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"This volume covers the most important aspects of biosynthesis, processing, and functions of RNA in trypanosomes, ranging from transcription to RNA editing, mRNA splicing/translation/turnover, processing of transfer and ribosomal RNA, RNA interference, and current transcriptome-wide analyses. Recent progress in RNA-focused research in trypanosomatids promises to yield novel insights into trypanosome-specific features, as well as to reveal in the process new potential therapeutic strategies for combating these parasitic diseases."

"This is the first comprehensive handbook entirely dedicated to all the aspects of antiplatelet therapy. The book is divided into three main sections, pathophysiology, pharmacology and therapy, for a total of 23 chapters. A large group of leading experts from different European countries and from the USA, both from academia and industry, have contributed to the book. Besides a detailed overview on the pharmacology and clinical applications of all the currently used or of the novel antiplatelet agents, innovative approaches (e.g. intracellular signalling as an antiplatelet target, small RNAs as platelet therapeutics, etc.) or unconventional aspects (e.g. pharmacologic modulation of the inflammatory action of platelets are also treated. "

"PLATELETS is the definitive current source of state-of-the-art knowledge about platelets and covers the entire field of platelet biology, pathophysiology, and clinical medicine. Recently there has been a rapid expansion of knowledge in both basic biology and the clinical approach to platelet-related diseases including thrombosis and hemorrhage. Novel platelet function tests, drugs, blood bank storage methods, and gene therapies have been incorporated into patient care or are in development. This book draws all this information into a single, comprehensive and authoritative resource. Comprehensive and definitive source of knowledge about platelets for clinicians, pathologists and scientists Integrates the entire field of platelet biology, pathophysiology, and clinical medicine Full color reference comprising 64 chapters, 1400 pages, and 16,000 references Contributions from 126 world leaders in their fields New chapters on topics such as the regulation of platelet life span, platelet microRNAs, GPVI and CLEC-2, monitoring of antiplatelet therapy, novel antiplatelet therapy, and making platelets ex vivo."

"Latar Belakang. Cedera Reperfusi Iskemia merupakan eksaserbasi paradoks mengakibatkan disfungsi dan kematian sel setelah aliran darah direstorasi ke jaringan yang sebelumnya iskemia. Pada iskemia tungkai akut, reperfusi menimbulkan reaksi kompleks melibatkan inflamasi lokal maupun sistemik dengan dampak lokal sindroma kompartemen dan dampak sistemik berupa disfungsi hingga kegagalan multi organ. Platelets activating factors (PAF) sebagai mediator inflamasi pospholipid mempunyai efek fisiologis yang poten dan beragam, sehingga meningkatkan respon inflamasi pada cedera reperfusi iskemik.Berbagai upaya untuk mencegah dan memperingan cedera reperfusi iskemik, antara lain penggunaan prosedur ischemic preconditioning, antioksidan dan terapi anti-sitokin telah diteliti namun hasil dan manfaat klinisnya belum memuaskan. PTX, phosphodiesterase nonspesifik derivat xanthine, memperlihatkan efek penekanan inflamasi dan menghambat interaksi lekositendotel yang menjanjikan dalam mencegah cedera reperfusi. Namun hasil penelitian mengenai peran pentoxifylinne dalam menekan reaksi inflamasi melalui penekanan PAF pada iskemia tungkai akut tidak konsisten. Sehingga penelitian ini bertujuan untuk menilai peran PTX dalam mengurangi cedera reperfusi melalui penekanan mediator inflamasi PAF pada hewan coba kelinci dengan Reperfusi Iskemia tungkai akut.Metodologi. Dilakukan tindakan iskemik tungkai kiri selama 3 jam yang diikuti 2 jam periode reperfusi pada 10 ekor kelinci New Zealand White jantan yang dibagi menjadi 2 kelompok (kelompok pentoksifin dan kelompok kontrol) secara acak. Pada kelompok perlakuan diberikan PTX 30 menit sebelum reperfusi dengan dosis initial bolus 40 mg/kgBB diikuti dengan dosis rumatan 1 mg/kg BB/jam hingga 3 jam periode reperfusi. Pada kelompok kontrol diberikan cairan garam fisiologis dengan kecepatan dan volume yang sebanding. Tindakan Iskemik dilakukan dengan oklusi arteri iliaka komunis sinistra mengunakan klem selama 3 jam kemudian dilanjutkan dengan restorasi aliran darah. Pengambialn sampel untuk pemeriksaan kadar PAF dilakukan pada 2,5 jam iskemik dan pada 2 jam reperfusi.Hasil. Pada periode Iskemik dua jam tiga puluh menit tidak mengakibatkan perbedaan bermakna (p=0,754), kadar rerata PAF pada kelompok PTX 13,09 ± 0,41 pg/mL dan kelompok kontrol I3,38 ± 0,28 pg/mL. Pada jam ke dua tindakan reperfusi ditemukan perbedaan bermakna (p=0,009) kadar rerata PAF dari kelompok PTX menurun menjadi 11,36±0,78 pg/mL dan kelompok kontrol meningkat menjadi 25,5±0,78 pg/dL.Kesimpulan. PTX menurunkan kadar PAF plasma kelinci dengan cedera reperfusi iskemikia tungkai akut.

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Background. Ischemic reperfusion injury is a paradoxical exacerbation of cell dysfunction and death following the restoration of blood flow to previously ischemic tissue. Restoration of blood flow is essential to salvage ischemic tissue, however reperfusion itself paradoxically causes further damage to the ischemic tissue, threatening function and viability both organ local and distal through the inflammation response.

In Acute limb ischemia, there are essentially two components: a local component that can result in increasing the regional damage from ischemia inflammatory responses which may result in local syndrome, compartment syndrome, and systemic syndrome, multi organ dysfunction and failure.

Several method and attempt had been studied and performed to prevent and attenuate reperfusion injury such as, ischemic preconditioning, antioxidant, and anti-cytokine therapy, but their clinical benefit were not satisfactory. Pentoxifylline has emerged as an agent that may attenuate inflammation response through several mechanisms. However, studies on PTX and its function to prevent and attenuate inflammation response through attenuating PAF in acute limb ischemic were not consistent. In this study the role of PTX and its function to prevent and attenuate inflammation response through attenuating PAF in acute limb ischemic was investigated.

Methods. Acute limb ischemia in the left lower limbs of 10 New Zealand White male rabbit were performed for 3 hour followed by 2 hours period of ischemia. The rabbits were randomly separated into 2 groups of five (group pentoxifylinne and group control). The Pentoxifylline group was given PTX 40 mg/kg bolus half an hour prior to reperfusion followed by maintenance dose 1 mg/kg/hour until 2 hour post reperfusion, while the control group was given normal saline solution with comparable volume and rate administration. Acute limb Ischemic procedure was performed by direct occlusion of the left femoral artery using non traumatic clamp and followed by releasing the clamp after 3 hours of occlusion. Level of PAF were measured after 2.5 hour of ischemic period and after 2 hours of reperfusion period.

Results. After 2.5 hours of ischemic period, the mean PAF levels did not show any significant difference (p=0.754). The mean PAF level of pentoxifylline group 13.09f0.41 pg/mL, while the mean PAF level of control group 13.38±0.28 pg/mL, After 2 hours period of reperfusion, there were significant differences of mean PAF level between the two groups (p=0.009). The mean PAF level in the control group increase by 12.1 110.79 to became 25.5±0.78 pg/dL, while the mean PAF level of the PTX group decrease by 1.73f1.1 pg/mL and became 11.36±0.78 pg/m L.

Conclusion. PTX decreased the PAF level in rabbits with acute limb ischemic reperfusion injury."

"ABSTRAKLatar belakang. Transfusi trombosit dibutuhkan pada pasien trombositopenia terkait kegagalan produksi ataupun akibat perdarahan. Konsentrat trombosit merupakan tempat yang baik untuk pertumbuhan bakteri karena kantong komponen trombosit disimpan pada suhu 20-24OC dan terdapat zat tambahan dekstrosa yang dapat digunakan sebagai sumber energi bagi bakteri. Selain itu kantong trombosit yang digunakan berpori sehingga memungkinkan pertukaran udara dengan lingkungan luar. Angka kejadian kontaminasi bakteri cukup tinggi, di Amerika berkisar 1:1000 dengan angka kematian 150 pasien setiap tahunnya, oleh karena itu diperlukan metode skrining bakteri yang cepat, akurat dan ekonomis. Penelitian ini bertujuan untuk membandingkan hasil pewarnaan Gram dengan metode biakan dalam mendeteksi kontaminasi bakteri pada komponen konsentrat trombosit.Metodologi. Penelitian ini menggunakan desain potong lintang pada 46 konsentrat trombosit. Dilakukan uji biakan menggunakan botol media BacT/ALERT serta pewarnaan Gram pada sampel penelitian di hari pertama dan kelima masa simpan komponen konsentrat trombosit.Hasil. Ditemukan 1 subjek penelitian yang terkontaminasi Staphylococcus epidermidis baik pada masa simpan hari pertama dan kelima subjek tersebut. Subjek positif terdeteksi oleh metode biakan dan tidak terdeteksi dengan metode pewarnaan Gram.Simpulan. Kontaminasi bakteri pada konsentrat trombosit dapat terdeteksi dengan metode kultur, tetapi tidak dengan metode pewarnaan Gram. Proporsi kontaminasi bakteri pada konsentrat trombosit pada penelitian adalah 2,1%.

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ABSTRACTBackground. Platelet transfusions is required in patients with thrombocytopenia associated production failure or due to bleeding. Platelet concentrate is a good place for the growth of bacteria because it is stored at a temperature of 20-24OC, the dextrose, part of additives, can be used as an energy source for bacteria. Furthermore, the bags are porous, allowing air exchange with the outside environment. The incidence of bacterial contamination is quite high, ranging from 1:1000 in America with a mortality rate of 150 patients per year, therefore it is necessary to have bacterial screening methods which is fast, accurate and feasible. This study aimed to compare the results of the Gram stain with culture methods in detecting bacterial contamination in platelet concentrates components.Methodology. This study used cross-sectional designs in 46 platelet concentrates. Samples were cultured and Gram staining was tested on the first and fifth day of the shelf life of platelet concentrate.Results. 1 subject was found contaminated by Staphylococcus epidermidis both on the first and fifth day of the subject shelf life. Positive subject was detected by culture method but not with the Gram stain method.Conclusion. Bacterial contamination in platelet concentrates can be detected by culture methods, but not with the Gram stain method. The proportion of bacterial contamination in platelet concentrate in this study is 2.1%."

"ABSTRAKRuang Lingkup dan Cara Penelitian: Kemampuan asam asetilsalisilat (ASA) dalam menghambat agregasi trombosit, sering dikaitkan dengan pencegahan infark jantung. Dewasa ini, dalam upaya menurunkan resiko terjadinya infark jantung, ada kecenderungan menggunakan ASA dengan dosis makin kecil. Sehubungan dengan itu, dilakukan penelitian yang bertujuan untuk mengetahui berapa lama, dan apakah ada perbedaan yang bermakna antara intensitas antitrombotik beberapa tingkat dosis ASA (50 mg, 100 mg, 200 mg, dan 300 mg). Kemampuan agregasi trombosit diukur dengan metode baru yang berdasarkan intensitas transmisi cahaya. Hasil pemeriksaan tercermin sebagai suatu kurva agregasi trombosit. Disain yang dipakai adalah rancangan pola silang, dengan 11 orang sukarelawan sehat yang setelah diacak, masing-masing mendapat 4 tingkat dosis ASA dengan selang waktu 2 minggu. Bahan pemeriksaan terdiri dari 'platelet rich plasma', 'platelet poor plasma' dan adenosin difosfat yang berkadar akhir 10 uM, sebagai agregator. Parameter hambatan agregasi trombosit adalah berkurangnya nilai agregasi maksimal dan atau meningkatnya reversibilitas kurva agregasi trombosit, disbanding nilai sebelum mendapat ASA. Data dianalisis dengan ANOVA dua arah dan 'Planned comparison'. Untuk data dengan distribusi tidak normal, dipakai tes non parametrik (tes Friedman).Hasil dan Kesimpulan: Bila berdasarkan adanya salah satu parameter hambatan agregasi trombosit, maka ASA 50 mg, 100 mg, dan 200 mg per oral dapat menghambat agregasi trombosit selama 4 hari, sedangkan ASA 300 mg selama 5 hari (p > 0,01). Namun bila berdasarkan adanya kedua parameter hambatan agregasi trombosit, maka ASA 50 mg dapat menghambat agregasi trombosit pada 3 jam sesudah pemberian obat, sedangkan ASA 100 mg dan 200 mg, sampai 4 hari sesudah pemberian ASA. Intensitas antitrombotik ke empat dosis ASA, pada hari yang sama setelah makan obat, tidak menunjukkan perbedaan yang bermakna (p}0,07). Untuk menyatakan hambatan agregasi trombosit, kriteria peningkatan reversibilitas kurva agregasi lebih peka di-banding kriteria pengurangan nilai agregasi maksimal.

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ABSTRACT

Scope and Method of Study: The ability of acetylsalicylic acid (ASA) to inhibit the platelet aggregation is related with its use to the prevention myocardial infarction. Currently there is a trend to use small doses of ASA for this purpose. In this context, the present trial was conducted to find out how long the antithrombotic effect persist after small oral doses of ASA, and also to observe whether in the same days different small doses of ASA exert significant difference in their anti-thrombotic intensity. The antithrombotic effect of ASA was measured according to the method described by Born which was based on light transmission. The results were recorded as platelet aggregation curve. Eleven healthy volunteers participated in this trial after giving their' informed consents. Each subject received single doses (i.e. 50, 100, 200 and 300 mg) of ASA in a randomized and cross-over design. Wash out period between doses was 2 weeks. Materials being tested included platelet rich plasma, platelet poor plasma and adenosine diphosphate (aggregating agent) with final concentration of 10 uM. Inhibition of platelet aggregation by ASA was evaluated using two parameters, i.e. decrease of maximal aggregation and/or increase of aggregation curve's reversibility (compared to their pre-ASA values). Data was analysed with two way ANOVA and planned comparison test. Friedman test was used for non-Gaussian data.

Results and conclusions: If criterion of platelet aggregation inhibition is based on one of the two criteria mention above, ASA 50, 100, and 200 mg inhibited platelet aggregation for four days; meanwhile the 300 mg dose did it for five days (p < 0,01). If criterion of platelet aggregation inhibition is based on both of the above mentioned criteria, however, ASA 50 mg inhibited plate-let aggregation at 3 hours after dosing; meanwhile the 100 and 200 mg doses did it for four days. There is no significant difference in antithrombotic intensity between the four doses in the same days after drug administrations (p > 0,01). In addition, reversibility of platelet aggregation curve is a more sensitive parameter than maximal aggregation for measuring platelet aggregation."

"Latar Belakang: Risiko perdarahan tidak berkorelasi linear dengan jumlah trombosit pada kondisi trombositopenia. Terdapat perbedaan fungsi trombosit pada trombositopenia gangguan produksi dengan destruksi perifer. Pada trombositopenia, hasil fungsi agregasi trombosit dengan light transmission aggregometry tidak valid. Diperlukan pemeriksaan fungsi trombosit yang dapat dikerjakan pada kondisi trombositopenia.Tujuan: Mengkaji fungsi agregasi trombosit pada pasien trombositopeniaMetode: Studi potong lintang terhadap 60 pasien trombositopenia gangguan produksi dan destruksi perifer di Rumah Sakit Cipto Mangunkusumo selama Desember 2023 sampai April 2024. Dilakukan pemeriksaan jumlah trombosit, IPF, dan fungsi agregasi trombosit.Hasil: Terdapat perbedaan fungsi agregasi antara trombositopenia gangguan produksi dengan destruksi perifer (40% vs 77,7%). Didapatkan perbedaan nilai IPF antara trombositopenia gangguan produksi dengan destruksi perifer (5,65% vs 21%). Tidak didapatkan korelasi antara jumlah trombosit dengan fungsi agregasi trombosit pada trombositopenia gangguan produksi maupun destruksi perifer (r=0,214, p=0,231; r=0,364 p=0,062). Tidak didapatkan korelasi antara jumlah trombosit dengan fungsi agregasi trombosit pada trombositopenia gangguan produksi maupun destruksi perifer. Didapatkan titik potong IPF 10,25% untuk membedakan trombositopenia gangguan produksi dan destruksi perifer dengan sensitivitas 80,8% dan spesifisitas 68%.Kesimpulan: Fungsi agregasi trombosit pada trombositopenia destruksi perifer lebih baik daripada trombositopenia gangguan produksi. Fungsi agregasi trombosit tidak berkorelasi dengan jumlah trombosit maupun dengan IPF.

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Background: The risk of bleeding does not linearly correlate with platelet count in thrombocytopenia.There is difference between platelet function in central and peripheral thrombocytopenia. Platelet aggregation function assay performed by light transmission aggregometry is not valid in thrombocytopenia. Platelet aggregation assay that can be performed in thrombocytopenia is needed.

Objective: To assess platelet function in thrombocytopenia patients.

Methods: A cross-sectional study was conducted on 60 thrombocytopenic patients at Cipto Mangunkusumo Hospital from December 2023 to April 2024. Platelet count and immature platelet fraction (IPF) were done by automatic blood cell counter while platelet aggregation by Plateletworks ADP Kit

Results: There was a difference in platelet aggregation function between central thrombocytopenia and peripheral thrombocytopenia (40% vs 77.7%). A difference in IPF values was found between central thrombocytopenia and peripheral thrombocytopenia (5.65% vs. 21%). No correlation between platelet count and platelet aggregation function in thrombocytopenia (r=0.214, p=0.231 vs. r=0.364, p=0.062). No correlation was found between IPF and platelet aggregation function (r=-0.139, p=0.498 vs. r=-0.282, p=0.171). The cut-off value of IPF was 10.25% to distinguish central and peripheral thrombocytopenia.

Conclusion: Platelet aggregation function in peripheral thrombocytopenia was better than central thrombocytopenia. Platelet aggregation function did not correlate neither platelet count nor IPF."

"Platelet merupakan fragmen sel berinti kecil beredar dalam darah yang dilepaskan dari megakariosit. Platelet  memainkan peranan penting dalam hemostasis, thrombosis, inflamasi, dan aterogenesis.  Produksi stres oksidatif dan reactive oxygen species (ROS) dapat mengaktifkan platelet dan berperan dalam patogenesis penyakit kardiovaskular. Hiperlipidemia merupakan salah satu faktor risiko penyakit kardiovaskular yang dapat menginisiasi terjadinya aktivasi platelet melalui produksi ROS yang berlebih. Tujuan penelitian ini adalah mengetahui pengaruh diet tinggi lemak terhadap karakteristik model hewan hiperlipidemia serta menganalisis pengaruh hiperlipidemia terhadap aktivasi platelet melalui parameter beta thromboglobulin. Sebanyak 24 tikus Wistar dibagi menjadi 4 kelompok, yaitu 1 kelompok normal dan 3 kelompok induksi diet tinggi lemak. Pemberian induksi diet tinggi lemak dilakukan selama 10 minggu. Hasil menunjukkan pemberian diet tinggi lemak selama 10 minggu meningkatkan profil lipid kolesterol total dan trigliserida secara signifikan jika dibandingkan kelompok normal. Model hewan hiperlipidemia  yang diinduksi diet tinggi lemak menghasilkan kadar beta-thromboglobulin yang lebih tinggi jika dibandingkan kelompok normal.  Beta thromboglobulin, kolesterol total, dan trigliserida menunjukkan korelasi yang sangat kuat dengan arah yang positif. Dapat disimpulkan bahwa pemberian diet tinggi lemak selama 10 minggu berhasil membentuk kondisi hiperlipidemia melalui parameter kolesterol total dan trigliserida. Model hewan hiperlipidemia yang diinduksi diet tinggi lemak selama 10 minggu menunjukkan terjadinya aktivasi platelet berdasarkan tingginya kadar beta-thromboglobulin jika dibandingkan dengan kelompok normal.

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Platelets are small nucleated cell fragments circulating in the blood that are released from megakaryocytes. Platelets play an important role in hemostasis, thrombosis, inflammation, and atherogenesis. Production of oxidative stress and reactive oxygen species (ROS) can activate platelets and play a role in the pathogenesis of the cardiovascular disease. Hyperlipidemia is one of the risk factors for cardiovascular disease that can initiate platelet activation through excessive ROS production. The purpose of this study was to determine the effect of variations in the composition of a high-fat diet on the characteristics of hyperlipidemic animal models and to analyze the effect of hyperlipidemia on platelet activation through beta thromboglobulin. A total of 24 Wistar rats were divided into 4 groups, 1 normal group and 3 high-fat diet groups. A high-fat diet was given for 10 weeks. The results showed that giving a high-fat diet for 10 weeks increased the lipid profile of total cholesterol and triglycerides significantly when compared to the normal group. An animal model of hyperlipidemia induced by a high-fat diet resulted in higher beta-thromboglobulin levels compared to the normal group. Beta thromboglobulin, total cholesterol, and triglycerides showed a very strong correlation in a positive direction. It can be concluded that giving a high-fat diet for 10 weeks succeeded in forming a hyperlipidemic condition through total cholesterol and triglyceride parameters. An animal model of hyperlipidemia induced by a high-fat diet for 10 weeks showed platelet activation based on high levels of beta-thromboglobulin  compared to the normal group. "

"Platelet yang teraktivasi dapat menyebabkan agregasi dan pembentukan trombus sehingga dapat menjadi faktor risiko penyakit kardiovaskular. Hiperlipidemia merupakan faktor risiko utama penyakit kardiovaskular yang dapat mengaktivasi platelet melalui berbagai jalur. Platelet yang teraktivasi akan mengeluarkan biomarker yang dapat dideteksi, salah satunya yaitu RANTES. Penelitian ini bertujuan untuk melihat pengaruh pemberian diet tinggi lemak terhadap profil lipid dan kadar RANTES sebagai parameter aktivasi platelet pada model hewan hiperlipidemia. Untuk menganalisis pengaruh diet tinggi lemak terhadap profil lipid plasma, hewan uji dibagi menjadi 4 kelompok; kelompok normal, dan 3 kelompok induksi yang diberi variasi diet tinggi lemak atau high-fat diet (HFD) yang mengandung kuning telur puyuh, lemak sapi, lemak kambing, mentega, minyak kelapa, fruktosa, kolesterol murni, dan asam kolat. Hasil menunjukkan terdapat peningkatan yang signifikan (p<0,05) pada kadar kolesterol total (HFD 1 = 139,68±11,88 mg/dL; HFD 2 = 161,14±14,42 mg/dL; HFD 3 = 248,80 ±7,49 mg/dL) dan trigliserida (HFD 1 = 142,06 ±14,03 mg/dL; HFD 2 = 185,94 ±13,36 mg/dL; HFD 3 = 236,85 ±7,53 mg/dL) pada semua kelompok diet tinggi lemak selama 10 pekan induksi diet tinggi lemak jika dibandingkan dengan kelompok normal (69,74±5,66 mg/dL dan 79,22 ±14,03 mg/dL). Pada pekan ke-10, terlihat perbedaan yang signifikan (p<0,05) baik antara kelompok normal dengan kelompok induksi maupun antar kelompok HFD 1, HFD 2, dan HFD 3. Hasil pengukuran kadar RANTES menunjukkan perbedaan yang signifikan antara kelompok HFD 3 dan kelompok normal (p<0,05). Peningkatan kadar kolesterol total dan trigliserida menunjukkan korelasi positif dan sedang dengan rasio RANTES (r = +0,474 dan r = +0,447).

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Activated platelets can cause aggregation and thrombus formation that can be a risk factor for cardiovascular disease. Hyperlipidemia is a major risk factor for cardiovascular disease and also can activate platelets through various pathways. Activated platelets will release detectable biomarkers such as RANTES. This study aimed to examine the effect of high-fat diet on lipid profile and RANTES levels as a parameter of platelet activation in hyperlipidemic animal models. To analyze the effect of a high-fat diet on the plasma lipid profile, the animals were divided into 4 groups, group 1 is the normal group and three induction groups that were given a variation of a high-fat diet (HFD) containing quail egg yolk, beef fat, goat fat, butter, coconut oil, fructose, pure cholesterol, and cholic acid. The results showed that there was a significant increase (p<0.05) in total cholesterol (HFD 1 = 139,68±11,88 mg/dL; HFD 2 = 161,14±14,42 mg/dL; HFD 3 = 248,80 ±7,49 mg/dL) and triglyceride levels (HFD 1 = 142,06 ±14,03 mg/dL; HFD 2 = 185,94 ±13,36 mg/dL; HFD 3 = 236,85 ±7,53 mg/dL) in HFD group during 10 weeks of high-fat diet induction compared to normal group (69,74±5,66 mg/dL and 79,22 ±14,03 mg/dL). At week 10, there was a significant difference (p<0.05) both between the normal group and the induction group as well as between the HFD 1, HFD 2, and HFD 3 groups. The results of the measurement of RANTES levels showed a significant difference (p<0,05) between HFD 3 and the normal group. Increased levels of total cholesterol and triglycerides showed a positive moderate correlation with the RANTES ratio (r = +0,474 dan +0,447)."