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Published by Universitas Gadjah Mada

ISSN : 01261312 EISSN : 23563931 DOI : http://dx.doi.org/10.19106/JMedSci005303202101

Core Subject : Science,

Immunology & microbiology Neuroscience

Journal of the Medical Sciences (JMedSci) or Berkala Ilmu Kedokteran (BIK) is an international, open-access, and double-blind peer-reviewed journal, published by Faculty of Medicine, Public Health and Nursing, Universitas Gadjah Mada Yogyakarta Indonesia. JMedSci aiming to communicate high-quality articles in the areas of biomedical science from basic to clinical sciences.The journal welcomes papers from original articles, case reports, reviews, and book reviews. All papers published in JMedSci are freely available as downloadable pdf files. The journal began its publication on March 1973 and published quarterly (January, April, July, and October). JMedSci is abstracted and indexed in DOAJ, Crossref, Google Scholar, Sinta, Indonesia One Search. JMedSci is accredited by Directorate of General Higher Education, the Ministry of Research, Technology, and Higher Education, Indonesia

Arjuna Subject : Kedokteran - Kedokteran (Lain-Lain)

Articles 2,170 Documents

159 160 161 162 163

Systemic provocation in doxycycline induced fixed drug eruption: a case report Anik Murwaningsih; Rosmarini Estri Sih Hananti; Niken Indrastuti
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 45, No 02 (2013)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Fixed drug eruption (FDE) is recurrent lesions that upon repeated uptake of causative drug, always appears at the same skin and mucosal site. Determination of causal relationship in drug allergy is very important. In this case report, cases of doxycycline-induced FDE was reported. The subject of the research was a 29-year-old male, referred by dermatologist, with history of reccurent FDE. Physical examination revealed an oval well demarcated patch hyperpigmentation. Patch test was perfomed on previous involved and uninvolved site. The result of the patch test was irrelevant. Retesting patch test gave similar result. Systemic provocation test or drug provocation test (DPT) with doxcycline were done with suspected drug under ambulatory survelance and gave positive result. In this case, the DPT succeeded to identify doxycycline as the causal agent of FDE. The work-up of a suspected drug hypersensitivity includes a detailed clinical history, physical examination, skin tests, and provocation tests. The DPT is recommended to confirm drug’s hypersensitivity reactions. Systemic provocation test is considered as the gold standard for diagnosing FDE.

Mechanism of cytotoxic activity of chalcone derivatives against K562 leukemia cell lines Arina Novilla; . Mustofa; Indwiani Astuti; . Jumina; Hery Suwito
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 49, No 4 (2017)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Two chalcone derivatives i.e. (E)-1-(4-aminophenyl)-3-(2,3dimethoxyphenyl)-prop-2-en-1-one (Compound-1), and (E)-1-(4-aminophenyl)-3-phenylprop-2-en-1-one) (Compound-2),has been proven to have potential cytotoxic activity. The aim of this study was toevaluate the effect of these compounds on PI3K/Akt signalling pathway in K562 celllines. After incubation with the tested compounds, AKT, caspase-3, STAT3 and cyclinD1 concentrations were measured using ELISA. Furthermore, cell cycle was analysedusing flowcytometry. Imatinib and isotretinoin were used as positive control, whereascell culture without treatment was used as negative control. The AKT concentration aftertreatment with Compound-1 and -2 was significantly lower than that control, imatiniband isotretinoin (p<0.05). The apoptotic indices after treatment with Compound-1 and-2 were significantly higher than control, however they were lower than imatinib andisotretinoin (p<0.05). The caspase-3 concentration after treatment with Compound-1 at5 and 10 μg/mL and Compound-2 at 10 μg/mL was significantly higher than that controland imatinib, however it was lower than isotretinoin (p<0.05). The STAT3 concentrationafter treatment with Compound-1 and -2 was significantly lower than that control andisotretinoin at 50 μg/mL (p<0.05) and similar with imatinib (p>0.05). The cyclin D1concentration after treatment with Compound-1 and -2 was significantly lower than thatcontrol, imatinib and isotretinoin (p<0.05). In addition, Compound-1 and -2 arrested G0/G1 and G2/M phase in K562 cell lines, with comparable results to imatinib and isotretinoin.In conclusion, the mechanism of cytotoxic activity of Compound-1 and -2 are through thePI3K/Akt signalling pathway inhibition, apoptosis induction by upregulation of apoptoticmarkers, and inhibition of cell cycle progression by regulating cell cycle-related factors.

Prolonged Kidney Ischemia-Reperfusion Injury Associates with Inflammation, Vascular Remodelling, and Myofibroblast Formation Nur Arfian*; Hilma Kholida Ats-tsani; Pratiwi Indah Sayekti; Dwina Agrila Lakabela; Amelia Amelia; Toni Febriyanto; Hana Rutyana Putri Antonio; Dian Prasetyo Wibisono; Dwi Cahyani Ratna Sari
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 50, No 1 (2018)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Prolonged kidney ischemia-reperfusion injury (IRI) is the important risk factor for leading to chronic kidney disease (CKD). Persistent hypoxia and inflammation are considered as the main pathogenesis of chronic injury, followed by myofibroblast expansion and fibrosis process. Tubular injury, cell proliferation, and vasoconstriction, as acute compensatory responses, are restored in chronic phase. The aim of the study was to investigate the relation between inflammation, vascular remodeling, and myofibroblast formation as response to ischemia injury after prolonged kidney ischemia-reperfusion (I/R). Fifteen male Swiss mice aged 3-4 months were used as kidney I/R injury model after bilateral pedicle renal clamping. Rats were divided into 3 groups with five rats in each group i.e. control group (sham operation/SO), acute I/R model (IR1), and chronic I/R model (IR12). PAS staining was used for scoring tubular injury. Fibrosis was assessed using sirius red and a-SMA immunostaining for myofibroblast expansion. PCNA and CD68 immunostaining were used for identifying cell proliferation and macrophage infiltration. RT-PCR was conducted for assessing MCP-1, HIF-1a, and ppET-1 expression, which were quantified using ImageJ software. Data were analyzed using one way ANOVA and Kruskal-Wallis test with significance level of p<0.05. Significantly increase of tubular injury score (p<0.001) and PCNA positive cell (p<0.001) in IR1 group compared to SO were observed, otherwise HIF-1a of IR12 enhanced (p<0.05). Macrophage cell count (p<0.01) and MCP-1 expression (p<0.05), were significantly increase in IR1 and IR12 injury, compared to SO. Wall thickness of arteries was significantly increase (p<0.05) as well as decrease of vascular lumen area (p<0.05), followed by enhancement of ppET-1 expression (p<0.01) in IR1 group and restored significantly (p<0.05) in IR12 group. Fibrosis fraction-area and myofibroblast expansion were significantly increase gradually from IR1 to IR12 injury (p<0.01). In conclusion, prolonged kidney I/R injury induces the sustainability of hypoxia and inflammatory response, which promotes myofibroblast formation, and decrease the response of vascular remodelling.

EFFECT OF 1,2-EPOXY-3[3-3[3,4-DIMETOXYI-PHENIL]-4H-1-BENZOPIRAN-4-ON] PROPANE (EPI) ON SIRTUIN-1 AND NUCLEAR FACTOR-κB EXPRESSION OF MAMMARY TUMORS INDUCED IN SPRAGUE DAWLEY RATS BY DMBA Ayyub Harly Nurung; Sri Herwiyanti; Dewi Kartikawati Paramita
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 48, No 3 (2016)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

ABSTRACT The main factors contribute to breast cancer development is the combination of exogenous and endogenous factors. Endogenous factors include both SIRT1 and NF-kB. Exogenous factor used in this research is 7.12 dimethylbenz(a)anthracene (DMBA). 1,2-epoxy-3[3- 3[3,4-dimetoxy-phenil]-4h-1-benzophiran-4-on] propane (EPI) is a derivative of isoflavone generate from clove leaf oil. To examine the effect of EPI on SIRT1 and NF-kB expression in DMBA-induced Sprague Dawley (SD) rats, and the correlation between SIRT1 and NFkB expressions. Tissue generated form 35 Sprague Dawley female rats aged 2 weeks old were used in this study. Those rats were divided into 7 groups (5 rats/group), namely normal control group; corn oil group; DMBA group; EPI treated groups with 1 mg/kgBW (EPI I), 2 mg/kgBW (EPI II), and 4 mg/kgBW (EPI III), respectively; and doxorubicin group. EPI and doxorubicin were administered from 1st until 15th week, while DMBA were administered from 3rd until 9th week. The paraffin block was prepared from all breast organ of the rats that terminated at the end of week 15th. Examination of SIRT1 and NF-kB expression was performed using light microscope at 400x magnifications, after immunohistochemistry (IHC) staining. Expression level of SIRT1 and NF-kB were analyzed using IHC-profiler plug-in in ImageJ software. SIRT1 and NF-kB expression in EPI treated groups were not significantly different with the one in Doxorubicin group, but lower than DMBA group (p=0.000). There was a positive correlation between SIRT1 and NF-kB expression (p=0.001; r=0.773) in EPI-treated group. EPI was able to prevent an increasing of SIRT1 and NF-kB expression in SD model breast cancer that induced with DMBA. There is a positive correlation between SIRT1 and NF-kB expression in EPI-treated SD rats that were induced by DMBA

Sensitivity and specificity of serum procalcitonin level compared to leucocyte count for diagnosis surgical site infection on patients undergoing major surgery in Dr. Sardjito General Hospital Yogyakarta Muhammad Sayuti; . Supomo; Umi Sholekah Intansari
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 45, No 01 (2013)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Surgical site infection (SSI) is one of the most serious complications on sugical procedure. However, its diagnosis is still based on the clinical and laboratory examination that take more time and less sensitive and specific. Therefore, early diagnosis that is more accurate and precise is needed. Some biomarker such as serum procalcitonin (PCT) is promoted for diagnosis SSI. The aim of the study was to evaluate the sensitivity and specificity of serum PCT compared with leucocyte for diagnosis SSI on patients undergoing major surgery. This was a descriptive analytical study with a prospective observational design. Patients who underwent a major surgery between October 30th and December 31rt, 2011 and fulfilled the inclusion and exclusion criteria were recruited. Clinical and laboratory examinations including leucocyte count were conducted presurgery. On 3rd day postsurgery, blood sample was taken for PCT and leucocyte count measurement. A blood bacterial culture was performed on patients suffering from SSI according to Centers for Disease Control (CDC) criteria. Patients were then followed until 30 days postsurgery. A total of 49 patients consisting of 22 men and 27 women were involved in this study. Surgical site infection was found in 16 patients consisting of 8 (50%) patients with clean surgical wound, 3 (19%) patients with clean surgical contamination wound, 4 (25%) patients with surgical contamination wound and 1 (6%) patient with dirty surgical wound. Furthermore, laboratory examination found that 9 patients had abnormal leucocyte with 5 of them suffering from SSI, whereas from 14 patients with serum PCT abnormal, 11 patients suffered from SSI. Diagnostic test showed that the sensitivity and specificity of serum PCT for diagnosis SSI were 68.75 and 90.90%, respectively, whereas the sensitivity and specificity of leucocyte were 31.25 and 87.87%, respectively. In conclusion, serum PCT has better sensitivity and specificity compared with leucocyte for the diagnosisof SSI in patients with major surgery.

Efek biji mahkota dewa terhadap ekspresi Anis Widyasari; Yudanti Riastiti; Indwiani Astuti; Rina Susilowati; . Harijadi
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 38, No 01 (2006)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

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The effect of mahkota dewa seed (Phaleria macrocarpa (Schaff. Bowl.) on active caspase-3 expression in WiDr Ca colon cell line Background: Mahkota dewa (MD, Phaleria macrocarapa (Schaff) BoerII.) is widely used for cancer therapy, but its mechanism as anticancer has not been known yet. Recently, ethanol extract of MD seed has been shown to have cytotoxic effect on WiDr Ca colon cell line. Objective: The purpose of this study is to know active caspase-3 expression in WiDr Ca colon cell fine after MD treatment. Methods: WiDr Ca colon cell line was incubated with ethanol extract of MD seed in three concentrations for 48 hours. Active caspase-3 expression was shown using immunohistochemistry method. Results: In the cell line treated with ethanol extract of MD seed 11.35 uglml (1/2 IC50), 22.7 ug/mI (IC,) and 45.4 ug/ml (2x1050), immunopositive cells had been found to be 20.4%, 49% and 63%, respectively. The cell line treated with 5-Fluorouracil (5-FU) in IC50 dosage only had 27.4% imunopositive cell. ConclUsion: Ethanol extract of MD seed had cytotoxic effect on WiDr cell line through the increased active caspase 3 expression. The effect was greater than 5-FU. Key words: Mahkota Dewa, WiDr cell line, Caspase 3, apoptosis, 5 FU

Mitochondrial Genetics and Cancer Safarina G. Malik
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 48, No 4 (2016): SUPPLEMENT
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

The first modern human, the Mitochondrial Eve, was traced back to Africa about 200,000 years ago, based on the variation in the mitochondrial DNA (mtDNA). An eruption of a super volcano, Mount Toba, in Sumatra 70,000 years ago may have led to a 'nuclear winter', followed by a 1,000-year ice age. This cold snap would have made life difficult; genetic evidence indicated a sharp reduction in population size around this time, reaching approximately 10,000 individuals. Once the climate started to improve, our ancestors recovered from this near-extinction event. The population expanded, and some courageous explorers ventured beyond Africa. Around 50,000 years ago some of these brave ancestors had successfully crossed the globe to South East Asia and Australia. Some of them settled in the Indonesian archipelago, forming the first settlement of prehistoric Indonesia. The second migration happened around 10,000 years ago, where a group of hunter-gatherers followed the now-submerged river systems that once ran from mainland Asia between the modern islands of Sumatera, Java, and Borneo. Then, around 4,000 years ago the third group of ancestors arrived. This agricultural community brought along their culture of pottery, plant cultivation, and animal domestication, co-inciding with the vast spread of Austronesian languages. Therefore, it is likely that the Indonesian archipelago hosts a wide range of linguistic, ethnic and genetic diversity.1 Nowadays, the modern Indonesia is home to around 700 ethnic populations, each with distinct cultural and linguistic characteristics, representing vast genome diversity.Our ancestors’ decision to embark on a sea travel and take on its related lifestyle has influenced the development of susceptibility and resistance to various diseases observed today. During the prolonged travel, our ancestors were subjected to changes in global climate and geographic dynamic, which strongly influenced and shaped the genetic background of modern humans, including the mtDNA genome. Mitochondria, a well-adapted endosymbiotic intracellular organelles, became efficient for energy production through-out the course of evolution. They are critical for survival and proliferation of living organisms under aerobic conditions and produce ATP through oxidative phosphorylation (OXPHOS). Adaptation to new environments that favor beneficial traits may have caused genetic risk differences that influence the crucial function of the mitochondria, consequently affecting many function in the cell.2 The altered function of the mitochondria might act as an important factor for disease susceptibility across many human populations, i.e. mtDNA variation that grouped together forming a certain type/group (the mtDNA haplogroup) was reported to modulate cancer susceptibility3-5 and resistance6 in Chinese population.Cancer cells are characterized in general by a decrease of mitochondrial respiration and OXPHOS, a consequence of disruptive mtDNA mutations commonly found in cancer cells, and thus one could say that the growth of cancer cells is directly limited by energetics.7 In order to survive, cancer cells must modify their mitochondrial physiology to optimize energy production to their changing environments. There are two types of advantageous mtDNA mutation in cancer cells: mutations that impair OXPHOS and serve to stimulate neoplastic transformation, and those that facilitate cancer cell adaption to changing bioenergetics environments.8 These mtDNA mutations would eventually lead to an enhanced generation of reactive oxygen species (ROS), which can act both as mutagens and cellular mitogens, and contribute directly to cancer progression.7 Therefore, it can be concluded that mitochondrial alterations are critical for cancer initiation, promotion, and metastasis (Fig 1). Figure 1. Integrated mitochondrial paradigm to explain genetic and phenotypic complexities of metabolic and degenerative disease, aging, and cancer.Top three arrows: factors that have impact on mitochondrial OXPHOS robustness, risk for developing disease symptoms. Central oval arrows: pathophysiological basis of disease processes and the basis of disease progression. Lower five arrows: summarized disease categories and phenotypic outcomes of disturbed mitochondrial energy transformation. Bottom arrow: effect of the problematic accumulation of somatic mtDNA mutations resulting in delayed onset and a progressive course of diseases and aging. Right arrow: clinical problems that can result from reduced energy production in the most energetic tissues: the brain, heart, muscle, and kidney. Left arrow: indicates the metabolic effects of mitochondrial dysfunction, which result in the perturbation of the body’s energy balance. Lower right arrow: mitochondrial alterations are critical for cancer initiation, promotion, and metastasis. Lower left arrow: the hypothesized inflammatory and autoimmune responses that may result from chronic introduction of mitochondria’s bacteria-like DNA and N-formylmethionine proteins into the bloodstream.9

Synergistic interaction between quercetin and doxorubicin on MCF-7 human breast cancer cell line Abdul Khairul Rizki Purba; . Mustofa; Indwiani Astuti
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 45, No 03 (2013)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

The effectiveness of doxorubicin has decreased due to resistance of cancer cells. One of thenatural ingredients that are proven to reduce the resistance to anticancer is quercetin. Quercetininteracts with doxorubicin via a competition of P-glycoprotein (P-gp) transporter activity. Theaim of this study is to evaluate the interaction of quercetin and doxorubicin as cytotoxicityeffect on MCF-7 cells. Cytotoxicity test was conducted by the MTT method. Mechanism ofinteraction between doxorubicin and quercetin was evaluated with isobologram analysis.Doxorubicin and quercetin inhibited the growth of MCF-7 cells significantly. Doxorubicin andquercetin respectively had IC50 of 21M and 103 M. The interaction of doxorubicin and quercetinwere characterized by the amount of doxorubicin IC50 equivalent and quercetin IC50 equivalentless than 1 and the point-intercept of each IC50 notation equivalent plotted on the graph belowthe additive line. Analysis of isobolograms indicated that the interaction doxorubisn and quercetinin each of the ratios had synergy. Quercetin can be considered to be in a combination wit

Cytotoxic activity of simvastatin in T47D breast cancer cell lines and its effect on cyclin D1 expression and apoptosis Bayu Putra; Mae Sri Hartati Wahyuningsih; Eti Nurwening Sholikhah
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 49, No 2 (2017)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Background: Statins (HMG-CoA Inhibitors) is a drug used for decreasing plasma cholesterol levels and used in therapy to prevent coronary artery disease. Research in animals and epidemiological studies showed that statin therapy can decrease risk against cancer associated with cholesterol. Based on that result then research of cytotoxic activity against simvastatin knowing cultur T47D breast cancer cells and his influence in decreasing expression of cyclin D1 and induction of apoptosis has been done.Research objectives: The aims of this research is to prove activities of simvastatin against T47D breast cancer cell culture, especially to examine cytotoxic activity, cyclin D1 expression, and simvastatin effect in apoptotic induction.Research method: The type of this research is quasi experiment with using posttest with non-equivalent control group design. Cytotoxicity test performed on T47D breast cancer cell cultures using MTT assay to determine IC50 values after given simvastatine. Expression of cyclin D1 and apoptosis induction test detected using flow cytometry with antibody monoclonal anti-cyclin D1 and Annexin V-Pi, then analyzed by FACS-Calibur program.Results: Simvastatin has cytotoxic effect against T47D breast cancer cells with IC50 values 25.25 µg/mL. Simvastatin with concentrations of 6.31; 12.62; 25.25 and 50.5 µg/mL was able to decrease the cyclin D1 expression. Furthermore, simvastatin can induce apoptosis with EC50 values 26.96 µg/mL in T47D breast cancer cells.Conclusion: Simvastatin has cytotoxic activity of in T47D breast cancer cells and decreasing cyclin D1 expression and inducing apoptosis activity in T47D breast cancer cells.Keywords: simvastatin, cytotoxic, cyclin D1, apoptotic, T47D.

Low CD4+ T cell counts are not risk factor for Malassezia species infection in HIV/AIDS patients Epi Panjaitan; Satiti Retno Pudjiati; Agnes Sri Siswati
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 46, No 04 (2014)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Human immunodefiiency virus (HIV) infection and aquired immunodeficiency syndrome (AIDS)cause a progressive depletion of CD4+ T cell populations accompanied by progressive impairmentof cellular immunity and increasing susceptibility to opportunistic infections. Seborrheic dermatitisis one of the most common skin opportunistic infections on HIV/AIDS patients. Malasseziaspecies is bilieved as the causative of seborrheic dermatitis. The aim of the study was to evaluatelow CD4+ T cell counts as risk factor for Malassezia sp. infection in HIV/AIDS patients. This wasan observational study with cross-sectional design conducted on HIV/AIDS patients who attendedin Department of Dermatology and Venereology, Faculty of Medicine Universitas Gadjah Mada/Dr Sardjito General Hospital, Yogyakarta and met the inclusion and exclusion criteria. Culture ofMalassezia sp. was conducted in Department of Microbiology and classified as high (>100 CFU/tape) and low (<100 CFU/tape) density colonies. CD4+ T cell counts were measured in Departmentof Clinical Pathology and classified as high (>200 cells/mm3) and low (<200 cells/mm3) CD4+ Tcell counts. A total of 83 subjects with HIV/AIDS comprising 54 (65.1%) males and 29 (34.9%)females aged 20 - >60 years were involved in the study. The number of Malassezia sp. colonyon subjects with high and low CD4+ T cell counts were 31.55 ± 26.21 and 25.2 ± 33.89 CFU/tape, respectively. No significantly relationship between between CD4+ T cell count and Malasseziasp. colony number was observed in the study (p=0.607; 95%CI=0.04-5.19; RP=0.452). Inconclusion, low CD4+ T cell counts is not risk factor for Malassezia sp. infection in HIV/AIDSpatients.

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Home Page

OAI Link

Editorial Team

Contact

Reviewer

Google Scholar

Contact Name
Nurhadiyahya

Contact Email
nurhadiyahya@ugm.ac.id

Phone
+6289672800034

Journal Mail Official
jmedscie@ugm.ac.id

Editorial Address
https://jurnal.ugm.ac.id/bik/about/editorialTeam

Location
Kab. sleman,

Daerah istimewa yogyakarta

INDONESIA

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Home Page

OAI Link

Editorial Team

Contact

Reviewer

Google Scholar

Contact Name Nurhadiyahya

Contact Email nurhadiyahya@ugm.ac.id

Phone +6289672800034

Journal Mail Official jmedscie@ugm.ac.id

Editorial Address https://jurnal.ugm.ac.id/bik/about/editorialTeam

Location Kab. sleman, Daerah istimewa yogyakarta INDONESIA

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Contact Name
Nurhadiyahya

Contact Email
nurhadiyahya@ugm.ac.id

Phone
+6289672800034

Journal Mail Official
jmedscie@ugm.ac.id

Editorial Address
https://jurnal.ugm.ac.id/bik/about/editorialTeam

Location
Kab. sleman,

Daerah istimewa yogyakarta

INDONESIA