Sesamin, a major lignin isolated from sesame ( Sesamum indicum ) seeds and sesame oil, is known to possess antioxidant and anti-inflammatory properties. Several studies have revealed that oxidative stress and inflammation play a major role in a variety of cardiovascular diseases (CVDs). This comprehensive review summarizes the evidence on the effects of sesamin on CVD and its risk factors, principally due to its antioxidant properties. Specifically, this review highlights the mechanisms underlying the anti-hypertensive, anti-atherogenic, anti-thrombotic, anti-diabetic, and anti-obesity, lipolytic effects of sesamin both in vivo and in vitro , and identifies the signaling pathways targeted by sesamin and its metabolites. The data indicates that RAS/MAPK, PI3K/AKT, ERK1/2, p38, p53, IL-6, TNFα, and NF-κB signaling networks are all involved in moderating the various effects of sesamin on CVD and its risk factors. In conclusion, the experimental evidence suggesting that sesamin can reduce CVD risk is convincing. Thus, sesamin can be potentially useful as an adjuvant therapeutic agent to combat CVD and its multitude of risk factors.

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Objective 1) To assess the incidence of cardiovascular disease (CVD) risk factors in a university population, and 2) to investigate the effects of an 8-week exercise intervention on CVD risk factors. Methods Forty-six students participated in this study. Baseline cardiorespiratory fitness was assessed using maximal oxygen uptake (VO2 max). Total cholesterol, high-density lipoprotein (HDL)-cholesterol and triglycerides were measured. Body mass index (BMI), waist-to-hip circumference ratio (WHR), blood pressure (BP) and arterial stiffness were also assessed. Participants performed 8weeks of exercise consisting of 60 min of moderate-high intensity exercise three times a week, and all parameters were repeated following the 8-week program. Results Participants were divided into an apparently healthy control group (BMI < 25 kg/m2) and an overweight/obese experimental group (BMI ≥ 25 kg/m2). Both groups had low cardiorespiratory fitness and clear evidence of risk for CVD. Following the 8-week program, participants demonstrated significant improvement in biochemical parameters and in overall fitness (p < 0.05). WHRs decreased whilst peak oxygen volumes increased when comparing baseline and post-exercise values (p < 0.05). BMI decreased in both groups following exercise (p < 0.05). Systolic BP was surprisingly elevated in nearly 30% of participants, but was comparatively lower in the control group (p < 0.05). There was a clear increase in HDL-cholesterol values post-intervention (p < 0.05). Conclusion Early detection of CVD risk factors, particularly in a young population, can lead to earlier prevention of disease through lifestyle changes. Moreover, short-term exercise can have important effects on reducing CVD risk factors, improving body composition and overall cardiorespiratory fitness.

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Sickle cell disease (SCD) is one of the commonest severe inherited disorders, but specific treatments are lacking and the pathophysiology remains unclear. Affected individuals account for well over 250,000 births yearly, mostly in the Tropics, the USA, and the Caribbean, also in Northern Europe as well. Incidence in the UK amounts to around 12–15,000 individuals and is increasing, with approximately 300 SCD babies born each year as well as with arrival of new immigrants. About two thirds of SCD patients are homozygous HbSS individuals. Patients heterozygous for HbS and HbC (HbSC) constitute about a third of SCD cases, making this the second most common form of SCD, with approximately 80,000 births per year worldwide. Disease in these patients shows differences from that in homozygous HbSS individuals. Their red blood cells (RBCs), containing approximately equal amounts of HbS and HbC, are also likely to show differences in properties which may contribute to disease outcome. Nevertheless, little is known about the behaviour of RBCs from HbSC heterozygotes. This paper reviews what is known about SCD in HbSC individuals and will compare the properties of their RBCs with those from homozygous HbSS patients. Important areas of similarity and potential differences will be emphasised.

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The opening of ion channels is proposed to arise from bending of the pore inner helices that enables them to pivot away from the central axis creating a cytosolic opening for ion diffusion. The flexibility of the inner helices is suggested to occur either at a conserved glycine located adjacent to the selectivity filter (glycine gating hinge) and/or at a second site occupied by glycine or proline containing motifs. Sequence alignment with other K ؉ channels shows that hERG possesses glycine residues (Gly 648 and Gly 657 ) at each of these putative hinge sites. In apparent contrast to the hinge hypotheses, substitution of both glycine residues for alanine causes little effect on either the volt- channels. Our findings indicate that the hERG inner helix glycine residues are required for the tight packing of the channel helices and that the flexibility afforded by glycine or proline residues is not universally required for activation gating.Potassium (K ϩ ) channels are integral membrane proteins that form a pore for conduction of K ϩ ions through the lipid bilayer membrane. They have evolved to perform a wide range of physiological processes and share a similar overall structure consisting of four subunits, which co-assemble to form a central pore coupled to additional regulatory domains that detect a huge variety of different signals. hERG (human ether-à-go-gorelated gene) belongs to the voltage gated family of potassium (K v ) 2 channels. It is widely expressed in the heart and nervous system. It may also be ectopically expressed in certain types of cancer (reviewed in Ref. 1). The physiological importance of hERG is illustrated by the discovery that block of the pore by medications or loss of channel function due to inherited mutations carries an increased risk of sudden cardiac death (2). Therefore, there is considerable interest in gaining further insight into the structural basis of hERG gating and drug binding (3, 4).In recent years, crystal structures have provided tremendous insight into how K ϩ channels function. The KcsA and KirBac1.1 structures correspond to channels in the closed conformation (5, 6). The inner helices of the pore that extend across the membrane and line the inner cavity are straight and come together to form a right-handed helical bundle constricting the channel at the intracellular entrance to the inner cavity, thus presenting a barrier to K ϩ movement. In contrast, MthK (7, 8), K v AP (9), and K v 1.2 (10) have all been crystallized in the open state. All these channels display a bend in the inner helices, which splays the C-terminal (intracellular) end of the inner helix away from the central axis of the pore to create a large aperture at the intracellular mouth of the channel.The inner helices appear to bend at a position, which is highly conserved as a glycine in K ϩ channels (Fig. 1). This led to the proposal that the glycine residue forms a kink or gating hinge that is required for the opening of the activation gate (7). An important feature of glycine is its ability to intro...