Konseptual Framework Untuk Pengukuran Kualitas Website Pada Sistem Informasi Akademik Dengan Metode Gqm

Konseptual framework yang diusulkan dalam penelitian ini berupa model konseptual yang merupakan gambaran proses pengukuran kualitas beserta tahapan yang dilakukan dalam pengukuran kualitas website sistem informasi akademik. Model konseptual yang sudah ada selama ini masih bersifat luas dan tidak spesifik pada domain tertentu. Terdapat banyak website yang dibangun oleh web developer, namun masih sedikit yang dibangun sesuai dengan kebutuhan pengguna. Salah satu website online dibidang pendidikan adalah sistem informasi akademik. Sistem informasi akademik merupakan layanan website oleh universitas dalam menyediakan informasi dan pengelolaan data-data akademik. Karakteristik dari sistem informasi akademik adalah academic content, periodic acccessibility, level of user authority, precission dan accurateness. Beberapa dari karakteristik tersebut kemudian dipetakan kedalam faktor-faktor kualitas yang diadopsi dari berbagai model, seperti ISO-9126, Website quality Model, dan academic website quality model. akademik. Hasil pemetaan tersebut memperoleh 5 faktor kualitas yang diusulkan untuk melakukan pengukuran kualitas, yaitu USAbility, functionality, content, efficiency dan reliability. Kelima faktor kualitas ini dijadikan sebagai tujuan pengukuran. Metode GQM digunakan untuk memperoleh metric internal agar menghasilkan pengukuran yang objektif dan kuantitatif. Metric-metric yang dihasilkan dari metode GQM divalidasi dengan menggunakan validasi empiris. Metric internal produk diterapkan dalam studi kasus sistem informasi akademik berbasis web universitas di Pekanbaru. Hasil validasi dari framework pengukuran yang dibangun adalah memiliki nilai baik pada faktor kualitas functionality, content dan reliability, dan nilai cukup pada faktor kualitas USAbility dan efficiency

Mean day of onset and arthritis score.

<p>To test the tolerogenic capacity of carvacrol-TS treated BMDC mice were treated as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0046336#pone-0046336-g004" target="_blank">figure 4</a>, although here, PG-unpulsed BMDC recipients are also shown. Values indicate mean ± SEM of n = 6 (PBS, untreated BMDC-pulsed, carvacrol-TS treated BMDC-pulsed and untreated BMDC-unpulsed) or n = 7 (TS treated BMDC-pulsed, TS treated BMDC-unpulsed and carvacrol-TS treated BMDC-unpulsed). * (p≤0.05) compared to PBS group.</p

Carvacrol-TS treated BMDC suppress PGIA.

<p>Arthritis was induced by two intraperitoneally immunizations with human PG on days 0 and 21. One day prior to the second PG immunization mice were intraperitoneally injected with 1×10⁶ PG pulsed untreated, TS treated or carvacrol-TS treated BMDC. As a control, mice received only PBS. Arthritis severity expressed as the mean and SEM of at least six mice per group. * (p<0.05) for area under the curve compared to PBS group.</p

DC fingerprint after TS and carvacrol-TS treatment.

<p>Mouse BMDC were incubated with 0.1 mM carvacrol or were left untreated. After two hours a one hour TS at 42.5°C followed. <b>A</b>. Experimental setup. <b>B-D:</b> Cells were collected at indicated time points and mRNA was isolated. With cDNA quantitative RT-PCRs were performed in untreated, TS treated (grey) and carvacrol-TS treated (black) BMDC. Results were depicted relative to untreated BMDC at the indicated time points. Data are representative of three independent experiments. <b>B.</b> Quantitative RT-PCRs for CCL2, CCL7 and CCL12. <b>C.</b> Quantitative RT-PCRs for LIF, AREG and IL-10. <b>D.</b> Quantitative RT-PCRs for HSP70 and MT1. <b>E.</b> After ON recovery at 37°C, intracellular HSP70 levels and extracellular CD40, CD86 and MHCII were analyzed. Grey solid: untreated BMDC; black line: TS treated BMDC; grey line: carvacrol-TS treated BMDC. Results are representative of at least 5 independent experiments.</p

Primer sequences used for quantitative real time PCR.

<p>Primer sequences used for quantitative real time PCR.</p

Genes with a high fold change or particularly interesting for DCs.

<p>BMDC were treated as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0046336#pone-0046336-g001" target="_blank">figure 1</a>. Genes that are particularly interesting for DC were selected and fold changes (F.C.) of gene expression in TS BMDC treated with or without carvacrol compared to that of fully untreated BMDC are shown.</p

Carvacrol-TS treated BMDC induce a less pro-inflammatory T cell.

<p>Mice were intravenously injected with 1×10⁷ CFSE labeled pOVA-specific T cells one day prior to intraperitoneally injection of 1×10⁶ pOVA pulsed untreated, TS treated or carvacrol-TS treated BMDC. Four days after BMDC injection spleen and mLN were harvested. <b>A.</b> Representative examples of CFSE dilution of pOVA-specific T cells in mLN (left) and percentage of undivided pOVA-specific T cells in spleen and mLN (right). <b>B.</b> Percentage of FoxP3 expression of pOVA-specific proliferating T cells (left) and percentage of replicated FoxP3⁺ cells of total FoxP3⁺ cells divided by the percentage of replicated FoxP3⁻ cells of total FoxP3⁻ cell population (right). Data are analyzed by flow cytometry. <b>C-D.</b> Splenic cell suspensions were restimulated with pOVA for 72 hours. Cytokine secretion for IL-2, IL-6, IFNγ and TNFα relative to non-stimulated cells are shown (C). Cytokine expression of IFNγ, IL-1β, IL-10 and TGFβ was measured by quantitative RT-PCR. Data are expressed as relative expression to the calibrator HPRT (D). White: untreated BMDC, grey: TS treated BMDC, black: carvacrol-TS treated BMDC. Values are the mean and SEM of three mice per group. * (p<0.05) and ** (p<0.01).</p

Endogenous and bacterial HSP60 in IIM and control muscles.

<p>Endogenous HSP60 is highly expressed in all IIM (<b>A–C</b>), mainly in association with inflammatory infiltrates (white arrows), vascular endothelial cells (red asterisk), myofibers surrounded or invaded by immune infiltrates (yellow arrow). In control muscles only occasional capillaries were positive for endogenous HSP60 (<b>D</b>). Bacterial HSP60 was occasionally observed associated with muscle infiltrates in all IIM muscles (<b>E–G</b>), particularly PM (<b>E</b>) and sIBM (<b>F</b>), but not controls (<b>H</b>). Original magnification x40; bar: 20 µm.</p

Interaction among HSP60, LC3 and TLR4 in IIM and control muscles.

<p>(<b>A</b>) LC3-positive autophagosomes (red) are present in infiltrating cells (white arrow), within muscle fibers (asterisks), and blood vessels (blue arrows) (<b>A</b>, top panel). Vesicles positive for endogenous HSP60 (green) and LC3 (red) are present mainly in association with infiltrates and capillaries (<b>A</b>, top panel). Cells positive for bacterial HSP60 (green) in IIM muscles are also immunopositive for LC3 (red) (<b>A</b>, top panel). (<b>B</b>) Endogenous HSP60 (green) co-expresses with TLR4 (red) on some muscle fibers (asterisks), blood vessels (blue arrows) and in extracellular matrix (yellow arrows). Original magnification x40; bar: 20 µm. Original magnification of the insets x120; bars: 5 µm (PM) and 10 µm (sIBM).</p

Autophagy, Inflammation and Innate Immunity in Inflammatory Myopathies

<div><p>Autophagy has a large range of physiological functions and its dysregulation contributes to several human disorders, including autoinflammatory/autoimmune diseases such as inflammatory myopathies (IIMs). In order to better understand the pathogenetic mechanisms of these muscular disorders, we sought to define the role of autophagic processes and their relation with the innate immune system in the three main subtypes of IIM, specifically sporadic inclusion body myositis (sIBM), polymyositis (PM), dermatomyositis (DM) and juvenile dermatomyositis (JDM). We found that although the mRNA transcript levels of the autophagy-related genes BECN1, ATG5 and FBXO32 were similar in IIM and controls, autophagy activation in all IIM subgroups was suggested by immunoblotting results and confirmed by immunofluorescence. TLR4 and TLR3, two potent inducers of autophagy, were highly increased in IIM, with TLR4 transcripts significantly more expressed in PM and DM than in JDM, sIBM and controls, and TLR3 transcripts highly up-regulated in all IIM subgroups compared to controls. Co-localization between autophagic marker, LC3, and TLR4 and TLR3 was observed not only in sIBM but also in PM, DM and JDM muscle tissues. Furthermore, a highly association with the autophagic processes was observed in all IIM subgroups also for some TLR4 ligands, endogenous and bacterial HSP60, other than the high-mobility group box 1 (HMGB1). These findings indicate that autophagic processes are active not only in sIBM but also in PM, DM and JDM, probably in response to an exogenous or endogenous ‘danger signal’. However, autophagic activation and regulation, and also interaction with the innate immune system, differ in each type of IIM. Better understanding of these differences may lead to new therapies for the different IIM types.</p></div