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"Leading authorities on percutaneous tumor ablation come together in this volume to provide a complete overview of everything physicians and other health professionals need to know to successfully implement and administer an image-guided ablation service. After an introduction to the protocols and attendant physics of ablation technology, concise organ-based chapters focus on a wide range of both straightforward and atypical cases to teach readers how to handle the unique clinical and technical challenges associated with percutaneous tumor ablation in different areas of the body. Succinct, step-by-step descriptions complement high-resolution images throughout to illustrate the nuances of each procedure. This must-have clinical reference will develop the technical and clinical tumor ablation skills of every fellow and practicing physician in interventional radiology, oncology, and surgical oncology."

"Kasus ?Primitive Neuro Ectodermal Tumor? (PNET) sangat jarang dan sangat sukar didiagnosis. Sebuah kasus PNET didiagnosis dengan teknik histopatologi dan pemeriksaan imunohistokimia. Seorang bayi laki-laki umur 4 bulan diperiksakan ke rumah sakit dengan benjolan pada dinding dada sejak bayi tersebut berumur 3 hari. Benjolan tersebut makin lama makin membesar hingga akhirnya mencapai diameter ± 10 cm, selanjutnya penderita dibawa ke klinik. Benjolan tersebut terfiksir pada dinding dada dengan batas tidak tegas, pada kulit diatas tumor tampak dua ulkus. Selanjutnya tumor tersebut didiagnosis sebagai suatu hemangioma. Secara makroskopis tumor berukuran 17 x 13 x 5,5 cm, berbatas tidak tegas, berwarna putih dan lunak. Secara mikroskopis massa tumor terdiri atas sel-sel berukuran kecil yang tidak berdiferensiasi, berbentuk bulat-oval, dengan inti hiperkromatik, dan sebagian membentuk struktur roset, Homer-Wright di antara bagian lainnya yang difus. Mitosis 7/10 HPF, nekrosis minimal kurang dari 25%. Gambaran ini sesuai dengan suatu ?malignant small round sel tumor?, Pada pemeriksaan imunohistokimia dengan panel antibodi meliputi Vimentin, NSE, Chromogranin dan CD99 menunjukkan Vimentin positif lemah-sedang, NSE negatif-positif lemah, Chromogranin negatif-positif lemah dan CD99 positif lemah-sedang. Secara keseluruhan, berdasarkan pemeriksaan makroskopis, histopatologik, dan imunohistokimia disimpulkan sebagai suatu ?Malignant Small Round Cell Tumor? yang sesuai dengan PNET / ES (Ewing?s sarcoma) yang perlu di konfirmasi dengan pemeriksaan sitogenetik. (Med J Indones 2007; 16:108-12).

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Primitive Neuro Ectodermal Tumor (PNET) is rare and difficult to diagnose. A case of PNET was diagnosed based on histopathological and immunohistochemical findings. A 4-month-old infant was admitted to the hospital with a tumor on the midline of his chest wall since he was 3 days old. The tumor was fixed on the chest wall and had ill-defined margin, enlarged over time and reached more than 10 cm in diameter when he was brought to a clinician. Two small ulcers were seen on the skin overlying the tumor. It was diagnosed as soft tissue tumor suggestive of a hemangioma. The tumor was 17 x 13 x 5.5 cm in size, white colored and firm to the touch. Microscopic examination revealed malignant small round cells with round to ovoid nuclei, coarse chromatin and scanty cytoplasm. Most cells were arranged in a solid pattern with scattered Homer-Wright rosettes. The mitotic count was 7/10 HPF, and necrosis was minimal (less than 25%). On immunohistochemical examination, the cells showed weak to moderate immunoreactivity to Vimentin and CD99, but showed negative to weak positive reactivity to NSE and Chromogranin. Based on the clinical features, gross findings, histopathologic and immunohistochemical examinations, the case was diagnosed as a malignant small round cell tumor consistent with PNET / ES (Ewing?s Sarcoma). To confirm the diagnosis, cytogenetic examination is suggested. (Med J Indones 2007; 16:108-12)."

"Percutaneous and coronary interventions, used to treat narrow arteries of the heart caused by/found in those with coronary heart disease. This book is a detailed guide for performing percutaneous procedures and it covers in-depth the procedures that cardiologists and interested specialists must be aware of in order to use the devices proficiently."

"Tumor necrosis factor alpha (TNF-alpha) adalah salah satu sitokin proinflamasi yang berperan pada timbulnya cedera iskemia-reperfusi pasien infark miokard akut yang menjalani tindakan intervensi koroner perkutan primer (IKPP). Kolkisin merupakan salah satu obat antiinflamasi yang diduga memiliki pengaruh terhadap TNF-alpha. Penelitian ini bertujuan untuk mengetahui peran kolkisin terhadap kadar TNF-alpha serum pasien infark miokard akut dengan tindakan intervensi koroner perkutan primer. Desain penelitian uji klinis acak tersamar ganda menggunakan sampel sisa serum penelitian dari subjek pasien infark miokard akut Rumah Sakit dr. Cipto Mangunkusumo. Subjek penelitian dibagi menjadi dua kelompok. Kelompok studi diberikan loading dose kolkisin 2 mg, kemudian dilanjutkan 2 x 0,5 mg per hari secara oral selama 48 jam, sementara kelompok kontrol diberikan plasebo. Analisis kadar TNF-alpha menggunakan metode ELISA yang diperiksa sebelum dan 48 jam pasca-IKPP untuk mendapatkan delta perubahan kadar TNF-alpha. Terdapat 64 subjek yang dianalisis terdiri dari 30 kelompok kontrol dan 34 kelompok studi. Delta kadar TNF-alpha pasca-IKPP kelompok kontrol (2,2) terhadap delta kadar TNF-alpha kelompok studi (0,7). Penelitian ini merupakan penelitian pertama tentang pengaruh kolkisin terhadap kadar TNF-alpha pada pasien infark miokard akut dengan tindakan intervensi koroner perkutan primer di Indonesia. Pengukuran TNF-alpha perlu dilakukan lebih dari dua kali untuk melihat dinamika kadar TNF-alpha pada pasien infark miokard akut yang menjalani tindakan intervensi koroner perkutan primer dan penelitian lanjutan diperlukan untuk menilai peran kolkisin sebagai obat antiinflamasi dengan pemeriksaan menggunakan metoda ELISA dengan reagen high-sensitive.

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Tumor necrosis factor alpha (TNF-alpha) is a proinflammatory cytokine that plays a role in the emergence of ischemia-reperfusion injury in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention (PCI). Colchicine is an anti-inflammatory drug believed to affect TNF-alpha. This study aimed to determine the role of colchicine on serum TNF-alpha levels in acute myocardial infarct patients undergoing primary percutaneous coronary intervention. The research design was a double-blind, randomized clinical trial using residual research serum samples from patients with acute myocardial infarction at Dr. Hospital. Cipto Mangunkusumo. The research subjects were divided into two groups. The study group was given a loading dose of 2 mg colchicine and then continued at 2 x 0.5 mg per day orally for 48 hours, whereas the control group was given a placebo. Analysis of TNF-alpha levels using the ELISA method was performed before and 48 hours after primary percutaneous coronary intervention to obtain the delta of changes in TNF-alpha levels. There were 64 subjects analyzed, comprising 30 control groups and 34 study groups. The delta of TNF-alpha levels post-PCI in the control group (2.2) compared with the delta of TNF-alpha levels in the study group (0.7). This is the first study on the effect of colchicine on TNF-alpha levels in acute myocardial infarction patients with primary percutaneous coronary intervention in Indonesia. TNF-alpha measurements need to be carried out more than twice to determine the dynamics of TNF-alpha levels in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention, and further research is needed to assess the role of colchicine as an anti-inflammatory drug by ELISA with high-sensitive reagents."

"Penelitian ini bertujuan memeriksa efek dosimetris dari pergerakan tumor untuk beberapa variasi besar ampiltudo pergerakan. Penelitian ini menggunakan fantom dinamik toraks yang dibangun berdasarkan CIRS Dynamic Thorax Phantom model 008A. Fantom ini mensimulasikan pergerakan secara translasi pada arah Superior dan Inferior (SI) serta rotasi pada bidang Lateral kanan-kiri (RL) dan Anterior Posterior (AP) untuk menirukan pergerakan akibat pernafasan manusia. Fantom ini didesain dan dikontrol menggunakan  linear actuator, servo motor, Adafruit motor shield L293D dan Arduino UNO R3. Fantom ini digunaan untuk mengevaluasi dosis titik menggunakan teknik 3D-CRT, IMRT, VMAT dan amplitudo translasi 5 mm; 10 mm; 15 mm  dengan amplitudo rotasi 90°. Pengukuran dosis titik menggunakan dosimeter film GafChromic EBT 3 dan thermoluminescence TLD LiF-100. Fantom toraks dinamik yang dibuat dapat meniru pergerakan translasi dengan amplitudo 5±0,2 mm; 10±0,5 mm; 15±0,4 mm dan pergerakan rotasi dengan amplitudo 89°±2°. Dari penelitian ini didapatkan penggunaan Internal Margin sebesar 5 mm mampu memberikan kompensasi deviasi dosis berkisar antara 0,6% sampai dengan 1%, penurunan dosis terbesar adalah pada arah Superior dan Inferior, gerak rotasi target tumor berpengaruh pada peningkatan deviasi dosis pada lateral kanan dan kiri akibat pebedaan kedalaman serta Teknik VMAT tidak disarankan untuk target bergerak karena memberikan deviasi terbesar yaitu berkisar pada -5% sampai dengan 9% akibat dari derajat kebebasan pergerakan antara gantry dan target semakin tinggi.

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This study aimed to investigate dosimetric effect of target movement for several translational amplitude. This work used in-house dynamic thorax phantom based on CIRS Dynamic Thorax Phantom model 008A. This phantom simulated translation in superior-inferior direction, rotational in the anterior-posterior and left-right lateral plane to mimic human respiratory motion. It was designed and controlled by linear actuator motor, servo motor, Adafruit motor shield L293D and Arduino UNO R3. It was implemented to evaluate point dose of 3D-CRT, IMRT, VMAT technique and for 5 mm; 10 mm; 15 mm translational motion amplitude 90° rotational target motion amplitude. The point dose measurement used GafChromic EBT 3 film and TLD LiF-100 as dosimeter. This in-house dynamic thorax phantom can mimicking NSCLC target movement for translational amplitude 5±0,2 mm; 10±0,5 mm; 15±0,4 mm and rotational amplitude 89°±2° From this study it found that the use of Internal Margin of 5 mm was able to compensate dose deviation about 0.6% to 1%, the largest decrease in dosage was in the Superior and Inferior direction, the rotational motion of the target tumor had an effect on increasing dose deviation on the right and left lateral due to the difference in depth and VMAT Technique it is not recommended for moving targets because it provides the largest deviation which ranges from -5% to 9% due to the higher degree of freedom of movement between the gantry and the target."

"PendahuluanTumor ganas maksila tidak sering dijumpai. Gejala permulaan samar-samar, dapat menyerupai radang sinus paranasal. Umumnya penderita datang telah ada benjolan sehingga penyakit telah meluas, dan telah mengenai struktur yang berdekatan. Diagnosa biasanya dibuat setelah stadium lanjut. Pengobatannya kompleks dan pronogsanya kurang baik. Penanganan tumor ganas maksila di RSCM, disamping oleh bagian bedah, juga dilakukan oleh bagian THT. Akan dilaporkan kasus tumor ganas maksila yang dirawat di bagian bedah RSCM 1985-1986. "

"DNA damage can have particularly severe carcinogenic influence if it incapacitates the cellular machinery normally protecting the cell from the effects of genomic damage. The protective functions involve not only DNA repair and apoptosis (programmed cell death), but also regulation of the cell cycle and proliferation. Therefore, carcinogenesis can be promoted by inactivating or altering key regulatory proteins like p16INK4a, which has the capability to arrest the cell cycle in the G1 phase and prevent inappropriate proliferation. Functional cyclin-dependent kinase (Cdk) inhibitor p16INK4a binds to Cdk-4 and Cdk-6, thereby preventing the Cdk-cyclin complexes from promoting phosphorylation of pRb and releasing the transcription factor E2F needed for the cell cycle to proceed to the S phase. Arrest in G1 accounts for a minority of arresting cells after DNA damage, the majority of arrests taking place in G2 without recognized p16INK4a contribution. However, inactivating alterations of p16INK4a are common in cancers, possibly because of additional functions of p16INK4a in senescence and inhibition of the spreading and migration of cancer cells. Since oncogenic initiation is insufficient for growing significant tumors without spreading and angiogenesis, this could partly explain why inactivated p16INK4a is frequently exhibited in clinical tumors in spite of apparently less exclusive role in cell cycle arrest. On the other hand, multiple oncogenic events are usually necessary to develop cancer, and generally both pRb and p53 pathways are impaired in tumors. This suggests that growth regulation in G1 and therefore also its key molecular components including p16INK4a are important in carcinogenesis."