Hubungan Kadar Apolipoprotein B Dengan Aterosklerosis Arteri Karotis Interna Pada Pasien Pasca Stroke Iskemik

Background: Ischemic stroke is caused by brain artery obstruction or narrowing called atherosclerosis. Its marker is the thickness of tunica intima-media (intima-media thickness / IMT) of the artery. Apolipoprotein B is the indicator of atherosclerosis diseases. Most previous studies find association between apolipoprotein B level with cardiovascular disease, while the association between apolipoprotein B with atherosclerosis in post ischemic stroke patients has not been studied yet. Objective: To investigate association between apolipoprotein B level and internal carotid artery atherosclerosis based on thickness of intima-media in patients post ischemic stroke. Method : This cross-sectional study was done in post ischemic stroke subjects in outpatient clinic of Neurology Department Kariadi Hospital Semarang, during December until February 2011. Apolipoprotein B level was measured with Integra method. The thickness of tunica intima-media of the internal carotid artery was measured by Ultrasonografi Duplex. Result: Fourty four patients post ischemic stroke that met the inclusion and exclusion criteria, comprise of 22 male (50%) and 22 female (50%). Atherosclerosis was defined as tunica intimamedia thickness >0.9 mm, was found in 24 subjects (54.6%). Apolipoprotein B level, which designated as high (apoB >105 mg/dl), was found in 25 subjects (56.8%). Multyvariat logistics regression test proved there was significant correlation between apolipoprotein B level with internal carotid artery atherosclerosis (p = 0.0001). Conclusion: Apolipoprotein B level significantly has correlation with atherosclerosis of internal carotid artery based on thickness of intima-media in patients post ischemic stroke. Key words: apolipoprotein B level, internal carotid artery atherosclerosis, ischemic stroke

結節性硬化性患者21名に認められた新規遺伝子異常とTSC1遺伝子エクソン14のタンデム型スプライスアクセプターサイトの変異に関する研究

博士（医学）神戸大

Commercializing oocytes in the era of therapeutic cloning; an extension of pro-life vs pro-choice debates

No Abstrac

Qualitative and Quantitative Analyses Of SMN 2 Gene Expression Upon Exposure with Histone De-acetylase Inhibitors and Polyphenols

Autosomal recessive SMA (Spinal Muscular Atrophy) is the second most common inherited disease, leading to early infancy death. The SMN1 mutations are leading cause of SMA. However, increasing expression of SMN2 has been exploited as therapeutic target for SMA. Several Histone Deacetylase Inhibitors (HDACIs) are known to increase SMN2 expression level. This study aimed to elucidate the effects of two hydroxamate-based HDACIs, SAHA and Dacinostat, and SRT1720, a synthetic SIRT1 activator with polyphenolic structure, on the SMN2 expression , CpG Islands (CGI) methylation and SMN protein levels in fibroblasts taken from SMA Type 1 and Type 11 patients. It was found that the levels of overall SMN2 gene expression (Overall-SMN2), SMN2 exon 7 inclusion (E7-SMN2) and SMN protein levels were significantly increased in 10 1-1M SAHA-treated Type 1 and Tvpe II cells. The mean methylation level was significantly lower. Accordingly, the level of Overall-SMN2 and E7-SMN2 transcript increase were also significant. The transcript increase induced by Dacinostat led to more increase of SMN protein compared to SAHA in Type 1 cells (2.54 ± 1.57 fold). SMN2 gene expression (Overall-SMN2 and E7-SMN2) was also increased upon exposure to SRT1720. The mean CGIs methylation percentage and SMN protein level alteration were decreased modestly SAHA-Dacinostat combination increased SMN2 express1on in Type I, but not Type II cells. SRT1 720-Dacinostat combination increase Overall-SMN2 and E7-SMN2 transcripts nearly double the increase induced by individual compounds. SRT1720-SAHA combination resulted in lower increase than that induced by SAHA alone but higher increase than that induced by SRT1720 alone. Furthermore, SMN protein was noted to be increased and CGIs was more demethylated in treated cells. In conclusion, SMN2 expression (Overall-SMN2 and E7 -SMN2), SMN protein level and methylation level of CGIs were significantly altered upon exposure to SAHA, Dacinostat and SRT1720-Dacinostat combination in SMA fibroblast Type I and Type II . This is the first report about Dacinostat and SRT1720 effect on SMN2 modulation

Intertextual Study of Main Characters on the Novel "Atheis" by Achdiat Karta Mihardja and "Ronggeng Dukuh Paruk" by Ahmad Tohari

Haryo Seto Saktiono. Intertextual Study of Main Characters on the Novel "Atheis" by Achdiat Karta Mihardja and "Ronggeng Dukuh Paruk" by Ahmad Tohari. Thesis, Surakarta: Faculty of Teacher Training and Education, Sebelas Maret University Postgraduate Program, February 2021. The purpose of this study is to explain: (1) To find the intrinsic element (character) in the novel "Atheis" by Achdiat Karta Mihardja; (2) Finding the intrinsic element (character) in the novel "Ronggeng Dukuh Paruk" by Ahmad Tohari; (3) Finding intertextual intrinsic elements (characters) from the novel "Atheis" by Achdiat Karta Mihardja and the novel "Ronggeng Dukuh Paruk" by Ahmad Tohari. This study uses a descriptive qualitative method and uses an intertextual approach. Researchers obtained data from the Atheis novel by Achdiat Karta Mihardja and the novel Ronggeng Dukuh Paruk by Ahmad Tohari, data in the form of direct analysis, interviews, and worksheets from teachers and students of SMA N 1 Gemolong. The technique used for sampling was done by purposive sampling. The data validity was obtained through source triangulation, while the data analysis technique used interactive analysis techniques. The conclusions of this study are (1) This study succeeded in finding the intrinsic element (character) of the novel "Atheis" by Achdiat Karta Mihardja. (2) This study succeeded in finding the intrinsic element (character) of the novel "Ronggeng Dukuh Paruk" by Ahmad Tohari. (3) This study succeeded in finding the intertextual intrinsic elements (characters) of the novel "Atheis" by Achdiat Karta Mihardja and the novel "Ronggeng Dukuh Paruk" by Ahmad Tohari

Kadar Apolipoprotein B dan Aterosklerosis Arteri Karotis Interna pada Pasien Pasca Stroke Iskemik

Relations between apolipoprotein B level with internal carotid artery atherosclerosis in post ischemic stroke patientBackground: Ischemic stroke is caused by brain artery obstruction or brain artery narrowing called atherosclerosis. Its marker is the thickness of tunica intima-media (intima-media thickness/IMT) of the artery. Apolipoprotein B is one of the indicator of atherosclerosis diseases. Most of the previous studies investigate association between apolipoprotein B level and cardiovascular disease, while the association between apolipoprotein B and atherosclerosis in post ischemic stroke patients has not been studied yet.Objective: To investigate association between apolipoprotein B level and internal carotid artery atherosclerosis based on thickness of intima-media in patients post ischemic stroke.Method: This cross-sectional study was done in post ischemic stroke (first attack) subjects in outpatient clinic of Neurology Department Kariadi Hospital Semarang, during December until February 2011. Apolipoprotein B level was measured with Integra method, during 1 month after the onset. The thickness of tunica intima-media of the internal carotid artery was measured by Ultrasonography Duplex.Result: Fourty four patients post ischemic stroke that met the inclusion and exclusion criteria, comprise of 22 male (50%) and 22 female (50%). Atherosclerosis which was defined as tunica intima-media thickness >0.9 mm, was found in 24 subjects (54.6%). Apolipoprotein B level, which designated as high if apoB >105 mg/dl, was found in 25 subjects (56.8%). Multivariate logistics regression test controlling lipid factor as confounding factors resulted in OR 142.1 (p=0.0001).Conclusion: Apolipoprotein B level significantly correlate with atherosclerosis of internal carotid artery represented by thickness of intima-media in patients post ischemic stroke

Genetic Background of β Thalassemia Modifier: Recent Update

Thalassemia has become major health problem among developing countries. Genetic background which contain enormous mutations and variations have lead in clinical problem differences. The genetic basis of thalassemia, beta specifically, is mutations of the gene encoding the β chain of the hemoglobin (Beta-Globin, HBB). However, today it is known that abnormalities in this gene do not necessarily determine the clinical appearance of β thalassemia patients. A set of genes has been found that can modify the primary β thalassemia disorder. Secondary modifier contains genes that have been associated with elevated levels of HbF and improvement ratio of α / β globin chain. The genes involved are HBA, HBG, BCL11A, HBS1L-MYB and other cofactor genes regulating erythropoiesis. Tertiary genetic modifier comes from other genes related to the disease severity including iron metabolism, redox activity, and clinical complications. The review aims to provide the latest updates regarding the known β Thalassemia modifier genes and some other genes involved in the changes of the clinical manifestations