloblastoma multikistik/padat tidak menunjukkan perbedaan bermakna. ......Ameloblastoma is a benign tumor that slow-growth, locally invasive and high rate of recurrence. Ameloblastoma multicystic/solid is the most commonly found. Cell adhesion molecules (CAMs) have an important role, in the process of tissue morphogenesis during development and maintaining tissue differentiation in the adult organism. Cellular adhesion and motility factor is the mechanism responsible for tumor initiation and progression. E-cadherin is the most important cell adhesion molecules in the adherens junctions that maintain epithelial cells attached to one another. Loss of function of E-cadherin as tumor suppresor protein associated with increased invasive and metastatic behavior of tumor. The purpose of this study was to analyze the expression of E-cadherin of multicystic/solid ameloblastoma in the follicular pattern, plexiform pattern, and mixed pattern. Method : E-cadherin expression of 52 cases of multicystic/solid ameloblastoma investigated by immunohistochemical. The results were evaluated semiquantitatively, by investigating the percentage immunopositive of tumor cells and intensity of staining. Results: 52 sample (18 follicular pattern, 14 plexiform pattern and 20 mixed pattern). E-cadherin expressed on more than 50% of tumor cells. Statistical analysis showed no significant difference among the three patterns ameloblastoma multicystic (p>0,05). Conclusion: The expression of Ecadherin among the three patterns ameloblastoma multicystic/solid showed no significant difference.

Abstrak :
Latar belakang: Mukopolisakaridosis (MPS) tipe II adalah kelainan genetik yang ditandai dengan gangguan metabolik berupa defisiensi enzim iduronat-2-sulfatase (I2S) karena adanya mutasi pada gen iduronat-2-sulfatase (IDS), sehingga heparan sulfat dan dermatan sulfat tidak terdegradasi dan terakumulasi pada jaringan. Penelitian ini dilakukan untuk menganalisis aktivitas spesifik enzim I2S dan kaitannya dengan varian mutasi gen IDS pada pasien MPS II di Indonesia. Metode: Data sekuen nukleotida gen IDS dari enam pasien MPS II dianalisis untuk melihat jenis mutasi serta dibuat model konformasi proteinnya. Sel peripheral blood mononuclear cell (PBMC) diisolasi menggunakan metode sentrifugasi bertingkat dan dikultur menggunakan medium RPMI. Nilai aktivitas spesifik I2S diperoleh dengan mengukur aktivitas I2S per miligram konsentrasi total protein. Aktivitas enzim I2S diukur menggunakan metode fluorometri, sementara konsentrasi total protein diukur menggunakan bicinchoninic acid (BCA) protein assay.  Hasil: Tiga varian mutasi yang ditemukan pada pasien MPS tipe II adalah missense (3/6), delesi (2/6), dan nonsense (1/6). Aktivitas enzim spesifik I2S pada pasien menunjukkan angka yang bervariasi. Mutasi dengan rata-rata aktivitas spesifik I2S paling rendah sampai paling tinggi secara berurutan adalah mutasi delesi (0,026 nmol/min/mg), missense (0,052 nmol/min/mg), dan nonsense (0,052 nmol/min/mg).  Kesimpulan: Aktivitas spesifik enzim I2S pada pasien MPS tipe II di Indonesia 0,044 nmol/min/mg, sedangkan pada kontrol adalah 0,172 nmol/min/mg. Nilai rata-rata aktivitas spesifik I2S pada pasien menurun empat kali lipat dibandingkan pada kontrol.

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Background: Mucopolysaccharidosis type II (MPS II) is an inherited metabolic disorder that caused by iduronate-2-sulfatase (I2S) enzyme deficiency due to mutations in the iduronate-2-sulfatase (IDS) gene, so that heparan sulfate and dermatan sulfate do not be degrade and accumulate in tissues. This study was conducted to analyze the specific activity of I2S and its relationship to IDS variant mutation of MPS II patients in Indonesia. Method: IDS gene nucleotide sequences from six MPS II patients were analyzed to see mutation type and protein conformation model was made. Peripheral blood mononuclear cell (PBMC) were isolated using a stratified centrifugation and cultured using the RPMI medium. I2S specific activity values are obtained by measuring I2S activity per milligram of total protein concentration. I2S enzyme activity was measured using fluorometry method, while total protein concentration was measured using bicinchoninic acid (BCA) protein assay. Result: There were three variant mutation in MPS II patients, such as missense (3/6), deletion (2/6), and nonsense (1/6). I2S specific enzyme activity shows varying numbers. IDS mutation based on I2S specific activity from lowest to highest mean value are deletion (0.026 nmol/min/mg), missense (0.052 nmol/min/mg), and nonsense (0.052 nmol/min/mg). Conclusion: I2S specific activity in MPS II patient is 0,044 nmol/min/mg, while the control is 0,172 nmol/min/mg based on the mean value. I2S specific activity in patients decreased four times compared to controls.

Abstrak :
[ABSTRAK
Doksorubisin merupakan salah satu antikanker golongan antrasiklin yang efektif, untuk keganasan di darah. Akan tetapi, seperti antikanker konvensional pada umumnya, penggunaan doksorubisin dapat menyebabkan berbagai efek samping pada organ lain, misalnya pada testis sehingga penggunaannya di klinis menjadi terbatas. Hal ini disebabkan karena mekanisme antikanker doksorubisin dapat juga menimbulkan toksisitas pada testis. Peningkatan stress oksidatif adalah salah satu mekanisme dapat menyebabkan kerusakan pada organ tersebut. Mangiferin sebagai zat antioksidan alami, terkandung dalam Mangifera Indica L. diperkirakan dapat digunakan untuk mengurangi toksisitas testis. Namun sampai saat ini, belum ada penelitian yang mengeksplor efek proteksi mangiferin terhadap kerusakan oksidatif testis yang diinduksi doksorubisin. Penelitian ini menggunakan tikus jantan Sprague Dawley, yang dibagi menjadi empat kelompok. Masing-masing kelompok terdiri dari enam ekor tikus. Tikus pada kelompok kontrol negatif diberikan doksorubisin secara intraperitoneal (dosis total 15 mg/kgBB) dan kelompok normal diberikan NaCl 0,9%. Mangiferin (dosis 30 dan 60 mg/kg BB) diberikan oral selama tujuh minggu. Setelah, tujuh minggu tikus dimatikan dan testis dikumpulkan untuk analisis parameter stress oksidatif biokimia kadar MDA (malonedyaldehide), aktivitas SOD (Superoxide Dysmutase), perubahan histologi dan apoptosis kaspase-9 dan kaspase-12. Hasil penelitian menunjukkan bahwa pemberian doksorubisin selama dua minggu dapat meningkatkan kadar MDA, menyebabkan kerusakan sel spermatogenik, sel Sertoli dan penciutan diameter tubulus seminiferus testis, peningkatan ekspresi kaspase-9 di sisi luminal yang diberikan doksorubisin. Pemberian mangiferin dosis 30 dan 60 mg/kg BB selama tujuh minggu dapat mengurangi kerusakan sel spermatogenik dan sel Sertoli tubulus seminiferus testis, penurunan kadar MDA dan penurunan ekspresi kaspase-9 pada kelompok perlakuan diberikan doksorubisin dan mangiferin. Perbaikan parameterparameter ini mengindikasikan bahwa mangiferin mempunyai efek proteksi terhadap kerusakan sel spematogenik dan sel sertoli tubulus seminiferus testis tikus yang diberikan doksorubisin.

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ABSTRACT
Doxorubicin, one of the anthracycline anticancer class, is effective especially in blood malignancy. However, as in the general use of the conventional anticancer-drugs. Doxorubicin can cause various side effects in other organs, such as the testes so that its use in clinical become limited. This is because of the anticancer mechanism can cause cytotoxicity on testes. The increased oxidative stress is the main mechanism that can be the causal. Mangiferin as a natural antioxidant substance, contained in Mangifera Indica L., is expected to reduce the toxicity. The Antioxidants are expected to reduce the toxicity of the testes. But until now, no studies have explored the effects of mangiferin protection against oxidative damage induced testicular doxorubicin. This study used male Sprague Dawley rats, which were divided into four groups. Each group consisted of six mice. Rats in the negative control group was given intraperitoneal doxorubicin (total dose 15 mg/kg) and the normal group was given normal saline 0.9%. Mangiferin (doses of 30 and 60 mg/kg) was administered orally for seven weeks to the treatment gtoups (both DOX and MAG were given). After seven weeks-off, testes of mice were collected for analysis of biochemical parameters i.e. oxidative stress levels of MDA and SOD activity, histology and apoptosis of the caspase-9 and of the caspase-12. The results showed that administration of doxorubicin for two-weeks can cause damage to Sertoli, spermatogenic cells and shrinking of diameter of testicular seminiferous tubules, increasing the levels of MDA, increasing in the expression of caspase-9 on the luminal side in the treatment group was given doxorubicin. This possibility of the doxorubicin dose given is too toxic to the testes in this study. Mangiferin dose administration of 30 and 60 mg / kg for seven-weeks can reduce the damage of Sertoli and spermatogenic cells of the testicular seminiferous tubules, decrease levels of MDA, reduce Sertoli, spermatogenic cell and diameter of the testicular seminiferous tubulus damage, decrease caspase-9 expression only on luminal side of the seminiferus tubulus in the groups given both of doxorubicin and mangiferin. these parameters indicate that mangiferin, which has antioxidant?s activity, provides protective effects against oxidative damage in spematogenic and Sertoli cell testicular seminiferous tubules of mice given doxorubicin, Doxorubicin, one of the anthracycline anticancer class, is effective especially in blood malignancy. However, as in the general use of the conventional anticancer-drugs. Doxorubicin can cause various side effects in other organs, such as the testes so that its use in clinical become limited. This is because of the anticancer mechanism can cause cytotoxicity on testes. The increased oxidative stress is the main mechanism that can be the causal. Mangiferin as a natural antioxidant substance, contained in Mangifera Indica L., is expected to reduce the toxicity. The Antioxidants are expected to reduce the toxicity of the testes. But until now, no studies have explored the effects of mangiferin protection against oxidative damage induced testicular doxorubicin. This study used male Sprague Dawley rats, which were divided into four groups. Each group consisted of six mice. Rats in the negative control group was given intraperitoneal doxorubicin (total dose 15 mg/kg) and the normal group was given normal saline 0.9%. Mangiferin (doses of 30 and 60 mg/kg) was administered orally for seven weeks to the treatment gtoups (both DOX and MAG were given). After seven weeks-off, testes of mice were collected for analysis of biochemical parameters i.e. oxidative stress levels of MDA and SOD activity, histology and apoptosis of the caspase-9 and of the caspase-12. The results showed that administration of doxorubicin for two-weeks can cause damage to Sertoli, spermatogenic cells and shrinking of diameter of testicular seminiferous tubules, increasing the levels of MDA, increasing in the expression of caspase-9 on the luminal side in the treatment group was given doxorubicin. This possibility of the doxorubicin dose given is too toxic to the testes in this study. Mangiferin dose administration of 30 and 60 mg / kg for seven-weeks can reduce the damage of Sertoli and spermatogenic cells of the testicular seminiferous tubules, decrease levels of MDA, reduce Sertoli, spermatogenic cell and diameter of the testicular seminiferous tubulus damage, decrease caspase-9 expression only on luminal side of the seminiferus tubulus in the groups given both of doxorubicin and mangiferin. these parameters indicate that mangiferin, which has antioxidant’s activity, provides protective effects against oxidative damage in spematogenic and Sertoli cell testicular seminiferous tubules of mice given doxorubicin]

Abstrak :
[ABSTRAK
Latar belakang: Proses pematangan sperma terjadi melalui interaksi spermatozoa dengan protein yang disekresikan ke lumen oleh sel epitel epididimis. Sekresi protein pada epididimis ditentukan oleh gen-gen yang terekspresi spesifik di epididimis. Ekspresi gen di epididimis dapat dipengaruhi oleh androgen atau faktor testikular. CD52 telah diketahui terekspresi di epididimis, namun regulasi yang mempengaruhi ekspresi gen CD52 di epididimis belum diketahui. Tujuan dari penelitian ini adalah untuk menganalisis ekspresi dan regulasi gen CD52 agar dapat memprediksi perannya di epididimis mencit. Metode: Analisis bioinformatika dilakukan untuk memprediksi sinyal peptida dan domain fungsional dari CD52. Quantitative real time RT-PCR digunakan untuk mengukur ekspresi relatif gen CD52 pada analisis spesifisitas jaringan, ketergantungan terhadap androgen dan faktor testikular, serta postnatal development. Hasil: CD52 memiliki sinyal peptida yang menunjukkan ciri protein sekretori dan terekspresi secara spesifik di epididimis. Ekspresi CD52 yang tertinggi terdapat di bagian cauda. Ekspresi CD52 pada mencit diregulasi oleh androgen yang ditandai dengan penurunan pada hari pertama dan ketiga setelah digonadektomi dan pemberian testosteron eksogen setelah gonadektomi dapat menjaga ekspresi CD52 50% dari kadar normalnya. Eksperimen dengan memberikan reseptor androgen antagonis (flutamide) juga mendukung bahwa ekspresi CD52 sangat tergantung terhadap androgen. Ekspresi CD52 menurun sangat bermakna hingga mencapai 93% dibandingkan dengan kontrol. Selain androgen, ekspresi CD52 juga dipengaruhi oleh faktor testikular. Ekspresi CD52 mengalami penurunan bermakna dari hari pertama hingga kelima setelah perlakuan efferent duct ligation (EDL) hingga mencapai 75% dari kontrol. Selain itu ekspresi CD52 juga dipengaruhi oleh perkembangan pasca lahir. Ekspresi CD52 meningkat di hari ke-15 hingga hari ke-60 pasca lahir. Kesimpulan: CD52 merupakan gen penyandi protein sekretori yang terekspresi spesifik di epididimis pada region cauda dan regulasinya dipengaruhi oleh androgen, faktor testikular, dan perkembangan pasca lahir.

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ABSTRACT
Background. Epididymal sperm maturation is occurs via interactions between sperm and proteins secreted by epididymal epithelium. These proteins are encoded by genes that are specifically expressed in a region-specific manner. Previous studies have demonstrated that epididymal genes are regulated by androgen and testicular factors. CD52 is an epididymal gene putatively involved in sperm maturation. However, the regulation of its expression in the epididymis has not been fully understood and little is known about its role during sperm maturation process. Therefore, this study was aimed to analyze the expression and regulation of CD52 in the mouse epididymis. Method. Bioinfomatic analyses were perfomed to predict signal peptides and functional domains of CD52. Quantitative real-time RT-PCR was used to analyze tissue distribution, androgen, testicular factors dependency and postnatal development. Results. CD52 amino acid sequence contains a signal peptide, indicating it is a secretory protein. CD52 exhibited region-spesific expression in the epididymis with the highest level was in cauda. Mice CD52 expression was regulated by androgen indicated by a decrease started at day 1 following a gonadectomy. Interestingly, testosterone replacement therapy was able to maintain the expression at 50% of normal level. Experiment by given androgen receptor antagonist, flutamide showed decrease of CD52 expression about 93% than control. It?s confirming that CD52 expression depend on androgen. Moreover, testicular factors also influenced CD52 expression. This was revealed by efferent duct ligation in which CD52 expression was reduced at day 1 to day 5 following the ligation. Finally, CD52 expression was developmentally regulated, this was indicated by increase in the level of expression start at day 15 postnatally. Conclusion: CD52 is a secretory protein and exhibited region-spesific expression in the cauda epididymis. It is regulated by androgen, testicular factors, and also affected by development stage. , Background. Epididymal sperm maturation is occurs via interactions between sperm and proteins secreted by epididymal epithelium. These proteins are encoded by genes that are specifically expressed in a region-specific manner. Previous studies have demonstrated that epididymal genes are regulated by androgen and testicular factors. CD52 is an epididymal gene putatively involved in sperm maturation. However, the regulation of its expression in the epididymis has not been fully understood and little is known about its role during sperm maturation process. Therefore, this study was aimed to analyze the expression and regulation of CD52 in the mouse epididymis. Method. Bioinfomatic analyses were perfomed to predict signal peptides and functional domains of CD52. Quantitative real-time RT-PCR was used to analyze tissue distribution, androgen, testicular factors dependency and postnatal development. Results. CD52 amino acid sequence contains a signal peptide, indicating it is a secretory protein. CD52 exhibited region-spesific expression in the epididymis with the highest level was in cauda. Mice CD52 expression was regulated by androgen indicated by a decrease started at day 1 following a gonadectomy. Interestingly, testosterone replacement therapy was able to maintain the expression at 50% of normal level. Experiment by given androgen receptor antagonist, flutamide showed decrease of CD52 expression about 93% than control. It’s confirming that CD52 expression depend on androgen. Moreover, testicular factors also influenced CD52 expression. This was revealed by efferent duct ligation in which CD52 expression was reduced at day 1 to day 5 following the ligation. Finally, CD52 expression was developmentally regulated, this was indicated by increase in the level of expression start at day 15 postnatally. Conclusion: CD52 is a secretory protein and exhibited region-spesific expression in the cauda epididymis. It is regulated by androgen, testicular factors, and also affected by development stage. ]

Abstrak :
ABSTRAK LATAR BELAKANG: Tatalaksana penyakit Graves (GD) lebih umum dilakukan dengan obat antitiroid, namun lebih dari 50% penderita GD dapat kambuh setelah kondisi remisi. Hal ini dapat dipengaruhi oleh faktor genetik dan lingkungan. Salah satu gen yang meregulasi respon imun GD adalah gen CD40 yang secara umum diekspresikan pada permukaan limfosit B. Penelitian ini bertujuan untuk mengetahui variasi genetik gen CD40 daerah 5?-UTR dan pengaruhnya terhadap kadar sCD40 dalam serum, serta peran faktor klinis dalam memengaruhi kekambuhan pada penderita GD. METODE: Penelitian ini merupakan studi kasus kontrol yang membandingkan 30 penderita GD yang kambuh dan 30 penderita GD yang tidak kambuh setelah obat antitiroid dihentikan. Analisis variasi genetik dilakukan dengan metode PCRRFLP dan pengukuran kadar sCD40 dalam serum dengan metode ELISA. Analisis statistik yang dilakukan adalah uji chi-square, uji t tidak berpasangan dan uji Mann Whitney, dengan kemaknaan p<0,05. HASIL: Variasi genotip dan alotip gen CD40 C/T-1 daerah 5?-UTR serta jenis kelamin tidak menunjukkan hubungan yang bermakna terhadap risiko kekambuhan GD (p>0,05), namun penelitian ini berhasil membuktikan adanya hubungan yang signifikan antara kadar sCD40 dalam serum (p<0,001) dan usia saat diagnosis (p=0,001) dengan risiko kekambuhan pada penderita GD. Hubungan antara variasi genotip gen CD40 dengan kadar sCD40 tidak menunjukkan perbedaan yang bermakna (p>0,05), namun genotip CC dan CT memiliki rerata kadar sCD40 yang lebih tinggi daripada genotip TT. KESIMPULAN: Variasi genetik gen CD40 C/T-1 daerah 5?-UTR tidak berperan dalam peningkatan kadar sCD40 dan risiko kekambuhan GD, namun kadar sCD40 dan usia diagnosis berperan pada kekambuhan GD.

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ABSTRACT Background: The most common of Graves? Disease (GD) treatment is antithyroid drug but more than 50% patients can relapse after remission period. This can be influenced by genetic and environment factors. One of the genes that have regulation on immune response is CD40 gene in the surface of Lymphocyte B. The aim of this research to determine genetic variation in 5?-UTR CD40 gene, association to sCD40 level in serum, and the role of clinical factors that influence the risk for relapse in GD patients. Methods: This research is a case-control study comparing 30 relapse patients and 30 non-relapse patients after treatment with anti-thyroid drug was terminated. Genetic variation was analyzed with PCR-RFLP. Measurement of sCD40 level in the serum had been analyzed by ELISA method. Statistical analyses were chisquare, independent t-test, Mann-Whitney test, a two-tailed p value less than 0.05 was considered significant. Results: Genotype and alleles 5?-UTR CD40 gene variation as well as sex shown no association with risk for relapse (p>0.05), but sCD40 level in serum and age of diagnosis were considered significant with risk for relapse (p=0.001). Association between genotype variation in CD40 gene and sCD40 level were not significant (p>0.05) but sCD40 level in genotype CC and CT were higher than TT. Conclusions: Genetic variation in 5?-UTR CD40 gene has no role to increase sCD40 level and risk for relapse but sCD40 level in serum and age of diagnosis have a role for relapse in GD patients.

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ABSTRAK
Latar Belakang: Kanker kolorektal merupakan perubahan patologis jaringan epitel kolon dan rektum normal menjadi massa jaringan yang abnormal, salah satunya disebabkan ekspresi berlebih pada protein siklin D1 sehingga menyebabkan proliferasi sel di kolorektal yang berlebihan. Upaya pencegahan dan pengobatan penyakit kanker kolorektal dapat dilakukan secara alami salah satunya dengan mengonsumsi ekstrak daun Annona muricata L. (sirsak). Sirsak diketahui banyak mengandung komponen fitokimia yang berperan sebagai anti-kanker. Metode: Penelitian ini menggunakan sel kultur kanker kolorektal HT-29 yang diberi paparan ekstrak etanol daun sirsak dan 5-Fluorourasil (5-FU) sebagai kontrol positif, kontrol pelarut, kontrol sel sebagai kontrol negatif untuk dicari konsentrasi optimumnya (CC50) dan dilanjutkan dengan konsentrasi ½ x CC50,1 x CC50, dan 2 x CC50. Parameter yang dinilai adalah viabilitas sel dengan MTT Assay dan analisis penambatan molekuler dari ekstrak etanol daun sirsak terhadap protein siklin D1 dengan molecular operating environment (MOE) 2013.08 software. Hasil: Konsentrasi optimum (CC50) ekstrak etanol daun sirsak sebesar 278 µg/mL dan 5-FU sebesar 88 µg/mL. Pemeriksaan viabilitas sel menunjukkan persentase sel HT-29 hidup menurun seiring dengan bertambahnya konsentrasi dan persentase terendah di konsentrasi 2 x dari cytotoxicity concentration 50 (CC50) setelah pemberian ekstrak etanol daun sirsak (40,4±1,3%) dibandingkan dengan 5-FU (52,8±4,3%), kontrol pelarut (97,2±1,4%) dan kontrol sel (100%). Analisis penambatan molekuler terhadap protein siklin D1 didapatkan molekul N-hexadecanoic acid dan phytol yang mempunyai energi bebas (ΔG) terendah, yaitu 9,7755 kkal/mol dan -7,2147 kkal/mol. Kesimpulan: Konsentrasi 5-FU memiliki CC50 tiga kali lebih rendah dibandingkan ekstrak etanol daun sirsak. Molekul N-hexadecanoic acid dan phytol mempunyai kemampuan berikatan dengan protein siklin D1.

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ABSTRACT
Introduction: Colorectal cancer is a pathological transformation of normal colon and rectum epithelial that becomes an abnormal tissue mass, due to the overexpression of cyclin D1 protein that inducing the high/excessive proliferation of colorectal cell. It accounted for about 1 million new cancer cases in 2002 (9.4% of the world total). The treatment and prevention of colorectal cancer could be done naturally by consuming leave extract of Annona muricata L. (soursop). Soursop is known for many phytochemical components that serve as an anti-cancer such as alkaloid, annonaceous acetogenin, megastigman, flavonoid glycosides, phenolic, and cyclopeptide. Methods: The study was used HT-29 colorectal cancer cell that treated with ethanolic leave extract of soursop and 5-Fluorourasil (5-FU) as positive control to find the cytotoxicity concentration that can inhibit 50% of HT-29 cell population (CC50) and the ½ x CC50,1 x CC50, and 2 x CC50 concentrations of them were treated for next treatment with MTT assay. Analysis of molecular docking of ethanolic leave extract of soursop to cyclin D1 protein used molecular operating environment (MOE) 2013.08 software. Results: CC50 of ethanolic leaf extract of soursop is 278 µg/mL dan 5-FU is 88 µg/mL. Percentage of viable HT-29 cell line decreased in accordance with increasing concentration and the lowest percentage of viable HT-29 cell is 2 x CC50 after ethanolic leave extract of soursop treatment (40,4±1,3%) was compared to 5-FU (52,8±4,3%), solvent control (97,2±1,4%), and cells control (100%). Analysis of molecular docking to cyclin D1 protein was obtained N-hexadecanoic acid and phytol molecules that have the lowest free energy (ΔG), i.e 9,7755 kkal/mol and -7,2147 kkal/mol and the highest affinity, i.e 7,219 and 5,975.

Abstrak :
Latar Belakang: Obesitas telah menjadi masalah kesehatan besar di dunia. PEMF merupakan modalitas penyembuhan obesitas karena mampu menghambat adipogenesis. Hingga kini, belum dapat dipahami proses molekuler yang mendasari mekanisme penghambatan adipogenesis oleh PEMF. Adipogenesis diketahui melibatkan faktor transkripsi PPARγ yang berperan dalam pengaktifan gen-gen adipogenik, di antaranya ADIPOQ. PPARγ terkekspresi tinggi pada tahap awal adipogenesis dan ADIPOQ terekspresi tinggi pada tahap terminasi adipogenesis. Kedua gen tersebut dapat dijadikan penanda terjadinya adipogenesis. Penelitian ini bertujuan untuk mengetahui tingkat ekspresi PPARγ dan ADIPOQ pada MSC yang dipajan PEMF dan MSC yang tidak dipajan PEMF. Metode: Sampel RNA diisolasi dari masing-masing kelompok perlakuan pada hari ke-0 (kalibrator), 2, 4, 7, dan 14. Ekspresi gen PPARγ dan ADIPOQ dianalisis menggunakan metode qRT-PCR. Pajanan PEMF diberikan dengan intensitas Bmax=2 mT, f= 75 Hz, dalam waktu 10 menit sehari selama 14 hari masa adipogenesis. Sebagai data pelengkap dilakukan pengamatan terhadap morfologi dan jumlah sel berdasarkan hasil gambaran menggunakan mikroskop. Hasil: Hasil analisis qRT-PCR menunjukkan ekspresi PPARγ dan ADIPOQ pada kelompok PEMF lebih rendah dibanding dengan kelompok kontrol. Pada hari ke-2 dan hari ke-14, terdapat perbedaan bermakna ekspresi PPARγ dan ADIPOQ antara kelompok PEMF dan kelompok kontrol (p<0,05). Pada hari ke-7, ekspresi PPARγ dan ADIPOQ mulai ditekan kembali pada kelompok PEMF, ditandai dengan tidak adanya perbedaan bermakna antara kenaikan ekspresi PPARγ dan ADIPOQ di hari ke-4 menuju hari ke-7 (p>0,05). Penghambatan ekspresi gen sejalan dengan hasil pengamatan morfologi dan jumlah sel. Kesimpulan: PEMF memiliki efek penghambatan terhadap adipogenesis sel punca mesenkimal. Hasil penelitian menunjukkan bahwa pajanan PEMF dapat menekan ekspresi PPARγ dan ADIPOQ, perkembangan morfologi, dan jumlah sel selama masa adipogenesis. ......Background: Obesity has become a major health problem in the world. PEMF is known as a modality for obesity treatment because its ability to inhibit adipogenesis. But until now, the molecular processes of adipogenesis inhibition by PEMF is remain unknown. Adipogenesis process involve the transcription factor, PPARγ, which plays a role in activating adipogenic genes, including ADIPOQ. PPARγ is highly expressed at the early stages of adipogenesis and ADIPOQ is highly expressed at the termination of adipogenesis. Both of these genes can be used as markers of adipogenesis. This study aimed to determine the level of PPARγ and ADIPOQ expression on MSC exposed by PEMF and MSC that are not exposed by PEMF. Method: Total RNA was extrected from samples of each treatment group on day 0 (calibrator), 2, 4, 7, and 14. The expression level of PPARγ and ADIPOQ were analyzed using the qRT-PCR method. Exposure to PEMF with Bmax = 2 mT, f = 75 Hz, for 10 minutes a day in 14 days of adipogenesis. Observations on the morphology and the number of cells were analyzed using a microscope imaging. Result: The results of the qRT-PCR analysis showed expression of PPARγ and ADIPOQ in the PEMF group is lower than the control group. On the day 2 anda day 14, there were significant differences in the expression of PPARγ and ADIPOQ between the PEMF group and the control group (p <0.05). On day 7, expression of PPARγ and ADIPOQ suppressed in the PEMF group, marked by a and no significant difference between increases PPARγ and ADIPOQ on day 4 to day 7 (p> 0.05). Inhibition of gene expression is in line with the results of morphology and number of cells. Conclusion: Adipogenesis inhibition in the PEMF group was better than the control group. The results showed that the effect of PEMF and length of exposure can suppress PPARγ and ADIPOQ expression, cell morphology, and the number of cells during the period of adipogenesis.