Moch. Istiadjid E.S.
Laboratorium Ilmu Bedah Fakultas Kedokteran UnibrawMalang

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PENGARUH DEFISIENSI FOLAT TERHADAP FERTILITAS INDUK DAN KUALITAS JANIN TIKUS E.S., Moch. Istiadjid
Jurnal Kedokteran Brawijaya Vol 20, No 1 (2004)
Publisher : Fakultas Kedokteran Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (479.777 KB) | DOI: 10.21776/ub.jkb.2004.020.01.2

Abstract

This experimental study was performed to reveals the association of folic acid deficiency with the rat’s fertility and also with life quality of baby’s rat. The level of folic acid deficiency were divided into two groups, consisted of severe and mild, based on the intake of folic acid, those were given to each groups that consist  of ten mature Sprague-Dawley rats. Other were givennormal folic acid as a control. Sixteen weeks after dietary suplly, rat’s  blood were evaluated to measure the contain of folic acid in the serum and erythrocyte and then the rats were forced mating. Baby rats were born with histerostomy. Rat’s fertility were evaluated by measured the number of delivered baby’s rat in 21th, 42th and 63th gestation or delivered days at each group. The quality of baby’s rats were evaluated by measured the body weight of each baby  and examined of any kind of congenital anomaly, such as spina bifida, encephalocele or anencephaly. The data analysis suggested the positive impact of maternal folic acid level in erythrocyte and maternal serum with the level of maternal fertilityand life quality of the baby,s, especially its body weight. Thus, the deficiency of folic acid will cause maternal infertility, lowered body weight of the baby’s rats and may be also congenital anomaly. Key words:Folic acid deficiency, infertility, low body weight, congenital anomaly.
LUAS DEFEK MENINGOKEL BERHUBUNGAN DENGAN KADAR TRANSFORMING GROWTH FACTOR β1 (TGF-β1)DAN INSULINE-LIKE GROWTH FACTOR-1 (IGF-1) DALAM TULANG E.S., Moch. Istiadjid
Jurnal Kedokteran Brawijaya Vol 20, No 3 (2004)
Publisher : Fakultas Kedokteran Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (535.775 KB) | DOI: 10.21776/ub.jkb.2004.020.03.4

Abstract

Meningocele pathogenesis is based on skull defect that occurs since the first three month of fertilization period. Through that defect, mening, cerebrospinal liquid, and cerebral parenchym is protruded. Meningocele can cause by folic aciddeficiency that had proved correlation with TGF-β1 and IGF-I level, both in maternal blood or baby rat’s skull. Folic acid deficiency also causes increasing the number of apoptosis and necrosis cells death in baby’s skull. TGF-β1 and IGF-I one growth factors thatstimulate bone synthesis. The purpose of this study is to explore the correlationbetween TGF-β1 and IGF-I level in skull on side defect of meningocele patients and the wide of skull defect to obtain the role of the  two growth factors in meningocele teratogenesis perspectively. Eight meningocele patients that were performed excision by standard procedure have taken a few of bone speciment on sidedefect to count TGF-β1 and IGF-I levels with immunochemistry technic. Wide defect was determined by measuring defect’s diameter, using Martin anthropometer. The correlation between TGF-β1 and IGF-I skull level and defect’s wide was analyzed by SEM (structuralequation modeling) statistic. There was significant negative-correlation between that variable, that mean the lower of the two growth factors level is wider of skull defect. TGF-β1: r = -0.648, p =0.009; IGF-I: r = -0.426, p =0.025. Key words:Meningoencephalocele, Skull defect, TGF-β1, IGF-I.