Text readability and legibility on iPad with comparison to paper and computer screen

U radu autori istražuju čitkost teksta na iPad uređaju i djelomično ga uspoređuju s čitanjem sa zaslona računala i papira. Na temelju ranijih istraživanja, mjerene su dvije nezavisne varijable: brzina čitanja (T) i subjektivna težina čitanja (Z). U istraživanju je sudjelovalo 220 studenata starih između 18 i 48 godina podijeljeno u 11 grupa od po 20 sudionika. Ključni rezultati su: Sans serif font Gotham čitkiji je i čitljiviji na iPadu od Minion Pro serifnog fonta, iako kad su veličine fonta veće, nema statistički značajne razlike između njih; zbog manjeg broja znakova po retku, dvostupačni prijelom najteže je čitljiv; tekst prelomljen u minimalno 79 znakova po retku i više dovoljno je čitak za čitanje na iPadu; s obzirom na kvalitetu čitanja, tekstovi prikazani na iPadu mogu zamijeniti tekstove tiskane na papiru.In this paper authors examine readability and legibility of text on iPad and compare it partially to reading from computer screen and paper. Following previous research, two independent variables were measured: speed of reading (T) and subjective difficulty of reading (Z). 220 university students aged 18÷48 participated in the experiment and were divided into 11 groups of 20 participants. Key findings are as follows: Sans serif Gotham font is more readable and legible on iPad than Minion Pro serif font, although, when presented in bigger font sizes there is no significant difference between the two letter cases; two column spread of text was the hardest to read, giving fewer number of characters per row; layout of text with 79 characters per row and above should be readable and legible enough for reading texts on iPad; considering quality of reading, texts displayed on iPad can replace texts printed on paper

Drug therapy used to treat HBV.

<p>Costing is based on the International Medical Products Price Guide: <a href="http://mshpriceguide.org/en" target="_blank">http://mshpriceguide.org/en</a> (data accessed May 2017. Price for lamivudine (3TC)—South Africa Department of Health; Price for tenofovir (TDF)—Supply Chain Management Project; price for HBV immunoglobulin (HBIG)—Sudan Medicins Sans Frontieres). WHO essential medicines: <a href="http://who.int/medicines/publications/essentialmedicines/EML_2015_FINAL_amended_NOV2015.pdf?ua=1" target="_blank">http://who.int/medicines/publications/essentialmedicines/EML_2015_FINAL_amended_NOV2015.pdf?ua=1</a>.</p

Ex vivo activation of HIV expression by RMD and VOR.

<p>CD4 T cells were isolated from virally suppressed HIV-infected patients and pulse-treated with RMD and VOR for 6 and 24 hours, respectively. Cell-associated total RNA was extracted, HIV RNA levels were quantified at the indicated time points, and fold increase in the cell-associated HIV RNA was determined relative to corresponding vehicle-treated control for each individual time point. The fold change for each donor and condition is based on mean number of HIV copies from 4 to 5 independent measurements. Red dashed line represents the mean fold HIV induction across all tested donors. Symbols # (p<0.01) and * (p<0.05) denote a statistically significant difference between fold HIV induction by RMD and VOR across all donors tested. Data for each individual donor and condition including results of statistical analysis are provided in Supplementary <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004071#ppat.1004071.s008" target="_blank">Table S4</a>. (<b>A</b>) Memory CD4 T cells were purified as the CD4(+)CD45RA(−) subset. (<b>B</b>) Resting CD4+ T cells were purified as the CD4(+)HLA-DR(−)CD69(−)CD25(−) subset.</p

Phylogenetic analysis of HIV sequences expressed ex vivo following the latency reversal.

<p>Resting CD4 T cells isolated from a cART-suppressed HIV-infected patient (high-responding patient from <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004071#ppat-1004071-g007" target="_blank">Fig. 7</a>) were treated continuously with RMD or activation control (anti-CD3/CD28 antibodies). Single-genome sequencing was used to analyze patient HIV proviral DNA and plasma RNA at the initiation of treatment (day 0), together with the ex vivo induced HIV RNA in cell culture supernatants at the end of treatment (day 7). Total of 43 sequences were recovered for proviral DNA. Eighty-eight, 11, and 4 sequences of HIV RNA were collected in culture supernatants following the treatment with activation control, 7.5 nM RMD, and 2.5 nM RMD, respectively. Grey arrows indicate examples of full concordance between the sequence of proviral DNA and viral RNA induced either by RMD or activation control. No HIV RNA sequences were recovered in supernatants from cultures treated with control vehicle or 2 µM SAHA. Identified HIV DNA and RNA sequences were aligned and the phylogenetic tree was constructed using Clustal W and MEAG5.</p

Resource gap in research funding allocations and academic publications for hepatitis B virus (HBV), hepatitis C virus (HCV), HIV, and malaria.

<p>Panels A/C: funding data from the United States National Institutes for Health (NIH) estimated funding for research, condition, and disease categories 2013–2018 (*projected figures for 2017 and 2018), available at <a href="https://report.nih.gov/categorical_spending.aspx" target="_blank">https://report.nih.gov/categorical_spending.aspx</a>, downloaded June 2017. For the projected funding allocation for 2018, HCV will receive 2.3-fold HBV funding, malaria 4.8-fold, and HIV 66.8-fold. Research into “malaria” and “malaria vaccine” are subdivided in the source data set but have been pooled in this graphic. Panels B/D: We recorded the number of publications listed on NCBI PubMed based on the search terms “HIV,” “HBV,” “HCV,” and “malaria” for each year from 2007–2016. Example search string for HBV publications in 2016: (HBV[Title]) AND ("2016/01/01"[Date—Publication]: "2016/12/31"[Date—Publication]). Data are represented as absolute numbers (panels A and B) and the proportion of the whole (panels C and D). For hepatitis delta virus (HDV), funding allocation data are not available, and we identified <25 publications/year (range 7–23).</p

RMD does not induce global activation of immune cell subsets.

<p>PBMCs isolated from four HIV-infected patients on suppressive cART were treated with a 4-hour pulse of RMD or continuously with vehicle control (DMSO), VOR, or PMA+ionomycin and stained for surface markers 48 hours after the treatment initiation. Fractions of CD69−, CD25−, and HLA-DR-positive cells in subsets of CD4+ T cells, CD8+ T cells, and CD19+ B cells were analyzed by flow cytometry as described in <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004071#s4" target="_blank">Materials and Methods</a>. Each symbol represents one donor.</p

RMD activates intracellular HIV expression at concentrations below the levels achieved by clinical dosing.

<p>Resting CD4 T cells were isolated from 3 cART-suppressed HIV-infected patients and pulse-treated with RMD for 4 hours with the indicated concentrations. Cell-associated HIV RNA levels were analyzed at each time point following the treatment initiation (t = 0 hour), and fold induction was determined relative to a background signal in vehicle-treated controls. Predicted i.v. dose and percentage of clinical exposure were calculated for each RMD concentration tested relative to the clinically approved dose of 14 mg/m²; calculations were performed based on the free fraction of drug in human plasma and cell culture media. Data represent mean ± SD from at least 3 HIV-infected donors. Data for each individual donor and condition including results of the statistical analysis are summarized in Supplementary <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004071#ppat.1004071.s008" target="_blank">Table S4</a>.</p

In vitro activation of HIV expression by HDAC inhibitors in an in vitro latency model.

<p>Primary CD4 T cells latently infected in vitro with reporter HIV were established as previously described <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004071#ppat.1004071-Bosque1" target="_blank">[29]</a>, <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004071#ppat.1004071-Bosque2" target="_blank">[30]</a> with additional minor modifications described in <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004071#s4" target="_blank">Materials and Methods</a>. The infected cells were incubated in the presence of the indicated HDACi. (<b>A</b>) A dose response of HIV activation by HDACi was determined by the quantification of luciferase reporter activity after a 48-hour treatment. <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004071#s2" target="_blank">Results</a> are mean ± SD from a representative experiment performed in quadruplicate. (<b>B</b>) Induction of p24 expression by RMD and VOR. Flow cytometry analysis of cells from a representative donor is shown with gating on the live cell population. Anti-CD3/CD28 antibodies conjugated to beads were used as a positive control. (<b>C</b>) Time course of the induction of p24 expression by RMD. Cells isolated from 2 independent donors were treated with 40 nM RMD or anti-CD3/CD28 antibodies for 24 to 72 hours in the presence of antiretrovirals. Percentage of p24-positive cells was determined by flow cytometry with gating on live cell population.</p

Activity and cytotoxicity of HDAC inhibitors in the in vitro HIV latency model.

<p>Latently infected primary CD4 T cells prepared from three independent healthy donors were treated with the indicated compounds continuously for 48 hours. EC₅₀ and CC₅₀ values were determined from each dose-dependent response using a multi-parameter algorithm. Data are mean ± SD from three independent experiments performed in quadruplicate.</p

Ex vivo response to RMD in multiple longitudinal samples from the same donors.

<p>Resting CD4 T cells isolated from 2 cART-suppressed HIV-infected patients were treated continuously with RMD or with anti-CD3/CD28 antibodies (AC, activation control) for 7 days. HIV RNA in cell culture supernatants was quantified by COBAS on day 7. Data for a high-responding (<b>A</b>) and a low-responding donor (<b>B</b>) to RMD is shown; each donor was tested at 3 different time points separated by at least 2 weeks (Exp 1–3). VC/NDC, vehicle control/no-drug control. Asterisk (*) indicates no value due to COBAS analysis failure. Dashed lines indicate the limit of HIV quantification by COBAS (20 copies/ml). Data for each individual donor and condition including results of the statistical analysis are summarized in Supplementary <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004071#ppat.1004071.s008" target="_blank">Table S4</a>.</p