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"RSJPDHK adalah RS pemerintah di bawah Kementerian Kesehatan yang ditetapkan sebagai rumah sakit BLU (Badan Layanan Umum) Kementerian Kesehatan yang telah melaksanakan remunerasi sejak tahun 2008. Implementasi kebijakan remunerasi di RSJPDHK ditetapkan melalui keluarnya KMK 165 tahun 2008. Pada tahun 2011 yang mengatur sistem tunjangan kinerja. Tujuannya adalah melaksanakan reformasi birokrasi maka perlu diberikan tunjangan kinerja. Tujuan penelitian ini yaitu melakukan kajian terhadap sistem remunerasi berdasarkan Keputusan Menteri Keuangan nomor 165 Tahun 2008 yang telah diterapkan di RSJPDHK dan sistem remunerasi berdasarkan Peraturan Menteri Pendayagunaan Aparatur Negara dan Reformasi Birokrasi nomor 63 Tahun 2011 yang akan diterapkan di Instansi Pemerintah. Penelitian ini melakukan analisis kesenjangan antara sistem remunerasi RSJPDHK berdasarkan KMK nomor 165 tahun 2008 dengan Permen PAN nomor 63 tahun 2011.Dari hasil FGD dengan para dokter spesiaslis jantung RSJPDHK dan wawancara mendalam para informan bahwa KMK nomor 165 tahun 2008 dasarnya adalah PP 23 tahun 2005 tentang BLU sedangkan Permen PAN nomor 63 tahun 2011 tidak berdasarkan PP 23 tahun 2005 tentang BLU. Sehingga Permen PAN nomor 63 tahun 2011 dapat dipergunakan pada tatanan birokrasi dan tidak bisa dipergunakan untuk RS BLU. Keadaan tersebut akan berdampak terjadinya kesenjangan pada segala aplikasi pelaksanaan sistem remunerasi pada RS BLU. Kesimpulan dari penelitian ini yaitu penerapan KMK nomor 165 tahun 2008 di RSJPDHK sudah tepat. Permen PAN nomor 63 tahun 2011tepat apabila diterapkan di institusi dengan tatanan birokrat.Saran yang diberikan yaitu melakukan monitoring dan evaluasi pelaksanaan sistem remunerasi yang berjalan di RSJPDHK berdasarkan KMK No. 165 Tahun 2008 sebagai upaya penyempurnaan. Permen Pan No. 63 tahun 2011 harus dilengkapi dengan peraturan yang sesuai jika akan dilaksanakan pada institusi BLU.

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National Cardiovascular Center Harapan Kita (NCCHK) is a public hospital which structurally located under Ministry of Health and defined as a Public Service Board. The Ministry of Health has been implemented the remuneration system since 2008. The implementation of these policies in NCCHK are set through a decree of the Minister of Finance No.165 in 2008. In 2011, the Minister of Administrative and Bureaucratic Reform published a decree No.63 to regulate the performance allowance.

The aim is, to implement a bureaucratic reform, it is necessary to give the performance allowance. To review the remuneration system based on a decree of the Minister of Finance No.165, 2008 which has been applied in NCCHK and the remuneration system based on a decree of the Minister of Administrative and Bureaucratic Reform No.63, 2011 which will be applied in governmental bodies. Perform a gap analysis between the remuneration system based on a decree of the Minister of Finance No.165, 2008 and a decree of the Minister of Administrative and Bureaucratic Reform No.63, 2011.

From the results of the focused group discussions with NCCHK cardiologists and in-depth interview with informants, it was conclude that a decree of the Minister of Finance No.165, 2008 is essentially based on a Government Ordinance No.23, 2005 about Public Service Board. However, a decree of the Minister of Administrative and Bureaucratic Reform No.63, 201 was not based on this Government Ordinance so that it cannot be used in a hospital that become a Public Service Board. This situation will end with the occurrence of gaps in the implementation of any applied system in the public-service-board hospital remuneration.

Conclusion. The application of the decree of the Minister of Finance No.165,2008 is appropriate for public-service-board hospitals. The decree of the Minister of Administrative and Bureaucratic Reform No.63, 2011 is applicable when it is applied in institutions with bureaucratic order.

Suggestion. To monitor and evaluate the implementation of the remuneration system that running on NCCHK based on a decree of the Minister of Finance No.165, 2008 as efforts to improve. The decree of the Minister of Administrative and Bureaucratic Reform No.63, 2011 should be equipped with appropriate regulations if it would be implemented on public-service-board institutions."

"Latar Belakang: Penyakit arteri perifer (PAP) merupakan penyakit yang sering dijumpai serta memiliki morbiditas dan mortalitas yang bermakna. Iskemia tungkai akut merupakan salah satu PAP yang menyebabkan stres retikulum endoplasma dan kematian sel melalui apoptosis atau autofagia. Aktivasi Caspase secara berurutan memainkan peran penting dalam suatu fase apoptosis sei. Sementara itu, Beclin-l memiliki peran utama dalam autofagia. Endotelin-1 (ET -1) sebagai faktor transkripsi Monocyte Chemoattractant Protein-1 (MCP-1) telah diteliti dengan baik dalam perkembangan aterosklerosis tetapi tidak pada iskemia tungkai. Tujuan penelitian ini adalah untuk mengetahui peran ET-1 dalam patogenesis iskemia tungkai akut melaIui MCPIP, Beclin-1, dan Caspase-3. Bahan dan Metode: Tiga belas kelinci umur 5 bulan galur Selandia Bam White (NZW) dipilih untuk penelitian ini. Arteri femoralis kanan semua kelinci kemudian diikat dan dilakukan reseksi pembedahan sampai alirannya hilang, dikonfirmasi oIeh Doppler Laser Fluximetry. Semua kelinci kemudian secara acak dialokasikan untuk kelompok perlakuan dengan pemberian intravena ECE-1 inhibitor (CGS26303) 5 mglkg berat badanlhari selama 26 hari dan kelompok kontrol. Jaringan diambiI dari daerah otot iskemik dan dilakukan pemeriksaan untuk ekspresi protein MCPIP, Beclin-1 untuk biomarker autofagia serta Caspase-3 untuk biomarker apoptosis menggunakan imunohistokimia. Ekspresi gen diperiksa menggunakan real time polymerase chain reaction (RT-PCR) dan dinyatakan sebagai ekspresi gen relatif. Hasil: Selama periode follow-up, 2 kelinci mati karena infeksi. Oleh karena itu, tersisa 11 kelinci yang menjadi subjek penelitian ini. Empat kelinci dialokasikan untuk kelompok kontrol sementara 7 kelinci diberikan ECE-I sebagai kelompok perlakuan. Semua kelompok perlakuan positif memiliki antibodi terhadap MCPIP, Beclin-1, dan Caspase-3 tetapi tidak untuk kelompok kontrol (p = 0,003). Meskipun demikian, ekspresi gen relatif dari MCP1P, Beclin-1 dan Caspase-3 ditemukan bervariasi antara 2 kelompok dan tidak berbeda bermakna seeara statistik. Simpulan: Pada iskemia tungkai akut, ET-1 diduga memiliki peran penting dalam mengatur MCP1P, Beelin-1, dan Caspase-3. Jalur tersebut merupakan suatu alternatif baru mekanisme kematian sei. Intervensi melalui inhibisi ET -1 diduga dapat menunda proses kematian sel.

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Background: Peripheral arterial disease (PAD) is common and causes significant morbidity and mortality. Acute limb ischemia is one of the PAD that will develops endoplasmic reticulum stress and subsequently cell death through apoptosis or autophagy. Sequential activation of Caspases plays a major role in the execution phase of cell apoptosis while Beclin-I has a central role in autophagy. Endothelin-I (ET -1) as atranscription factor of Monocyte Chemoattractant Protein-I (MCP-1) has been well studied in the progression of atherosclerosis but not in limb ischemia. The aim of the study is to investigate the role of ET -1 in the pathogenesis of acute limb ischemia through MCPIP, Beclin-1 and Caspase-3 . Materials and Methods: Thirteen of 5-month-old New Zealand White (NZW) rabbits are chosen for this study. The right femoral artery of all rabbits are ligated and resected surgically until its flow disappear and confirmed by laser Doppler Fluximetry. All are then randomly. allocated for intravenous administration of ECE-I inhibitor (CGS26303) 5 mglkg body weight/day for 26 days (n=7) and control group (n=6). The tissue taken from ischemic muscle area was examined for protein expression of MCPIP, Beclin-1 for autophagy biomarker as well as Caspase-3 for apoptotic biomarker using immunohistochemistry technique. Gene expressions are examined using real time Polymerase Chain Reaction (PCR) and expressed as relative gene expression. Result: During period of follow-up, 2 rabbits died because of infection. Therefore there were still remain II rabits for subject of this study. Four were allocated for non-intervention as control group while 7 were for ECE-1 administration as intervention group. All of the intervention group has positive on antibody for MCPIP, Beclin-I and Caspase-3 but not for the control group (p = 0.003). However, the relative gene expression on MCPIP, Becline-1 and Caspase-3 varied between 2 groups and were not statistically different. Conclusion: In acute limb ischemia, ET-1 maya play major role in regulating MCPIP, Beclin-l and Caspase-3. This pathway may be proposed as a new alternative mechanism of cell death in this situation. Intervention of ET-I may delay the process of cell death."

"Percutaneous transluminal coronary angioplasty ( PTCA) isknown as the mechanical alternative intervention forrevascularization of coronary artcry stenosis.Unfortunately reocclusion and coronary spasm is seen on quite anumber of patients. This process is said due to an imbalance ofvasoactive substances at the cellular endothelial level which cause vasoconstriction of the smooth muscle cells. It's believed that endothelin and lipid peroxidc ( oxigen frec radicals) has a significant role in this process. This study is designed to prove the hypothesis that there is anincrease of endothclin and lipid peroxide concomitantlyimmediately after PTCA proseduce. On 37 patients with stenosis at left coronary artery, local plasma endothelin and lipid peroxide were measured before and after PTCA. Blood was obtained at side of coronary sinus. Endothelin was measured by specific competitive protein binding radioimmunoassay ( RIA Technique ), while lipid peroxide was measured by using Malonaldehyde (MDA) concentration. Local plasma MDA was measured by fuorosense spectrofotometri.The results showed a significant increase of local plasma endothelin after PTCA (5,28+1-3,33 to 8,53 +1- 4,5 . Pglml, p = 0,0001) and a significant increase of local plasma MDA concentration after PTCA ( 0,540+1-0,279 to 0,868+1-0,438. Umol/L, p = 0,0001). There was no correlation found between the increase of local plasma endothelin with the duration of balloon inflation, peak pressure of balloon inflation, diameter of the balloon, length of the balloon, the number of balloon inflation. This finding suggest that beside endothelial injury during PTe" other unknown factor contribute to the increasing level of endothelin. However correlation was found between the increase of local plasma MDA and the number of the balloon inflation.Conclusions: Local plasma endothelin and lipid peroxide were significantely increased immediately after PTCA, and there was correlation between the increase of local plasma lipid peroxide with the number of the balloon inflation."