Caroline L. Smith

Virtual laboratory simulations are commercially available to train students; these creative resources are available to complete remotely without traditional time and safety restrictions of laboratory-based practical classes. We introduced a Health and Safety virtual laboratory simulation to a core large first-year science module. Having surveyed students using a combination of Likert-type responses, multiple answer questions and free text responses, students reported that it had increased understanding and knowledge. Additionally, students reported that the laboratory simulation was motivating and had increased confidence for actual practical classes. We also surveyed students one year after completing the simulation finding a similar pattern of responses; the simulation had been useful, increasing confidence and knowledge about Health and Safety. Our data show that the virtual laboratory simulation improved student understanding and was still perceived to have been useful one year after completion, providing evidence of a longer term impact of the simulation on student learning.

Poly(3-hydroxyoctanoate)/poly(3-hydroxybutyrate), P(3HO)/P(3HB), blend films loaded with aspirin were prepared, and the influence of aspirin loading on the surface properties, mechanical, thermal and degradation properties were investigated. Scanning electron microscopy images revealed that the addition of aspirin introduced a new topography on the surface of the blend films. Aspirin contributed to the increase in the hydrophilic nature of the blend films compared with the unloaded blend films. This was complemented by a considerable increase in the total protein adsorption in the aspirin-loaded blend films. The percentage cell viability was higher in the aspirin-loaded blend films compared with the unloaded blend films. There was a decrease in the tensile strength and the Young’s modulus with the addition of the aspirin. However, the percentage elongation at break, a measure of elasticity, was higher in the aspirin-loaded films, indicating an increase in their flexibility compared with the unloaded blend films. There was a decrease in the melting temperature (T_m), glass transition temperature (T_g) and the crystallization temperature (T_c) due to the decrease in the crystallinity of the aspirin-loaded blend films in comparison with the unloaded blend films. Finally, controlled release of aspirin was observed without any burst release, and 96·6% release was achieved within 25 d, ideal for the development of biodegradable drug-eluting stents.

Several factors influence the severity of Plasmodium falciparum; here, we investigate the impact of alpha+-thalassaemia genotype on P. falciparum parasitemia and prevalence of severe anaemia amongst microcytic children from Kumasi, Ghana. Seven hundred and thirty-two children (≤10 years) with P. falciparum were categorised into normocytic and microcytic (mean cell volume ≤76 fL). Microcytic individuals were genotyped for the -α(3.7) deletional thalassaemia mutation and parasite densities determined. Amongst microcytic patients both parasite densities and prevalence of severe malaria parasitemia (≥100 000/μL) were significantly lower (P < 0.001) in the presence of an alpha+-thalassaemia genotype compared with non-alpha+-thalassaemia genotype. There was no evidence that alpha+-thalassaemia protected against severe anaemia. The protection conferred by alpha-thalassaemia genotype against severe P. falciparum parasitemia did not change with increasing age. The severity of P. falciparum parasitemia was significantly lower in both the homozygous and heterozygous alpha+-thalassaemia groups compared with microcytic individuals with non-alpha+-thalassaemia genotype. The protective effect, from severe malaria, of the alpha+-thalassaemia allele does not alter with age.

Novel poly(3‐hydroxyoctanoate), P(3HO), and bacterial cellulose composites have been developed. P(3HO) is hydrophobic in nature whereas bacterial cellulose is extremely hydrophilic in nature. Therefore, homogenized bacterial cellulose has been chemically modified in order to achieve compatibility with the P(3HO) matrix. Modified bacterial cellulose microcrystals and P(3HO) have been physically blended and solvent casted into two‐dimensional composite films. Mechanical characterization shows that the Young's modulus of the P(3HO)/bacterial cellulose composites is significantly higher in comparison to the neat P(3HO) film. The melting temperature (T_m) of the composites is lower while the glass transition temperature (T_g) is higher than the neat P(3HO) film. Also, the composite film has a rougher surface topography as compared to the neat P(3HO) film. A month's in vitro degradation study has been carried out in Dulbeccos modified eagle medium and in phosphate buffer saline. The incorporation of modified bacterial cellulose microcrystal in the P(3HO) film has increased the degradability of the composite film. Finally, in vitro biocompatibility studies using human microvascular endothelial cells established the biocompatibility of the P(3HO)/bacterial cellulose microcrystal films. The cell proliferation was 50–110% higher on the P(3HO)/bacterial cellulose composites as compared to the neat P(3HO) film. Hence, in this study, for the first time, P(3HO)/bacterial cellulose composites have been developed. The addition of bacterial cellulose has resulted in properties that are highly desirable for medical applications including the development of biodegradable stents.

5,6,7,8-Tetrahydrobiopterin (BH₄) is an essential cofactor of nitric oxide synthases (NOSs). Oxidation of BH₄, in the setting of diabetes and other chronic vasoinflammatory conditions, can cause cofactor insufficiency and uncoupling of endothelial NOS (eNOS), manifest by a switch from nitric oxide (NO) to superoxide production. Here we tested the hypothesis that eNOS uncoupling is not simply a consequence of BH₄insufficiency, but rather results from a diminished ratio of BH₄vs. its catalytically incompetent oxidation product, 7,8-dihydrobiopterin (BH₂). In support of this hypothesis, [³H]BH₄binding studies revealed that BH₄and BH₂bind eNOS with equal affinity ( K_d≈ 80 nM) and BH₂can rapidly and efficiently replace BH₄in preformed eNOS-BH₄complexes. Whereas the total biopterin pool of murine endothelial cells (ECs) was unaffected by 48-h exposure to diabetic glucose levels (30 mM), BH₂levels increased from undetectable to 40% of total biopterin. This BH₂accumulation was associated with diminished calcium ionophore-evoked NO activity and accelerated superoxide production. Since superoxide production was suppressed by NOS inhibitor treatment, eNOS was implicated as a principal superoxide source. Importantly, BH₄supplementation of ECs (in low and high glucose-containing media) revealed that calcium ionophore-evoked NO bioactivity correlates with intracellular BH₄:BH₂and not absolute intracellular levels of BH₄. Reciprocally, superoxide production was found to negatively correlate with intracellular BH₄:BH₂. Hyperglycemia-associated BH₄oxidation and NO insufficiency was recapitulated in vivo, in the Zucker diabetic fatty rat model of type 2 diabetes. Together, these findings implicate diminished intracellular BH₄:BH₂, rather than BH₄depletion per se, as the molecular trigger for NO insufficiency in diabetes.

Abstract: C-reactive protein (CRP) has received much attention as a cardiovascular risk factor and has been recommended to be used in screening to assist in predicting the occurrence of cardiovascular disorders. There are numerous association studies documenting changes in circulating CRP concentrations, there are, however, fewer studies providing evidence that CRP mediates the progression of cardiovascular pathologies. Elucidating the potential mechanisms for CRP has been confounded by recent reports that contaminants of CRP are partially responsible for observed effects. In this review the use of CRP as a tool to predict cardiovascular disorders will be discussed alongside a more recently described cardiovascular risk factor asymmetric dimethylarginine (ADMA). An endogenously occurring nitric oxide synthase inhibitor, ADMA, is formed by the action of protein arginine methyltransferases and subsequent proteolysis and it is metabolised in vivo by the dimethylarginine dimethylaminohydrolases (DDAH). The evidence available documenting the effects of CRP and ADMA, the regulatory mechanisms and the genetic influences, will be discussed in order to determine whether CRP and ADMA are mediators in the progression of cardiovascular disorders or merely useful biomarkers.