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

Hyperglycaemia significantly and in a dose-dependent fashion affected neurite outgrowth.

<p>(A) Exposure to increasing glucose concentrations induced a significant dose-dependent decrease of neurite outgrowth in neuron-SC co-cultures (B) but not in neuron monocultures. (C) Exposure of neuron monocultures to hyperglycaemia-conditioned SC monoculture medium caused a significant decrease of the neurite outgrowth. All data are normalized to control and presented as mean±SEM of independent experiments (<i>n</i> = 8) *p<0.05; **p<0.005; ***p<0.0005 vs control. (D) Cytokine array of hyperglycaemia-conditioned SC monoculture medium showing increase of VEGF compared to control. (E) Data are expressed as relative levels of VEGF.</p

Bevacizumab prevented and restored peripheral nerve functions in diabetic rats.

<p>Control and STZ-diabetic rats were treated with bevacizumab according to the prevention (A, B, C) or therapeutic (D, E, F) schedule. (A) Bevacizumab prevented in a dose-dependent fashion thermal hypoalgesia, (B) mechanical threshold decrease and (C) nerve conduction velocity decrease in diabetic rats. In the therapeutic schedule, bevacizumab restored (D) thermal hypoalgesia (E) mechanical threshold and (F) nerve conduction velocity decrease in diabetic rats. Data are expressed as mean±SEM (<i>n</i> = 8 animals per group) *p<0.05 vs controls; **p<0.01 vs controls; ****p<0.001 vs controls; #*p<0.05 vs STZ; ##p<0.01 vs STZ.</p

Hyperglycaemia did not increase DRG neuron or Schwann cell (SC) apoptosis.

<p>(A) Neuron-SC co-cultures showed a modest increase of apoptosis rate only at the highest glucose concentration; paclitaxel (tax) and cisplatin (cis) exposition was used as positive controls. (B) In DRG neuron monocultures, hyperglycaemia did not induce apoptosis. (C) Tubulin-III and GFAP staining demonstrated that apoptosis mainly involved SC. (D) SC monocultures showed a mild increase of apoptosis rate at the highest glucose concentrations, similar to that observed in co-cultures (see C). (E) Flow cytometry by annexin V/PI assay confirmed the absence of apoptosis in co-cultures exposed to hyperglycaemia. (F) Representative cytogram showing the absence of apoptosis in control co-culture (ctrl) and after 24 hour exposition to hyperglycaemia 45 mM (hg), compared to the high apoptosis rate after exposition to anti-neoplastic compounds (tax, cis). Data are expressed as mean±SEM of independent experiments (<i>n</i> = 8) *p<0.05; **p<0.005; ***p<0.0005 vs controls; #p<0.05; ##p<0.005; ###p<0.0005 vs SC controls.</p

Hyperglycaemia-induced post-translational regulation of VEGF.

<p>(A) Exposure to glucose 45 mM for 24 hours increased the level of secreted VEGF in neuron-SC co-cultures and SC monocultures. Data are express as percentage difference between their own control in independent experiments (<i>n</i> = 5) *p<0.05. (B) Hyperglycaemia significantly increased VEGF mRNA only in neuron monocultures (<i>n</i> = 5). (C) Representative and (D) quantitative western blot (WB) demonstrating VEGF decrease in hyperglycaemia-conditioned SC monocultures compared with control SC monocultures. VEGF level was not affected in neuron monocultures. Data are expressed as mean±SEM of independent experiments (<i>n</i> = 4) *p<0.05 vs controls. (E) VEGF induced a significant reduction in axonal outgrowth in neuron/Schwann cells coculture. Data are expressed as mean±SEM of independent experiments (<i>n</i> = 3) *p<0.05 vs controls.</p

Bevacizumab prevented hyperglycaemia-mediated neurite outgrowth impairment and normalized FLT-1.

<p>(A) bevacizumab prevented the decrease of hyperglycaemia-mediated neurite outgrowth in neuron-SC co-cultures (<i>n</i> = 5) and (B) the increase of FLT-1 mRNA in neurons monocultures (<i>n</i> = 5). (C) Representative and (D) quantitative western blot (WB) (<i>n</i> = 5) showing the significant decrease of FLT-1 in hyperglycaemia-conditioned SC monocultures and the preventive effect of bevacizumab. (E) sFLT-1 decreased in the medium of all neuron and SC monocultures and co-cultures exposed to hyperglycaemia (<i>n</i> = 5). (F) Bevacizumab did not affect sFLT-1 level in hyperglycaemia-conditioned co-cultures (<i>n</i> = 3). Data are expressed as mean±SEM of independent experiments. *p<0.05 vs controls; #p<0.05 vs hyperglycaemia; ##p<0.01 vs hyperglycaemia.</p

Additional file 9: Figure S5. of Network topology of NaV1.7 mutations in sodium channel-related painful disorders

Eccentricity centrality variation (∆E ct ) in NaV1.7 mutations compared to WT. (DOCX 2709 kb

Additional file 16: Figure S6. of Network topology of NaV1.7 mutations in sodium channel-related painful disorders

Structural modelling variants and their interatomic bonds of I848T and N395K. (DOCX 747 kb

MOESM1 of Laser capture microdissection for transcriptomic profiles in human skin biopsies

Additional file 1: Table S1. Summary of characteristics of subjects and skin components. Quality parameters on extracted RNA (RIN and DV200), RNA input amount used for library preparation, RNA concentration of pre-pooled samples, amount of hybridized cDNA, final concentration of libraries and million of reads sequenced for sample are shown. Subjects are indicated by the sample ID. Samples from number 1 to 8 were patients and from number 9 to 14 were healthy controls. Samples pooled together are indicated by the same capital letter (from A to O) in the pool row. The samples that did not reach the requested amount for hybridization were excluded from the experiment (marked as “X”)

MOESM2 of Laser capture microdissection for transcriptomic profiles in human skin biopsies

Additional file 2: Figure S1. Base sequence quality score. The two graphs show the Phred quality score (Q score) on y axis across all sequenced based on x axis at each position in the FASTQ file for the different skin layers, flow cells (FC) and reads (1 and 2). All the values were reported as mean ± standard deviation. A) Q score distribution across different tissues (ELF: enriched layer of fibers, G: glands, D: dermis and WS: whole section); B) Q score distribution across the different FC used for sequencing