The hydration characteristics and utilization of slag obtained by the vitrification of MSWI fly ash.

This study investigated the effects of slag composition on the hydration characteristics of slag blended cement (SBC) pastes. Synthetic slag samples were prepared by melting CaO-modified and Al(2)O(3)-modified municipal solid waste incinerator (MSWI) fly ash. MSWI fly ash was mixed with 5% CaO and 5% Al(2)O(3) (by weight), respectively, resulting in two fly ash mixtures. These mixtures were then melted at 1400 degrees C for 30 min to produce two types of slag with different contents, designated at C-slag and A-slag. Both the C-slag and A-slag samples exhibited a pozzolanic activity index higher than the unmodified slag sample. The results show that the synthetic slags all met the Taiwan EPA's current regulatory thresholds. These synthetic slags were then blended with ordinary Portland cement (OPC) at various weight ratios ranging from 10 to 40%. The 28-day strength of the C1 paste was higher than that developed by the OPC paste, suggesting that the C-slag contributed to the earlier strength of the SBC pastes. At curing times beyond 28 days, the strength of the A1 paste samples approached that of the OPC paste samples. It can be seen from this that increasing the amount of calcium and aluminum oxide increases the early strength of SBC. The C-slag blended cement paste samples showed an increase in the number of fine pores with the curing time, showing that the C-slag enhanced the pozzolanic reactions, filling the pores. Also, the incorporation of a 10% addition of C-slag also tended to enhance the degree of hydration of the SBC pastes during the early ages (3-28 days). However, at later ages, no significant difference in degree of hydration between the OPC pastes and the SBC pastes was observed with the 10% C-slag addition. However, the incorporation of A-slag did decreased the degree of hydration. A slag blend ratio of 40% significantly decreased the hydration degree.

Does balloon mitral valvuloplasty improve cardiac function? A mechanistic investigation into impact on exercise capacity.

Procedural technical success of balloon mitral valvuloplasty (BMV) is indicated by an increase in valve area and a reduction in transvalvar gradient, but there are conflicting results regarding whether these indicators correlate with subsequent improvements in exercise capacity. We conducted a study to explore the effects of valvuloplasty on cardiac function to gain insight into the mechanisms responsible for the impact on exercise ability. Sixteen patients with mitral stenosis participated in the study and the five who did not proceed to valvuloplasty served as the control group. All patients performed maximal cardiopulmonary exercise tests before and 6 weeks after valvuloplasty (without valvuloplasty in controls). Central haemodynamics including cardiac output were measured non-invasively at rest and peak exercise. At baseline, the cardiopulmonary exercise test results were similar in the two groups. Following valvuloplasty, cardiac output did not alter at rest, but increased significantly at peak exercise (8.7+/-1.7 to 10.5+/-2.1 l min(-1), P<0.01), as did peak cardiac power output (1.88+/-0.55 to 2.28+/-0.74, P<0.05) and cardiac reserve (1.07+/-0.33 to 1.45+/-0.55 watts, P<0.05). Aerobic exercise capacity improved (13.9+/-4.2 to 16.4+/-4.3 ml kg(-1) min(-1), P<0.01) as did exercise duration (354+/-270 to 500+/-266 s, P<0.01). There were no significant changes in the controls. There was a significant correlation between the changes in peak VO(2) and changes in cardiac reserve (r=0.62, P<0.01) but not with changes in resting haemodynamics. These changes did not correlate with changes in peri-procedural mitral valve haemodynamics, despite increases in mitral valve area from 1.05+/-0.16 to 1.74+/-0.4 cm(2) (P<0.0001), accompanied by falls in the transvalvar gradient and pulmonary artery pressure (12.4+/-4.7 to 4.5+/-3 mmHg, and 26.8+/-8.4 to 17.4+/-5.2 mmHg, respectively, all P<0.0001). In conclusion, we found that successful mitral valvuloplasty in our patient cohort led to improved cardiac and physical functional capacity but not resting haemodynamics. Neither indicators of technical success nor resting haemodynamics were very reliable in predicting functional improvement.

Palladium(II) and platinum(II) analogues of luminescent diimine Triangulo complexes supported by triply bridging sulfide ligands: structural and spectroscopic comparisons.

Reaction of [M(L-L)Cl(2)] [M = Pd, Pt; L-L = 4,4'-di-tert-butyl-2,2'-bipyridine ((t)Bu(2)bpy), 4,4'-dimethylcarboxylate-2,2'-bipyridine ((CO(2)Me)(2)bpy), bis(diphenylphosphino)methane (dppm)] with Na(2)S in refluxing methanol afforded [M(3)((t)Bu(2)bpy)(3)(mu(3)-S)(2)](2+) [M = Pd (1a), Pt (2a)], [M(3)((CO(2)Me)(2)bpy)(3)(mu(3)-S)(2)](2+) [M = Pd (1b), Pt (2b)], and [Pt(3)(dppm)(3)(mu(3)-S)(2)](2+) (3) as perchlorate salts. X-ray crystal analysis revealed that 1a, 1b, 2a, and 3 have triangular M(3)S(2) core structures. The three metal atoms in 1a, 2a, and 3 form virtual equilateral triangles with intramolecular Pd-Pd and Pt-Pt separations of 3.027(1)-3.065(1) and 3.104(1)-3.154(1) A, respectively. An isosceles triangle of Pd(3) atoms is observed in the molecular structure of 1b. The (1)MLCT absorption of 2a and 2b appears at 415 and 448 nm, respectively, in dichloromethane and is significantly red-shifted from the lowest energy absorption band of the Pd(3) analogues. Complex 1a exhibits weak photoluminescence in the solid state at 77 and 298 K (uncorrected lambda(max) 760 and 730 nm, respectively) while the 77 K solid-state emission of 1b (uncorrected lambda(max) 760 nm) is also weak. At 77 K, complexes 2a, 2b, and 3 display broad unstructured emissions at lambda(max) 616-630 nm in the solid state. Ligand-field excited states are tentatively assigned for these emissions.

What is the signal for the posttranslational arginylation of proteins?

The N-terminal, posttranslational arginylation of proteins is ubiquitous in eukaryotic cells. Previous experiments, using purified components of the reaction incubated in the presence of exogenous substrates, have shown that only those proteins containing acidic residues at their N-terminals are arginylation substrates. However, data from experiments that used crude extracts of brain and nerve as the source of the arginylating molecules, suggest that the in vivo targets for arginylation are more complex than those demonstrated using purified components. One of the proposed functions for arginylation is as a signal for protein degradation and proteins that have undergone oxidative damage have been shown to be rapidly degraded. In the present experiments we have tested the hypothesis that the presence of an oxidatively damaged residue in a protein is a signal for its arginylation. These experiments have been performed by adding synthetic oxidized peptides to crude extracts of rat brain, incubating them with [3H]Arg and ATP and assaying for arginylated peptides using RP-HPLC. Results showed that while the oxidized A-chain of insulin was arginylated in this system, confirming previous experiments, other peptides containing oxidized residues were not. When a peptide containing Glu in the N-terminus was incubated under the same conditions it too was not a substrate for arginylation. These findings show that neither the presence of an N-terminal acidic residue nor an oxidized residue alone are sufficient to signal arginylation. Thus, another feature of the oxidized A-chain of insulin is required for arginylation. That feature remains to be identified.

Rapid spongiform degeneration of the cerebrum and cerebellum in Creutzfeldt-Jakob encephalitis: serial MR findings.

We report the cerebral MR imaging findings in a patient with pathologically proved Creutzfeldt-Jakob disease in whom predominant gray and white matter degeneration was seen within 1 year of symptom onset. The initial MR signal abnormalities in the basal ganglia were subtle. A follow-up MR examination revealed diffuse cerebral and cerebellar atrophy and demyelination.

Recovery of antioxidants and reduction in lipid hydroperoxides in murine epidermis and dermis after acute ultraviolet radiation exposure.

In previous studies we have found that a single acute dose of ultraviolet radiation to murine skin causes a large degree of destruction of enzymic and non-enzymic antioxidants immediately after irradiation. In the present study, we wished to elucidate the recovery of antioxidants after a single dose of ultraviolet (UV) radiation. We measured antioxidants and lipid hydroperoxides (as a marker of membrane damage) in murine epidermis and the dermis at 0, 3, 12, 24, 72 and 120 h after exposure to UV radiation (25 J/cm2, UVA+UVB). Lipid hydroperoxides showed the highest values immediately after UV exposure and returned to control values within 24 h in both epidermis and dermis. The activities of catalase, glutathione peroxidase and glutathione reductase showed the lowest activities immediately after UV exposure; superoxide dismutase activities reached a minimum at 3 h postexposure. The pattern of recovery was different for each enzyme and for epidermis and dermis. The activities of superoxide dismutase and catalase decreased remarkably and recovered slowly. Superoxide dismutase in the dermis recovered full activity by 120 h and in the epidermis by 12 h. Catalase activity in both epidermis and dermis had returned to only 50% of control activity at 120 h, although the epidermis showed a temporary increase (to 93%) at 24 h. Glutathione peroxidase and glutathione reductase were slightly decreased immediately after irradiation, recovered to 100% at 3 h and then increased to 200-250% in both the epidermis and the dermis at various times; values had returned to 100% in epidermis by 120 h but remained elevated in dermis.(ABSTRACT TRUNCATED AT 250 WORDS)