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  1. Gunadi, Juwitasari T, Damayanti NNR, Kaniashari DS, Kencana SMS, Hastuti J
    Med J Malaysia, 2020 05;75(Suppl 1):28-31.
    PMID: 32483104
    INTRODUCTION: Despite various definitive methods that are used for treating Hirschsprung's disease (HSCR), there are few studies comparing the effect of different pull-through methods on the growth outcomes of patients. We aimed to compare the effect of three different pull-through methods, namely Duhamel, Soave and transanal endorectal pullthrough (TEPT), on HSCR growth outcomes of patients.

    METHODS: Medical records of all HSCR patients who underwent pull-through at the Dr. Sardjito Hospital, Indonesia between January 2010 and August 2016 were reviewed for their growth outcomes before and after the surgery.

    RESULTS: We included 64 HSCR patients, 45 males and 19 females, of which 14, 17, and 33 patients underwent Duhamel, Soave, and TEPT respectively. There were no nutritional status differences in HSCR patients after Duhamel, Soave, and TEPT surgery (p=0.07, 0.17, and 0.79, respectively). Z-score average of weight-for-age did not differ between three surgical methods (p=0.77 and 0.15 for preoperative and postoperative, respectively). In addition, the improvement of nutritional status was achieved in 21.2% HSCR patients after TEPT, 14.3% post Duhamel and 5.9% following Soave procedure, but these differences did not reach a significant level (p=0.34).

    DISCUSSION: Our study shows no difference in effect on the growth outcomes in HSCR patients following Duhamel, Soave and TEPT procedure. Further study with a larger sample size is important to give valuable long-term growth outcomes for HSCR patients after pull-through.

  2. Munawaroh F, Arfian N, Saputri LAAWS, Kencana SMS, Sari DCR
    Med J Malaysia, 2023 Jul;78(4):476-483.
    PMID: 37518915
    INTRODUCTION: Diabetes Mellitus (DM) is a chronic disease with many complications, one of which is diabetic encephalopathy which is characterised by memory dysfunction. Hyperglycaemia that occurs in DM will activate inflammatory pathways in neurons, including NF-κB pathway. Activation of this pathway produce proinflammatory agents such as MCP-1 and IL-6, which activate glial cells. Activation of glial cells is characterised by Glial Fibrillary Acid Protein (GFAP). Chlorogenic acid (CGA) has been reported to have anti-inflammatory effects and can improve memory function. This research aimed to determine the effect of CGA as anti-inflammation, its effect on memory function, mRNA expression of NF-κB, MCP-1, IL- 6, and GFAP of frontal lobe.

    MATERIALS AND METHODS: A total of 24 male rats were randomly divided into six groups: control, DM 1.5 month (DM1.5), DM 2 months (DM2) and the group with three different doses of CGA 12.5 (CGA1), 25 (CGA2), and 50 (CGA3) mg/KgBW. Frontal lobe tissue is taken for analysis of mRNA expression for NF-κB, MCP-1, IL-6, and GFAP using Reverse Transcriptase PCR (RT-PCR). Samples were also taken for histopathology preparation and stained by immunohistochemistry method using anti-GFAP antibodies to observe glial cell activation in frontal lobe tissue.

    RESULTS: The group that was given CGA at all doses have statistically significant better memory function, i.e. DM2 versus CGA1 (p = 0.036), CGA2 (p = 0.040), and CGA3 (p = 0.021). The result of mRNA expression in NF-κB was lower in the group given CGA, i.e. DM2 compared to CGA2 (p = 0.007). mRNA expression of MCP-1 was significantly lower in all CGA treatment groups compared to the non-CGA group (p = 0.000). IL-6 mRNA expression was lower than the group not given CGA, DM compared to CGA2 (p = 0.028). GFAP mRNA expression was lower than the group given CGA in DM, DM2 group compared to CGA1 (p = 0.04) and CGA3 (p = 0.004).

    CONCLUSION: Administration of CGA can improve memory function at all doses given, and can reduce brain inflammatory activity, especially in the CGA2 group.

  3. Yuniartha R, Arfian N, Setyaningsih WAW, Kencana SMS, Sari DCR
    Malays J Med Sci, 2022 Dec;29(6):46-59.
    PMID: 36818894 DOI: 10.21315/mjms2022.29.6.5
    BACKGROUND: Chronic hyperglycaemia of diabetes causes long-term damage and impaired function of multiple organs. However, the pathological changes in the liver following long-term diabetes remain unclear. This study aimed to determine the pathological complications of long-term diabetes in the rat liver.

    METHODS: Intraperitoneal injection of streptozotocin (STZ) was used to induce diabetes in rats at a single dose (60 mg/kg body weight [BW]). Rats were euthanised at 1 month (DM1 group), 2 months (DM2 group) and 4 months (DM4 group) following diabetes induction with six rats in each group. Immunohistochemistry was performed against SOD1, CD68, p53 and p16 antibodies. Messenger RNA (mRNA) expressions of SOD1, SOD2, GPx, CD68, p53, p21 and caspase-3 genes were measured by reverse transcription-polymerase chain reaction.

    RESULTS: Hepatic p53 mRNA expression was significantly higher in DM1, DM2 and DM4 groups compared to the control group. The p21 and caspase-3 mRNA expressions were significantly upregulated in the DM2 and DM4 groups. The p16-positive cells were obviously increased, particularly in the DM4 group. Bivariate correlation analysis showed mRNA expressions of p21 and caspase-3 genes were positively correlated with the p53 gene.

    CONCLUSION: Diabetic rats exhibited increased apoptosis and senescence in the liver following a longer period of hyperglycaemia.

  4. Arfian N, Nugraha GC, Kencana SMS, Alexandra G, Eliyani ND, Dewi KC, et al.
    Med J Malaysia, 2024 Aug;79(Suppl 4):72-76.
    PMID: 39215419
    INTRODUCTION: Inflammation caused by diabetes can damage multiple organs, including the lungs. Vitamin D (VD) has been shown to potentially reduce inflammation and boost the immune system. VD might play a role in diabetes' inflammatory response. This study aims to elucidate the evidence regarding the lung as the target organ for DM and the possible role of VD in preventing pulmonary damage progression in the diabetes rat model.

    MATERIAL AND METHODS: Thirty Sprague Dawley rats (3-monthold, 200 to 300 gm) were randomly divided into six groups, namely control (C), 4 weeks diabetes mellitus (DM1), 8 weeks DM (DM2) and three DM1 groups (VD1, VD2, and VD3) who received Vitamin D doses of 0.125, 0.25 and 0.50 μg/kg BW, respectively. After 4 weeks, daily VD was administered intraperitoneally for 30 days. Lung tissues were taken for IL- 6, MCP-1, NFKB and CD68 mRNA expression analysis and paraffin embedding. Immunohistochemical staining against CD68 and MCP-1 was conducted. Data were analysed using one-way ANOVA. p < 0.05 was considered statistically significant.

    RESULTS: DM2 group represented significantly higher IL6, MCP1, NFKB and CD68 mRNA expression than Control group (p < 0.05). Meanwhile, VD2 and VD3 groups revealed significantly lower mRNA expression of IL-6, MCP1, NFKB and CD68 than DM2 (p < 0.05). Immunostaining revealed the spreading of MCP1 protein expression in lung tissue along with macrophage infiltration in the DM2 group, which was reduced in the VD2 and the VD3 groups.

    CONCLUSION: VD shows a protective effect on diabetesinduced lung damage by regulating inflammation factors.

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