Factors perceived to influence risky sexual behaviours among university students in the United Kingdom: a qualitative telephone interview study

Background In the United Kingdom people under the age of 25 years are at increased risk of contracting sexually transmitted infections. Most university students belong to this age group but little is known about their sexual behaviours. The aim of the study was to explore university students’ perspectives of factors and mechanisms that influence risky sexual behaviours among university students in the United Kingdom. Methods All students at a university in a northern city of England were invited via email to participate in qualitative telephone interviews. Interviews were audio recorded and transcribed verbatim. Framework analytical approach was used. Results Twenty interviews were conducted with a diverse sample of students. The social context of university lifestyle was perceived to affect risky sex through high levels of alcohol consumption, increased sexual opportunities, liberation from moral surveillance and expectations of the stereotypical highly sexually active student. Individual and cultural differences were also perceived to account for some patterns of risky sex with older students, overseas students and religious students perceived to be less likely to engage in risky sex due to academic priorities and a tendency to be more likely to adhere to moral values. Risk denial was also a key factor that led students to engage in risky sex. Poor access to sexual health services including inconvenient opening times, lack of confidentiality and stigma were perceived to contribute to the limited use of sexually transmitted infections testing and contraceptive services. Conclusions Lifestyle, individual and structural factors seem to play an important role in influencing the risky sexual behaviours of university students. Therefore preventive interventions that focus on these factors could be very useful in this sub-population of young people. This study provides useful baseline information that helps us understand how and why some United Kingdom university students engage in risky sexual behaviours that puts them at risk of contracting sexually transmitted infections

Hypoxia Differentially Regulates Arterial and Venous Smooth Muscle Cell Migration.

Intimal hyperplasia (IH) is a clinical concern leading to failure of up to 50% of vein grafts and 10% of arterial grafts after 10 years with no known current treatment. Recent studies have shown that hypoxia differentially regulates proliferation of vein derived smooth muscle cells (V-SMC) compared to artery derived smooth muscle cells (A-SMC). The objective of this study is to evaluate the effect of hypoxia on cellular migration and the mechanisms underlying the differential effects of hypoxia on A-SMC and V-SMC migration.Hypoxic treatment (3-5% O2) of Smooth Muscle Cells (SMC) resulted in differential migration in scratch wound and electric cell substrate impedance sensing (ECIS) assays. Hypoxia led to greater migration compared to normoxia with venous derived wound closure (V-SMC 30.8% Normoxia to 67% Hypoxia) greater than arterial wound closure (A-SMC 6.2% Normoxia to 24.7% Hypoxia). Paracrine factors secreted by hypoxic endothelial cells induced more migration in SMC compared to factors secreted by normoxic endothelial cells. Migration of V-SMC was greater than A-SMC in the presence of paracrine factors. Neutralizing antibody to Vascular Endothelial Growth Factor Receptor -1 (VEGFR-1) completely inhibited V-SMC migration while there was only partial inhibition of A-SMC migration. A-SMC migration was completely inhibited by Platelet Derived Growth Factor BB (PDGF-BB) neutralizing antibody. p38 Mitogen Activated Protein kinase (p38 MAPK) inhibitor pre-incubation completely inhibited migration induced by paracrine factors in both A-SMC and V-SMC.Our study determines that SMC migration under hypoxia occurs via both an autocrine and paracrine mechanism and is dependent on Vascular Endothelial Growth Factor-A (VEGF-A) in V-SMC and PDGF-BB in A-SMC. Migration of both A-SMC and V-SMC is inhibited by p38 MAPK inhibitor. These studies suggest that pharmacotherapeutic strategies directed at modulating p38 MAPK activity can be exploited to prevent IH in vascular grafts

Schematic diagram showing paracrine and autocrine stimulation of SMC migration.

<p>The diagram shows a differential increase in VEGFR-1 in V-SMC and A-SMC under hypoxia, which results in phosphorylation of p38 MAPK, leading to increased migration in V-SMC compared to A-SMC.</p

VEGFR-1 and PDGF-BB play a role in SMC migration.

<p><b>A. and B.</b> Real-time tracings of A-SMC and V-SMC, normalized to the time of wounding, representing average cellular migration over a period of 5 hours, with or without pre-incubation with VEGFR-1 and PDGF-BB neutralizing antibody, in the presence of HECM are shown.</p

Hypoxia induced migration of V-SMC and A-SMC.

<p>Scratch wound assays were used to determine relative migration of cells under normoxia or hypoxia. <b>A.</b> Representative phase contrast images of V-SMC and A-SMC immediately after the scratch (0 hour) are shown. Cells were fixed and stained with DAPI after 24-hour treatment with normoxia or hypoxia. Representative images are shown. <b>B.</b> Relative migration and wound closure was determined in three independent experiments. Error bars indicate S.D. Data are the mean ± SD of at least three independent experiments. * represents <i>P</i><0.05.</p

Real-time cell migration.

<p>ECIS was used to determine TER. <b>A.</b> Flow chart of the experimental design. <b>B.</b> Real-time tracings of V-SMC and A-SMC, normalized to the time of wounding, representing average cellular migration over a period of 15 hours are shown. The tracings represent average TER (quadruplicates) of V-SMC and A-SMC. <b>C.</b> Histogram shows average rate of SMC migration from quadruplicate cultures over 5 hours. * indicates statistical significance (<i>P</i> <0.05).</p

p38 MAPK pathway is involved in the paracrine-stimulation of SMC by endothelial cells.

<p><b>A.</b> Upper panel: Representative western blot shows the levels of phosphorylated p38 MAPK and total p38 MAPK in A-SMC and V-SMC, when incubated with EBM-2, NECM and HECM under hypoxia for 3 hours. Lower panel: The figure represents relative levels of phosphorylated p38 MAPK normalized to total p38 MAPK levels. Error bars indicate S.D. Data are the mean ± SD of at least three independent experiments. <b>B. and C.</b> Real-time tracings of V-SMC and A-SMC, normalized to the time of wounding, representing average cellular migration with or without SB203580 (p38MAPK inhibitor), in the presence of HECM, over a period of 8 hours. The tracings represent average TER (quadruplicates) of V-SMC and A-SMC in the presence or absence of SB203580.</p

Hypoxia Differentially Regulates Arterial and Venous Smooth Muscle Cell Migration

Intimal hyperplasia (IH) is a clinical concern leading to failure of up to 50% of vein grafts and 10% of arterial grafts after 10 years with no known current treatment. Recent studies have shown that hypoxia differentially regulates proliferation of vein derived smooth muscle cells (V-SMC) compared to artery derived smooth muscle cells (A-SMC). The objective of this study is to evaluate the effect of hypoxia on cellular migration and the mechanisms underlying the differential effects of hypoxia on A-SMC and V-SMC migration.Hypoxic treatment (3-5% O2) of Smooth Muscle Cells (SMC) resulted in differential migration in scratch wound and electric cell substrate impedance sensing (ECIS) assays. Hypoxia led to greater migration compared to normoxia with venous derived wound closure (V-SMC 30.8% Normoxia to 67% Hypoxia) greater than arterial wound closure (A-SMC 6.2% Normoxia to 24.7% Hypoxia). Paracrine factors secreted by hypoxic endothelial cells induced more migration in SMC compared to factors secreted by normoxic endothelial cells. Migration of V-SMC was greater than A-SMC in the presence of paracrine factors. Neutralizing antibody to Vascular Endothelial Growth Factor Receptor -1 (VEGFR-1) completely inhibited V-SMC migration while there was only partial inhibition of A-SMC migration. A-SMC migration was completely inhibited by Platelet Derived Growth Factor BB (PDGF-BB) neutralizing antibody. p38 Mitogen Activated Protein kinase (p38 MAPK) inhibitor pre-incubation completely inhibited migration induced by paracrine factors in both A-SMC and V-SMC.Our study determines that SMC migration under hypoxia occurs via both an autocrine and paracrine mechanism and is dependent on Vascular Endothelial Growth Factor-A (VEGF-A) in V-SMC and PDGF-BB in A-SMC. Migration of both A-SMC and V-SMC is inhibited by p38 MAPK inhibitor. These studies suggest that pharmacotherapeutic strategies directed at modulating p38 MAPK activity can be exploited to prevent IH in vascular grafts