Item assessment in the development of a diagnostic motor performance test for myopathy in children

The authors conducted an assessment study of newly developed motor performance items for the diagnosis of myopathy. 17 children who had had muscle biopsy for this diagnosis in the recent past were administered 14 items based on the measurement of static, dynamic and explosive muscle strength and muscle endurance. Individual items did not have perfect discriminative power, but the results were encouraging enough to warrant detailed study with combinations of the items, so that in future fewer children will have to undergo unnecessary muscle biopsies.     

Modification of hypoxia-induced injury in cultured rat astrocytes by high levels of glucose

BACKGROUND AND PURPOSE: Preexisting hyperglycemia exacerbates central nervous system injury after transient global and focal cerebral ischemia. Increased anaerobic metabolism with resultant lactic acidosis has been shown to cause the hyperglycemic, neuronal injury. The contribution of astrocytes in producing lactic acidosis under hyperglycemic/ischemic conditions is unclear, whereas the protective role of astrocytes in ischemic-induced neuronal injury has been documented. The ability of astrocytes to maintain energy status and ion homeostasis under hyperglycemic conditions could ultimately reduce neuronal injury. Therefore, we determined the effects of increased glucose concentrations on glucose utilization, lactate production, extracellular pH, and adenosine triphosphate concentrations in hypoxia-treated astrocyte cultures. METHODS: Primary astrocytes were prepared from neonatal rat cerebral cortices. After 35 days in vitro, cultures were incubated with 0-60 mmol/L glucose and subjected to hypoxic conditions at 95% N2/5% CO2 for 24 hours. In addition, under high-glucose conditions (30 mmol/L), astrocytes were exposed to up to 72 hours of hypoxia. Determination of lactate dehydrogenase efflux, adenosine triphosphate concentrations, and extracellular lactate concentrations defined astrocyte status. Equiosmolar levels of mannitol were added in place of high glucose concentrations to distinguish hyperosmotic effect. RESULTS: When physiological concentrations of glucose (7.5 mmol/L) or lower concentrations were used, significant cell damage occurred with 24 hours of hypoxia, as determined by increased efflux of lactate dehydrogenase and loss of cell protein. When higher glucose concentrations (15-60 mmol/L) were used, efflux of lactate dehydrogenase was similar to that observed in normoxic cultures, despite an increased utilization of glucose. Lactate concentrations in the media at low or normal glucose concentrations exceeded normoxic levels, but higher glucose concentrations (15-30 mmol/L) failed to increase lactate levels further. Values of adenosine triphosphate for hypoxic astrocytes treated with high glucose concentrations were significantly higher than those of astrocytes with zero or low glucose levels. In cultures exposed to hypoxia and high glucose levels (30 mmol/L), no cellular injury was observed before 48 hours of hypoxia. Lactate concentrations in the media increased during the first 24 hours of hypoxia and reached steady state. The pH of the media decreased to 6.4 after 24 hours and 5.5 at 48 hours. The latter pH was concomitant with a marked increase in extracellular lactate dehydrogenase activity. Hyperosmotic mannitol failed to protect cultured astrocytes against hypoxia. CONCLUSIONS: Hypoxic injury to mature astrocytes was reduced by the presence of 15-60 mmol/L glucose in the medium during 24-30 hours of hypoxia. Injury occurred when the pH of the medium was < 5.5. This protection was not afforded by the hyperosmotic effect of high glucose concentrations, nor was the hypoxic injury at later time periods with 30 mmol/L glucose mediated solely by lactate accumulation.     

Characterization of C-S-H from Highly Reactive β-Dicalcium Silicate Prepared from Hillebrandite

β-dicalcium silicate synthesized by thermal dissociation of hydrothermally prepared hillebrandite (Ca₂(SiO₃)(OH)₂) exhibits extremely high hydration activity. Characterization of the hydrates obtained and investigation of the hydration mechanism was carried out with the aid of trimethylsilylation analysis, ²⁹Si magic angle spinning nuclear magnetic resonance, transmission electron microscopy selected area electron diffraction, and XRD. The silicate anion structure of C-S-H consisted mainly of a dimer and a single-chain polymer. Polymerization advances with increasing curing temperature and curing time. The C-S-H has an oriented fibrous structure and exhibits a 0.73-nm dreierketten in the longitudinal direction. On heating, the C-S-H dissociates to form β-C₂S. The temperature at which βC₂S begins to form decreases with increasing chain length of the C-S-H or as the Ca/Si ratio becomes higher. The high activity of β-C₂S is due to its large specific surface area and the fact that the hydration is chemical-reaction-rate-controlled until its completion. As a result, the hydration progresses in situ and C-S-H with a high Ca/Si ratio is formed.     

Pressurized fluidized-bed hydro retort ing of raw and beneficiated Eastern oil shales

Bench-scale tests were conducted with raw and beneficiated shales in an advanced multi-purpose research reactor. Raw Alabama shale and raw and beneficiated Indiana shales were retorted at 515 °C using hydrogen pressures of 4 and 7 MPa. Shale feed rates were 15 to 34 kg h⁻¹. High oil yields and carbon conversions were achieved in all tests. Oil yield from Alabama shale hydroretorted at 7 MPa was 200% of Fischer assay. Raw and beneficiated Indiana shales hydroretorted at 7 MPa produced oil yields of 170 and 195% of Fischer assay respectively. Total carbon conversions were >70% for all tests conducted at 7 MPa.     

Elevation of serum cholesterol levels in mice by the antioxidant butylated hydroxyanisole

The food antioxidants butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) are structurally related to the hypocholesterolemic drug probucol. The purpose of this study was to determine if BHA can lower serum cholesterol levels as is observed with probucol. Treatment of mice with 0.75% BHA in their feed for 10 days resulted in a significant (P < or = 0.01) elevation of serum cholesterol levels. This effect contrasts with the cholesterol-lowering effect of probucol. Further, the degree of cholesterol elevation was comparable to that observed in mice administered 3% cholesterol in their feed for 7 days. The enzyme acyl CoA:cholesterol acyltransferase (ACAT) was decreased significantly (P < or = 0.01) in liver microsomes from BHA-treated mice. In contrast, hepatic microsomal ACAT activity was increased significantly (P < or = 0.01) in cholesterol-fed mice. These results suggested that the increased serum cholesterol observed in BHA-treated mice was not accompanied by an increase in hepatic cholesterol levels. Indeed, hepatic microsomal cholesterol levels were reduced in BHA-treated mice, but were increased significantly (P < or = 0.01) in cholesterol-fed mice. These results demonstrate that the common food additive BHA elevates serum cholesterol levels by a mechanism that apparently involves the decreased uptake of cholesterol by the liver.