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All Journal BALI MEDICAL JOURNAL (BMJ) journal of internal medicine INDONESIAN JOURNAL OF BIOMEDICAL SCIENCES E-Jurnal Medika Udayana Jurnal Teknik ITS IPTEK Journal of Proceedings Series R.E.M (Rekyasa Energi Manufaktur) Jurnal Berkala Kedokteran The Indonesian Biomedical Journal Jurnal Administrasi Pendidikan Indonesia Jurnal Penyakit Dalam Udayana Jurnal Kelautan Nasional Wave: Jurnal Ilmiah Teknologi Maritim ISM (Intisari Sains Medis) : Jurnal Kedokteran International Journal of Marine Engineering Innovation and Research Jurnal Sosial dan Teknologi MAHESA : Malahayati Health Student Journal GANESHA MEDICINA Public Health and Preventive Medicine Archive Makara Journal of Technology Jurnal Penyakit Dalam Indonesia WAVE: Jurnal Ilmiah Teknologi Maritim
I Ketut Suastika
Institut Teknologi Sepuluh Nopember Surabaya
Humanities Automotive Engineering Biochemistry, Genetics & Molecular Biology Chemical Engineering, Chemistry & Bioengineering Civil Engineering, Building, Construction & Architecture Computer Science & IT Control & Systems Engineering Decision Sciences, Operations Research & Management Dentistry Earth & Planetary Sciences Education Electrical & Electronics Engineering Energy Engineering Environmental Science Health Professions Immunology & microbiology Industrial & Manufacturing Engineering Law, Crime, Criminology & Criminal Justice Materials Science & Nanotechnology Mechanical Engineering Medicine & Pharmacology Nursing Physics Public Health Transportation

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Journal : indonesian journal of biomedical sciences

 1 
INTERLEUKIN-1?, INTERLEUKIN-6, AND ANTAGONIST INTERLEUKIN-1RECEPTOR AS MEMORY IMPAIRMENT RISK FACTOR IN COMPLEX PARTIAL EPILEPSY Purwa-Samatra, D. P. G.; Sudewa-Djelantik, A. A. G.; Suastika, and K.
INDONESIAN JOURNAL OF BIOMEDICAL SCIENCES Vol 7 No 1 (2013): IJBS Vol.7 No.1 January-June 2013
Publisher : Udayana University

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Abstract

Memory impairment is one of the most common adverse following epilepsy, particularly complex partial epilepsy. Cytokines physiologically play an important role in memory impairment by preventing long term potentiation process in hypocampus. Several literatures have mentioned that IL-1b, IL-6 and antagonist receptor IL-1Ra are crucial cytokines in complex partial epilepsy. This study aims to find out whether high level of IL-1b and IL-6 as well as low level of IL-1Ra might be risk factors of memory impairment in complex partial epilepsy patient. This was a case control study, enrolling 30 complex partial epilepsy patients with memory impairment as case group and 30 complex partial epilepsy patients without memory impairment as control group. In this study, it was obtained that the mean of IL-1? level in case group was significantly higher compared to the control (2.74 ± 4.36 vs. 0.42 ± 0.18 pg/ml, p = 0.007). The mean of IL-6 in case group was significantly higher compare to control (5.89 ± 6.32 vs. 2.34 ± 1.80 pg/ml, p = 0.006). The mean of IL-1Ra level of the case group was not significantly higher compared to the control (519.81 ± 262.64 vs. 413.28 ± 106.85, p = 0.767). By applying bivariate analysis, McNemar’s test, we observed that IL-1? with cut off point 0.63 pg/ml and OR = 70 is a risk factor of memory impairment in complex partial epilepsy indicated by p = 0.001. Similar result was also gained for IL-6 with cut off point 2.87 pg/ml and OR = 4.57 as a risk factor of memory impairment in complex partial epilepsy indicated by p = 0.007. Meanwhile, IL- 1Ra with cut off point 471 pg/ml and OR = 0.727 was not as a risk factor of memory impairment in complex partial epilepsy indicated by p = 0.573. It can be concluded that the high level of IL-1B and IL-6 were the risk factors of memory impairment in complex partial epilepsy patients. High level 1L-1B patient was 70 times higher risk of becoming memory impaired. High IL-6 patients will have the risk nearly 5 times higher. The low level of IL-1Ra does not as a risk factor in epilepsy patients for having the following memory impairment.
LOW PLASMA CORTISOL LEVEL IS A RISK FACTOR FOR ADULT ATOPIC DERMATITIS AND NEGATIVELY CORRELATED TO PLASMA LEVELS OF NOREPINEPHRINE AND INTERLEUKIN-4 Wardhana, Made; Suata, Ketut; Suastika, Ketut
INDONESIAN JOURNAL OF BIOMEDICAL SCIENCES Vol. 4, No. 1 Januari 2010
Publisher : Udayana University

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Abstract

Atopic dermatitis is a skin inflammatory disease characterized by hyperactivity of the humoral immune system with a typical onset in infancy or early childhood. Many studies have focused on the patho-physiological role of the immune system in atopic dermatitis, but since the stress hormone receptor was recognized on the surface of immune cells, it appeared that cortisol was prominent stress hormones in regulating the immune system. Some studies have shown that individuals with atopic diseases such as atopic dermatitis, allergic rhinitis and bronchial asthma had lower concentration of saliva cortisol than those with non-atopic conditions. With this evidence, it can be assumed that lower concentration of cortisol as the result of hypo-response of hypothalamus-pituitary-adrenal to stressor can increase and interleukin (IL-4) concentrations. Both substances stimulate lymphocyte T helper 2 (Th2) cells to synthesize IL-4, which has an important role in atopic dermatitis pathogenesis to increase hypersensitivity to various environmental allergens. Until recently, few studies are available concerning the low concentration of plasma cortisol as a risk factor for atopic dermatitis, as well as its correlation with plasma levels of and IL-4. The purpose of this study was to show that low concentration of plasma cortisol is a risk factor for atopic dermatitis and it is negatively correlated with and plasma IL-4. Matched pair case control design, involving 36 cases and 36 controls, was used to show that low concentration of cortisol is a risk factor for atopic dermatitis, and cross sectional design was applied to find out the negative correlation between cortisol and IL-4 in 88 samples consisting of 52 patients with atopic dermatitis and 36 healthy person or persons without atopy. The result of the case-control study showed that plasma cortisol concentration of the case group was significantly lower (4.89 + 2.1 ug/dl; CI 95 %; p < 0.001) than in those of the control group (9.12 + 2.33 ug/dl) at confidence level of 95%; p < 0.001. Multiple logistic regression analysis showed odd ratio of cortisol 3.45, which was higher than the ratio of other parameters such as IL-4, history of atopy and skin moisture. Plasma and IL-4 concentrations of the patients with atopic dermatitis were significantly higher than in the subjects without atopy. The correlation test indicated that plasma cortisol was negatively correlated to norepinephrine (r = - 0.68; p < 0.05), and IL-4 (r = - 0.55; p = 0.05) levels in patients with atopic dermatitis. Based on the above findings, it can be deduced that low concentration of plasma cortisol, being correlated to increased plasma levels of norepinephrne and interleukin-4, is a risk factor for atopic dermatitis in adult
HUBUNGAN POSITIF ANTARA ULKUS KAKI DIABETIK DENGAN PERSENTASE SEL BERMARKAH CD4+ PEMBAWA MALONDIALDEHID Putu SutirtaYasa, I Wayan; Suastika, Ketut; Sudewa Djelantik, Anak AgungGede; Mantik Astawa, I Nyoman
INDONESIAN JOURNAL OF BIOMEDICAL SCIENCES Vol. 3, No. 1 Januari 2009
Publisher : Udayana University

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Abstract

Tingginya angka kejadian ulkus kaki diabetik (UKD) dan luka di kaki yangsulit sembuh memberi petunjuk kemungkinan ada proses kematian sel imun yangsangat banyak dan belum jelas mekanismenya secara molekuler pada jaringan UKD.Telah diteliti hubungan antara derajat UKD dengan persentase sel bermarkahCD4+ pembawa malondialdehid (MDA). Penelitian ini adalah penelitianobservasional dengan rancangan cross sectional analytic study yang dilakukan diRumah Sakit pemerintah dan swasta di Denpasar, Badung, Tabanan, dan Gianyar.Parameter yang diukur dari bahan darah adalah kadar gula darah memakai metodeenzimatik (heksokinase), dan dari bahan jaringan kaki, dihitung sel bermarkah CD4+pembawa MDA memakai metode imunohistokimia (reagen dari Biodesign danAbcam ). Dari 80 sampel UKD didapatkan 49 (61,2%) penderita laki-laki dan 31(38.8%) penderita wanita, berdasarkan tingkat keparahan UKD, sampel dipilah lagimenjadi: 29 (31,9%) derajat 2; 20 (21,9%) derajat 3; 13 (14,3%) derjat 4; dan18(19,8%) derajat 5, rata-rata persentase sel bermarkah CD4+MDA adalah 75,0 ±20,5 %, Didapatkan korelasi positif kuat antara persentase sel bermarkah CD4+pembawa malondialdehid dengan derajat UKD (r = 0,71; p < 0,01). Pada penelitianini membuktikan ada mekanisme kematian sel imun dan sekaligus menjawabpermasalahan bahwa pada penderita UKD mudah terkena infeksi dan sulit untukdisembuhkan, dengan dibuktikan bahwa ada korelasi positif kuat antara derajat UKDdengan persentase pembentukan MDA dari sel bermarkah CD4+, ini menyatakanbahwa semakin berat derajat UKD semakin banyak mengalami kematian sel imun..
ALDEHYDE DEHIDROGENASE LEVEL AND FATTY ACID ETHYL ESTER AS BIOCHEMICAL MARKERS PERSIST LONGER THAN ETHANOL IN WISTAR RATS AFTER CHRONIC ALCOHOL CONSUMPTION Suaniti, Ni Made; Sudewa Djelantik, A. A. Gde; Suastika, Ketut; Mantik Astawa, Nyoman
INDONESIAN JOURNAL OF BIOMEDICAL SCIENCES Vol. 4, No. 2 Juli 2010
Publisher : Udayana University

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Abstract

Alcohol consumption in human has increased from year to year in Indonesia and more recently, anincreasing number of cases of alcohol intoxication, alcoholic liver disease, and death were observed.The purpose of this experimental study was to examine the significance of two known biochemicalmarkers of alcohol given by mouth in the Wistar rats. The study design used was the “Truerandomized experimental post test only control group design". The rats were randomly distributedaccording to the experimental design and were treated daily for six weeks (chronic intake) with 5%and 20% alcohol. This study used 15 rats with 5 rats for treatment group treated with 5% alcohol, 5rats for treatment group treated with 20% alcohol, and 5 rats as control group treated with distilledwater. The biochemical markers were aldehyde dehydrogenase (ALDH) and Fatty Acid Ethyl Esters(FAEE). ALDH and FAEE were two biochemical markers of ethanol which are sensitive and specificfor alcohol consumption. The study was conducted in two phases. Initially, rats were treated orallyeveryday for six weeks with 5% and 20% alcohol, and then the blood level of ethanol, ALDH andFAEE were measured. Blood samples were collected at 6 and 24 hours after the last oral intake ofchronic alcohol administration. Qualitative analysis was carried out to detect the presence of ethanol,ALDH, and FAEE in the treatment groups and quantitative analysis to determine their levels in theblood of Wistar rats. Statistical analysis of ALDH was done by using parametric test and the presenceof FAEE persisting longer than ethanol by non-parametric test. The results showed that ALDHpersisted and increased significantly following chronic consumption of alcohol in the rats. Similarly,FAEEs persisted longer than ethanol after alcohol intake. After six hours, the ALDH level increasedby 108.14% in the rat treated chronically with 5% alcohol and by 85.07% in rat treated with 20%alcohol. After 24 hours, FAEE also persisted longer in the blood than ethanol following treatmentwith alcohol 5%. ALDH levels increased by 83.11% after chronic treatment with 5% alcohol and by112.05% in the rats treated with 20% alcohol. In the blood collected 24 hours after the last treatmentwith 5% alcohol, ALDH increased by 95.11% and by 86.79% in the rats treated with 20% alcohol.FAEE persisted longer than ethanol in the blood following administration of 5 % and 20% alcoholboth at 24 hours following chronic treatment. The longer persisting ALDH and FAEE were new andgood biochemical blood markers for chronic alcohol consumption in the Wistar rats.
THE HIGH PLASMA RETINOL BINDING PROTEIN 4 LEVEL AS A RISK FACTOR CONSEQUENTLY OF TYPE 2 DIABETES MELLITUS OF ABDOMINAL OBESITY Budhitresna, AAG; Suastika, Ketut; Mantik Astawa, Nyoman; Santoso, Anwar
INDONESIAN JOURNAL OF BIOMEDICAL SCIENCES Vol. 5, No. 1 Januari 2011
Publisher : Udayana University

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Abstract

Abdominal obesity (Ab-Ob) related to cardiometabolic risk, that is riskfactor constellation for succeeded cardiovasculer disease and type 2 DiabetesMellitus (DM). That factors such as atherogenic dislipidemia, hypertension,hyperglycemia, protrombotic state, and proinflammation state. Type 2 DMcharacterised by insulin resistance (IR). Plasma levels of retinol binding protein 4(RBP4) that is secreted by adipocytes are increased in insulin resistance (IR) state.Experiment in mice suggest that elevated RBP4 level cause IR. Although theunderlying mechanism is not clearly understood, RBP4 considered playimportance role consequently of type 2 DM in Ab-Ob.This research was carried out to determine the role of high plasma RBP4level as a risk factor consequently of type 2 DM in Ab-Ob. The research wasconducted by cross sectional analytic in 81 patients with Ab-Ob and case controlstudy with matching on 33 patients with Ab-Ob type 2 DM as cases and 33patients with Ab-Ob non type 2 DM as control. The plasma of TNF-?, sTNFR1,and RBP4 levels was measured by ELISA. IR status of the patients wasdetermined by HOMA-IR, whereas the ?-cell function was determined byHOMA-B. Ab-Ob was defined by using criteria for Asian peoples (male WC ? 90cm; female WC ? 80 cm). The result of 81 patients with Ab-Ob showed that bothplasma of TNF-? and sTNFR1 levels were significant positive correlated withplasma RBP4 level (coeficient correlation r = 0,294; p = 0,008 dan r = 0,458; p =<0,001 respectively). In addition, the plasma of RBP4 level significantly positivecorrelation with HOMA-IR (r = 0,450; p = 0,000) and significantly negativecorrelation with HOMA-B (r = -0,564; p = <0,001). In the matched case-controlstudy, it was shown that mean plasma of RBP4 level of type 2 DM group (76,08 ±16,84 ?g/ml) statistically higher than that without type 2 DM group (41,13 ±14,75 ?g/ml) (p = <0,001). The odds ratio higher plasma of RBP4 level was 5,426(CI 95%; 1,343 – 21, 928) statistically significant for increases risk type 2 DM (p= < 0,05). It has been proven that RBP4 was a dominant and consisten risk factor(66.9%, p = < 0.001) which influenced the incidence of type 2 DM in Ab-Ob. It can be concluded that high plasma of RBP4 level have a greater risk tosuffered from type 2 DM compared to low plasma of RBP4 in Ab-Ob. The highplasma of RBP4 level is most dominant and consistent risk factor consequently oftype 2 DM. These mechanism could behind the association between high plasmaof RBP4 level and type 2 DM.
THE ROLE OF INTENSIVE INSULIN THERAPY ON SUPEROXIDE DISMUTASE (SOD), TUMOR NECROSIS FACTOR-? (TNF-?), AND INTERLEUKIN-6 (IL-6) ON HYPERGLYCEMIA IN CRITICALLY ILL PATIENTS Wiryana, Made; Suastika, Ketut; Bagianto, Hari; Bakta, Made
INDONESIAN JOURNAL OF BIOMEDICAL SCIENCES Vol. 4, No. 1 Januari 2010
Publisher : Udayana University

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Abstract

Hyperglycemia and insulin resistance are common in critically ill patientsin the ICU, although they have not previously had diabetes. It has been reportedthat pronounced hyperglycemia may lead to complications in such patients, andcause the reactive oxygen species (ROS) production, although controlled trial dataare still lacking. The current debatable issue, focusing on whether the intensiveinsulin therapy, aimed at normalizing blood glucose, may improvepatients’prognosis. Then, the debate is mainly about the time to start the therapy,and target of blood glucose level. Therefore, this research is mainly designed andaimed at knowing the difference between intensive insulin therapy andconventional insulin therapy on the increase of superoxide dismutase (SOD),decrease of cytokine production (TNF-? and IL-6), increase of albumin level, andevent of SIRSThis study was carried out in a randomly pre and post-test control groupdesign, involving 40 adult patients being nursed through the ICU Sanglah hospitalDenpasar. They were randomly assigned to receive intensive insulin therapy, inwhich blood glucose was decreased and maintained at the level between 80-110mg/dl, or conventional insulin therapy in which the insulin was infused only if theblood glucose level exceeded 215 mg/dl, decreased and maintained then at thelevel between 180-200 mg/dl.The result of the study showed that there was (1) significant increase ofSOD mean level (370. 70 vs 98.50 U/gHb, p=0.001); (2) no significant decreaseof TNF-? mean level; (3) significant decrease of IL-6 mean level (10.26 vs 2.25;p=0.023); (4) significant increase of albumin mean level ( 0.62 vs 0.22); (5)significant decrease of SIRS (10 % vs 40 %, p=0.000) on intensive insulin therapygroup compared to conventional insulin therapy group. It can be concluded thatintensive insulin therapy could maintain blood glucose level between 80 – 110mg/dl, increase SOD level, decrease IL-6 level, increase albumin level, anddecrease SIRS on hyperglycemia in critically ill ICU patients.
THE ROLE OF INTENSIVE INSULIN THERAPY ON SUPEROXIDE DISMUTASE (SOD), TUMOR NECROSIS FACTOR-? (TNF-?), AND INTERLEUKIN-6 (IL-6) ON HYPERGLYCEMIA IN CRITICALLY ILL PATIENTS Wiryana, Made; Suastika, Ketut; Bagianto, Hari; Bakta, Made
INDONESIAN JOURNAL OF BIOMEDICAL SCIENCES Vol. 3, No. 1 Januari 2009
Publisher : Udayana University

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Abstract

Hyperglycemia and insulin resistance are common in critically ill patientsin the ICU, although they have not previously had diabetes. It has been reportedthat pronounced hyperglycemia may lead to complications in such patients, andcause the reactive oxygen species (ROS) production, although controlled trial dataare still lacking. The current debatable issue, focusing on whether the intensiveinsulin therapy, aimed at normalizing blood glucose, may improvepatients’prognosis. Then, the debate is mainly about the time to start the therapy,and target of blood glucose level. Therefore, this research is mainly designed andaimed at knowing the difference between intensive insulin therapy andconventional insulin therapy on the increase of superoxide dismutase (SOD),decrease of cytokine production (TNF-? and IL-6), increase of albumin level, andevent of SIRSThis study was carried out in a randomly pre and post-test control groupdesign, involving 40 adult patients being nursed through the ICU Sanglah hospitalDenpasar. They were randomly assigned to receive intensive insulin therapy, inwhich blood glucose was decreased and maintained at the level between 80-110mg/dl, or conventional insulin therapy in which the insulin was infused only if theblood glucose level exceeded 215 mg/dl, decreased and maintained then at thelevel between 180-200 mg/dl.The result of the study showed that there was (1) significant increase ofSOD mean level (370. 70 vs 98.50 U/gHb, p=0.001); (2) no significant decreaseof TNF-? mean level; (3) significant decrease of IL-6 mean level (10.26 vs 2.25;p=0.023); (4) significant increase of albumin mean level ( 0.62 vs 0.22); (5)significant decrease of SIRS (10 % vs 40 %, p=0.000) on intensive insulin therapygroup compared to conventional insulin therapy group. It can be concluded thatintensive insulin therapy could maintain blood glucose level between 80 – 110mg/dl, increase SOD level, decrease IL-6 level, increase albumin level, anddecrease SIRS on hyperglycemia in critically ill ICU patients.
HIGH PLASMA TNF-? LEVELS AND MONONUCLEAR CELLS iNOS AND TNF-? EXPRESSION AS RISK FACTORS FOR PAINFUL DIABETIC NEUROPATHY Eko Purwata, Thomas; Suastika, Ketut; Raka Sudewi, A. A.; Widjaja, Djoenaidi
INDONESIAN JOURNAL OF BIOMEDICAL SCIENCES Vol. 4, No. 2 Juli 2010
Publisher : Udayana University

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Abstract

Painful Diabetic Neuropathy (PDN) is one of the most common and annoyingcomplications of diabetes mellitus. The pathogenesis of PDN is complex and still unclear.Recently it has become clear that nitric oxide (NO) and proinflammatory cytokines playan important role in the pathogenesis and maintenance of pain in PDN. Based on thisphenomenon, this study was conducted to investigate whether the cytokine tumornecrosis factor-alpha (TNF-?) and NO, in this case inducible Nitric Oxide Synthase(iNOS), play a role in PDN pathogenesis.The study was carried in two steps. The first step was a cross sectional and thesecond step was a case-control study. The study was performed in 110 type-2 diabeticpatients. The plasma TNF-? levels were determined by ELISA while the expression ofTNF-? and iNOS in mononuclear cells were analyzed immunohistochemically.Of 110 subjects, 59 patients suffered from Painful DN (case) and the remaining51 patients were Painless DN (control). Cross sectionally, plasma TNF-? levels andimmunoreactivity for iNOS and TNF-? were higher in patients with more severe pain inthe Visual Analog Scale (VAS). There were statistically significant differences (p <0.05) between mild and severe pain in regard to TNF-? level (15.24 pg/ml ± 5.42 vs.20.44 pg/ml ± 10.34 ); to iNOS immunoreactivity (9.72 % ± 8.61 vs. 15.6% ± 11.84); andto TNF-? immunoreactivity (13.0 % ± 9. 48 vs. 20.44% ± 11.75).The case control study showed that TNF-? had an odd ratio of 5.053 [CI 95%(2.241-11.392); p < 0.001]. TNF-? immunoreactivity of 4.125 [CI 95% (1.805-9.425); p< 0.001]; and iNOS immunoreactivity of 3.546 [CI 95% (1.613-7.795); p = 0.002]. There were correlations between TNF-? level, TNF-? and iNOS immunoreactivity andVAS with coefficient correlation: 0.330; 0.285 and 0.275 (p < 0.05) respectively.It is concluded that Diabetic Neuropathy patients with high TNF-? levels, iNOSand TNF-? immunoreactivity of mononuclear cells have higher risk for painful DN thanpainless DN. The higher TNF-? level, iNOS and TNF-? immunoreactivity the moresevere was the pain. This supports the hypothesis that TNF-? and iNOS have role inPDN pathogenesis. The results of this research could be applied as a basic for furtherresearch in pursuit of better management of PDN.
Co-Authors A Santoso A. A. Mas-Putrawati AAG Budhiarta AAG Budhitresna Ade Reza Hariyadi Agung Pranoto Agus Joko Purwanto An Apriyani Tebiary Anak Agung Ayu Mirah Adi Anak Agung Gde Budhiarta Anak Agung Gde Budhiarta Anak Agung Gede Sudewa Djelantik Angga Yustiawan Anwar Santoso Ardi Nugroho Yulianto Aries Sulisetyono Aryana, I Gust Putu Suka Aryawan, Wasis Dwi Askandar Tjokroprawiro Astika, I Nyoman Buana Ma'ruf Buana Ma'ruf Budhiarta, Anak Agung Gde Dedi B. Purwanto Dewa Putu Gede Purwa Samatra Dian Purnamasari Dian Purnamasari Dikantoro, Regi Y. Djoenaidi Widjaja Djoko W. Soeatmadji Dwija Sanjaya Ericson Estrada Sipayung Gede Kambayana Gede Putu Arsana Gede Sukrawan Giles Anthony Thomas Gunanta, Julhari H Taniguchi H. S. Habiba Muhiddin, H. S. Habiba Hari Bagianto I Gusti Agung Dewi Sarihati I Gusti Ayu Mardewi I Gusti Putu Suka Aryana I Ketut Aria Pria Utama I Made Bakta I Made Jawi I Made Jawi I Made Pande Dwipayana I Made Siswadi Semadi I Made Siswadi Semadi I Made Siswadi Semadi I Nyoman Astika I NYOMAN MANTIK ASTAWA I Nyoman Wande I Nyoman Wande I P G. Adiatmika I Putu Gede Adiatmika I Wayan Mustika I Wayan Mustika I Wayan Putu Sutirta Yasa I Wayan Weta I Wayan Wita Ida Bagus Aditya Nugraha Ida Bagus Ekaputra Ida Bagus Ekaputra, Ida Bagus Ida Bagus Ngurah Wises Ida Bagus Putu Putrawan IGN Gunadi Ignatius Ferdi Yuatmadja IMR Saraswati Iswara, Ni Putu Ayu Astri Prana K Badjra Nadha K Rina K Tangking Widarsa Kadek Ngurah Hariawa Ketut Adi Jaya Sutana Ketut Suata Komang Ayu Kartika Sari Kurniawan, I Made Dwi Luh Gede Sri Yenny Luh Seri Ani Made Ratna Saraswat MADE RATNA SARASWATI . Made Wardhana Made Wiryana Malik, Safarina G. Marisye Christantia Ma’ruf, Buana N Kajiwara N. K. Niti Susila, N. K. Ni Ketut Rai Purnami Ni Made Suaniti Ni Nyoman Trisna Yuliharti Tersinanda Ni Putu Ayu Astri Prana Iswara Noor Virliantarto Nurhadi Nurhadi Nym Astika Oktavianthi, Suksma Pradana Soewondo Purnami, Ni Ketut Rai Purwanto, Dedi B. Putra, Wing H. A. Putri Virliani Putri Virliani Putri Virliani R. A.T. Kuswardhani R. Prawira Bayu Putra Dewa Raka-Sudewi A. A. Regi Y. Dikantoro Regi Yudha Dikantoro S. Soetjiningsih, S. S., Hantono Saraswati, Putu Ayu Indah Setyawan, Dony Sidartawan Soegondo Siorcani, Putu Tasha Sri Trisnawati Sri Trisnawati Sri Yuniari Sri Yuniari, Sri Sutanegara - Sutjahjo Suherman, Sutjahjo Teguh Putranto Thomas Eko Purwata Tuty Kuswardani Virliantarto, Noor W Wita Wasis Akriananta Wibowo Harso Nugroho Wibowo Nugroho, Wibowo Wing H. A. Putra Wira Gotera Wisnu Firstdhitama