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"Aneurisma intrakranial sakular terjadi akibat lemahnya dinding pembuluh darah karena hilang atau rusaknya tunika muskularis. Belum ada penelitian yang bertujuan memperkuat dinding aneurisma intrakranial dengan cara menumbuhkan kembali lapisan tunika muskularis. Penelitian-penelitian Mesenchymal Stem Cells (MSC) pada hewan coba berhasil menumbuhkan otot polos vaskular pada aneurisma aorta dan arteri karotis. Diharapkan MSC dapat berperan dalam pembentukan tunika muskularis pada aneurisma intrakranial.Penelitian ini bertujuan menganalisis hubungan pertumbuhan tunika muskularis aneurisma intrakranial pada hewan coba dengan perlakuan pemberian Bone Marrow Mesenchymal Stem Cells (BM MSC) dan manipulasi tekanan darah tikus, dengan penanda SM-actin dan calponin.Sebanyak 40 tikus Wistar diinduksi aneurisma selama 16 minggu. Modifikasi penurunan tekanan darah dan pemberian BM MSC pada minggu ke16, 18. Tikus dialokasi random ke dalam empat kelompok, yaitu hipertensi tanpa BMMSC, normotensi tanpa BMMSC, hipertensi dengan BMMSC, dan normotensi dengan BM MSC. Pada akhir minggu ke18 dilakukan nekropsi untuk pemeriksaan histopatologi, ekspresi SM-actin dan calponin terhadap aneurisma intrakranial, serta penilaian histopatologi pembuluh darah ekstrakranial.Sebanyak 27 tikus memenuhi kriteria sampel dengan 62 aneurisma intrakranial. Pada kelompok dengan pemberian BMMSC didapatkan 8 (53,33%) aneurisma memberikan ekspresi SMα-actin (p = 0,014; OR = 14,86) dan 8 (70,00%) ekspresi calponin (p = 0,008; OR = 7,78). Terdapat 4 (57,14%) aneurisma dengan ekspresi SMα-actin (p = 0,070, OR = 2,33) dan 7 (87,5%) dengan ekspresi calponin (p = 0,01, OR = 42,00) pada kelompok normotensi dengan pemberian BM MSC. Pada keempat kelompok tidak didapatkan perbedaan luas dan tebal tunika media arteri karotis (p = 0,616 dan p = 0,222) dan arteri iliaka (p = 0,452 dan p = 0,325). Pemberian BMMSC berhubungan dengan ekspresi SMα-actin dan calponin positif pada dinding aneurisma, menunjukkan pertumbuhan tunika muskularis. Faktor tekanan darah berhubungan dengan ekspresi calponin namun tidak berhubungan dengan ekspresi SMα-actin. Pemberian BM MSC tidak memberikan efek terhadap tunika media pembuluh darah ekstrakranial.

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Saccular intracranial aneurysm is a weak arterial wall caused by degeneration of tunica muscularis. There is still no research focused on strengthening intracranial aneurysm wall by restoring or regenerating tunica muscularis. The mesenchymal stem cells research in animal model had successfully regenerate vascular smooth muscle in abdominal aorta and carotid artery aneurysm. MSC is expected to have a role in regeneration of tunica muscularis in intracranial aneurysm.The objective of this study is to analyze the association between regeneration of tunica muscularis in intracranial aneurysm by BM MSC administration and blood pressure manipulation with SMα-actin dan calponin marker.Forty male Winstar rats were subjected to intracranial aneurysm induction for sixteen weeks. Then, the rats were randomly assigned into four groups, which were hypertension, normalized blood pressure, bone marrow mesenchymal stem cells BM MSC administration and hypertension group, and normalized blood pressure and BM MSC administration group. At the end of 18th week, all rats were sacrificed and evaluated for histopathology, immunohistochemistry (SMα-actin dan calponin), and extracranial artery structure.Twenty-seven rats with 62 aneurysms were eligible for sample criteria. Eight (53.3%) and fourteen (70.0%) aneurysms in group with BM MSC administration expressed SMα-actin (p = 0.014, OR = 14.86) and calponin (p = 0.008, OR = 7.78). In normotension and BM MSC administration group there were 4 (57.1%) aneurysm with SMα-actin expression (p = 0.070, OR = 2.33) and 7 (87.5%) with calponin expression (p = 0.01, OR = 42.00). There were no significant differences of wall area and thickness of carotid artery (p = 0,616 and p = 0,222) and iliac artery (p = 0.452 and p = 0.325) among four groups. In conclusion BM MSC administration was associated with SMα-actin and calponin expression on aneurysm wall, indicating regeneration of tunica muscularis. BM MSC administration was related to tunica muscularis regeneration, Blood pressure manipulation and BM MSC administration was related to calponin expression but was not related to SMα-actin expression. No effect of BM MSC administration was found on extracranial arteries."

"ABSTRAKLatar belakang: Pada semua sindrom epilepsi, epilepsi lobus temporal ELT memiliki kemungkinan paling besar untuk menjadi resisten terhadap obat.Polimorfisme gen multidrug resistant-1 MDR1 C3435T dicurigai sebagai salahsatu penyebabnya. Di RS Cipto Mangunkusumo RSCM , sebagai pusat rujukannasional, prevalensi ELT potensial resisten obat adalah 84.51 dan duapertiganya dalam terapi karbamazepin KBZ .Tujuan: Mengetahui polimorfisme dan ekspresi gen MDR1 C3435T serta kadarplasma KBZ pada penderita epilepsi yang responsif dan resisten terhadap obat.Metode: Penelitian potong lintang komparatif dilakukan di RSCM dari Juni 2015sampai Desember 2016. Penderita ELT dipilih secara konsekutif. Kelompokkontrol terdiri dari subjek sehat tanpa riwayat epilepsi. Identifikasi genotipemenggunakan teknik restriction Fragment Length Polymorphism PCR denganenzim restriksi Mbo1. Pemeriksaan kadar plasma KBZ menggunakan HighPerformance Liquid Chromatography. Ekspresi mRNA dengan metodesequencing and real time quantitative PCR.Hasil: Didapatkan 61 subjek dan 25 kontrol. Sebaran genotipe TT 71,43 danalel T genotipe CT dan TT lebih tinggi pada grup resisten x= 10,41; p =0,001 . Terdapat korelasi sangat kuat antara dosis dan kadar plasma KBZ padagrup responsif r = 0,75; p = 0,000 dengan rerata dosis 405,21 226,50mg dankadar plasma 7,59 2,32mcg/mL. Ekspresi kuantitatif relatif Rq mRNA palingtinggi pada grup kontrol diikuti resisten dan responsif. Genotipe TT menunjukkanRq yang berbeda pada tiap grup. Terdapat perbedaan bermakna antara dosis dankadar plasma KBZ pada masing-masing genotipe tiap grup, terutama antaragenotipe CT reponsif dengan semua genotipe grup resisten.Kesimpulan: Genotipe TT dan alel T MDR1 C3435T secara statistik berhubungandengan dosis dan kadar plasma KBZ yang lebih tinggi pada ELT resisten obat.

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ABSTRACTBackground Among epilepsy syndrome, temporal lobe epilepsy TLE has thehighest probability to become drug resistant. Multidrug resistant 1 MDR1 C3435T polymorphism was suspected to be one of the caused. In CiptoMangunkusumo hospital RSCM , as the national reference hospital, potentialdrug resistant epilepsy prevalence was 84.51 and carbamazepine CBZ usagein two third of the patients.Objective This study was performed to learn about MDR1 C3435T polymorphismand expressions, and CBZ plasma concentration in drug responsive and resistanttemporal lobe epilepsy patients.Methods A comparative cross sectional study was performed in RSCM. TLEpatients were selected consecutively. Healthy people were also selected as thecontrol group. Restriction Fragment Length Polymorphism PCR technique withMbo1 restriction enzyme was used to identify the genes. High Performance LiquidChromatography method was used to determine CBZ concentration in plasma.mRNA expressions identification were using sequencing and real timequantitative PCR methods.Result There were 61 subjects in study group and 25 in control group. Frequencyof TT genotype 71.43 and T allele CT and TT genotype were higher inresistant one x2 10.41, p 0.001 . There was a very strong correlationsbetween CBZ plasma concentration in drug responsive epilepsy r 0.75, p 0.000 in mean dosage of 405,21 226,50mg and plasma concentration of 7,59 2,32mcg mL. mRNA expressions were highest in control group followed byresistant and responsive ones. TT genotype expression was relatively different ineach group. There were signifant differences between genotype in each groupwith CBZ dosage and plasma concentration, especially in CT responsivecompare to all genotypes in resistant group.Conclusion TT genotype and T allele of MDR1 C3435T statistically associatedwith higher CBZ dosage and plasma concentration in drug resistant TLE patients."

"Latar belakang. Infeksi HIV dapat memicu inflamasi kronik dan reaktifasi CMV yang dan dapat mempengaruhi limfosit T. Gambaran seperti ini juga ditemukan pada usia lanjut dan berhubungan dengan penyakit degeneratif termasuk gangguan kognitif. Penelitian ini bertujuan untuk mengetahui pengaruh CMV dan limfosit T terhadap fungsi kognitif pada pasien HIV usia muda.Metode. JakCCANDO JAKarta CMV and Candida in HIV patients on ART, evaluation in CArdiology, Neurocognitive, Dentistry and Ophthalmology study, merupakan studi prospektif yang dilakukan di RSUPN. dr. Cipto Mangunkusumo. Studi ini melibatkan 80 pasien HIV 19-44 tahun yang belum pernah mendapat terapi antiretroviral ARV dengan limfosit T CD4

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Background. HIV can trigger chronic inflammation and CMV reactivation that affect T cell. These feature is also found in old age population and associated with degenerative disease including cognitive impairment. In this study we investigated the effects of CMV and T cells on cognitive function of younger HIV patients.Methods. JakCCANDO JAKarta CMV and Candida in HIV patients on ART, evaluation in CArdiology, Neurocognitive, Dentistry and Ophthalmology is a prospective study of patients at Cipto Mangunkusumo hospital. This study involved 80 HIV antiretroviral therapy ART naive patients 19 44 years with baseline CD4 T cell counts "

"Cedera otak pada perdarahan intraserebral spontan (PIS) terdiri dari cedera primer kerusakan struktural karena proses mekanis dan cedera sekunder akibat respons patofisiologis subklinis mencakup inflamasi, stress oksidatif dan sitotoksik terhadap komponen serta produk degradasi darah. Proses subklinis PIS yang sedang berlangsung tersebut masih belum terpantau secara lengkap, sehingga penelitian ini ditujukan untuk mengidentifikasi perjalanan proses subklinis cedera otak sekunder perdarahan intraserebral spontan dan pengaruhnya terhadap perubahan luaran respons klinis kasus (LRK) PIS pasca-intervensi bedah saraf. Penelitian ini menggunakan desain observasional prospektif, mulai Agustus 2016-April 2018 terhadap 20 subjek yang baru pertama kali mengalami perdarahan intraserebral spontan yang disertai perdarahan intraventricular dan menjalani intervensi bedah saraf external ventricular drainage (EVD). Data tercatat mencakup skor Full Outline of UnResponsiveness (SF), TIK, dan kadar hari ke-1 dan hari ke-7 Tumor Necrosis Factor alpha (TNFα), Superoxide Dismutase (SOD) dan zat besi dalam LSS. Analisis bivariat menggunakan uji Ttak berpasangan atau uji Mann-Whitney. Data skala kategorik diuji dengan Chisquare atau Fisher's exact test, dan untuk data kategorik berpasangan dengan uji McNemar.TIK pasca-intervensi semua subjek menurun secara gradual menjadi normal dan ada lima subjek yang tidak mengalami perbaikan LRK SF hari 1-7. Semua subjek kelompok 'tanpa perbaikan' mempunyai kadar TNFα LSS hari ke-1 tinggi, sebaliknya yang kadarnya normal mengalami perbaikan LRK (P=0,003). Selisih nilai peningkatan TNFα hari 1-7 juga lebih besar bermakna pada yang 'tanpa perbaikan' (P=0,005). Kadar SOD LSS hari ke-1 dan perubahannya tidak terbukti berbeda bermakna antara kedua kelompok. Pengamatan klinis memperlihatkan 80% subjek 'perbaikan', mempunyai kadar zat besi LSS hari ke-1 normal dalam status saturasi transferin < 50%. Semua subjek yang mempunyai kadar zat besi hari ke-1 tinggi dalam status saturasi transferin ≥ 50% mengalami LRK 'tanpa perbaikan'. Terdapat perbedaan bermakna dari selisih peningkatan status saturasi transferin antara kedua kelompok subjek. (P=0,05). Penelitian ini menyimpulkan bahwa subjek PIS dengan kadar TNFα LSS hari ke-1 tinggi dan/atau zat besi LSS tinggi dalam status saturasi transferin ≥ 50%, mempunyai LRK 'tanpa perbaikan'. Semakin besar peningkatan kadar TNFα LSS pada hari ke-7 dan/atau kadar zat besi yang disertai peningkatan saturasi transferrin, mempunyai LRK 'tanpa perbaikan'. Kadar SOD hari ke-1 dan perubahan kadar hari 1-7 belum dapat dimanfaatkan sebagai penanda prognosis dan proses subklinis PIS.

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Brain injury of spontaneous intracerebral hemorrhage caused by primary injury of structural damage due to mechanical processes and secondary injuries resulting from subclinical pathophysiological responses of inflammation, oxidative stress and cytotoxicity to components and blood degradation products including iron. The subclinical pathophysiology processes still cannot be monitored explicitly. This study is aimed at identifying the course of ICH subclinical secondary brain injury process and finding its relations with the days 1-7 trend of clinical response outcomes after neurosurgical intervention. This study is a prospective observational designed study done from August 2016 until April 2018. Twenty subjects were diagnosed as spontaneous intracerebral hemorrhage and underwent neurosurgical intervention external ventricular drainage (EVD). Recorded data consist of everyday Full Outline of UnResponsiveness (FOUR) score, intracranial pressure, and cerebro-spinal fluid (CSF) Tumor Necrosis Factor alpha (TNFα), Superoxide Dismutase (SOD), iron and transferrin saturation at day-1 and day-7. Bivariate analysis performed with unpaired T-test or Mann-Whitney test. Unpaired categorical scale data tested by Chi-square or Fisher's exact test, and McNemar test for paired categorical data.All 'unimproved' subjects had high levels of day-1 CSF TNFα, whereas all subjects with normal TNFα have clinical improvement response (P=0.003). Subsequently those subjects had significantly greater increasing levels (P=0.005). No significant difference of CSF SOD between of 'unimproved' and 'improved' group. Clinical observation clearly showed that 80% of 'improved' subjects have normal day-1 iron levels in controlled by transferrin saturation < 50%. There will be no improvement of those high iron levels with transferrin saturation ≥ 50%. A significant difference results were also noted of increasing transferrin saturation status (P=0,05). This study concluded that SICH with high level of day-1 CSF TNFα and/or high CSF iron with transferrin saturation ≥ 50%, would have an 'unimproved' trend of clinical response outcome. Greater increasing level of those biomarkers in days 1-7, tend to have an unimproved outcome. CSF SOD could not to be use as a significant clinical prognostic and process biomarker."