Nucleation particles in diesel exhaust: composition inferred from in situ mass spectrometric analysis.

Mass spectrometric measurements of size and composition of diesel exhaust particles have been performed under various conditions: chassis dynamometer tests, field measurements near a German motorway, and individual car chasing. Nucleation particles consisting of volatile sulfate and organic material could be detected both at the chassis dynamometer test facility and during individual car chasing. We found evidence that if nucleation occurs, sulfuric acid/water is the nucleating agent. Low-volatile organics species condense only on the preexisting sulfuric acid/water clusters. Nucleation was found to depend strongly on various parameters such as exhaust dilution conditions, fuel sulfur content, and engine load. The latter determines the fraction of the fuel sulfur that is converted to sulfuric acid. The organic compounds (volatile and low-volatile) condense only on preexisting particles, such as both sulfuric acid nucleation particles and larger accumulation mode soot particles. On the latter, sulfuric acid also condenses, if the conditions for nucleation are not given. The overall ratio of sulfate to organic (volatile and low-volatile) is also strongly dependent on the engine load. It was found that the production of nucleation particles even at high engine load can be suppressed by using low-sulfur fuel.

Phenol/cresol degradation by the thermophilic Bacillus thermoglucosidasius A7: cloning and sequence analysis of five genes involved in the pathway.

Bacillus thermoglucosidasius A7 degraded phenol at 65 degrees C via the meta cleavage pathway. Five enzymes used in the metabolism of phenol were cloned from B. thermoglucosidasius A7 into pUC18. Nine open reading frames were present on the 8.1kb insert, six of which could be assigned a function in phenol degradation using database homologies and enzyme activities. The phenol hydroxylase is a two-component enzyme encoded by pheA1 and pheA2. The larger component (50kDa) has 49% amino acid identity with the 4-hydroxyphenylacetate hydroxylase of Escherichia coli, while the smaller component (19kDa) is most related (30% amino acid identity) to the styrene monoxygenase component B from Pseudomonas fluorescens. Both components were neccessary for activity. The catechol 2, 3-dioxygenase encoded by pheB has 45% amino acid identity with dmpB of Pseudomonas sp. CF600 and could be assigned to superfamily I, family 2 and a new subfamily of the Eltis and Bolin grouping. The 2-hydroxymuconic acid semialdehyde hydrolase (2HMSH), encoded by pheC, revealed the highest amino acid identity (36%) to the equivalent enzyme from Pseudomonas sp. strain CF600, encoded by dmpD. Based on sequence identity, pheD and pheE were deduced to encode the 2-hydroxypenta-2,4-dienoate hydratase (2HDH), demonstrating 45% amino acid identity to the gene product of cumE from Pseudomonas fluorescens and the acetaldehyde dehydrogenase (acylating) demonstrating 57% amino acid identity to the gene product of bphJ from Pseudomonas LB400.

Heart rate variability in time and frequency domains: effects of gallopamil, nifedipine, and metoprolol compared with placebo.

OBJECTIVE: To assess the effects of three different antianginal drugs on heart rate, blood pressure, and heart rate variability. DESIGN: Randomised, single blind, placebo controlled, cross over study. SETTING: University hospital. PARTICIPANTS: Nine healthy male volunteers. INTERVENTIONS: Oral administration of either 50 mg gallopamil, 20 mg nifedipine, 100 mg metoprolol, or placebo according to a random crossover plan. MAIN OUTCOME MEASURES: Time intervals between consecutive R waves in electrocardiograms measured with an accuracy of 5 ms from digital Holter recordings. Blood pressure monitored continuously by finger plethysmography. RESULTS: Metoprolol lowered heart rate from 62(6) to 51(5) beats/min (p = 0.003) after 78(23) minutes. Nifedipine provoked reflex tachycardia from 56(5) to 94(18) beats/min (p < 0.001) at 10(3) minutes after treatment followed by an exponential decline in heart rate to baseline values with a time constant of 34(7) min in seven subjects but 83 minutes in one volunteer. One subject showed no exponential decline in heart rate. Nifedipine significantly lowered the supine mean arterial pressure from 86(6) to 67(6) mm Hg (p = 0.004) after 11(2) minutes, indicating an acute reduction in arterial resistance. Gallopamil did not significantly change mean heart rate or blood pressure. In the sitting position three hours after administration gallopamil and metoprolol significantly lowered power spectral density in the low frequency band (0.03 Hz to 0.15 Hz) compared with placebo (p < 0.05). Nifedipine did not produce such an effect. CONCLUSIONS: Gallopamil and metoprolol both inhibit cardiac sympathetic activation compared with placebo, whereas nifedipine causes reflex sympathetic activation.