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"Latar belakang: Antrasiklin diketahui dapat menimbulkan toksisitas pada jantung melalui mekanisme peningkatan pembentukan advanced glycation end-products (AGEs), yakni pentosidine dan Nε-(carboxylmethyl)lysine (CML).Penelitian ini bertujuan mengetahui efek telmisartan (TLM) suatu antagonis reseptor angiotensin II (ARB) terhadaptoksisitas jantung yang diinduksi oleh antrasiklin.Metode: Tikus galur Sprague Dawley dibagi secara acak menjadi 3 kelompok: kelompok pertama mendapat daunorubisin(DNR) 3 mg/kgBB dua hari sekali hingga mencapai dosis kumulatif 9 mg/kgBB. Kelompok kedua mendapat DNR ditambahTLM 10 mg/kgBB/hari, secara oral selama 6 minggu, sedangkan kelompok kontrol (CTL) hanya mendapat pelarut DNR.Rerata tekanan darah (MBP), tekanan ventrikel kiri (LVP), tekanan diastolik akhir ventrikel kiri (LVEDP), dan kontraktilitasventrikel (±dP/dt) diukur dengan menggunakan Powerlab. Sedangkan fraksi ejeksi (EF) dan fraksi pemendekan (FS) dinilaidengan ekokardiografi. Ekspresi reseptor AGE (RAGE), pentosidin, dan CML diperiksa dengan imunohistokimia danwestern blot.Hasil: DNR menyebabkan perburukan beberapa parameter hemodinamik yang dapat diperbaiki oleh TLM, yakni :LVP : 124,3 ± 6,0; 111 ± 7; dan 115,1 ± 5,4 mmHg, untuk kelompok CTL, DNR, dan DNR-TLM. LVEDP: 7,5 ± 0,9;10,7 ± 0,3; 8,7 ± 0,4 mmHg, dan ; +dP/dt: 6813 ± 541; 4800 ± 345; 5950 ± 398 mmHg/s. Hal yang sama juga terlihatpada parameter ekokardiografi, yakni: EF: 78,9 ± 1,8; 59.6 ± 1,4; 76,2 ± 2,75 %; FS: 42,8 ± 1,7; 29,1 ± 1,3; 41 ±2,7 % untuk kelompok CTL, DNR and DNR-TLM. Ekspresi protein RAGE, pentosidine dan CML meningkat padapemberian DNR yang kemudian dihambat dengan pemberian bersama TLM.Kesimpulan: AGE berperan pada toksisitas jantung akibat pemberian DNR. Telmisartan dapat menghambat efek tersebutdengan menurunkan ekspresi RAGE.

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AbstractBackground: Anthracyclines have been reported to induce cardiotoxicity through mechanisms involving formation ofadvanced glycation end-products (AGEs), including pentosidine and Nє-(carboxymethyl) lysine (CML). We investigated thepotential utility of telmisartan (TML), an angiotensin II receptor antagonists (ARB) on anthracycline-induced cardiotoxicity.Methods: Three groups of Sprague-Dawley rats were treated as follows: The first group received daunorubicin (DNR)3 mg/kgBW every alternating day to reach a cumulative dose of 9 mg/kg DNR . The second group received DNR plusTLM at a dose10 mg/kgBW, by oral gavage for 6 weeks, and the third group served as control group (CTL) which onlyreceived vehicle of DNR. Mean blood pressure (MBP) peak left ventricular pressure (LVP), LV end-diastolic pressure(LVEDP), and intra-ventricular contractility (±dP/dt) were recorded by using Powerlab instrumentation. Ejectionfraction (EF), and fractional shortening (FS) were measured by echocardiography. Expression of receptor of AGE(RAGE), pentosidine and CML were measured by immunohistochemistry and Western blot in LV tissue.Results: DNR treatment was associated with significant weakening of some hemodynamic parameters which couldbe reversed by TML (LVP: 124.3 ± 6.0; 111 ± 7; and 115.1 ± 5.4 mmHg, respectively in CTL, DNR and DNR-TLMgroups; LVEDP: 7.5 ± 0.9; 10.7 ± 0.3; 8.7 ± 0.4 mmHg, respectively; +dP/dt: 6813 ± 541; 4800 ± 345; 5950 ± 398mmHg/s, respectively). The same phenomenons were also observed on echocardiographic parameters (EF: 78.9 ± 1.8;59.6 ± 1.4; 76.2 ± 2.75 %, resepectively; FS: 42.8 ± 1.7; 29.1 ± 1.3; 41 ± 2.7 %) respectively. Expression of RAGE aswell as pentosidine and CML were increased in DNR-rats. TML treatment ameliorated these changes.Conclusion: These results suggested the role of AGE formation in DNR-induced cardiotoxicity and telmisartan couldinhibit the progression of cardiac toxicity at least in part by reduction RAGE expressiom."

"Golongan antrasiklin merupakan kemoterapi pilihan pertama untuk penanganan kanker payudara, khususnya pada pasien lanjut usia. Namun beberapa penelitian melaporkan terkait kejadian tidak diharapkan pada penggunaan antrasiklin. Penelitian ini dilakukan bertujuan untuk mengidentifikasi kejadian tidak diharapkan. Selain itu untuk mengetahui hubungan variabel bebas terhadap kejadian tidak diharapkan pada penggunaan rejimen berbasis antrasiklin. Penelitian ini merupakan penelitian observasional dengan rancang penelitian potong lintang (cross-sectional).  Pengambilan sampel dilakukan secara retrospektif, pada pasien lanjut usia (≥60 tahun) di Rumah Sakit Kanker Dharmais. Pengambilan data mulai Januari 2018-Desember 2020. Identifikasi kejadian tidak diharapkan dari penggunaan kemoterapi berbasis antrasiklin menggunakan metode trigger tool khusus untuk pasien kanker. Analisis statistik digunakan untuk memperoleh karakteristik variabel bebas, selain itu untuk mengetahui hubungan variabel bebas terhadap kejadian tidak diharapkan. Pada 107 subjek, sebanyak 71% (n=76 pasien) teridentifikasi dengan trigger tool, seluruh subjek mengalami 122 trigger.rigger pemberian transfusi darah paling banyak ditemukan pada penelitian ini, yaitu pada 39% (n=30 pasien). Netropenia dan anemia merupakan KTD terbanyak yang teridentifikasi pada penggunaan kemoterapi berbasis antrasiklin. Seluruh KTD yang teridentifikasi merupakan kategori E sebanyak 251 kejadian. Pemberian transfusi darah merupakan variabel bebas yang mempunyai hubungan signifikan (p<0,05) dengan kejadian tidak diharapkan dari penggunaan kemoterapi berbasis antrasiklin pada pasien lanjut usia kanker payudara.

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Anthracycline are the first choice chemotherapy for the treatment of breast cancer, particularly in elderly patients. However, several studies reported adverse events in the treatment of using anthracyclines. This study aims to identify adverse events. Furthermore, to find out more about how independent variables related to adverse event. An observational retrospective study of elderly patient (≥ 60 years) was conducted in a tertiary cancer hospital in Jakarta. Data were collected from January 2018 to December 2020. We used trigger tool specific for cancer patients to identify adverse event during anthracycline base regimen. Independent variables were evaluated in univariate analysis: age, weight loss, marital status, total cumulative dose, polypharmacy, types of anthracycline, metastatic status. Bivariate and multivariate analysis to find out relationship between independent variable and adverse event. In total, 107 subject records were collected and reviewed, there were 71% (n=76 patients) identified with trigger tool. Trigger were totally identified 122 times in 86 medical records. Neutropenia and anemia were the most common adverse events identified in our study. Adverse events with category E identified in all of the subject, as many as 251 events. Blood transfusion had significantly relationship (p<0,05) with adverse events in elderly breast cancer patients."

"BACKGROUND:proliferative diabetic retinopathy (DR) is an advanced form of DR that eventually could lead to blindness. Levels of vitreous advanced glycation end products (AGEs) and D-dimer may reflect the pathological changes in the retina, but only few studies have assessed their correlation with blood hemoglobin A1C (HbA1c) levels. This study aimed to find the association between blood HbA1c levels with vitreous AGEs and D-dimer levels in patients with proliferative DR. METHODS:an analytical cross-sectional study was performed in subjects with proliferative DR who underwent vitrectomy. Subjects were divided into 2 subgroups, i.e. uncontrolled (HbA1c >7%) and controlled (HbA1c <7%) groups. Vitreous AGEs and D-dimer levels were assessed; the levels were compared between uncontrolled and controlled hyperglycemic patients. Statistic correlation tests were also performed for evaluating blood HbA1c, vitreous AGEs, and D-dimer levels.RESULTS:a total of 47 patients were enrolled in this study and 32 (68.1%) of them were women. Median vitreous AGEs level was 11.0 (3.0 - 48.0) µg/mL; whereas median vitreous D-dimers level was 5,446.0 (44.0 - 37,394.0 ) ng/mL. The median vitreous AGEs levels was significantly higher in patients with uncontrolled vs. controlled hyperglycemia (14.0 vs. 4.0 mg/mL; p<0.001). There was a significant positive correlation with moderate strength between blood HbA1c level and vitreous AGEs level (r=0.524; r2=0.130; p=0.0001). Blood HbA1c level could be used to predict vitreous AGEs level by using the following calculation: vitreous AGEs = -1.442+ (1.740xblood HbA1c). Vitreous D-dimer levels were not significantly different between uncontrolled and controlled hyperglycemia (median 4607.5 vs. 5701.6 ng/mL; p = 0.458). There was a positive significant correlation between blood HbA1c and vitreous D-dimer levels (r = 0.342; p = 0.019); however the correlation was weak. Vitreous AGEs level had a positive significant correlation with vitreous D-dimer levels (r = 0.292; p = 0.046) and the correlation strength was also weak.CONCLUSION:median vitreous AGEs levels were significantly higher in proliferative DR patients with uncontrolled than those with controlled hyperglycemia. Blood HbA1c level can be used to assess vitreous AGEs level in patients with proliferative DR by using the following calculation: vitreous AGEs = -1.442+(1.740 x HbA1c). However, the blood HbA1c level can not be used to predict vitreous D-dimer level in patients with proliferative DR.

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Latar belakang: retinopati diabetik (RD) tipe proliferatif merupakan bentuk lanjut RD yang selanjutnya dapat menyebabkan kebutaan. Kadar produk akhir glikasi/advanced glycation end products (AGEs) dan D-dimer cairan vitreus dapat menggambarkan perubahan patologi pada retina, tetapi hanya ada sedikit penelitian yang menilai korelasi antara kedua parameter tersebut dengan kadar HbA1c dalam darah. Tujuan penelitian ini menemukan hubungan antara kadar HbA1c darah dengan kadar AGEs dan D-dimer cairan vitreus pada pasien dengan RD tipe proliferatif. Metode: penelitian bersifat analitik potong lintang pada pasien dengan RD tipe proliferatif yang menjalani vitrektomi. Pasien dibagi dalam 2 kelompok yaitu hiperglikemi tidak terkendali (HbA1c > 7%) dan terkendali (HbA1c < 7%). Kadar AGEs dan D-dmer cairan vitreus diukur dan kadarnya dibandingkan antara pasien hiperglikemi tidak terkendali dan terkendali. Uji korelasi statistik juga dilakukan antara kadar HbA1c darah dengan kadar AGEs dan D-dimer cairan vitreus.

Hasil: pasien berjumlah 47, dengan 32 (68.1%) pasien adalah wanita. Nilai median kadar AGEs cairan vitreus 11.0 (3.0 – 48.0) μg/mL, dan nilai median kadar D-dimer cairan vitreus 5,446.0 (44.0 – 37,394.0 ) ng/mL. Nilai median kadar AGEs cairan vitreus lebih tinggi bermakna pada pasien dengan hiperglikemia tidak terkendali dibandingkan dengan hiperglikemia terkendali (14.0 vs. 4.0 mg/mL; p<0.001). Terdapat korelasi positif bermakna dengan kekuatan sedang antara kadar HbA1c darah dan kadar AGEs cairan vitreus (r = 0.524; r2 = 0.130; p=0.0001). Kadar HbA1c darah dapat digunakan untuk memperkirakan kadar AGEs cairan vitreus dengan menggunakan rumus: kadar AGEs cairan vitreus = -1.442+(1.740xHbA1c darah). Kadar D-dimer cairan vitreus pasien dengan hiperglikemia tidak terkendali tidak berbeda bermakna dengan pasien hiperglikemia terkendali (median 4607.5 vs. 5701.6 ng/mL; p = 0.458). Terdapat korelasi positif bermakna tetapi dengan kekuatan lemah antara kadar HbA1c darah dengan kadar D-dimer cairan vitreus (r = 0.342; p = 0.019). Kadar AGEs cairan vitreus memiliki korelasi positif bermakna dengan kekuatan lemah dibandingkan dengan kadar D-dimer cairan vitreus (r = 0.292; p = 0.046).

Kesimpulan: nilai median kadar AGEs cairan vitreus lebih tinggi bermakna pada pasien RD proliferatif dengan hiperglikemia tidak terkendali dibandingkan hiperglikemia terkendali. Kadar HbA1c darah dapat digunakan untuk memperkirakan kadar AGEs cairan vitreus pada pasien RD proliferatif dengan menggunakan rumus: kadar AGEs cairan vitreus = -1.442+ (1.740x HbA1c darah). Kadar HbA1c darah pada pasien RD proliferatif tidak dapat digunakan untuk memperkirakan kadar D-dimer cairan vitreus."

"Achilles tendinopathy merupakan sebuah penyakit degeneratif yang dapat disebabkan oleh diabetes mellitus tipe 2 (DMT2). Penyakit ini disebabkan oleh akumulasi dari advanced glycation end products (AGEs). Akumulasi AGEs pada tendon dapat menyebabkan mekanisme cross-link dengan kolagen dan aktivasi jalur persinyalan receptor of advanced glycation end products (RAGE) yang menyebabkan struktur kolagen menjadi tidak teratur. Pembuatan model DMT2 dilakukan dengan hewan model tikus dengan metode high fat diet dan induksi streptozotocin (STZ) pada galur tikus Sprague Dawley. Studi pendahuluan yang dilakukan menunjukkan pada dosis STZ 30 mg/Kg tidak menunjukkan hewan model DMT2. Oleh karena itu, tujuan pada penelitian ini adalah untuk melakukan studi histologis achilles tendinopathy yang disebabkan oleh DMT2 pada ketiga dosis (30 mg/Kg, 40 mg/Kg dan 65 mg/Kg) dan dilanjutkan dengan studi ekspresi gen efek gen RAGE. Studi ini menggunakan sampel tendon achilles tikus yang sudah dibuat model DMT2 dengan metode high fat diet dan induksi streptozotocin (STZ) pada galur tikus Sprague Dawley yang telah dibentuk dalam blok parafin. Terdapat tiga kelompok perlakuan diabetes dengan induksi streptozotocin yang berbeda, yakni dosis STZ 30 mg/Kg, 40 mg/Kg, dan 65 mg/Kg. Metode yang digunakan untuk membuat preparat histologis adalah dengan metode parafin dengan dua pewarnaan, yakni hematoksilin dan eosin Harris dan masson trichrome untuk melihat struktur kolagen. Untuk identifikasi ekspresi gen RAGE menggunakan metode quantitative real time polymerase chain reaction. Hasil penelitian menunjukkan bahwa achilles tendinopathy yang disebabkan oleh diabetes memberikan hasil gambaran histologis dengan terjadinya kerusakan jaringan tendon yang ditandai dengan disorganisasi kolagen yang terlihat pada dosis STZ 65 mg/Kg. PaPada dosis STZ 30 mg/Kg dan 40 mg/Kg, kondisi kolagen masih dalam kolagen yang mirip dengan tendon sehat dengan beberapa daerah mulai mengalami disorganisasi kolagen. Ekspresi gen RAGE dengan menggunakan qRT-PCR menghasilkan tingkat ekspresi gen RAGE yang meningkat sebanyak 2,71 kali pada kelompok perlakuan diabetes dibandingkan dengan kelompok normal. Kesimpulan yang didapatkan pada penelitian ini adalah model tikus DMT2 menunjukkan perubahan dan disorganisasi tendon. Pada sampel tikus dosis STZ 65 mg/Kg menghasilkan disorganisasi tendon paling parah dibandingkan dengan dosis injeksi STZ 30 mg/Kg dan 40 mg/Kg. Selain itu, pada tendon perlakuan diabetes didapatkan tingkat ekspresi gen RAGE yang meningkat sebanyak 2,71 kali dibandingkan dengan tendon normal.

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Achilles tendinopathy is a degenerative condition that can be caused by type 2 diabetes mellitus (DMT2). This disease is caused by the accumulation of advanced glycation end products (AGEs). The buildup of AGEs in the tendon can lead to cross-linking mechanisms with collagen and activation of the receptor for advanced glycation end products (RAGE) signaling pathway, resulting in irregular collagen structure. The disease model was created using a rat model with a high-fat diet and streptozotocin (STZ) induction in Sprague Dawley rats. Preliminary studies showed that the STZ dose of 30 mg/kg did not result in a DMT2 model. Therefore, the aim of this research was to conduct a histological study of Achilles tendinopathy caused by DMT2 at three different doses (30 mg/kg, 40 mg/kg, and 65 mg/kg), followed by studying the gene expression of RAGE-related genes.The study used Achilles tendon samples from rats that were induced with DMT2 using a high-fat diet and STZ induction in Sprague Dawley rats, which were then embedded in paraffin blocks. There were three diabetes treatment groups with different STZ induction doses: 30 mg/kg, 40 mg/kg, and 65 mg/kg. Histological preparations were made using the paraffin method with two staining techniques, namely Harris hematoxylin and eosin staining and Masson trichrome staining to visualize collagen structure. The quantitative real-time polymerase chain reaction (qRT-PCR) method was used to identify RAGE gene expression. The results showed that Achilles tendinopathy caused by diabetes resulted in histological changes in the tendon tissue, characterized by collagen disorganization, particularly evident at the STZ dose of 65 mg/kg. At doses of STZ 30 mg/kg and 40 mg/kg, collagen appeared similar to that of a healthy tendon, but some areas showed signs of collagen disorganization. The qRT-PCR analysis revealed that RAGE gene expression was 2.71 times higher in the diabetes treatment group compared to the normal group.In conclusion, the DMT2 rat model exhibited changes and disorganization in the tendon. The 65 mg/kg STZ injection in rat samples resulted in the most severe tendon disorganization compared to the 30 mg/kg and 40 mg/kg STZ injection doses. Additionally, diabetes treatment of the tendon showed a 2.71-fold increase in RAGE gene expression compared to the normal tendon."

"ABSTRAK Latar Belakang: Pasien Diabetes Mellitus DM tipe 2 memiliki peningkatan risiko terjadinya fraktur yang dikenal dengan istilah diabetoporosis. Pemeriksaan Bone Mass Densitometry BMD dinilai tidak superior dalam mendiagnosis diabetoporosis mengingat nilai BMD pada DM tipe 2 dapat normal bahkan meningkat. Beberapa penanda diharapkan dapat menggambarkan kualitas tulang secara non invasif. Peran AGEs dan reseptornya dinilai penting dalam proses diabetoporosis. Namun demikian, penelitian mengenai penanda AGEs dan reseptornya pada pasien DM tipe 2 masih tergolong sangat sedikit serta belum adanya penelitian yang membandingkan kadar AGEs dan reseptornya pada pasien DM tipe 2 dan subjek normal.Tujuan: Penelitian ini bertujuan untuk mengetahui perbedaan kadar pentosidine serum, esRAGE serum, rasio esRAGE/pentosidine serum antara pasien DM tipe 2 dan subjek normal, serta korelasi rasio esRAGE/pentosidine serum terhadap P1NP serum sebagai penanda peningkatan risiko diabetoporosis.Metode: Penelitian ini merupakan studi potong lintang terhadap 38 perempuan DM tipe 2 belum menopause, berusia 35 tahun dengan diagnosis DM tipe 2 yang berobat di Poli Metabolik Endokrin RSCM, Klaster Diabetes Kencana RSCM, RSUP Persahabatan, RSUK Tugu Koja, RSUK Kemayoran, dan Puskesmas Jatinegara. Sebagai kelompok non DM adalah 36 perempuan non DM dengan rentang usia yang sama. Pengambilan sampel dilakukan secara simple random sampling terhadap darah yang terkumpul. Pemeriksaan Pentosidine serum dan esRAGE dilakukan dengan metode ELISA sedangkan pemeriksaan P1NP dilakukan dengan menggunakan metode ECLIA.Hasil Penelitian: Pasien DM tipe 2 memiliki kadar pentosidine lebih tinggi p=0,028 , kadar esRAGE yang lebih rendah p=0,248 , serta rasio esRAGE/pentosidine yang lebih rendah p=0,001 daripada subjek normal. Rerata kadar pentosidine serum pada DM tipe 2 dan subjek normal adalah 5406 1911 pmol/ml dan 3145 1892 pmol/ml; sedangkan median rasio esRAGE/pentosidine serum adalah 0,03 pg/pmol dan 0,06 pg/pmol. Tidak terdapat korelasi antara rasio esRAGE/pentosidine dengan kadar P1NP serum.Kesimpulan: Kondisi hiperglikemia pada DM tipe 2 menyebabkan tingginya kadar pentosidine serum yang tidak diimbangi dengan peningkatan kadar esRAGE serum. Secara khusus, terjadi penurunan rasio esRAGE/pentosidine serum pada pasien DM tipe 2 perempuan dan tidak ditemukan korelasi antara rasio esRAGE/pentosidine serum dengan kadar P1NP serum sebagai penanda formasi tulang.

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ABSTRACT Background: Diabetes Mellitus type 2 T2DM patients have an increased risk of fracture known as diabetoporosis. Examination of Bone Mass Densitometry BMD is considered not superior in diagnosing diabetoporosis since the BMD value in type 2 DM can be normal and even increased. Some markers are expected to describe bone quality in a non invasive manner. The role of AGEs and their receptors is considered important in the process of diabetoporosis. However, research on the role of AGEs and their receptors in T2DM patients is still lacking and there was no study comparing AGEs and their receptors in T2DM and non T2DM patients before.Aim: The aim of this study is to determine the difference of serum pentosidine level, serum esRAGE, serum esRAGE/pentosidine ratio between T2DM and non T2DM patients, and correlation of serum esRAGE/pentosidine ratio to serum P1NP as a marker of increased risk of diabetoporosis.Method: This is a cross-sectional study on 38 premenopausal females with T2DM with a minimum age of 35 years with symptoms or diagnosis of T2DM for more than 5 years, seen for treatment at Endokrin Metabolik Klinik at RSCM, Klaster Diabetes RSCM Kencana, RSUP Persahabatan, RSUK Tugu Koja, RSUK Kemayoran, and Puskesmas Jatinegara. Healthy controls are 36 non-DM females with similar age range. Sampling was done by simple random sampling. Serum pentosidine and serum esRAGE measurement were done by ELISA method and serum P1NP measurement was done by ECLIA method.Results: T2DM patients had higher serum pentosidine levels p=0.028 , lower serum esRAGE p=0.248 , as well as lower esRAGE/pentosidine p=0.001 ratios than non T2DM. Serum pentosidine in T2DM and non T2DM is 5406 1911 pmol/ml and 3145 1892 pmol/ml; whereas median ratio of serum esRAGE/pentosidine was 0.03 pg/pmol and 0.06 pg/pmol. There was no correlation between ratio serum esRAGE/pentosidine and serum P1NP in T2DM patients.Conclusions: Hyperglycemia in T2DM patients lead to high serum pentosidine levels that are not followed by elevated serum esRAGE levels. In combination, there was a decrease level of serum esRAGE/pentosidine ratio in T2DM patients. No correlation was seen between level of serum esRAGE/pentosidine ratio and level of P1NP as a marker for bone formation in T2DM patients. "

"This book describes in detail the background to and objective of the development, materials, manufacturing processes, functions and future prospects of a number of ceramic products. Not merely about the science and technology of ceramic manufacturing, the book is about the products themselves, as it tries to clarify how ceramics continue to contribute to our lives. It is the first such work to show advanced ceramic products in detail, from the technologies used to their application, and can be seen as a kind of illustrated reference book for modern advanced ceramic products as it is filled with easy-to-understand illustrations and photos. "

"Latar Belakang: Kanker nasofaring (KNF) adalah keganasan yang terjadi pada epitel mukosa daerah nasofaring dengan angka kejadian di dunia sekitar 1,2 per 100.000 penduduk. Perkembangan mekanisme penanda molekuler yang berhubungan dengan proliferasi, apoptosis, dan invasi tumor yaitu Ki-67 dan p16, dapat memberikan indikasi tentang tingkat proliferasi sel dan status penghambatan siklus sel.Metode: Penelitian ini menggunakan disain kohort retrospektif dengan subjek pasien KNF stadium local lanjut yang berobat di RSCM pada periode 2015-2020. Penelusuran data klinis dilakukan bersamaan dengan pewarnaan imunohistokimia p16 dan Ki-67 menggunakan antibodi monoklonal. Ekspresi dihitung secara manual menggunakan piranti imageJ. Analisis hubungan p16 dan Ki-67 terhadap progression-free survival (PFS) 3 tahun menggunakan kurva Kaplan Meier dan uji log rank dengan batas kemaknaan p<0,05.Hasil: Angka PFS 3 tahun pada subjek sebesar 44% dengan median 29 bulan. Ekspresi p16-negatif dideteksi pada 56 (56,0%) sampel, dan peningkatan ekspresi Ki-67 pada 53 (53,0%) sampel. Kurva Kaplan-Meier menunjukkan PFS 3 tahun untuk p16-negatif yaitu 8,9% (p<0,0001). PFS untuk peningkatan ekspresi Ki-67 11,3% (p<0,0001).Simpulan: Penelitian ini menunjukkan pasien KNF stadium ocal lanjut dengan peningkatan ekspresi Ki-67 dan p16-negatif memiliki progression-free survival 3 tahun yang lebih rendah.

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Background: Nasopharyngeal cancer (NPC) is a malignancy that occurs in the mucosal epithelium of the nasopharyngeal area with a worldwide incidence of around 1.2 per 100,000 population. To date, the development of molecular marker mechanisms, including Ki-67 and p16 which are related to proliferation, apoptosis, and tumor invasion can indicate the level of cell proliferation and status of cell cycle inhibition.

Methods: A retrospective cohort study was conducted in subjects of NPC patients at RSCM from 2015 until 2020. Clinical data was collected from hospital registries, and immunohistochemistry staining of Ki-67 and p16 was perfomed by using monoclonal antibody. The expression of Ki-67 and p16 were calculated manually using the imageJ tool. Association of Ki-67 and p16 expression with 3 years- progression-free survival (PFS) was analyzed using Kaplan Meier with log-rank test p<0.05.

Results: The 3-years PFS in subjects was 44% with a median of 29 months. p16-negative expression was detected in 56 (56,0%) samples, and Ki-67 overexpression in 53 (53,0%) samples. The Kaplan-Meier curve shown the 3-years PFS for p16-negative was 8,9 (p<0,0001). PFS for Ki-67 overexpression was 11,3%, (p<0,0001).

Conclusion: This study shows that locally advanced NPC patients with Ki-67 overexpression and p16-negative have lower 3-year progression-free survival."

"Cardiomyopathy is a primary disease of the myocardium, unrelated to hypertension, congenital defect, or disorders of the valves, coronary blood flow, arteries, or pericardium.

In developing nations, Cardiomyopathy makes up 30% of all deaths due to heart disease, while in developed nations, Cardiomyopathy is not the main cause of heart disease.

Cardiomyopathy is classified according to etiology and clinical findings. From the etiology, Cardiomyopathy is classified into two types, the primary tipe, where the myocardiac disease is unknown/idiopathic, and the secondary type, with a clear cause, or is related with a disease of other organ systems. Based on clinical findings, Cardiomyopathy is classified into dilatation cardiomyopa-thy or congestive, restrictive, and hypertrophic Cardiomyopathy."

"Summary:Focuses specifically on doctoral level advanced nursing practice. This revision encompasses both the historical advanced nursing practice role and the evolution of the new doctoral level roles, and delineates and highlights the variety of roles new DNP graduates have assumed and will assume, along with coverage of actual skills that will advance the role of the doctoral level APRN"