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The sexual enslavement of Korean women has been an ongoing human rights issue in South Korea since WW2, with sexual slavery also occurring during the Korean War, within the US military camp-towns, and in contemporary Korean society. Consequently, women have been marginalised and silenced, with victim-survivors struggling to receive full legal redress from their perpetrators. This is despite a redress movement that appeared alongside the first public testimony of WW2 sex slave survivor, Kim Hak-sun, in 1991. Since Kim Hak-sun’s testimony, the experiences of South Korean sex slaves have been contested. This has resulted in the Korean state “fighting” to control survivors’ narratives, victimhood, and the wider victimhood of the nation. Whilst this approach has led to WW2 sex slave survivors and their redress movement receiving support, the effect has been a creation of a hierarchy of victimhood that seemingly values one collective experience of sexual slavery (WW2) over others, further marginalising Korean women. This thesis examines the silencing of South Korean victim-survivors of sexual slavery from WW2 to the present day. It analyses the provision of redress for Korean sexual slaves through the lens of an “ideal” victim, one used to separate “legitimate” victims from perceived “willing prostitutes”. It unravels this “ideal” victim construct – how it came about and for what purpose - and assesses its impact upon the survivors’ pursuit of redress. It argues that this construct is the result of a combination of socio-cultural norms and the state’s desire to build national identity after decades of colonialism, war, and authoritarianism. Combined, these factors influence the development of Korean law and determine whether redress is provided to female victims. Ultimately, this thesis contends that analysing the “ideal” victim provides an explanation as to why all Korean sexual slavery victim-survivors remain marginalised and have yet to receive truth and justice.

Aims\ud To test if 6 months' intervention with dietary nitrate and spironolactone could affect carotid subclinical atherosclerosis and stiffness, respectively, vs. placebo/doxazosin, to control for blood pressure (BP).\ud \ud Methods\ud A subgroup of participants in our double-blind, randomized-controlled, factorial VaSera trial had carotid imaging. Patients with hypertension and with/at risk of type 2 diabetes were randomized to active nitrate-containing beetroot juice or placebo nitrate-depleted juice, and spironolactone or doxazosin. Vascular ultrasound for carotid diameter (CD, mm) and intima–media thickness (CIMT, mm) was performed at baseline, 3- and 6-months. Carotid local stiffness (CS, m/s) was estimated from aortic pulse pressure (Arteriograph) and carotid lumen area. Data were analysed by modified intention to treat and using mixed-model effect, adjusted for confounders.\ud \ud Results\ud In total, 93 subjects had a baseline evaluation and 86% had follow-up data. No statistical interactions occurred between the juice and drug arms and BP was similar between the juices and between the drugs. Nitrate-containing vs. placebo juice significantly lowered CIMT (−0.06 [95% confidence interval −0.12, −0.01], P = .034), an overall difference of ~8% relative to baseline; but had no effect on CD or CS. Doxazosin appeared to reduce CS from baseline (−0.34 [−0.62, −0.06]) however, no difference was detected vs. spironolactone (−0.15 [−0.46, 0.16]). No differences were detected between spironolactone or doxazosin on CIMT and CD.\ud \ud Conclusions\ud Our results show that 6 months' intervention with dietary nitrate influences vascular remodelling, but not carotid stiffness or diameter. Neither spironolactone nor doxazosin had a BP-independent effect on carotid structure and function.

Background: Interesterified (IE) fats are widely used in place of trans fats; however, little is known about their metabolism. \ud Objective: To test the impact of a commonly consumed IE versus a non-IE equivalent fat on in vivo postprandial and in vitro lipid metabolism, compared with a reference oil (rapeseed oil; RO).\ud Design: A double-blinded, 3-phase crossover, randomized controlled trial was performed in healthy adults (n=20) aged 45-75 years. Postprandial plasma triacylglycerol (TG) and lipoprotein responses (including stable isotope tracing) to a test meal (50g fat) were evaluated over 8 hours. The test fats were IE 80:20 palm stearin/palm kernel fat, an identical non-IE fat, and RO (control). In vitro, mechanisms of digestion were explored using a dynamic gastric model (DGM). \ud Results: Plasma TG 8h incremental area under the curves were lower following non-IE versus RO (-1.7 mmol/L.h (95% confidence interval -3.3, -0.0)), but there were no differences between IE and RO nor IE and non-IE. Low density lipoprotein (LDL) particles were smaller following IE and non-IE versus RO (P=0.005). Extra, extra large (XXL)-, extra large (XL)- and large (L)- VLDL particle concentrations were higher following IE and non-IE versus RO at 6-8 h (P

Aims:\ud Dietary nitrate from sources such as beetroot juice lowers blood pressure (BP) via the nitrate-nitrite-nitric oxide (NO) pathway. However, NO and nitrite are inactivated via re- oxidation to nitrate, potentially limiting their activity. Cytochrome P450-3A4 inhibition with troleandomycin prevents nitrite re-oxidation to nitrate in rodent liver. Grapefruit juice contains the CYP3A4 inhibitor furanocoumarin. We therefore hypothesized that grapefruit juice would enhance BP-lowering with beetroot juice by maintaining circulating [nitrite].\ud Methods:\ud We performed a randomized, placebo-controlled, 7-hour crossover study in 11 healthy volunteers, attending on 3 occasions, receiving: a 70ml-shot of active beetroot juice (Beet- It®) and either (i) 250 ml grapefruit juice (“Active Beet+GFJ”), or (ii) 250 ml water (Buxton®, “Active Beet+H2O”); or (iii) Placebo Beet+GFJ.\ud Results:\ud The addition of grapefruit juice to active beetroot juice lowered systolic BP (SBP): Active Beet+GFJ versus Active Beet+H2O (P=0.02), and pulse pressure, PP (P=0.0003). Peak mean differences in SBP and PP were seen at T=5 hours: -3.3mmHg (95% CI -6.43 to -0.15) and at T=2.5 hours: -4.2 mmHg (95% CI -0.3 to -8.2), respectively. Contrary to the hypothesis, plasma [nitrite] was lower with Active Beet+GFJ versus Active Beet+H2O (P=0.006), as was salivary nitrite production (P=0.002) and saliva volume (-0.34 ml/min (95% CI -0.05 to - 0.68)). The taste score of Beet+GFJ was 1.4/10 points higher than Beet+H2O (P=0.03).\ud This article is protected by copyright. All rights reserved.\ud Conclusions:\ud Grapefruit juice enhanced beetroot juice’s effect on lowering SBP and PP despite decreasing plasma [nitrite]. Besides suggesting more complex mechanisms, there is potential for maximising the clinical benefit of dietary nitrate and targeting isolated systolic hypertension.