Garuda - Garba Rujukan Digital

Article Per Year (5 Year)

All

Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

bik
Website

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 41 Documents

1 2 3 4 5

Search results for , issue "Vol 48, No 4 (2016)" : 41 Documents clear

Expression of Circulating microRNA-141 and mRNA of PTEN (Phosphatase and Tensin Homolog) in Blood Plasma of Ovarian Tumor and Epithelial Ovarian Cancer Patient AS. Fitriawan; SN Chasanah; FK Pakun; AI Kartika; R. Oktriani; A. Trirahmanto; H. Prajatmo; A. Ghozali; T. Aryandono; SM. Harjana
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 48, No 4 (2016): SUPPLEMENT
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Epithelial Ovarian Cancer (EOC) is the most lethal gynecological malignancies among woman. The majority of this disease is diagnosed at the advanced stage due to lack of specific symptoms and effective screening methods. Therefore, an adequate biomarker for early detection is needed and may improve patient survival. microRNA is a small non-coding RNA that regulates gene expression in post-transcriptional level. Several studies have shown the ability to detect microRNA in blood circulation so microRNA may be used as a minimally invasive biomarker for EOC. microRNA-141 (miR-141) plays a major role in EOC by regulating expression of several tumor suppressor gene. Previous study have confirmed that miR-141 regulated PTEN gene directly by interacting with 3’UTR sequence of PTEN mRNA, and upregulation of miR-141 caused downregulation of PTEN expression in vivo. PTEN is important tumor suppressor gene that its inactivation found in various human cancer. PTEN is protein with lipid phosphatase activity that negatively regulate PI3K-AKT signaling pathway, thus playing a important role in various cellular process such as proliferation, growth, cell survival, EMT, cell motility, and angiogenesis. When various studies found that PTEN mRNA and protein expression is significantly downregulated in EOC tissue, little is known about the expression of PTEN mRNA in blood circulation of EOC patient, especially in Yogyakarta population.The aims of this study is to measure and to investigate the correlation of miR-141 and mRNA PTEN expression in plasma of ovarian tumor patient and EOC patient.This study used cross-sectional design. 25 blood plasma of ovarian tumor and 25 blood plasma of EOC were collected. Total RNA was isolated and reverse transcribed to obtain cDNA. The expression of miR-141 and mRNA PTEN were measured by quantitative real-time polymerase chain reaction assay (qPCR). The 2^(-∆∆cq) method was used to calculate relative quantification of miR-141 and mRNA PTEN using miR-16 as reference gene for microRNA and beta-actin mRNA as reference genes for PTEN mRNA. Expression of miR-141 is significantly elevated in blood plasma of epithelial ovarian cancer patient compared to the ovarian tumor (p=0,001, fold change=7,59). Expression of PTEN mRNA significantly downregulated in blood plasma of epithelial ovarian cancer patient compared to the ovarian tumor (p=0,001, fold change=11,63). There was a significant negative correlation between miR-141 expression and mRNA PTEN expression in blood plasma of epithelial ovarian cancer patient (p=0,033; r=-0,428).miR-141 and mRNA PTEN differentially expressed in blood plasma of ovarian tumor and epithelial ovarian cancer patient. There was a negative correlation between miR-141 and mRNA PTEN expression in blood plasma of epithelial ovarian cancer patient. Keywords: Epithelial ovarian cancer, circulating microRNA, miR-141, PTEN mRNA

A Comprehensive Exploration of Java Man: Bio-Cultural Evolution from Homo erectus to Homo sapiens Samuel J Haryono; Sri Utami; Restu Ambar Rahayuningsih
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 48, No 4 (2016): SUPPLEMENT
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

ABSTRACTAn overlap of time period between Homo erectus and Homo sapiens has not been confirmed. In the history of man, there have been two missing links: one between man and ape, and one between progressive Homo erectus and archaic Homo sapiens. Specimen dating on Java Man has been discrepant among research groups, and the use of molecular biology in ancient specimens has been a novelty. This study intends to use fossilised specimens, to harvest DNA to be sequenced for ribosomal DNA analysis for comparative phylogeny among ancient and modern man and other hominids. Dental calculus will be analysed to identify starch, carbohydrate, and protein to illustrate paleo dietary pattern. Soil samples will be examined for pollen and phytoliths to elaborate on ancient ecosystem. Blood samples will be procured from indigenous people along the riverflow region of Bengawan Solo to analyse modern human DNA. We hope that we may reconstruct the evolution pathway, construct the phylogenetic tree between ancient and modern hominids, and discover the uniqueness of Homo sapiens sapiens.Keywords: Java Man, Ribosomal DNA, Hominid Phylogenetic,

BRCA1 and BRCA2 Germline Mutations in Asian and European Populations Ute Hamann
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 48, No 4 (2016): SUPPLEMENT
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Women who carry a pathogenic mutation in the breast cancer susceptibility genes BRCA1 or BRCA2 (BRCA) have markedly increased risks of developing breast and ovarian cancers during their lifetime. It has been estimated that their breast and ovarian cancer risks are in the range of 46-87% and 15-68%, respectively. Therefore it is of utmost clinical importance to identify BRCA mutation carriers in order to target unaffected women for prevention and/or close surveillance and to help affected women choose the best chemotherapy regimen.Genetic testing for BRCA germline mutations is expanding in clinical oncology centers worldwide. Given the high costs of complete BRCA gene screens, a lot of effort has been expended on deciding upon whom to test. Relevant issues involved in decision making include the prior probability of a woman having a BRCA mutation, which is a function of her age and her disease status, her ethnic group, and her family history of breast or ovarian cancer.The frequency and spectrum of mutations in these genes show considerable variation by ethnic groups and by geographic regions. Most studies have been conducted in European and North American populations, while studies in Asian, Hispanic, and African populations are fewer. In most populations, many BRCA mutations were identified, which were distributed all over the genes. However, in some populations, a relatively small number of specific BRCA mutations are recurrent and account for the majority of all mutations in that population. Many of the recurrent mutations are founder mutations, which were derived from a common ancestor. Founder mutations are present in Ashkenazi Jewish, European, and Islander (Faroe, Easter, and Pitcairn) populations. Such mutations have also been identified in patients from several Asian, South American, and African countries. Population-specific genetic risk assessment and genetic mutation screening have been facilitated at low costs. Given that mutations in the BRCA genes are distributed in populations throughout the world, it is important that the benefits of genetic testing and of targeted therapies be made available not only to women from developed countries in Europe and North America, but also to those from less developed countries in Asia, Africa and South America.

The Expression of Homo Sapiens microRNA-21 (Hsa-miR-21-5p) and mRNA Reversion Inducing Cysteine Rich Protein with Kazal Motifs (RECK) in Plasma of Epithelial Ovarian Cancer Aprilia Indra Kartika; SN Chasanah; AS Fitriawan; DS Tanjung; MS Ftria; FK Pakun; R Oktriani; A Trirahmanto; H Prajatmo; T Aryandono; SM Haryana
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 48, No 4 (2016): SUPPLEMENT
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

ABSTRACT Epithelial Ovarian Cancer (EOC) is malignant cancer that caused death for most women in Indonesia. The emergence of EOC showed no specific symptoms in its early stages; that makes the screening mostly occur when patients are in advanced stage. Treatment of EOC at an advanced stage will be more challenging with poor prognosis. Therefore, minimally invasive biomarkers are needed to diagnose at the early stage. microRNA is one of the potential biomarkers which not only expressed inside the cell but also secreted outside the cell with exosome protection. This protection makes microRNA stable. Moreover, several studies have shown the ability to detect microRNA in the blood sample. microRNA-21 (miR-21) is oncomiR which targeted tumor suppressor mRNA RECK based on in silico analysis.The first aim is to determine the expression of miR-21 in plasma samples of EOC patients compared with healthy controls. The second aim is to investigate the expression correlation between miR-21 and RECK mRNA.Blood samples were collected from 30 patients and 30 healthy controls. Plasma was then obtained from centrifugated blood samples. The total RNA was isolated and reverse transcribed to produce cDNAs. cDNAs were then quantified using qPCR using specific primer for miR-21 and RECK mRNA. The expression analysis was done relative expression method by Livak. The expression of miR-21 was calculated using the miR-16 expression as the reference gene. Also, Beta-actin was used as reference gene for RECK mRNA calculation. The correlation between the expression of miR-21 and mRNA RECK was analyzed using the Spearman rho correlation analysis.In this study showed the expression of miR-21 in patients with EOC increased 4.7579-fold compared with healthy controls (p <0.05). On the other hand, the miR-21 target, RECK mRNA, decreased 4,2 times with fold change 0.237665 on plasma EOC patients compared with healthy controls (p <0.05). The statistical calculation of the expression of miR-21 and mRNA RECK was inversely proportional to mRNA RECK with a strong correlationThis study has been able to prove that the expression of miR-21 is up-regulated in EOC patients and confirmed by the down-regulation of RECK expression. The next research challenge is to make anti-miR-21 to suppress the expression of miR-21 in EOC, which can be analyzed the effect of miR-21 in the development of EOC.

ROLE OF DNA METHYLATION AS A DIAGNOSTIC BIOMARKER OF SPORADIC BREAST CANCER Wirsma Arif Harahap
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 48, No 4 (2016): SUPPLEMENT
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

The initiation and progression of breast cancer have been recognized for many years to be secondary to the accumulation of genetic mutations which lead to aberrant cellular function. Genetic mutations, either inherited or sporadic, may result in the activation of oncogenes and the inactivation of tumor suppressor genes. The more recent discovery that reversible alterations in histone proteins and deoxyribonucleic acid (DNA) can also lead to tumorigenesis has introduced a novel term to the field of cancer research: epigenetics. Epigenetics refers to the study of heritable changes in gene regulation that do not involve a change in the DNA sequence. The most often studied in epigenetics of breast cancer is DNA methylation. That a promoter methylation result in transcription blockade supports the notion that cellular inhibition takes place. Compared to normal tissues, hypermethylation occurs from double to triple in cancerous ones. DNA methylation plays a crucial role in oncogenesis and is one of the hallmarks of cancer.Detection of aberrantly methylated CpG islands in promoter region of several genes in DNA sample derived from nipple aspirates, serum, or cancer tissue associated with down regulation of expression or loss of function of these genes has been associated with early stages of breast cancer, where hypermethylation of CpG island points to poorer prognosis in breast cancer. DNA methylation has been identified as signature for TNBC. Methylation of BRCA1 gene is frequently demonstrated in young, estrogen receptor-negative breast cancer patients. Methylation of specific genes is known to differ across race and socioeconomic status. BRCA1 methylation in premenopausal women with sporadic breast cancer in West Sumatra region has been higher than in Western women.DNA methylation may be used to enhance current breast cancer classification. There is such a distinction between methylation and gene expression profiles of breast cancer that not all methylation profiles fit within the same molecular subtype. Specific gene methylation profiles are identified for basal-like, luminal A and HER2-overexpressing breast cancers. A number of studies have analyzed the methylation status of BRCA1, a key player in TNBC. One study demonstrated that BRCA1 promoter was methylated in TNBC. It was discovered that the sensitivity of TNBC cell lines to PARP inhibitors was increased when BRCA1 was methylated. Concurrently, BRCA1 methylation quantity was higher in patients with complete response than in those who are non-responders of neoadjuvant chemotherapy.Epigenetics is now the cutting edge of cancer research. Advances in this field will have major implications in diagnosis, prevention, treatment of cancer, and formulation of new epigenetically targeted cancer drugs.

Management of hereditary breast cancer: Surgeon's perspective Ava Kwong
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 48, No 4 (2016): SUPPLEMENT
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Mutations due to hereditary related genes such as BRCA1, BRCA2, TP53 and PTEN confer greater risk of developing breast cancer and for BRCA mutations, also ovarian cancer. The risk assessment based on genetic testing allows options of high risk surveillance, prevention and may now also guide use of specific therapies for treatment such as targeted therapies and use of platinum base chemotherapy. The choice of management, once an individual has been found to carry the BRCA mutation may also vary. Moreover the availability of genetic testing, method of testing such as the transition into the use of Next Generation Sequencing techniques has also increased options of clinicians to the choice of testing.Breast Surgeons are most likely to be the first person who encounters the first presentation of a breast cancer patient. It is important for breast surgeons to be actively involved in the referrals of patients for genetic testing and subsequently planning of the management of such high risk individuals in a multidisciplinary setting. Basic principles of genetic testing and choice of management will be discussed in reference to the surgeon’s perspectives. Keywords: mutations, BRCA1. BRCA2. TP53, PTEN, NGS, multidisciplinary setting

BRCA1 and BRCA2: Lack of Certainty and Its Clinical Implications Samuel J Haryono
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 48, No 4 (2016): SUPPLEMENT
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

AbstractIn this time of amounting cancer incidence and mortality, genetic testing may be greatly valuable in deciding on appropriate clinical management. It is unfortunate that the test is not a practical interrogative problem. When positive, the patients can settle down with what to do next, whereas when negative, their family members may breathe out in relief from unnecessary intensive surveillance and prophylaxis, and then there is VUS (Variants of Uncertain Significance). How should a health provider deliver the elaboration and implication of VUS to a patient who had expended a lump sum of and had expected a level of certainty? Variants of UncertainSignificance have nowadays become a challenging spoiler in the setting of clinical management of cancer. How would one inform someone else on anything uninformative? BRCA1 and BRCA2 are two genes with high penetrance in breast cancer. Since their functions as tumor suppressor genes and DNA repair regulators, their mutation effects are only visible when there is Loss of Heterozygosity. Mutation of BRCA1/2 gene can be demonstrated within the tissue specimen and blood sample DNA; that would mean it has occupied all tissues and is inheritable. In the case of BRCA1 and BRCA2 mutations, 10-20% of all genetic test results will read VUS, In one previous study of sixteen Indonesian patients, 13 (81,25%) patients had VUS. There were variants that had not been found in other population. Trans-academically speaking, the reclassification of VUS in BRCA1/2 gene is not merely a challenge to clarify its clinical impacts, but also an obligation to accomplish our community contribution to science.There can be a set of factors to suggest that a VUS may be a deleterious mutation:Co-segregation: when the variant comes with multiple and multigenerational incidence of cancer, it is possible.Epidemiology: when a case control study demonstrates prevalence discrepancy, it is possible.Co-occurrence with deleterious mutation: when the variant is shared within the same gene in other individuals, it is possible.Evolutionary data: when the sequence is carried across species, it is possible.Amino acid substitution: when the substitute is structurally similar, it is impossible.Loss of heterozygosity: when there is loss of a wild type allele in tumor specimen, it is possible.Functional analysis: should an in vitro assay demonstrate a loss of protein function, it is probable.The ultimate solution is not yet available. However, there is clinical significance for families with VUSs, only if that can confidently be classified as the presence or absence of the associated disease. That condition may be achieved by increasing the availability of genetic testing so that there can be a larger, open-access repertoire of VUSs.

One Step Nucleic Acid Amplification (OSNA) Study in Indonesia Samuel J Haryono; Lenny Sari; Sony Sugiharto; I Gusti Bagus Datasena; Raymond Mulyarahardja; . Rudianto
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 48, No 4 (2016): SUPPLEMENT
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

ABSTRACTSentinel lymph node (SLN) is defined as the first of a few selected lymphatic nodes, into which lymphatic fluid from a primary tumor drains. Streamlined processing of sentinel lymph nodes (SLN) for detection of lymph node metastasis involves the able command over methodical blocks of SLN identification, surgical removal of SLN and SLN analysis. One Step Nucleic Acid Amplification (OSNA) method, which relies on CK19 mRNA expression to detect intraoperatively lymph node metastases in breast cancer cases, emerged as a plausible alternative to the current gold standard that uses histopathological node analysis. Sixty selected axillary sentinel lymph nodes from thirty breast cancer patients. Sentinel lymph nodes were directly bi-halved after collection using customized lymph node cutting device (Sysmex), or scalpel. The first halves were subjected to histopathological examination and were stored in specimen containers containing fresh formaldehyde prior to processing. The adjacent halves were weighed to comply with the required mass by OSNA detection in the range of 50 – 600 mg and wrapped in clean foils for storage in -80°C prior to OSNA analysis. 60 SLNs were same diagnosis using both methods. 25 SLNs were negative and 25 SLNs were positive using both methods. 3 SLNs were positive on OSNA but negative on histology. Other 7 SLNs were negative on OSNA but positive on histology, and these 1 nodes contained only micrometastasis lesion. These results suggest that OSNA is a useful for detecting SLNs metastasis, but a copy number of CK19 might be an indepedent factor from prediction and prognosis of breast cancer.

THE EXPRESSION OF Hsa-miR-21-5p AS MINIMAL INVASIVE MARKER TO ADJUVANT CHEMOTHERAPY IN BREAST CANCER PATIENTS Dewi Safitri Tanjung; MS. Fitria; AI. Kartika; D. Rakhmina; SL. Anwar; R. Oktriani; . Irianiwati; SM. Harjana; T. Aryandono
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 48, No 4 (2016): SUPPLEMENT
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

AbstractBreast cancer remains the leading cause of death among women, and there is a need to develop minimally invasive marker. In our previous study based on clinicopathologic in pre-chemotherapy patients showed miR-21 was upregulated 1.32 times higher at advanced stage compared with early stage. Therefore the matched patients for post-chemotherapy samples were used. The aim of this research is to examine the expression of miR-21 as potential marker to adjuvant chemotherapy in breast cancer patients. The samples were taken by using cross sectional method with total 39 blood plasma samples from breast cancer patients in adjuvant chemotherapy and 12 healthy control samples. Plasma was obtained from blood samples and then RNA isolated were performed. Total RNA was reverse transcribed using cDNA synthesis. The expression of miR-21 was then analyzed using specific primer for miR-21 and miR-16 as the reference gene. Livak Method was used to calculate the expression level in each group. The result showed that there is significant downregulated expression of miR-21 in postchemotherapy 2.61 fold compared with pre-chemotherapy (p<0.05). The expression of miR-21 upregulated 2.2 folds (p<0.05) in pre-chemotherapy compared with healthy control, while in post-chemotherapy compared with healthy control, the expression of miR-21 was 0.8 fold (p<0.05). In conclusion, Hsa-miR-21-5p can be used as marker for adjuvant chemotherapy response in breast cancer because there is significant different expression between prechemotherapy, post-chemotherapy and healthy control. The continuation research in the near future for detecting the expression of tumor suppressor protein regulated by miR-21 is needed.Keywords: breast cancer, adjuvant chemotherapy, miR-21, minimal invasive marker

Bacterionomics and vironomics in carcinogenesis Pratiwi Sudarmono
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 48, No 4 (2016): SUPPLEMENT
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Virus and bacteria are microbes which are very common cause human infection. Most of the bacterial infection can be eradicated by antibiotics and infection symptoms disappear. But for virus infection, once infected, the virus will persistently stay in the host, even undergo not only a lytic cycle but also integrated into host genome. Nowadays, at least 6 virus type are consistently related to human cancer, such as EBV,HPV,HTLV,HBV,HCV,HKSV, and the new one Merkel Virus (MCV). Although not every infected people will get cancer, but around 20% of the whole cancer in human are caused by viral oncogene.Class one oncogenic bacterial is Helicobacter pylori. Infection with this bacteria can cause persistent gastro duodenal inflammation which cause some alteration in gastric cell growth into transformation. Expression of Cag gene and Vac gene and some expression of OMP protein usually link to gastric cancer.Molecular mechanisms of carcinogenesis for every virus which cause infection is a very complex , which include several processes caused by cell transformation. Besides, other host and environmental factors are also play a significant role in cancer development. Some scientist put a Hallmark analysis as a model to quickly summarize what pathobiology process will happen and what gene or protein caused the process. The Hallmark analysis comprise of several process which may happen simultaneously because some of the Hallmark is caused by the same protein. The Hallmark consists of various virus strategies in oncogenesis such as promoting angiogenesis, avoiding immune destruction, genome instability and mutation, deregulating cellular energetic, resisting cell death, sustaining proliferative signaling, evading growth suppressors, enabling cellular immortality, promoting inflammation and activation metastasis. For example, infection by HPV, will cause low grade dysplasia which can continue to invasive cervical cancer. After host cell transformation, in the long control region genes, E6 and E7 protein will cause several strategies in oncogenesis including resisting cell death and evading growth suppressors. HBV infection will end without any serious liver damage, but after cell transformation, almost all Hallmark strategies of viral oncogenesis are happening step by step in line with the severity of liver cell damage.As the onset of cancer development after infection can last years, there are an opportunity to design either vaccine or genetic therapy to minimalize further risk of cancer in human

Page 3 of 5 | Total Record : 41

1 2 3 4 5

Filter by Year

2016 2016

Filter By Issues

All Issue Vol 55, No 4 (2023) Vol 55, No 3 (2023) Vol 55, No 2 (2023) Vol 55, No 1 (2023) Vol 54, No 4 (2022) Vol 54, No 3 (2022) Vol 54, No 2 (2022) Vol 54, No 1 (2022) Vol 53, No 4 (2021) Vol 53, No 3 (2021) Vol 53, No 2 (2021) Vol 53, No 1 (2021) Vol 52, No 3 (2020): Special Issue: COVID-19 Vol 52, No 4 (2020) Vol 52, No 3 (2020) Vol 52, No 2 (2020) Vol 52, No 1 (2020) Vol 51, No 4 (2019) Vol 51, No 3 (2019) Vol 51, No 2 (2019) Vol 51, No 1 (2019) Vol 50, No 4 (2018) Vol 50, No 3 (2018) Vol 50, No 2 (2018) Vol 50, No 1 (2018): SUPPLEMENT Vol 50, No 1 (2018) Vol 49, No 4 (2017) Vol 49, No 3 (2017) Vol 49, No 2 (2017) Vol 49, No 1 (2017) Vol 48, No 4 (2016) Vol 48, No 4 (2016): SUPPLEMENT Vol 48, No 3 (2016) Vol 48, No 2 (2016) Vol 48, No 1 (2016) Vol 47, No 01 (2015) Vol 47, No 4 (2015) Vol 47, No 3 (2015) Vol 47, No 2 (2015) Vol 46, No 04 (2014) Vol 46, No 04 (2014) Vol 46, No 03 (2014) Vol 46, No 03 (2014) Vol 46, No 02 (2014) Vol 46, No 02 (2014) Vol 46, No 01 (2014) Vol 46, No 01 (2014) Vol 45, No 04 (2013) Vol 45, No 04 (2013) Vol 45, No 03 (2013) Vol 45, No 03 (2013) Vol 45, No 02 (2013) Vol 45, No 02 (2013) Vol 45, No 01 (2013) Vol 45, No 01 (2013) Vol 44, No 02 (2012) Vol 44, No 02 (2012) Vol 44, No 01 (2012) Vol 44, No 01 (2012) Vol 43, No 02 (2011) Vol 43, No 02 (2011) Vol 43, No 01 (2011) Vol 43, No 01 (2011) Vol 42, No 01 (2010) Vol 42, No 01 (2010) Vol 41, No 04 (2009) Vol 41, No 04 (2009) Vol 41, No 03 (2009) Vol 41, No 03 (2009) Vol 41, No 02 (2009) Vol 41, No 02 (2009) Vol 41, No 01 (2009) Vol 41, No 01 (2009) Vol 40, No 04 (2008) Vol 40, No 04 (2008) Vol 40, No 03 (2008) Vol 40, No 03 (2008) Vol 40, No 02 (2008) Vol 40, No 02 (2008) Vol 40, No 01 (2008) Vol 40, No 01 (2008) Vol 39, No 04 (2007) Vol 39, No 04 (2007) Vol 39, No 03 (2007) Vol 39, No 03 (2007) Vol 39, No 02 (2007) Vol 39, No 02 (2007) Vol 39, No 01 (2007) Vol 39, No 01 (2007) Vol 38, No 04 (2006) Vol 38, No 01 (2006) Vol 37, No 04 (2005) Vol 37, No 04 (2005) Vol 37, No 03 (2005) Vol 37, No 03 (2005) Vol 37, No 02 (2005) Vol 37, No 02 (2005) Vol 37, No 01 (2005) Vol 37, No 01 (2005) Vol 36, No 4 (2004) Vol 36, No 4 (2004) Vol 36, No 3 (2004) Vol 36, No 3 (2004) Vol 36, No 2 (2004) Vol 36, No 2 (2004) Vol 36, No 1 (2004) Vol 36, No 1 (2004) Vol 35, No 4 (2003) Vol 35, No 4 (2003) Vol 35, No 3 (2003) Vol 35, No 3 (2003) Vol 35, No 2 (2003) Vol 35, No 2 (2003) Vol 34, No 04 (2002) Vol 34, No 04 (2002) Vol 34, No 03 (2002) Vol 34, No 03 (2002) Vol 34, No 02 (2002) Vol 34, No 02 (2002) Vol 34, No 01 (2002) Vol 34, No 01 (2002) Vol 33, No 04 (2001) Vol 33, No 04 (2001) Vol 33, No 03 (2001) Vol 33, No 03 (2001) Vol 33, No 02 (2001) Vol 33, No 02 (2001) Vol 31, No 04 (1999) Vol 31, No 04 (1999) Vol 31, No 03 (1999) Vol 31, No 03 (1999) Vol 31, No 02 (1999) Vol 31, No 02 (1999) Vol 31, No 01 (1999) Vol 31, No 01 (1999) Vol 30, No 03 (1998) Vol 30, No 03 (1998) Vol 30, No 02 (1998) Vol 30, No 02 (1998) Vol 30, No 01 (1998) Vol 30, No 01 (1998) Vol 29, No 04 (1997) Vol 29, No 04 (1997) Vol 29, No 03 (1997) Vol 29, No 03 (1997) Vol 29, No 02 (1997) Vol 29, No 02 (1997) Vol 29, No 01 (1997) Vol 29, No 01 (1997) Vol 28, No 04 (1996) Vol 28, No 04 (1996) Vol 28, No 03 (1996) Vol 28, No 03 (1996) Vol 28, No 02 (1996) Vol 28, No 02 (1996) Vol 28, No 01 (1996) Vol 28, No 01 (1996) Vol 27, No 04 (1995) Vol 27, No 04 (1995) Vol 27, No 03 (1995) Vol 27, No 03 (1995) Vol 27, No 02 (1995) Vol 27, No 02 (1995) Vol 27, No 01 (1995) Vol 27, No 01 (1995) Vol 26, No 03 (1994) Vol 26, No 03 (1994) Vol 26, No 02 (1994) Vol 26, No 02 (1994) Vol 26, No 01 (1994) Vol 26, No 01 (1994) Vol 25, No 04 (1993) Vol 25, No 04 (1993) Vol 25, No 03 (1993) Vol 25, No 03 (1993) Vol 25, No 02 (1993) Vol 25, No 02 (1993) Vol 25, No 01 (1993) Vol 25, No 01 (1993) Vol 24, No 04 (1992) Vol 24, No 04 (1992) Vol 24, No 03 (1992) Vol 24, No 03 (1992) Vol 24, No 02 (1992) Vol 24, No 02 (1992) Vol 24, No 01 (1992) Vol 24, No 01 (1992) Vol 23, No 04 (1991) Vol 23, No 04 (1991) Vol 23, No 03 (1991) Vol 23, No 03 (1991) Vol 23, No 02 (1991) Vol 23, No 02 (1991) Vol 23, No 01 (1991) Vol 23, No 01 (1991) Vol 22, No 04 (1990) Vol 22, No 04 (1990) Vol 22, No 03 (1990) Vol 22, No 03 (1990) Vol 22, No 02 (1990) Vol 22, No 02 (1990) Vol 22, No 01 (1990) Vol 22, No 01 (1990) Vol 21, No 04 (1989) Vol 21, No 04 (1989) Vol 21, No 03 (1989) Vol 21, No 03 (1989) Vol 21, No 02 (1989) Vol 21, No 02 (1989) Vol 21, No 01 (1989) Vol 21, No 01 (1989) Vol 20, No 04 (1988) Vol 20, No 04 (1988) Vol 20, No 03 (1988) Vol 20, No 03 (1988) Vol 20, No 02 (1988) Vol 20, No 02 (1988) Vol 20, No 01 (1988) Vol 20, No 01 (1988) Vol 19, No 04 (1987) Vol 19, No 04 (1987) Vol 19, No 03 (1987) Vol 19, No 03 (1987) Vol 19, No 02 (1987) Vol 19, No 02 (1987) Vol 19, No 01 (1987) Vol 19, No 01 (1987) Vol 18, No 04 (1986) Vol 18, No 04 (1986) Vol 18, No 03 (1986) Vol 18, No 03 (1986) Vol 18, No 02 (1986) Vol 18, No 02 (1986) Vol 18, No 01 (1986) Vol 18, No 01 (1986) Vol 17, No 03 (1985) Vol 17, No 03 (1985) Vol 17, No 02 (1985) Vol 17, No 02 (1985) Vol 17, No 01 (1985) Vol 17, No 01 (1985) Vol 16, No 04 (1984) Vol 16, No 04 (1984) Vol 16, No 02 (1984) Vol 16, No 02 (1984) Vol 16, No 01 (1984) Vol 16, No 01 (1984) Vol 15, No 03 (1983) Vol 15, No 03 (1983) Vol 15, No 02 (1983) Vol 15, No 02 (1983) Vol 13, No 04 (1981) Vol 13, No 04 (1981) Vol 13, No 03 (1981) Vol 13, No 03 (1981) Vol 13, No 02 (1981) Vol 13, No 02 (1981) Vol 13, No 01 (1981) Vol 13, No 01 (1981) Vol 12, No 04 (1980) Vol 12, No 04 (1980) Vol 12, No 03 (1980) Vol 12, No 03 (1980) Vol 12, No 02 (1980) Vol 12, No 02 (1980) Vol 12, No 01 (1980) Vol 12, No 01 (1980) Vol 10, No 04 (1978) Vol 10, No 04 (1978) Vol 10, No 03 (1978) Vol 10, No 03 (1978) Vol 10, No 02 (1978) Vol 10, No 02 (1978) Vol 10, No 01 (1978) Vol 10, No 01 (1978) Vol 9, No 04 (1977) Vol 9, No 04 (1977) Vol 9, No 03 (1977) Vol 9, No 03 (1977) Vol 9, No 02 (1977) Vol 9, No 02 (1977) Vol 9, No 01 (1977) Vol 9, No 01 (1977) Vol 8, No 04 (1976) Vol 8, No 04 (1976) Vol 8, No 03 (1976) Vol 8, No 03 (1976) Vol 8, No 02 (1976) Vol 8, No 02 (1976) Vol 8, No 01 (1976) Vol 8, No 01 (1976) Vol 7, No 04 (1975) Vol 7, No 04 (1975) Vol 7, No 03 (1975) Vol 7, No 03 (1975) Vol 7, No 02 (1975) Vol 7, No 02 (1975) Vol 7, No 01 (1975) Vol 7, No 01 (1975) Vol 6, No 04 (1974) Vol 6, No 04 (1974) Vol 6, No 03 (1974) Vol 6, No 03 (1974) Vol 6, No 02 (1974) Vol 6, No 02 (1974) Vol 6, No 01 (1974) Vol 6, No 01 (1974) Vol 5, No 04 (1973) Vol 5, No 04 (1973) Vol 5, No 03 (1973) Vol 5, No 03 (1973) Vol 5, No 02 (1973) Vol 5, No 02 (1973) Vol 5, No 01 (1973) Vol 5, No 01 (1973) More Issue

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