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"Penyakit Graves merupakan penyakit autoimun pada kelenjar tiroid dengan manifestasi berbagai sistem organ, termasuk sistem kardiovaskular akibat hipertiroid. Pada pasien hipertiroid terjadi peningkatan fungsi sistolik ventrikel kiri dibandingkan populasi normal. Beberapa penelitian tentang kadar hormon tiroid mendapatkan hasil yang berbeda-beda. Hipotesis pada penelitian ini adalah peningkatan kadar hormon tiroid akan diikuti peningkatan fungsi ventrikel kiri.TujuanDiketahui korelasi kadar tiroksin bebas dan fraksi ejeksi ventrikel kiri pada pasien Graves yang belum diobati.MetodePada penelitian potong lintang ini digunakan kadar tiroksin bebas sebagai parameter hormon tiroid dan fraksi ejeksi ventrikel kiri (LVEF) menurut cara Simpson yang dimodifikasi dengan ekokardiografi sebagai parameter fungsi sistolik ventrikel kiri. Kadar tiroksin bebas diperiksa di laboratorium sedangkan fraksi ejeksi ventrikel kiri cara Simpson dinilai dengan alat ekokardiografi.HasilDidapatkan 10 pasien, 7 laki-laki dan 3 perempuan, dengan usia 18-52 tahun. Lama gejala dirasakan pasien 2-12 bulan. Pada pasien didapatkan rerata kadar fT4 5,75 (SB 0,96) ngldL dan rerata fraksi ejeksi ventrikel kiri 70,57 (SB 4,50) %. Didapatkan koefisien korelasi positif antara kadar tiroksin bebas dan fraksi ejeksi ventrikel kiri (r=0,711, p=0,021) pada pasien Graves yang belum diobatiKesimpulanPada penelitian ini didapatkan korelasi positif kuat antara kadar tiroksin bebas (fT4) dan fraksi ejeksi ventrikel kiri (LVEF) pada pasien Grave yang belum mendapat pengobatan.

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Graves' disease is an autoimmune disease of thyroid gland which can be manifested in many organ system, especially cardiovascular system due to hyperthyroid. Hyperthyroid patients have a higher left ventricular systolic function than normal. Several studies of correlation between thyroid hormone level and cardiac function have showed different results. The hypotesis tested in this study is the increasing thyroid level will followed by the increase of left ventricular systolic function in Graves' disease.

Objective

To determine the correlation between thyroid hormone level and left ventricular ejection fraction in newly diagnosed Graves' patients.

Methods

In this cross-sectional study, we use the free thyrosine level as a parameter of thyroid hormon and use left ventricular ejection fraction as a parameter of left ventricular systolic function. Free thyroxine level was measured in the laboratory and the LVEF were assessed by Simpson's methods of echocardiography study.

Results

Ten patients (7 men and 3 women; age 18-52 years old) were studied. Their average of ff4 was 5.75 (SD 0.96) ngldL and their average of LVEF was 70.57 (SD 4.50) %. There was positive correlation coefficient between free thyroxine level and left ventricular ejection fraction (r=0.711, p=0.021) in newly diagnosed Graves' patients.

Conclusion

In this study there was strong positive correlation between free thyroxine (fT4) and left ventricular ejection fraction (LVEF) in newly diagnosed Graves' patients."

"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."