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All Journal Jurnal Kedokteran Brawijaya International Journal of Cell and Biomedical Science
Yusrina Istanti
Laboratorium Ilmu Kesehatan Anak Fakultas Kedokteran Universitas Diponegoro/Rumah Sakit Umum Pusat Dr. Kariadi Semarang
Biochemistry, Genetics & Molecular Biology Immunology & microbiology Medicine & Pharmacology

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Korelasi Antara Transforming Growth Factor -Î’1 Monosit dengan Kebocoran Vaskuler pada Demam Berdarah Dengue Supriatna, Mohamad; Tondy, Haryson; Ermin, Tatty; Istanti, Yusrina; RMD, Kisdjamiatun
Jurnal Kedokteran Brawijaya Vol 26, No 1 (2010)
Publisher : Fakultas Kedokteran Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (1126.587 KB) | DOI: 10.21776/ub.jkb.2010.026.01.1

Abstract

ABSTRAKSel monosit merupakan target utama infeksi virus Demam Berdarah Dengue (DBD) yang dapat memproduksi faktor vasoaktif yang mempengaruhi fungsi sel endotel dan berperan dalam kebocoran vaskuler. Transforming growth factor beta 1 (TGF-1) merupakan salah satu sitokin yang mempunyai banyak peran dalam patogenesis DBD. Penelitian ini dilakukan untuk mengidentifikasi hubungan antara TGF-1 terhadap indeks efusi pleura (IEP), total protein, albumin dan hematokrit sebagai indikator kebocoran vaskular. Studi dilakukan dengan desain cross sectional pada pasien DBD usia 13-14 tahun di RS dr. Kariadi selama Juli 2005 hingga Juli 2006. Sampel pemeriksaan adalah kultur whole blood supernatant culture yang diinduksi LPS pada subyek penelitian. Kadar monosit TGF-1, PEI, total protein, albumin dan hematokrit diukur pada hari 0 dan 2. Data di analisis dengan uji Wilcoxon dan korelasi Spearman. Pada hari 0 dan 2 dianalisis korelasi antara kadar monosit TGF-1, PEI juga protein total, albumin dan hematokrit. Rerata kadar TGF-1 monosit pada hari ke 2 (43.29±28.012 pg/ml) lebih tinggi dari hari 0 (35.27 ± 34.642 pg/ml, p=0.09, Wilcoxon test). Pada hari 0 terdapat korelasi signifikan level TGF-1 monosit dengan PEI (r=-0.31, p=0.04), tetapi tidak dengan total protein (r=0.19, p=0.2), albumin (r=0.11, p=0.5 ; r=--.08, p=0.6). Pada hari kedua tidak ada korelasi signifikan antara level TGF-1 monosit level dan PEI (r=-0.2,p=0.3), total protein (r=0.2, p=0.2), albumin (r-0.2, p=0.2) dan hematokrit (r=-0.04, p=0.8). Dapat di simpulkan bahwa TGF-1 mungkin berperan dalam proses inflamasi DBD melalui PEI sebagai salah satu indikator kebocoran plasma.Kata Kunci : Albumin, DBD, hematokrit, IEP, TGF-1, protein totalβ
Time-Dependent Simulation Identifies Critical Hour Phase of Intestinal Acute Injury in Sepsis Mouse Model Istanti, Yusrina; Anggoro, Naufal Sebastian; Husain, Sofian Azalia; Azzahara, Salma Yasmine
International Journal of Cell and Biomedical Science Vol 3 No 9 (2024)
Publisher : Stem Cell and Cancer Research (SCCR)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.59278/cbs.v3i9.64

Abstract

Background: Understanding the dynamic process of intestinal injury and repair during sepsis is essential for identifying optimal therapeutic windows. This study aimed to determine the critical time phase of intestinal acute injury by analyzing histological changes over a 24-hour period in a sepsis mouse model. Methods: Mice were divided into four groups—Control, 9 h, 12 h, and 24 h—and intestinal tissue samples were assessed using the Chiu histological scoring system. A time-dependent simulation was conducted to evaluate average changes in tissue damage and to identify key transition points between injury and recovery phases. Statistical analysis was performed using one-way ANOVA followed by post hoc comparisons to determine significant differences among time points. Results: The simulation demonstrated a marked increase in intestinal damage between 9 h and 12 h, followed by partial recovery at 24 h. Statistical analysis revealed a significant difference (p < 0.05) corresponding to this shift. These findings suggest that peak tissue injury occurs around 12 hours post-sepsis induction, preceding the onset of repair mechanisms. Conclusion: The study provides quantitative insight into the temporal progression of intestinal injury in sepsis, identifying the 12–24 hour period as a critical therapeutic window for potential interventions.
Co-Authors Anggoro, Naufal Sebastian Azzahara, Salma Yasmine Haryson Tondy Husain, Sofian Azalia Kisdjamiatun RMD Mohamad Supriatna Tatty Ermin