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"Latar Belakang. Terdapat dua hipotesis mengenai terjadinya diabetes melitus tipe 2 yaitu kegagalan sel beta pankreas dan resistensi insulin. Mengingat pengaruh faktor genetik pada kejadian DM tipe 2 maka diperkirakan resistensi insulin juga dipengaruhi faktor genetik. Sejauh ini data prevalensi resistensi insulin dan gambaran metabolik pads saudara kandung subyek DM tipe 2 di Indonesia belum ada.Tujuan. Mendapatkan angka prevalensi resistensi insulin pada saudara kandung subyek dengan DM tipe 2 dan mendapatkan data profil metabolik (profil lipid, IMT, lingkar perut, konsentrasi asam urat darah), tekanan darah dan distribusinya pads seluruh saudara kandung subyek dengan DM tipe 2Metodologi. Studi pendahuluan dan potong lintang dilakukan pada 30 saudara kandung subyek DM tipe 2 yang datang berobat di Poliklinik Metabolik dan Endokrinologi RSUPN Dr Cipto Mangunkusumo, untuk dilakukan wawancara, pemeriksaan fisik, konsentrasi insulin darah puasa, glukosa puasa, trigliserida, kolesterol HDL dan asam urat. Resistensi insulin ditentukan dari persentil 75 dari HOMA-IR.Hasil. Nilai cut-off HOMA-IR pada penelitian ini sebesar 2,04. Frekuensi resistensi insulin pads saudara kandung subyek DM sebesar 26,67% dengan proporsi di tiap keluarga bervariasi dari 0-75%. Semua subyek dengan resistensi insulin memiliki obesitas sentral dan sebanyak 75% memiliki IMT > 25. Komponen metabolik yang paling banyak ditemukan adalah obesitas sentral (56,7%), menyusul hipertensi (46,7%), hipokolesterol HDL dan hipertrigliseridemia masing-masing 26,6%, dan hiperglikemia (20%).Simpulan. Frekuensi resistensi insulin pada saudara kandung subyek DM tipe 2 sebesar 26,67% dengan proporsi yang bervariasi di setiap keluarga antara 0-75%. Komponen metabolik paling banyak ditemukan adalah obesitas sentral.

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Backgrounds. There are two hypothesis in the pathogenesis of type 2 DM, beta cell failure and insulin resistance. As genetic background has significant role in type 2 DM cases, insulin resistance is also suspected to be influenced by genetic factor. Thus far, there are no insulin resistance prevalence data and metabolic abnormalities among siblings of subjects with type 2 DM available in Indonesia.Objectives. To obtain prevalence figure of insulin resistance among siblings of subjects with type 2 DM and to obtain their metabolic abnormality profiles as measured by their BMI, waist circumference (WC), blood pressure, glucose intolerance, concentration of triglyceride, HDL cholesterol and uric acid.Methods. Cross-sectional study is conducted to 30 siblings of subjects with type 2 DM who are still alive and agree to participate in this study. The subjects are interviewed, physically examined and go through laboratory examination (fasting plasma insulin, plasma glucose, serum triglyceride, HDL cholesterol and uric acid concentration). Insulin resistance is derived from 75 percentile of HOMA-IR.Results. The HOMA-IR cut-off value found in this study is 2,04. The frequency of insulin resistance is 26,67% among siblings of subjects with type 2 DM within variation range of 0-75%. All of subjects with insulin resistance have central obesity. About 75% subjects with insulin resistance have BMI ? 25. The metabolic components which are frequently found in this study can be ranked as follows; central obesity (56,7%), hypertension (46,7%), hypocholesterol HDL (26,6%), hypertriglyceridemia (26,6%) and hyperglycemia (20%).Conclusion. The frequency of insulin resistance is 26,67% among siblings of subjects with type 2 DM within variation range of 0-75%. Among the metabolic components found in this study, central obesity is the most frequent."

"ABSTRAKSkripsi ini bertujuan untuk menguji secara empiris pengaruh kinerja modalintelektual dan performa klub terhadap tingkat pengungkapan modal intelektual.Selain itu, penelitian ini juga menguji pengaruh kinerja modal intelektual tahunberjalan terhadap performa klub di tahun depan. Sampel penelitian yang digunakandalam penelitian ini adalah klub-klub sepakbola yang terdaftar pada Divisi UtamaLiga Eropa untuk periode musim 2007/2008 hingga 2012/2013 dan terpilih 26 klubyang menjadi sampel. Hasil regresi menyimpulkan bahwa kinerja modal intelektualdan performa klub berpengaruh positif terhadap tingkat pengungkapan modalintelektual, sedangkan kinerja modal intelektual tahun berjalan berpengaruh negatifterhadap performa klub di tahun depan.

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ABSTRACTThe objective of this research is to investigate the effect of intellectual capitalperformance and club’s performance on intellectual capital disclosure level.Moreover, this research also aims to investigate the effect of current intellectualcapital performance on future club’s performance. This research examines intellectualcapital disclosure of First Division European football clubs for season 2007/2008until 2012/2013. The result shows that there is positive relationship betweenintellectual capital performance and club’s performance on intellectual capitaldisclosure level, while current intellectual capital performance has negativerelationship on future club’s performance."

"Latar belakang. Pada penyakit graves (GD), konsentrasi vitamin D berbanding terbalik dengan titer antibodi dan berbanding lurus dengan status remisi. Pembentukan autoantibodi diawali dari pajanan self antigen oleh sel dendritik (DC), sebagai antigen presenting cell (APC), ke sel T naif. Kemampuan DC sebagai APC ditentukan oleh tingkat kematangannya. Sel dendritik, APC utama pada GD, bersifat lebih aktif dalam respons imun dibandingkan dengan subjek sehat. Studi pada SLE, MS, dan penyakit crohn menunjukkan efek imunoregulator vitamin D terutama melalui hambatan pematangan DC sehingga fungsi imunogenitasnya berkurang.Tujuan. Mengetahui efek 1,25-D3 in vitro dan 1α-D3 in vivo terhadap pematangan DC pasien GDMetode. Pada periode Mei 2014 sampai dengan Maret 2015 dilakukan studi eksperimental dan klinis, masing-masing pada 12 dan 25 pasien GD fase hipertiroid. Pada studi eksperimental, dilakukan kultur monocyte derived dendritic cell (MDDC) pasien GD dengan atau tanpa intervensi 1,25-D3 in vitro pada tahap monosit dan maturasi distimulasi dengan lipopolysaccharide (LPS). Pada studi klinis, sebanyak 12 dan 13 pasien GD, masing-masing mendapatkan 1α-D3 dan plasebo selama 8 minggu, di samping mendapatkan terapi standar PTU 100 mg 3 kali sehari. Kultur MDDC dilakukan sebelum dan sesudah suplementasi dan dilakukan perbandingan pematangan DC sebelum dan sesudah suplementasi pada kedua kelompok. Pematangan DC dilihat dari ekspresi penanda DC (HLA-DR, CD80, CD40, CD83, CD14, dan CD206) dan rasio sitokin IL-12/IL-10 pada supernatan kultur.Hasil. Pada studi in vitro, pascastimulasi LPS, DC yang dikultur dengan 1,25-D3 menunjukkan ekspresi HLA-DR, CD80, CD40, dan CD83 lebih rendah serta ekspresi CD14 dan CD206 yang lebih tinggi dibandingkan dengan DC yang dikultur dengan LPS saja. Pada DC yang dikultur dengan 1,25-D3, didapatkan rasio IL-12/IL-10 lebih rendah daripada DC tanpa 1,25-D3. Pada studi klinis, apabila dibandingkan antara ekspresi penanda DC serta rasio IL-12/IL-10 sebelum dan sesudah suplementasi 1α-D3 selama 8 minggu, belum didapatkan perbedaan yang bermakna pada ekspresi penanda DC dan rasio sitokin IL-12/IL-10.Simpulan. Pemberian 1,25-D3 in vitro menghambat pematangan DC pasien GD, sedangkan efek pemberian 1α-D3 in vivo terhadap pematangan DC belum dapat ditunjukkan pada penelitian ini.

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Background. In graves? disease (GD), vitamin D levels is inversely proportional to antibody titer and proportionally associated with remission status. The development of autoantibody is initiated by self-antigen exposure by dendritic cells (DC) as the antigen presenting cells (APC) to the naïve T cells. The ability of DC as APC is determined by its maturity level. Dendritic cells, the major APC in GD, have more active immune responses than those in healthy subjects. Studies on systemic lupus erythematosus (SLE), multiple sclerosis (MS) and crohn?s disease have demonstrated immunoregulator effects of vitamin D, mainly through inhibition of DC maturation, which may lead to lower immunogenic function.

Aim. To identify the effect of 1,25-D3 in vitro and 1α-D3 in vivo on DC maturation in patients with GD.

Method. Our study consisted of an experimental and a clinical study started from May 2014 until March 2015, which was conducted in 12 and 25 GD patients with thyrotoxicosis, respectively. In the experimental study, cultures of monocyte derived dendritic cell (MDDC) of GD patients were performed, with or without intervention of 1,25-D3 in vitro at monocytic phase and the maturation was stimulated by lipopolysaccharide (LPS). In the clinical study, there were 12 GD patients who received 1α-D3 supplementation and 13 GD patients who received placebo for 8 weeks, in addition to the standard treatment of PTU 100 mg three times a day. MDDC cultures and comparison of DC maturation were performed before and after the supplementation for both groups. DC maturation was evaluated based on the expression of DC markers (HLA-DR, CD80, CD40, CD83, CD14 and CD206) and the ratio of cytokines IL-12/IL-10 levels in the culture supernatants.

Results. In the in vitro study and following the LPS stimulation, DC cells cultured with 1,25-D3 showed lower expression of HLA-DR, CD80, CD40 and CD83 and higher expression of CD14 and CD206 compared to DC cultured with LPS alone. DC, which were cultured with 1,25-D3 had lower ratio of IL-12/IL-10 levels than those cultured without 1,25-D3. In the clinical study, when the expression of DC marker as well as the ratio of IL-12/IL-10 levels between before and after the 8-week supplementation of 1α-D3 were compared, we found no significant difference on the expression of DC markers and the ratio of IL-12/IL10.

Conclusion. In vitro 1,25-D3 supplementation inhibits DC maturation in patients with GD; while the effects of in vivo 1α-D3 treatment on DC maturation have not been clearly demonstrated in the present study yet."