Syncope with and without convulsion was studied in unselected blood donors in a community blood center. Convulsive syncope occurred in 0.03% of all blood donors and was more commonly observed when nursing personnel were alerted to its possible occurrence. It was more common in men. Although tonic extensor spasm was the most common convwithout convulsion was studied in unselected blood donors in a community blood center. Convulsive syncope occurred in 0.03% of all blood donors and was more commonly observed when nursing personnel were alerted to its possible occurrence. It was more common in men. Although tonic extensor spasm was the most common convwithout convulsion was studied in unselected blood donors in a community blood center. Convulsive syncope occurred in 0.03% of all blood donors and was more commonly observed when nursing personnel were alerted to its possible occurrence. It was more common in men. Although tonic extensor spasm was the most common convulsive movement, other complex convulsive phenomena occurred, some simulating epileptic seizure. No statistical difference in changes of pulse or blood pressure was found between subjects with convulsive versus nonconvulsive syncope. Similarly, no difference was found between subjects with tonic spasm and those with other convulsive phenomena, nor between those with "early" and those with "delayed" reactions. Marked individual variation may exist in the susceptibility of the central nervous system to ischemia. Some individuals appear to be predisposed to development of seizures in situations of global cerebral ischemia such as occur in hypotension and bradycardia.
Nucleic acid and protein synthesis were studied in temperature-sensitive mutants defective in phospholipid synthesis. The defect is due to a single mutation in glycerol 3-phosphate acyltransferase (EC 2.3.1.15). The results show that at the restrictive temperature not only does phospholipid synthesis cease, but DNA, RNA, and protein synthesis also cease. Active transport continues, however, indicating that the cells do not become leaky or lose their energy supply. These results suggest that phospholipid synthesis is coupled to DNA, RNA, and protein synthesis.Since lipid synthesis, and consequently membrane synthesis, is necessary for growth of cells, it is reasonable that cells would have regulatory mechanisms to couple the synthesis of lipids with the synthesis of macromolecules in order to maintain balanced cell growth. The availability of mutants in lipid biosynthesis has helped to elucidate the contribution of phosl)holipids to membrane structure and function (1). In particular, one apparent result was that protein synthesis and cell growth could continue for a significant amount of time in the absence of lipid synthesis. When an unsaturated fattyacid auxotroph of Escherichia coli was deprived of unsaturated fatty acids, growth, as well as DNA, RNA, and protein synthesis, continued for several hours (2-5). Similar results were obtained when 3-decynoyl-N-acetylcysteamine was used to inhibit unsaturated fatty-acid synthesis (4, 6, 7). Bacillus subtilis (8-10), Staphylococcus aureus (11), and E. coli (12) glycerol auxotrophs have been studied. When these mutants were deprived of glycerol, net phospholipid synthesis stopped immediately. However, macromolecular synthesis and cell growth continued for some time.Recently this laboratory has described a temperaturesensitive mutant of E. coli, CV15, that does not grow or make phospholipid at the restrictive temperature (13). The defect is due to a single mutation in glycerol 3-phosphate acyltransferase (EC 2.3.1.15), which catalyzes the first reaction unique to phospholipid biosynthesis. In this paper, detailed studies of the synthesis of phospholipid, DNA, RNA, and protein are reported for mutants with a thermolabile glycerol 3-phosphate acyltransferase. The results show that DNA, RNA, and protein synthesis do not continue at the restrictive temperature; the shutoff of the synthesis of these macromolecules parallels the shutoff of phospholipid synthesis. Active transport continues, however, indicating that the cells do not become leaky or lose their energy supply. MATERIALS AND METHODSBacterial Strains, Mfedia, and Growth Conditions. CV15 and its parent, strain 8, were described previously (13).Abbreviations: TMG, methyl-l-thio-j-D-galactopyranoside; IPTG, isopropyl-l-thio-,f-D-galactopyranoside.
The post-antibiotic effect (PAE) may allow for more widely spaced dosing of antibiotics than is currently employed without loss of efficacy. Antimicrobial combinations are widely used in clinical medicine. However, dosing schedules are usually based on pharmacological profiles of the drugs used alone. Previously we have demonstrated significant prolongation of the PAE induced by antimicrobial combinations in vitro as compared to PAEs induced by the agents alone. We examined this issue further in vivo in a neutropenic mouse thigh infection model, by exposing Staphylococcus aureus, Pseudomonas aeruginosa, Escherichia coli and Klebsiella pneumoniae to several antimicrobials, either singly or in combination. The PAE in vivo was defined as the difference in time needed for the organisms in the treated animals to grow 1 log10 as compared with controls after serum drug concentrations had fallen below the MIC. Drug concentrations exceeded the MIC for 1.2-3.2 h, but bactericidal activity occurred mainly during the first hour. When the agents were used singly a negative PAE was produced by ceftazidime against P. aeruginosa, a PAE of approximately 0 h by imipenem against E. coli and K. pneumoniae, a PAE of 2-4 h by cefazolin against S. aureus, gentamicin against E. coli and K. pneumoniae, and imipenem and tobramycin against P. aeruginosa, and a PAE of 6-7 h by gentamicin against S. aureus and rifampicin against P. aeruginosa. The beta-lactam/aminoglycoside combinations when used against S. aureus and P. aeruginosa prolonged the PAE by 1.0-3.3 h, compared with the longer of the individual drug PAEs, but no prolongation was observed against E. coli and K. pneumoniae. Ceftazidime reduced the PAE when used with tobramycin against P. aeruginosa. The long PAE of rifampicin against P. aeruginosa was 'carried over' to the combination, thus prolonging the growth suppression achieved by imipenem and tobramycin alone or in combination by 5.5-8.0 h. This effect on the PAE was additive only, and synergy was not observed. In conclusion, a potentially significant prolongation of the PAE by combination of drugs was observed in vivo, but only if both (or all) agents induced a PAE when used alone. The impact of this observation needs to be examined further in studies involving multiple and different dosing regimens in an infection model.
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