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"Blood vessels of tumors display many structural and functional abnormalities. Their unusual leakiness, potential for rapid growth and remodeling, and expression of distinctive surface molecules mediate the dissemination of tumor cells in the bloodstream and maintain the tumor microenvironment. Like normal blood vessels, they consist of endothelial cells, mural cells and their enveloping basement membrane. Common features, irrespective of their origin, size and growth pattern, are absent hierarchy, formation of large-caliber sinusoidal vessels, markedly heterogeneous density, increased permeability, decreased and abnormal pericyte-endothelial cell adhesion, irregular basement membrane structure, and the incorporation of bone-marrow-derived endothelial progenitor cells in the microvasculature. A number of specific tumor endothelial markers have been identified, as well as chromosomal abnormalities. These markers may be used to deliver drugs specifically and selectively to the tumor microvasculature."

"This book explores the development and use of innovative computational and mathematical approaches for modeling the vascular development of tumors. Covers modeling of the angiogenesis cascade, and integrates vasculature development with tumor growth dynamics."

"Background: lactate clearance and central venous oxygen saturation (ScvO2) are two methods for determining tissue oxygenation adequacy. There is a controversy regarding method better associates with and predicts sepsis and septic shock patients’ mortality. This study address the association of achieving one or two targets of microcirculatory resuscitation endpoints and early mortality in sepsis and septic shock. Methods: a cohort study was conducted in adult sepsis and septic shock patients in Intensive Care Unit, Cipto Mangunkusumo Hospital, Indonesia. Patients’ resuscitation endpoints data and outcome were observed during the first 120 hours of hospitalization. Cox’s proportional hazard regression analysis was used to analyse the early mortality risk in subject groups achieving lactate clearance target only, ScvO2 target only, both targets, and not achieving any target in 6 hours after onset of resuscitation adjusted for number of organ dysfunction. Results: subjects consisted of 268 patients. There were significant differences in the mortality risk between subjects who achieved both targets with subjects who achieved ScvO2 target only (adjusted hazard ratio [aHR] 13.47; 95% confidence interval [CI] 5.17-35.08) and subjects who not achieve any target (aHR 16.12; 95%CI 7.43-34.95). There were insignificant difference the early mortality risk between subjects who achieved both targets with subjects achieved lactate clearance target only (aHR 2.29; 95%CI 0.83-6.32). Conclusion: in patients with sepsis and septic shock, achievement of lactate clearance and ScvO2 targets associates with similar early mortality risk compared to achievement of lactate clearance target only. However, it associates with lower early mortality risk compared with ScvO2 target only

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Latar belakang: bersihan laktat dan saturasi oksigen vena sentral (ScvO2) adalah dua metode untuk menentukan kecukupan oksigenasi jaringan. Di antara kedua metode tersebut, terdapat kontroversi metode yang lebih berhubungan dengan dan dapat memprediksi mortalitas pasien sepsis dan renjatan sepsis. Penelitian ini bertujuan untuk menilai hubungan pencapaian target parameter akhir resusitasi mikrosirkulasi dan mortalitas dini pasien sepsis dan renjatan sepsis.

Metode: penelitian ini merupakan studi kohort pada pasien sepsis dan renjatan sepsis dewasa di Unit Perawatan Intensif RS Cipto Mangunkusumo, Indonesia. Data parameter akhir resusitasi dan luaran pasien diamati dalam 120 jam pertama perawatan. Analisis Cox’s proportional hazard regression digunakan untuk menilai risiko mortalitas dini pada kelompok subjek yang mencapai target bersihan laktat saja, target ScvO2 saja, kedua target dan tidak mencapai target apapun dalam 6 jam pertama sesudah awitan resusitasi, dengan penyesuaian terhadap jumlah disfungsi organ.

Hasil: subjek terdiri atas 268 pasien. Terdapat perbedaan risiko mortalitas yang bermakna antara kelompok subjek yang mencapai kedua target dibandingkan kelompok subjek yang mencapai target ScvO2 saja (adjusted hazard ratio [aHR] 13,47; 95% interval kepercayaan [IK] 5,17-35,08) dan yang tidak mencapai target apapun (aHR 16,12; 95% CI 7,43-34,95). Tidak terdapat perbedaan risiko mortalitas yang bermakna antara kelompok subjek yang mencapai kedua target dibandingkan kelompok subjek yang mencapai target laktat saja (aHR 2,29; 95%CI 0,83-6,32).

Kesimpulan: pada pasien sepsis dan renjatan sepsis, pencapaian target bersihan laktat dan ScvO2 berhubungan dengan risiko mortalitas dini yang tidak berbeda dengan dengan pencapaian target bersihan laktat saja, namun berhubungan dengan peningkatan risiko mortalitas dini dibandingkan dengan pencapaian target bersihan ScvO2 saja"

"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."