Ahmad Aulia
Department Of Histology, Faculty Of Medicine, Universitas Indonesia, Jakarta 10430, Indonesia

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Location and distribution pattern of nitric oxide synthesizing neuronal cells in the digestive tract and urinary bladder of mice Jusuf, Ahmad Aulia
Medical Journal of Indonesia Vol 9, No 4 (2000): October-December
Publisher : Faculty of Medicine Universitas Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (1072.008 KB) | DOI: 10.13181/mji.v9i4.618

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[no abstract available]
LOW VITAMIN B12 DIET INCREASES LIVER HOMOCYSTEINE LEVELS AND LEADS TO LIVER STEATOSIS IN RATS Sianipar, Imelda Rosalyn; Ujianti, Irena; Yolanda, Sophie; Jusuf, Ahmad Aulia; Kartinah, Neng Tine; Amani, Patwa; Murti, Krishna Aditya; Soeria Santoso, Dewi Irawati
Universa Medicina Vol 38, No 3 (2019)
Publisher : Faculty of Medicine, Trisakti University

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (821.825 KB) | DOI: 10.18051/UnivMed.2019.v38.194-201

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Background Nonalcoholic fatty liver disease (NAFLD) is one of the most widespread chronic liver diseases, caused by the development of insulin resistance. One of the mechanisms involved is a disturbance in insulin signaling by certain toxic substances that interact with one of the proteins responsible for the insulin signaling pathway. Increased homocysteine level, upon disruption of the methionine pathway, is associated with insulin resistance. The aim of this study was to evaluate the effect of hyperhomocysteinemia and insulin resistance (HOMA-IR level) induced by dietary vitamin B12 restriction on liver steatosis. Methods A study of laboratory experimental design was conducted involving 18 male Sprague Dawley rats (age 36-40 weeks, BW 300-350 g), that were randomly divided into 3 groups: control, 8-week treatment, and 16-week treatment. Standard AIN-93 diet was administered to the control group, whereas rats in the treatment groups were fed vitamin B12 deficiency-AIN-93M. At the end of treatment, liver homocysteine levels were determined by ELISA, HOMA-IR values were calculated, and steatosis degree of the liver was determined histologically. Statistical analysis was performed using independent t-test. Results A significant increase in liver homocysteine levels was found between the control and both the 8- and 16-week treatment groups (p<0.001). HOMA-IR levels were significantly higher in both treatment groups compared to controls (p<0.001). The area of liver steatosis in both treatment groups was significantly larger than that of the control group (p<0.001). Conclusion Increased homocysteine levels due to dietary vitamin B12 deficiency induces liver steatosis due to insulin resistance in rats.
PCS-5 Nitric Oxide Induced Basal Cell Hyperplasia and Lamina Propria Elongation in Rat Gastroesophageal Junction Tena Djuartina; Bambang Pontjo Priosoeryanto; Ari Fahrial Syam; Ahmad Aulia; Tri Isyani Tungga Dewi
Hemera Zoa Proceedings of the 20th FAVA & the 15th KIVNAS PDHI 2018
Publisher : Hemera Zoa

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NO (Nitric Oxide) is an inorganic compound composed of nitrogen and oxygen, NO is also produced in various places on various types of mammalian cells. NO as a radical compound is important in mediating physiological and pathological events in mammals including humans [1].GEJ (gastroesophageal junction) is a transition zone between the surface of esophagus which is covered by stratified squamous epithelium to the gastric mucosa which consists of simple columnar epithelium (z-line), where circular muscle of esophagus fuse with oblique muscle and lipid layer of the gaster. At the lower part of GEJ, there is the lower esophageal sphincter (LES) that not only allow food to move into stomach and works as an exit passage of the gas, but also inhibit reflux of any substances that potentially can cause harm to the esophagus [2].Petersson et al, found that chronic exposure to cytotoxic levels of NO can cause inflammation, intestinal metaplasia and neoplasia. Although it is known that gastric acid, pepsin and bile acids can cause adenocarcinoma of distal esophagus and GEJ, NO exposure and nitrosative stress role in this phenomenon is yet to be fully understood and further study is needed [3].The purpose of this was to identify and compare the histopathological changes occurring in GEJ in relation to administration of physiological concentration of nitrate dissolved in HCl and ascorbic acid. As such, the animal model used in this study can be used to study and represent the changes microscopically, because obtaining a full thickness biopsy from a human subject can be difficult to perform.
Efek Proteksi Ekstrak Air Tanaman Akar Kucing (Acalypha Indica Linn) Terhadap Perubahan Struktur Neuron Hipokampus Paska Hipoksia Serebri Nurhadi Ibrahim; Ahmad Aulia Jusuf; Lina Marlina
JURNAL KESEHATAN BHAKTI HUSADA Vol 1 No 01 (2015): Jurnal Kesehatan Bhakti Husada
Publisher : UP3M AKPER-AKBID BHAKTI HUSADA CIKARANG

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Latar Belakang : Beberapa penelitian telah membuktikan bahwa ekstrak air akar kucing memiliki kemampuan neuroterapi dan neuroprotektor baik secara in vivo maupun in vitro. Telah terbukti juga ekstrak akar kucing dapat mengatasi berbagai masalah kesehatan sebagai antidiuretik, anti emetik dan anti toksin. Akar kucing juga mengandung antioksidan sehingga pemberian ekstrak tanaman ini mampu mencegah kerusakan sel akibat hipoksia. Atas dasar penelitian – penelitian tersebut, akan dibuktikan bahwa pemberian ekstrak akar kucing prahipoksia akan mencegah kerusakan struktur neuron hipokampus . Tujuan : Menganalisis perubahan struktur neuron hipokampus yang mendapat ekstrak air tanaman akar kucing sebelum perlakuan hipoksia yang dilaksanakan selama 7 hari Metode : Lima kelompok tikus sprage dawley yang terdiri dari masing – masing 5 tikus dikelompokan menjadi kelompok kontrol negatif hanya diberi aqua, kontrol positif dengan diberikan vitamin B1 dan 3 kelompok yang diberikan ekstrak air akar kucing dengan dosis 300 mg/kgBB, 400 mg/kgBB dan 500 mg/kgBB selama 7 hari sebelum paparan hipoksia.Setelah perlakuan hipoksia diambil jaringan hipokampusnya dan dilihat struktur neuronnya dengan pewarnaan hematoksilin eosin dan sel yang masih normal dihitung dengan menggunakan optilab viewer dan image raster. Hasil : Ekstrak akar kucing dengan dosis 300 mg/kgBB, 400 mg/kgBB dan 500 mg/kgBB menunjukan struktur neuron dan jumlah sel neuron dengan kelompok kontrol negatif ( tanpa ekstrak akar kucing) secara signifikan di area CA3 dan lapisan dalam girus dentatus hipokampus (p= 0,000) Kesimpulan : Ekstrak akar kucing dengan dosis 300, 400 dan 500 mg/kgBB mempunyai efek protektif terhadap kerusakan neuron di hipokampus
Mitochondrial Adaptations of Obese Adult Rat Visceral Adipocytes which Differ in Nutritional Status during Childhood Lailan Safina Nasution; Ahmad Aulia; Sri Widia A. Jusman; Mohamad Sadikin
eJournal Kedokteran Indonesia Vol 9, No. 3 - Desember 2021
Publisher : Faculty of Medicine Universitas Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (243.296 KB) | DOI: 10.23886/ejki.9.48.197-202

Abstract

Mitochondria are highly dynamic organelles that can adapt to different environmental stimuli. This study aims to analyze differences in the function and biogenesis of mitochondria and anaerobic glycolysis activity between obese adult rats that were undernourished in childhood (LCD28) and those which were normal (SD28) or already fat (HFD28). Sprague-dawley rats were assigned groups and given diet treatments from December 2017 until August 2018 in the Laboratory Animal Management Unit, Faculty of Veterinary Medicine, Bogor Agricultural Institute. To observe mitochondrial function and biogenesis, MnSOD activity and PGC1α levels were analyzed using ELISA. To investigate the existence of anaerobic glycolysis, LDH activity was analyzed using a spectrophotometry method. The results showed that MnSOD activity and PGC1α levels of LCD28 increased compared to the other groups, signifying higher mitochondrial function and biogenesis. Meanwhile, no significant difference in LDH activity was found, signifying similar levels of anaerobic glycolysis.
CD34+ UCB stem cells attenuate TGF-β signaling and inhibit liver fibrosis: A new avenue for liver cirrhosis-carcinogenesis prevention Septiana, Wahyunia Likhayati; Antarianto, Radiana Dhewayani; Louisa, Melva; Jusuf, Ahmad Aulia; Barasila, Atikah Chalida; Pawitan, Jeanne Adiwinata; Fasha, Iqbal
Makara Journal of Health Research Vol. 24, No. 2
Publisher : UI Scholars Hub

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Background: The liver microenvironment plays a key role in liver fibrosis and carcinogenesis. This study aimed to fill the gap in knowledge on the interaction between hepatic stellate cells and endothelial progenitor cells with biomarkers of liver fibrosis and/or carcinogenesis, including Col1A1, TGF-β, and tenascin-C. Methods: CD34+ stem cells were isolated from umbilical-cord-blood mononuclear cells. 2D and 3D co-culture of CD34+ UCB SCs and LX2 was performed. The cells were incubated in a CO2 incubator for three days. Morphological observation, qRT-PCR of TGF-β1 and COL1A1, and immunocytochemistry of tenascin-C were performed. Results: CD34+ UCB SCs were viable in the 2D and 3D co-culture for 24 h. 3D co-culture of CD34+ UCB SCs and LX2 inhibited in vitro liver fibrosis by lowering Col 1A1 expression as compared to control. We observed lower TGF-β expression in 3D co-culture on days 1 and 2 followed by higher expression of TGF-β on day 3. 2D co-culture of CD34+ UCB SCs and LX2 showed a different level of COL1A1 and TGF- β expression compared with 3D co-culture. Spheroids from 2D co-culture of CD34+ UCB SCs and LX-2 showed immunoreactivity against tenascin-C. Conclusion: Interaction between LX-2 and CD34+ UCB SCs in 3D co-culture inhibits in vitro liver fibrosis. The viability of CD34+ UCB SCs is essential for attenuation of TGF-β signaling in LX-2.