Subcellular localization and some biochemical properties of the flavivirus Kunjin nonstructural proteins NS2A and NS4A

1. The mean incidence of deaths from ascites in the UK in 1993 was 1.4% (0.7% in 1991 and 0.9% in 1992) and 0.8% from sudden death syndrome (SDS). In total, the economic loss to the UK Broiler Industry in 1993 as a result of these 2 conditions was 24 Pounds M. 2. Clear geographical differences emerged in the occurrence of ascites, with, not only the lowest incidences being observed in Northern Ireland, but also the peak of the mortality from ascites occurring much later in the rearing cycle than in other regions on the mainland. 3. In all regions the incidence of SDS was lower than that of ascites but the reason for this disparity remains to be established. 4. Some of the variables associated with the road transportation of day-old chicks from the hatchery to the farm appeared to influence the incidence of ascites. These included distance or time travelled, stocking density, internal lorry temperature and the length of time the lorry was heated before transport as well as the time the shed was heated before chick arrival. Temperature was also an important factor during growth (brooding and finishing). 5. Negative pressure-powered ventilation was preferred in most organisations but more ascites was seen with positive pressure ventilation. However, the lowest incidence of ascites occurred with natural ventilation. There was more ascites relative to shed orientation when the wind direction was from the west compared to the east. 6. This survey identifies the extent of the problem of broiler ascites in the UK and also highlights the importance of good management control of day-old chicks, not only following placement, but even before their arrival on the farm.     

The impact of treatment time and smoking on local control and complications in T1 glottic cancer

Low frequency impedance measurements of pure egg lecithin (phosphatidylcholine) bilayers have revealed the presence of four layers which can be attributed to the acyl chain, carbonyl, glycerol bridge and phosphatidylcholine regions of the lecithin molecule. Measurements on bilayers formed in the presence of unoxidised-cholesterol revealed that cholesterol molecules were located in the hydrocarbon region of the bilayer with its hydroxyl groups aligned with the carbonyl region of the lecithin molecules. Measurements of oxidised-cholesterol lecithin bilayers revealed that these molecules protruded less into the hydrocarbon region and their polar hydroxyl group aligned with the glycerol bridge region of the lecithin molecule.     

Hearing loss in community-dwelling older persons: national prevalence data and identification using simple questions

OBJECTIVE: To estimate the prevalence of hearing loss among community-dwelling older persons according to clinical criteria and to develop a brief self-report screening instrument to detect hearing loss. DESIGN: Survey. SETTING: National probability sample of noninstitutionalized older persons. PARTICIPANTS: A total of 2506 persons aged 55 to 74 who participated in the National Health and Nutrition Examination Survey. MAIN OUTCOME MEASURES: Hearing loss as defined by Ventry and Weinstein (VW) criteria and by the High Frequency Pure-Tone Average (HFPTA) scale. RESULTS: Hearing loss by VW criteria was present in 14.2% and by HFPTA criteria in 35.1% of those surveyed. The prevalence increased with advancing age and was higher among men and those with less education. A logistic regression model identified six independent factors for hearing loss by VW criteria: age > or = 70 years (adjusted odds-ratio (AOR) 2.7, 95% confidence interval (95% CI) 1.6, 4.4), male gender (AOR 3.0, 95% CI 1.9, 4.8), < or = 12th grade education (AOR 3.8, 95% CI 1.8, 7.7), having seen a doctor for deafness or hearing loss (AOR 8.9, 95% CI 5.3, 14.9), unable to hear a whisper across a room (AOR 3.2, 95% CI 2.0, 5.1), and unable to hear a normal voice across a room (AOR 6.2, 95% CI 2.6, 14.9). A clinical scale based on the logistic model had 80% sensitivity and 80% specificity in predicting hearing loss using VW criteria and 59% sensitivity and 88% specificity in predicting hearing loss using HFPTA criteria. CONCLUSIONS: Hearing loss, as defined by two clinical criteria, is common and can be screened for accurately using simple questions that assess sociodemographic and hearing-related characteristics.     

Overexpression of human superoxide dismutase inhibits oxidation of low-density lipoprotein by endothelial cells

Oxidation of LDL in the subendothelial space has been proposed to play a key role in atherosclerosis. Endothelial cells produce superoxide anions (O2.-) and oxidize LDL in vitro; however, the role of O2.- in endothelial cell-induced LDL oxidation is unclear. Incubation of human LDL (200 microg/mL) with bovine aortic endothelial cells (BAECs) for 18 hours resulted in a 4-fold increase in LDL oxidation compared with cell-free incubation (22.5+/-1.1 versus 6.3+/-0.2 [mean+/-SEM] nmol malondialdehyde/mg LDL protein, respectively; P<0.05). Under similar conditions, incubation of LDL with porcine aortic endothelial cells resulted in a 5-fold increase in LDL oxidation. Inclusion of exogenous copper/zinc superoxide dismutase (Cu/ZnSOD, 100 microg/mL) in the medium reduced BAEC-induced LDL oxidation by 79%. To determine whether the intracellular SOD content can have a similar protective effect, BAECs were infected with adenoviral vectors containing cDNA for human Cu/ZnSOD (AdCu/ZnSOD) or manganese SOD (AdMnSOD). Adenoviral infection increased the content and activity of either Cu/ZnSOD or MnSOD in the cells and reduced cellular O2.- release by two thirds. When cells infected with AdCu/ZnSOD or AdMnSOD were incubated with LDL, formation of malondialdehyde was decreased by 77% and 32%, respectively. Two other indices of LDL oxidation, formation of conjugated dienes and increased LDL electrophoretic mobility, were similarly reduced by SOD transduction. These data suggest that production of O2.- contributes to endothelial cell-induced oxidation of LDL in vitro. Furthermore, adenovirus-mediated transfer of cDNA for human SOD, particularly Cu/ZnSOD, effectively reduces oxidation of LDL by endothelial cells.