SUMMARY : Biophysical studies of the virus system of vesicular stomatitis passaged in eggs showed that the major part ofthe infectivity was associated with a component of sedimentation coefficient 625 S. A component of sedimentation coefficient 330 S was observed also, and is probably a non-infective product of the disintegration of the 6 2 5 s component. These components contribute about 35 yo of the total complement-fixing activity of the virus system. All infective materials were handled in subdued light (Skinner & Bradish, 1954). Electron micrographs of concentrates of the infective fraction revealed rods, of length 175 mp. and diameter 69 m p , and almost spherical granules of diameter 65 mp. These particles are identified with the 6 2 5 s and 330s sedimentation components. The remaining 65 Yo of the total complement-fixing activity was associated with two discrete components of sedimentation coefficients about 2 0 s and 6 s . The first of these components may contribute up to 0.1 yo of the total infectivity of the virus system. The structure of the virus system is discussed in relation to the data obtained.Ultracentrifugal studies of the virus system of foot-and-mouth disease (Bradish, Brooksby, Dillon & Norambuena, 1952) demonstrated that infectivity and complement-fixing activity were associated with discrete components of sedimentation coefficients 70 S and 8 S, respectively. These values correspond with equivalent particle diameters of about 20 and 7 mp., respectively. The extension of studies of this type to the virus system of vesicular stomatitis presents advantages because of the greater mass of the infective particle which, on the basis of earlier ultrafiltration and ultracentrifugation data (Galloway & Elford, 1933; Elford & Galloway, 1937) has an equivalent diameter of about 75 mp. This larger particle facilitates the use of certain biophysical methods which were not employed in the previous study (Bradish et al. 1952). Of particular value is the comparison which may be made between the data obtained by the biological assay of ultracentrifugal fractions and those derived by direct optical-analytical ultracentrifugation and by electron microscopy. The results obtained are presented in this paper. METHODS Handling in subdued lightIt was observed by Skinner & Bradish (1954) that the infectivity of suspensions of many viruses, including those of the virus of vesicular stomatitis, was decreased significantly by exposure to light. Special precautions were taken

The burden of non-alcoholic fatty liver disease (NAFLD) worldwide is a significant clinical and public health issue, affecting approximately one third of the Western population. This review assesses the effect and impact lifestyle interventions have on the treatment of this common condition. We review studies comparing the effect of calorie restriction and exercise programs, as well as comparison of lifestyle intervention with pharmaceutical intervention. Both calorie restriction and exercise programs are shown to be beneficial in improving features of metabolic syndrome and surrogate markers of NAFLD. The paucity of studies using histological improvement hinders the ability to conclude a benefit on improvement of histological NAFLD, although this is shown in a small number of studies. There is a need to extend the intervention period to show a sustained improvement with intervention as most studies have a follow up period of 12 months of less.

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This abstract was presented as the Cellular and Molecular Nutrition Theme highlight.Elevated levels of methylglyoxal (MG), a highly reactive glycating agent forming advanced glycation endproducts (AGEs), have been associated with diabetes, obesity and vascular disease (1) . However, its role in the hepatic manifestation of metabolic syndrome, nonalcoholic fatty liver disease (NAFLD), is still a novel inquiry. The objective of these experiments was to assess MG levels in response to lipid loading in the liver.Immortalised human hepatocytes (HepG2 cells) cultured in physiological levels of glucose (5 mM) were treated with either saturated (400 μM palmitic acid, PA) or mono-unsaturated (500 μM oleic acid, OA) fatty acids (n = 3). Fatty acid-induced lipid loading was confirmed by Nile red staining. MG content of cells and in culture medium was measured by stable isotopic dilution liquid chromatography-mass spectrometry (LC-MS/MS) (2) . The MG-derived major AGE, hydroimidazolone MG-H1, was assessed by competitive ELISA in serum samples from a cohort of biopsy-confirmed adult NAFLD patients (n = 62). Sample collection was under full NHS ethical approval and conducted in accordance with the Declaration of Helsinki. One-way ANOVA with Dunnett's test was used to analyse the in vitro data. Pearson or Spearman correlations were used to examine MG-H1 relationship to histological features and clinical biochemistries, followed by multiple linear regression analyses.Fatty acid treatment resulted in a 4-fold increase of intracellular lipid in the OA-treated cells ( Fig. 1; P < 0·01). MG increased by 44 % in OA-treated cells compared to vehicle ( Fig. 2; P < 0·05), while culture medium MG increased by 46 % and 45 % in PA-and OA-treated cells, respectively ( Fig. 3; P < 0·05). Serum MG-H1 (n = 59) was inversely correlated with alanine aminotransferase levels, lobular inflammation and hepatocyte ballooning (P < 0·001). MG-H1 was positively correlated with body mass index (BMI) (P < 0·0001) however, there was no correlation between MG-H1 and steatosis or fibrosis score and, surprisingly, in this cohort BMI was inversely correlated to inflammation and ballooning. The multiple regression analyses resulted in no conclusive relationships between MG-H1 and variables to predict NAFLD activity.Accumulation of MG, as measured by LC-MS/MS, in fatty acid-treated cells and their associated medium suggests lipid accumulation increases MG formation and/or decreases MG metabolism. In contrast, serum MG-H1 from patients with fatty liver measured by ELISA did not correlate with extent of steatosis. If these findings can be corroborated by robust measurement of MG-H1 by LC-MS/MS, increased MG and AGEs formation in hepatic steatosis in vivo may be localised to the liver where proteolysis likely releases increased MG-H1 free adduct into plasma.