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"Lipoprotein (a) adalah suatu lipoprotein plasma yang mempunyai struktur dan komposisi yang mirip dengan lipoprotein berdensitas rendah (LDL) dengan tambahan apo(a) yang terikat pada apo B100. Struktur apo(a) mirip dengan plasminogen, suatu proenzim dalam sistem fibrinolitik. Oleh karena kemiripan ini, diduga Lp(a) dapat menghambat aktivitas plasminogen dan menurunkan aktivitas fibrinolitik. Penelitian ini bertujuan untuk membuktikan bahwa penambahan Lp(a) ke dalam plasma normal dapat menghambat aktivitas fibrinolitik.Subyek penelitian terdiri atas 4 orang sehat dengan kadar fibrinogen, aktivitas plasminogen dan masa lisis bekuan euglobulin dalam batas normal. Pada percobaan pertama, penambahan Lp(a) dilakukan sebelum sentrifugasi untuk memperoleh endapan euglobulin, sedang pada percobaan kedua Lp(a) ditambahkan pada endapan euglobulin. Sebagai kontrol, masa lisis bekuan euglobulin dikerjakan pada plasma yang ditambahkan NaCl 0,9% dengan volume yang sama seperti Lp(a).Hasil penelitian menunjukkan bahwa pada percobaan pertama tidak ada bekuan yang terbentuk. Diduga Lp(a) dapat mengikat fibrinogen dan keduanya berada di supernatan, sehingga tidak ada fibrinogen dalam endapan euglobulin yang dapat dibekukan oleh trombin. Pada percobaan kedua, sampai hari ke empat bekuan belum lisis. Kesimpulan: Penambahan Lp(a) ke dalam plasma normal dapat menghambat aktivitas sistem fibrinolitik. (Med J Indones 2004; 13: 135-9)

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Lipoprotein(a) is a plasma lipoprotein whose structure and composition are similar with low density lipoprotein (LDL) with an addition of apo(a) that is bound to apo B100. The structure of apo(a) is similar with plasminogen, a proenzym in fibrinolytic system. Due to this similarity, it is assumed that Lp(a) can inhibit plasminogen activity and decreases fibrinolytic activity. The purpose of this study is to prove that addition of Lp(a) to normal plasma can inhibit fibrinolytic activity.

Four healthy people whose fibrinogen levels, plasminogen activities and euglobulin clot lysis time were within normal range were enrolled in this study. Fibrinolytic activity were assessed by euglobulin clot lysis time (ECLT). In the first experiment, the addition of Lp(a) was done before centrifugation to obtain euglobulin precipitates, while in the second experiment, Lp(a) was added to the euglobulin precipitates. As a control, ECLT was performed in the plasma with the addition of NaCl 0.9% in the same volume with Lp(a).

The results of the study showed that in the first experiment, there was no clot formation. It is assumed that Lp(a) can bind fibrinogen and both of them floated in the supernatant, so there was no fibrinogen in the euglobulin precipitate that can be clotted by thrombin. In the second experiment, the clot did not dissolve until the fourth day. In conclusion, the addition of Lp(a) to normal plasma can inhibit the activity of fibrinolytic system. (Med J Indones 2004; 13: 135-9)"

"Stroke iskemik merupakan suatu disfungsi jaringan otak yang disebabkan oieh penurunan aliran darah ke otak. Penyebab tersering penurunan aliran darah ke otak adalah aterotrombosis dan emboli serebral. Untuk mencegah stroke diperlukan pengenalan dan pengendalian terhabap faktor risiko stroke. Seat ini peningkatan kadar plasminogen activator inhibitor-I (PAI-I) telah dinyatakan sebagai faktor risiko penyakit jantung iskemik. Peningkatan kadar, PAI-1 telah dihubungkan dengan penurunan aktivitas sistem fibinolisis. Mengenai hubungan antara kadar PAI-1 dengan stroke iskemik masih belum jelas.Pada penelitian ini ingin diketahui hubungan antara kadar PAI-1 dengan stroke iskemik. Selain itu, pada penelitian ini juga ingin diketahui hubungan antara kadar PAI-1 dengan faktor risiko stroke iskemik Iainnya seperti usia, jenis kelamin, status metabolik glukosa terganggu, hipertrigliseridemia, obesitas dan hipertensi. Oleh karena keterbatasan jumlah subjek penelitian, maka kami mengawalinya dengan suatu penelitian pendahuluan. Penelitian pendahuluan ini dilakukan dengan rancangan kasus kontrol, melibatkan 38 subjek penderita stroke iskemik dan 38 subjek kontrol yang telah memerwhi kriteria penelitian. Kadar PAI-1 diperiksa dengan metode ELISA menggunakan reagen Asserachrom PAI-1 dari Stago.Hasil penelitian menunjukkan hubungan antara kadar PAI-1 dengan stroke iskemik mempunyai nilai rasio odds sebesar 3.1, tetapi secara statistik hubungan ini tidak bermakna karena nilai 95 % interval kepercayaan adalah 0.757 - 12.790 (p = 0.103). Hasil analisis multivariat dengan regresi multipel menunjukkan adanya hubungan yang Iemah namun bermakna antara kadar PAI-i dengan usia (r = -0.2; p = 0.020), hipertensi (r = -0.2; p = 0.042) dan hipertrigliseridemia (r = 0.3; p = 0.004), tetapi tidak didapatkan hubungan yang bermakna antara kadar PM-1 dengan jenis kelamin (p = 0.616), status metabolik glukosa terganggu (p = 0.653) dan obesitas (p = 0.328). Hubungan antara kadar PAI-1 dan faktor risiko stroke Iainnya dapat digambarkan melalui persamaan berikut yaitu kadar PAI-1 = 55.4 - 0.5 x (usia) - 5.3 x (hipertensi) + 11.1 x (hipertrigliseridemia). Untuk mendapatkan kesimpulan, penelitian pendahuluan ini sebaiknya dilanjutkan dengan jumlah sampel yang cukup.

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Ischemic stroke is a cerebral dysfunction caused by decreased cerebral blood flow. The main causes of decreased cerebral blood flow are atherothrombosis and cerebral emboli. In attempt on stroke prevention, risk factors of stroke should be recognized and controlled_ Recently increased plasminogen activator inhibitor--1 (PAI-1) has been established as a risk factor for ischemic heart disease. Increased PAI-1 level is associated with decreased fibrinolytic activity. The association of increased PAI-1 level with ischemic stroke remains unclear.

The aim of this study was to analyze the relationship between PAI-1 level and ischemic stroke_ In addition, the relationship between PAI-1 level and other risk factors of ischemic stroke such as age, gender, uncontrolled blood glucose, hypertriglyceridemia, obesity and hypertension, would also be analyzed. Due to the limitation of sample size, we begin with a preliminary study. This preliminary study was a case control design, involved 38 patients of ischemic stroke and 38 control subjects who fulfilled the criteria. The level of PAI-1 was determined by ELISA method using Asserachrom PAI-1 from Stago. The results indicated that the odds ratio of the relationship between PAI-1 level and ischemic stroke was 3.1, but this relationship was not statistically significant since the 95 % confidence interval was 0.757 - 12.790 (p = 0.103).

The result of multivariate analysis with multiple regression showed that there were significant weak correlation between PAM level with age (r = -0.2; p = 0.020), hypertension (r = -0.2; p = 0.042), and hypertriglyceridemia (r = 0.3; p = 0.004) but there were no correlation between PAI-1 level with gender (p = 0.616), uncontrolled blood glucose (p = 0.653), and obesity (p = 0.328). The relationship of PAI-1 level and other risk factors could be described by this formula, PAI-1 level = 55.4 - 0.5 x (age) - 5.3 x (hypertension) + 11.1 x (hypertrygliceridemia). To obtain a conclusion, this preliminary study should be continued with adequate sample size."

"ABSTRAKKanker paru berkaitan dengan prognosis yang buruk. Oleh karenanya, diperlukan penanda sirkulasi untuk memprediksi respons terapi dan prognosis. Ekspresi mikroRNA 10b miR-10b dan aktivitas fibrinolitik, sebagaimana dicerminkan oleh soluble urokinase-type plasminogen activator receptor suPAR dan plasminogen activator inhibitor 1 PAI-1 , merupakan kandidat biomarker yang menjanjikan.Penelitian ini bertujuan mengevaluasi peran ekspresi miR-21, miR-10b, kadar suPAR dan PAI-1 plasma sebagai prediktor progresi dan respons terapi pada pasien kanker paru stadium lanjut.Penelitian ini merupakan studi kohort dan kesintasan di RS Kanker Dharmais RSKD , Jakarta. Subjek penelitian adalah pasien kanker paru karsinoma bukan sel kecil KPBBSK yang didiagnosis antara bulan Maret 2015 dan September 2016. Ekspresi miR-21 dan miR-10b dikuantifikasi dengan metode real-time polymerase chain reaction RT-PCR . Kadar suPAR dan PAI-1 diperiksa dengan metode enzyme-linked immunosorbent assay ELISA . Respons terapi dievaluasi berdasarkan kriteria RECIST 1.1. Pasien ditindaklanjuti sampai meninggal atau satu tahun setelah terapi.Terdapat 40 pasien yang dilibatkan dalam studi; 25 orang menyelesaikan sedikitnya4 siklus kemoterapi dan 15 lainnya meninggal selama terapi. Ekspresi miR-21 tidak berhubungan dengan progresi atau respons terapi. Kadar absolut miR-10b >592,145 copies/mL atau FC miR-10b > 0.066 bersifat protektif terhadap progresi dan respons buruk, sedangkan kadar suPAR > 4,237 pg/mL merupakan faktor risiko progresi dan respons buruk. Oleh karena dianggap penting, FC miR-10b juga dimasukkan dalam model prediksi progresi. Kadar PAI-1 > 4,6 ng/mL merupakan faktor protektif untuk respons buruk. Kadar suPAR merupakan faktor risiko independen untuk progresi dan respons buruk, sedangkan kadar PAI-1 merupakan faktor protektif independen untuk respons buruk.Simpulan: Model prediksi untuk progresi dapat dibuat dari ekspresi relatif miR-10b dan kadar suPAR, sedangkan respons terapi dapat diprediksi dari kadar suPARdan PAI-1. Dibutuhkan studi lebih lanjut untuk validiasi model-model prediksi ini.Kata kunci: kanker paru karsinoma bukan sel kecil KPKBSK , miR-10b, miR-21, overall survival, plasminogen activator inhibitor 1 PAI-1 , respons terapi, soluble urokinase-type plasminogen activator receptor suPAR

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ABSTRACTLung cancer is associated with poor prognosis. Circulating markers to predict treatment response and prognosis is needed. Expression of microRNA10b miR 10b and fibrinolytic activity, as reflected by soluble urokinase type plasminogen activator receptor suPAR and the plasminogen activator inhibitor 1 PAI 1 , were promising as biomarker candidates.This study aimed to evaluate the role of miR 21, miR 10b expression, suPAR and PAI 1 levels as predictors of progression during treatment and treatment response in advanced lung cancer patients.This was cohort and survival study in Dharmais Cancer Hospital DCH . The subjects were non small cell lung cancer NSCLC patients diagnosed between March 2015 and September 2016. Expression of miRNAs were quantified using real time polymerase chain reaction RT PCR method. Levels of suPAR and PAI 1 were assayed using the enzyme linked immunosorbent assay ELISA method. Treatment response was evaluated based on RECIST 1.1. Patients were followed up until death or one year after treatment.Forty patients were enrolled 25 completed at least 4 cycles of chemotherapy and15 patients died during treatment. Absolute and FC miR 21 were not associated with progression or treatment response. Absolute MiR 10b expression 592,145 copies mL or FC miR 10b 0.066 were protective for progressive disease and poor treatment response, while suPAR levels 4,237 pg mL was a risk factor for progressive disease and poor responders. Since FC miR 10b was an important predictive factor, it was included in the prediction model of progression. PAI 1 levels 4.6 ng mL was a protective factor for poor response group of patients. suPAR level was an independent risk factors for progression and poor response, while PAI 1 level was an independent protective factor of poor response.Conclusion A model to predict progression can be developed using miR 10b expression and suPAR levels, while treatment response can be predicted by suPAR and PAI 1 levels. Further studies are needed to validate this model.Key words miR 10b, miR 21, non small cell lung cancer NSCLC , overall survival, plasminogen activator inhibitor 1 PAI 1 , soluble urokinase type plasminogen activator receptor suPAR , treatment response"