MOESM2 of Use of the Hippocratic or other professional oaths in UK medical schools in 2017: practice, perception of benefit and principlism

Additional file 2: Appendix S2. Edinburgh Medical Oath

Supplemental information from Excavation and aggregation as organizing factors in de novo construction by mound-building termites

Materials and method

Experimental and Theoretical Polarized Raman Linear Difference Spectroscopy of Small Molecules with a New Alignment Method Using Stretched Polyethylene Film

This paper reports the development of the new technique of Raman linear difference (RLD) spectroscopy and its application to small molecules: anthracene and nucleotides adenosine-5′-monophosphate, thymidine-5′-monophosphate, guanosine-5′-monophosphate, and cytidine-5′-monophosphate. In this work we also present a new alignment method for Raman spectroscopy where stretched polyethylene films are used as the matrix. Raman spectra using light polarized along the orientation direction and perpendicular to it are reported. The polyethylene (PE) film spectra are consistent with powder samples and films deposited on quartz. RLD spectra determined from the difference of the parallel and perpendicular polarized light Raman spectra are also reported. The equations describing RLD are derived, and RLD spectra of anthracene and thymidine are calculated from these equations using Density Functional Theory and assuming perfect orientation of the samples. Because of the wealth of spectroscopic information in the vibrational spectra of biomolecules together with our ability to calculate spectra as a function of orientation, we conclude that RLD has the potential to provide structural information for biological samples that currently cannot be extracted from any other method

Suppression of viral replication in PBECs from asthmatic donors by neutralization of endogenous TGF-β.

<p>PBECs from asthmatic donors were pretreated for 24 h in the presence of a neutralizing anti pan TGF-β antibody or isotype control antibody before infection with RV1B (1000 units/10⁵ cells) for 48 h. In A, viral titre was determined as TCID₅₀/ml using culture supernatants obtained 48 h p.i. In B, IFN-β protein was measured at 48 h and was expressed as a ratio of the viral load measured as TCID₅₀ units. The data were analyzed using Wilcoxon’s rank sum test.</p

The effect of neutralizing endogenous TGF-β on RV replication.

<p>PBECs from 8 asthmatic donors or 6 non-asthmatic control subjects were pretreated for 24 h in the presence of a neutralizing anti pan TGF-β antibody or isotype control antibody before infection with RV1B (1000 units/10⁵ cells) for 48 h. The fold-decrease in viral replication by the neutralizing antibody was plotted as a ratio of the TCID₅₀/ml of antibody-treated versus isotype controls. The figure shows median and interquartile range, with individual data points superimposed. Data were analysed using a Mann Whitney U test.</p

The effect of TGF-β neutralization on basal SMAD2 activation.

<p>PBECs from asthmatic donors were treated with RV and anti TGF-β antibody, as indicated, as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0044580#pone-0044580-g005" target="_blank">Figure 5</a>. Cell lysates were harvested at 1, 4, and 6 hours post-virus infection and Smad-2 phosphorylation was analysed by Western blotting. A representative Western blot is shown in (A) and densitometric quantification of the experiment repeated using PBECs from 3 different asthmatic subjects is shown in (B).</p

Exogenous TGF-β₂ suppresses IFN-β release from virally infected (A) or poly IC exposed (B) PBEC cultures from non-asthmatic donors.

<p>PBEC cultures were infected with RV1B (5000 TCID₅₀ units/10⁵ cells) (n = 10) or treated with poly IC (n = 5) in the presence or absence of TGF-β₂ which was used at 1 (black bars in B) or 10 ng/ml (panel A and grey bars in B). Culture supernatants were harvested 48 hours p.i (A) or 8 h post stimulation (B) and IFN-β protein levels were measured by ELISA. In B, the data are expressed as a % of control cultures treated with poly IC in the absence of TGF-β₂ (median (IQR) IFN-β release  = 346 (1135) and 369 (1390) pg/ml for cells treated with 1 or 10 µg/ml Poly IC, respectively. The data were analyzed using Wilcoxon’s rank sum test (A) or using a paired t-test for normally distributed data (B).</p

The effect of anti-TGF-β antibodies on release of IFN-β and IFNλ1/IL-29 protein in response to poly IC.

<p>PBECs from 6 asthmatic donors were treated with 0.1–10 µg/ml poly IC in the presence of neutralizing anti-TGF-β antibodies (black bars) or an IgG isotype control (open bars) and incubated for 24 h. Supernatants were removed and IFN-β (A) or IFN-λ1/IL-29 protein levels (B) were measured by ELISA. Graphs show (mean±SEM) IFN produced in pg/ml the presence of the control or anti TGF-β antibodies.</p

Neutralizing endogenous TGF-β suppresses RV1B mediated SOCS-1 and SOCS-3 gene expression in asthmatic PBECs.

<p>Samples were treated as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0044580#pone-0044580-g005" target="_blank">Figure 5</a>. SOCS-1 (A) and SOCS-3 (B) gene expression were measured in 7 asthmatic subjects at 48 h p.i. by RT-qPCR and normalized to housekeeping genes. Results were plotted as relative fold-induction using the ΔΔCt method. The Wilcoxon rank sum test was used to analyse statistical significance.</p

Exogenous TGF-β₂ suppresses IFN-λ1/IL-29 release from virally infected (A) (n = 10) or poly IC (n = 4) exposed (B) PBEC cultures from non-asthmatic donors.

<p>IFNλ1/IL-29 protein levels were measured by ELISA from RV-infected or poly IC exposed PBECs treated with TGF-β₂ as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0044580#pone-0044580-g002" target="_blank">Figure 2</a>. Median (IQR) IFN-λ₁ release  = 3896 (2766) and 4932 (4941) pg/ml for cells treated with 1 or 10 µg/ml Poly IC, respectively.</p