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"Latar belakang: Pada era intervensi koroner perkutan primer (IKKP), angka kematian akibat infark miokard akut dengan elevasi segmen ST (IMA-EST) berhasil ditekan. Peningkatan angka sintasan tersebut berbanding dengan peningkatan insiden gagal jantung. Proses remodeling pascamiokard infark yang belum sepenuhnya dihambat oleh standar terapi saat ini akan berujung pada kondisi gagal jantung. Doksisiklin sebagai anti-matriks metaloproteinase (MMP) menunjukkan hasil yang baik dalam mencegah proses remodeling. Biomarker remodeling merupakan surrogate dini yang baik untuk memprediksi kejadian remodeling. Namun, efek doksisiklin terhadap biomarker remodeling dan luaran klins pasien IMA-EST belum diketahui.Tujuan: Penelitian ini bertujuan untuk mengetahui efek doksisiklin terhadap penurunan kadar biomarker remodeling pascainfark miokard.Metode: Penelitian ini menggunakan desain uji klinis tersamar tripel. Pasien IMA-EST dengan keterlibatan anterior atau Killip 2-3 dengan onset kurang dari 12 jam yang menjalani IKKP terbagi acak kedalam grup yang mendapat doksisiklin 2x100 mg selama 7 hari sebagai tambahan dari standar terapi dan grup dengan standar terapi. Pemeriksaan biomarker (netrofil, hs-Troponin T, hs-CRP, NT-pro BNP) dilakukan saat admisi rumah sakit dan evaluasi intraperawatan. Ekokardiografi dilakuan saat admisi dan hari ke-5 untuk menilai dimensi dan fungsi ventrikel kiri.Hasil: Terdapat 94 subyek yang diikutkan dalam penelitian dan terbagi rata ke dalam kedua grup. Karakteristik demografis dan klinis kedua grup homogen. Grup doksisiklin menujukkan nilai netrofil jam ke-24 yang lebih rendah dibanding grup kontrol (69,1±5,8% vs 71,9±8,0%, p=0,049). Peningkatan hs-Troponin T didapatkan lebih rendah pada kelompok dengan onset lebih dari 6 jam yang mendapatkan doksisiklin, namun tidak pada grup kontrol. Insiden gagal jantung 11,3% lebih rendah pada grup doksisiklin. Perbaikan fraksi ejeksi signifikan didapat pada grup doksisiklin dibanding grup kontrol (4,5±10,4% vs 0,3±10,3%, p=0,05). Peningkatan tersebut lebih besar pada pasien dengan onset lebih dari 6 jam dengan rerata peningkatan 5,9% (95%IK 0,05-11,7%, p=0,048).Kesimpulan: Doksisiklin memiliki efek perbaikan biomarker remodeling ventrikel, terutama netrofil dan hs-troponin T, serta fraksi ejeksi ventrikel kiri. Jumlah insiden gagal jantung lebih rendah pada grup doksisiklin.

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Background: In era of primary percutaneous coronary intervention (PPCI), mortaliry rate was reduced significantly. The increament in survival rate was followed by increament in heart failure cases. Cardiac remodelling after myocardial infarction was not fully anticipated by current therapy hence the patent would suffer for hear failure. Doxycycline as antimatrix metaloproteinase (MMP) inhibitor showed a promising results in modulation cardiac remodelling. Cardiac biomarkers for remodelling are surrogate parameters for early indentifying of remodelling. However, the effect of doxycyline to cardiac remodelling and its clinical implication are unknown.

Objective: To determine the effect of doxycycline on cardiac remodelling biomarkers after myocardial infarction.

Methods: We conducted triple blinded-randomized control trial. Patients with STEMI anterior or with Killip class 2-3 who underwent PPCI were randomly assigned to doxycycline (100 mg b.i.d for 7 days) in addition to standard therapy or to standar care. Cardiac remodelling biomarkers (neutrophils, hs-Troponin T, hs-CRP, NT-proBNP) were obtained on admission and during hospitalization. Echocardiography were assessed on admission and at 5 days to evaluate left ventricle dimmension and function.

Results: There were 94 patients assigned into doxycycline and control group. Baseline demographics and clinical characteristics were comparable between 2 groups. Doxycycline group showed lower percent neutrophils at 12 hours compare to control group (69.1±5.8% vs 71.9±8.0%, p=0.049). hs-Troponin T changes were lower in patients with onset >6 hours who received doxycycline and there were no differences among control group. Heart failure incidence was 11.3% lower in doxycycline group to control group. The improvement of left ventricle ejection fraction was sifnificantly higher in doxycycline group than in control group (4.5±10.4% vs 0.3±10.3%, p=0.05). The imrpovement was even higher in those with onset >6 hours with mean increament of 5.9% (95%CI 0.05-11.7%, p=0.048).

Conclusion: Doxycycline had effect in improving cardiac remodelling biomarkers, ie percent neutrophils and hs-Troponin T and left ventricle ejection fraction. Incidence of heart failure was lowe in doxycycline group."

"Latar belakang: Remodeling jantung pasca Infark Miokard Akut (IMA-ST) dipercayasebagai penyebab masih tingginya angka komplikasi gagal jantung walaupun sudahdiberikan terapi standar dan tatalaksana revaskularisasi. Matriks ekstraseluler (EKM)memiliki peranan penting dalam proses remodeling. Nekrosis miokard menyebabkanpeningkatan kadar matriks metalloproteinase (MMPs) yang akan mendegradasi EKM.Berbagai studi eksperimental, menunjukkan bahwa inhibisi MMPs memberikan manfaatpada proses remodeling. Doksisiklin merupakan penghambat MMPs poten yang telahmemberikan efek menjanjikan terhadap remodeling pada hewan coba dan uji klinis tidaktersamar.Tujuan: Mengetahui efek doksisiklin terhadap struktur dan fungsi ventrikel sebagaipenanda remodeling pada IMA-ST yang telah menjalani IKPP.Metode: Penelitian ini menggunakan desain uji klinis acak tersamar ganda. Pasien IMASTdengan keterlibatan anterior atau Killip 2-3 dengan onset kurang dari 12 jam yangmenjalani IKPP terbagi secara acak pada grup Doksisiklin (2x100 mg tablet selama 7hari) sebagai terapi tambahan dari standar tatalaksana dan grup kontrol. Pemeriksaanekokardiografi dasar pada saat awal perawatan segera setelah IKPP. Ekokardiografievaluasi dilaksanakan pada bulan ke 4.Hasil: Terdapat 134 subjek yang masuk dalam penelitian ini. Setelah evaluasi lanjutan,terdapat 8 pasien drop out pada masing-masing grup karena meninggal dan lost to followup 58 subjek masuk dalam Grup Doksisiklin dan 60 subjek Grup Kontrol. Karakteristikdemografis dan klinis kedua grup homogen. Parameter ekokardiografi menunjukkanadanya peningkatan Left Ventricle End-Diastolic Volume Index (D LVEDVi) yang lebihrendah dibandingkan grup kontrol (9,2 (-21-45) mL/m2 vs 16 (-13-62) mL/m2,p=0,008). Selain itu, fungsi fraksi ejeksi (DLVEF) mengalami peningkatan pada grupDoksisiklin (2,36 ± 8,5 vs -2,6 ± 8,4; p 0,005). Persentase Adverse Remodeling lebihsedikit pada grup Doksisiklin. Rentang perbaikan Global Longitudinal Strain (DGLS)lebih besar pada grup Doksisiklin, walaupun statistik tidak bermakna. Angkarehospitalisasi tidak berbeda bermakna pada kedua grup.Kesimpulan: Doksisiklin memberikan efek perbaikan terhadap struktur dan fungsiventrikel kiri pada pasien IMA-ST yang telah menjalani IKPP

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Background: Cardiac remodeling after acute myocardial infarction with ST elevation(STEMI) had been proved as the cause of the increased of heart failure complicationsdespite standard therapy and revascularization management. Extra cellular matrix (ECM)has an important role in the remodeling process. Myocardial necrosis causes increasedlevels of matrix metalloproteinase (MMPs) which will degrade ECM. Variousexperimental studies, showed that MMPs inhibition provides benefits in the remodelingprocess. Doxycycline is a potential MMPs inhibitor that has a promising effect onremodeling in experimental animals and clinical trials.Objective: To determine the effect of doxycycline on the structure and function ofventricles as a remodeling marker in STEMI that had undergone Primary PercutaneousCoronary Intervention (PPCI)Methods: We conducted a double-blind randomized control trial. Patients with STEMIanterior or with Killip class 2-3 with onset of less than 12 hours undergoing PPCI wererandomly assigned to the group that receiving Doxycycline (100 mg b.i.d for 7 days) asadjunctive therapy from standard management and the group without adjunct therapy. Aninitial echocardiographic examination was done after PPCI. Further evaluation was heldin 4 months after PPCI with an echocardiographic examination, which will be comparedbetween the initial examination and the evaluation.Results: There were 134 subjects included in this study. After further evaluation, therewere 8 patients drop out due to death and lost to follow up. Doxycycline group has 58and 60 subjects in Control group. Demographic and clinical characteristics of both groupsare homogeneous. Echocardiographic parameters showed change in Left Ventricle End-Diastolic Volume Index (D LVEDVi) significantly lower in Doxycycline group (9.2 (-21-45) mL/m2 vs. 16 (-13-62) mL/m2, p 0.008). In addition, the change of ejectionfraction (D LVEF) increased in the doxycycline group (2.36 ± 8.5 vs -2.6 ± 8.4, p0.005).The percentage of Adverse Remodeling is smaller in the Doxycycline group (70%vs 83%) and the range of D Global Longitudinal Strain (DGLS) is greater in Doxycyclinegroup, although both not statistically significant. Rehospitalization was not significantlydifferent between two groups.Conclusion: Doxycycline had effect in improving structure and function of the leftventricle in STEMI patients who have undergone PPCI"

"Belakang: Polimorfisme gen MMP-9 berperan dalam degradasi kolagenase tipe IV pada matriks ekstraselular yang memicu terjadinya destruksi tulang pada periodontitis. Tujuan: Untuk membandingkan distribusi polimorfisme gen MMP-9 -1562 C/T rs3918242 pada penyakit periodontitis dengan kontrol. Metode: Polimorfisme gen MMP-9 -1562 C/T di analisis menggunakan metode PCR-RFLP dengan enzim restriksi SphI. Hasil: Mayoritas frekuensi alel T ditemukan pada sampel periodontitis 11 dibandingkan dengan sampel kontrol 2. Sedangkan untuk frekuensi genotipe CT pada sampel periodontitis 22 ditemukan lebih tinggi dibandingkan dengan sampel kontrol 4. Kesimpulan: Ditemukan gambaran polimorfisme Gen MMP-9 ndash;1562 C/T pada penyakit periodontitis dan terdapat hubungan bermakna antara distribusi polimorfisme gen tersebut pada penyakit periodontitis dan individu sehat p = 0,018.

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Background: MMP 9 gene polymorphism is involved in degradation of type IV collagenases in the extracellular matrix ECM that leads to bone destruction in periodontitis.

Objectives: To compare the distribution of the MMP 9 1562 C T rs3918242 polymorphism in Indonesian males with and without periodontitis.

Methods: The MMP 9 1562 C T polymorphism was investigated by the PCR ndash RFLP method with SphI restriction enzyme digestion.

Results: The T allele in periodontitis sample 11 are higher than the healthy controls 2 . As well as the CT genotype, was found higher in periodontitis sample 22 than the healthy controls 4.

Conclusion: MMP 9 1562 C T gene polymorphism was found in this study and significantly associated with periodontitis p 0.018. "

"ABSTRAKLatar Belakang: Trombositosis pada pasien kanker payudara KPD diduga berkontribusi pada penyebaran dan sifat invasi sel punca kanker payudara. Modifikasi lingkungan mikro tumor dapat dilakukan untuk meningkatkan efektivitas terapi anti kanker. Belum diketahui apakah platelet derived growth factor PDGF -AB dalam lisat trombosit LT juga berperan terhadap cancer stem cell CSC payudara CD24-/CD44 .Tujuan: Penelitian ini bertujuan untuk menganalisis efek LT dan PDGF-AB didalamnya sebagai lingkungan mikro tumor pada proliferasi dan sifat invasi sel punca kanker payudara CD24-/CD44 yang ditandai dengan kadar matrix metalloproteinase-9 MMP-9 dan epithelial-cadherin E-cadherin . Metode: Penelitian ini merupakan studi eksperimental pada kultur sel punca KPD yang diberi LT dari pasien KPD dan donor sehat. Darah semua donor dilakukan pemeriksaan hematologi dan diproses untuk mendapatkan platelet rich plasma PRP . Jumlah trombosit per ?L PRP setiap donor dihitung. PRP diproses untuk mendapatkan LT. Kadar PDGF-AB LT diukur. LT 0,01 ditambahkan ke dalam medium dulbecco rsquo;s modified eagle rsquo;s medium DMEM -F12 untuk kultur sel punca KPD. Setelah inkubasi 48 jam, total jumlah sel, population doubling time PDT dan viabilitas sel dihitung dan dinormalisasikan terhadap nilai kontrolnya. Ekspresi MMP-9 dan E-cadherin dipilih sebagai penanda biologi sifat invasi dan diukur dengan metode enzyme-linked immunosorbent assay ELISA . Jumlah total sel, PDT, viabilitas sel, kadar MMP-9 dan E-cadherin dibandingkan antara pasien KPD dan donor sehat lalu dianalisis korelasinya dengan jumlah trombosit dan kadar PDGF-AB dalam lisat trombosit. Hasil: Jumlah trombosit dan kadar PDGF-AB dalam LT pasien KPD lebih tinggi dibandingkan LT donor sehat, keduanya dengan nilai p=0,02. LT pasien KPD memicu proliferasi sel punca KPD lebih baik dibandingkan LT donor sehat p

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ABSTRACTBackground Thrombocytosis in breast cancer BC patient is supposed to play a role in the invasiveness of breast cancer stem cells. Modification of tumor microenvironment was proposed to increase the efficacy of anticancer therapy. Aim This study aimed to analyze the effect of platelet lysate PL as well as its platelet derived growth factor PDGF AB content as a tumor microenvironment on the CD24 CD44 breast cancer stem cell BCSC proliferation and invasiveness. Methods This experimental study treated BCSC culture with PL from BC patients or healthy donors. Venous blood from all donors were subjected to hematology test and processed to obtain PRP. Platelet counts in PRP were determined. PRP was processed to obtain PL. PDGF AB contents in PL were measured. PL 0.01 was supplemented into dulbecco rsquo s modified eagle rsquo s medium DMEM F12 medium and used for culturing the CD24 CD44 BCSCs . After 48 hours, total cell count, population doubling time PDT , and cell viability were calculated and normalized to its control. Matrix metalloproteinase 9 MMP 9 and E cadherin was used as biological marker for CSC invasiveness and measured by enzyme linked immunosorbent assay ELISA method. Total cell count, PDT, cells viability as well as MMP 9 and E cadherin levels between BCSC, healthy donor platelet lysate and control group were compared and their correlation with platelet count in PRP and PDGF AB levels in platelet lysates were analyzed. Results Platelet counts and PDGF AB levels were higher in BC patient PL compared to healthy donor group, both with a p value of 0.02. BC patient PL could stimulate the proliferation of BCSCs higher than healthy donor PL p"