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T M Cook

Publications and source records attributed to T M Cook.

121 records · Page 7Linked to original sources
PubMed1971

Antibacterial nitroacridine, Nitroakridin 3582: effects on bacterial growth and macromolecular biosynthesis in vivo.

The antibacterial drug Nitroakridin 3582 inhibited the growth of selected grampositive bacteria more strongly than it inhibited the growth of gram-negative bacilli. Nitroakridin at concentrations of the order of 5 x 10(-5)m induced lysis of Bacillus licheniformis and Micrococcus lysodeikticus. At concentrations less than 10(-4)m, Nitroakridin 3582 reduced the exponential growth rate of Escherichia coli C-2; at 10(-4)m the drug was bacteriostatic, and, at concentrations greater than 10(-4)m, it was bactericidal. Prolonged bacteriostasis resulted in the formation of long filaments by E. coli, Serratia marcescens, Shigella sonnei, and Proteus mirabilis. The reversible effects of Nitroakridin 3582 on the growth of E. coli correlated with partial inhibitions of deoxyribonucleic acid biosynthesis; ribonucleic acid and protein syntheses were inhibited less strongly. Nitroakridin 3582 at concentrations greater than 2 x 10(-4)m, which block deoxyribonucleic acid biosynthesis, produced an accelerated bactericidal action.

Acridines↗
PubMed1971

Antibacterial nitroacridine, Nitroakridin 3582: binding to nucleic acids in vitro and effects on selected cell-free model systems of macromolecular biosynthesis.

Nitroakridin 3582 (NA) formed complexes with native deoxyribonucleic acid (DNA) and with transfer ribonucleic acid (tRNA) species from Escherichia coli. Spectrophotometric titrations of NA with these nucleic acids produced numerical results from which nonlinear adsorption isotherms were derived. These curves indicated the existence of more than one class of binding sites on the polymers to which NA was bound by more than one process. The stoichiometry of strong binding of NA to double helical DNA was in agreement with a conventional value (1 ligand molecule per 4.2 component nucleotides) for complete intercalation binding. NA inhibited the DNA-dependent DNA polymerase I and RNA polymerase reactions, the first strongly and the second appreciably. These inhibitions corresponded to the extents to which NA inhibits DNA and RNA biosyntheses in vivo. Evidently, NA interferes with the template function of DNA. The drug also inhibited the polymerization of phenylalanine in a cell-free E. coli ribosome-polyuridylic acid [poly (U)] system. The effect paralleled an inhibition of the poly (U)-directed binding of phenylalanyl tRNA to ribosomes. Ethidium bromide acted similarly. The antimalarial drug, chloroquine, stimulated polyphenylalanine synthesis, apparently as a result of stimulating the poly (U)-directed binding of phenylalanyl tRNA to ribosomes.

Acridines↗
PubMed1969

Mechanism of action of nalidixic acid on Escherichia coli. Vi. Cell-free studies.

The effects of nalidixic acid in vitro on deoxyribonucleic acid (DNA)- polymerase (deoxyribonucleosidetriphosphate: DNA deoxynucleotidyltransferase, EC 2.7.7.7), deoxyribonucleotide kinases (ATP: deoxymono- and diphosphate phosphotransferases), and deoxyribosyl transferase (nucleoside: purine deoxyribosyltransferase, EC 2.4.2.6) were examined employing partially purified and crude extracts of Escherichia coli ATCC 11229 and E. coli 15TAU. Nalidixic acid had no inhibitory effect on the DNA-polymerase of the wild-type strain E. coli ATCC 11229 at concentrations of 1.4 x 10(-3) to 2.8 x 10(-3)m. No inhibition of deoxyribonucleotide kinase activity was observed at concentrations of nalidixic acid ranging from 2 x 10(-3) to 8.6 x 10(-3)m. Nalidixic acid (0.43 x 10(-4) to 0.43 x 10(-3)m) had no inhibitory effect on the deoxyribosyl transferase activity of crude extracts obtained from E. coli ATCC 11229 or E. coli 15TAU. Analytical CsCl density gradient centrifugation demonstrated that the DNA obtained after treatment of E. coli 15TAU with nalidixic acid was not cross-linked. These results suggest that the prevention of DNA synthesis in vivo by nalidixic acid is not attributable to inhibition of DNA polymerase, deoxyribonucleotide kinase, deoxyribosyl transferase, or to cross-linking of the DNA of treated cells.

Carbon Isotopes↗
PubMed1967

Induction of excessive deoxyribonucleic acid synthesis in Escherichia coli by nalidixic acid.

Prior treatment of Escherichia coli with nalidixic acid in nutritionally complete medium altered the subsequent pattern of deoxyribonucleic acid (DNA) synthesis normally observed in nutritionally deficient medium. Transfer of E. coli 15 TAU to an amino acid- and pyrimidine-deficient medium usually resulted in a 40 to 50% increase in DNA content. Previous treatment with nalidixic acid caused a 200 to 300% increase in DNA content under these conditions. The extent of this DNA synthesis depended on the duration of prior exposure to nalidixic acid. The maximal rate of synthesis was obtained after a 40- to 60-min exposure to nalidixic acid and was two to three times that of the control. The induction of this excessive DNA synthesis was prevented by chloramphenicol or phenethyl alcohol, but the synthesis of this DNA was only partially sensitive to these agents. With E. coli TAU-bar, the rate of DNA synthesis, after removal of nalidixic acid, was similar to that of E. coli 15 TAU, but the maximal amount of DNA synthesized was 180 to 185% of that initially present. Cesium chloride density gradient analysis demonstrated that DNA synthesis after removal of nalidixic acid occurs by a semiconservative mode of replication. The density distribution of this DNA was similar to that obtained after thymine starvation. These results suggest that nalidixic acid treatment may induce additional sites for DNA synthesis in E.coli.

Arginine↗
PubMed1966

Mechanism of action of nalidixic acid on Escherichia coli. 3. Conditions required for lethality.

Deitz, William H. (Sterling-Winthrop Research Institute, Rensselaer, N.Y.), Thomas M. Cook, and William A. Goss. Mechanism of action of nalidixic acid on Escherichia coli. III. Conditions required for lethality. J. Bacteriol. 91:768-773. 1966.-Nalidixic acid selectively inhibited deoxyribonucleic acid (DNA) synthesis in cultures of Escherichia coli 15TAU. Protein and ribonucleic acid synthesis were shown to be a prerequisite for the bactericidal action of the drug. This action can be prevented by means of inhibitors at bacteriostatic concentrations. Both chloramphenicol, which inhibits protein synthesis, and dinitrophenol, which uncouples oxidative phosphorylation, effectively prevented the bactericidal action of nalidixic acid on E. coli. The lethal action of nalidixic acid also was controlled by transfer of treated cells to drug-free medium. DNA synthesis resumed immediately upon removal of the drug and was halted immediately by retreatment. These studies indicate that nalidixic acid acts directly on the replication of DNA rather than on the "initiator" of DNA synthesis. The entry of nalidixic acid into cells of E. coli was not dependent upon protein synthesis. Even in the presence of an inhibiting concentration of chloramphenicol, nalidixic acid prevented DNA synthesis by E. coli 15TAU.

Anti-Bacterial Agents↗
PubMed1966

Mechanism of action of nalidixic acid on Escherichia coli. IV. Effects on the stability of cellular constituents.

Cook, Thomas M. (Sterling-Winthrop Research Institute, Rensselaer, N.Y.), William H. Deitz, and William A. Goss. Mechanism of action of nalidixic acid on Escherichia coli. IV. Effects on the stability of cellular constituents. J. Bacteriol. 91:774-779. 1996.-Treatment of Escherichia coli 15TAU with nalidixic acid resulted in degradation of the nucleic acids of the cells, whereas protein was unaffected. Deoxyribonucleic acid (DNA) degradation appeared to be more extensive than ribonucleic acid degradation during periods of comparable bactericidal action. The onset of DNA degradation was evident prior to a measurable bactericidal effect. However, within the range of 2 to 20%, DNA degradation was accompanied by a decrease in viable cell numbers. Degradation of DNA to acid-soluble material occurred only under conditions permitting the bactericidal action of nalidixic acid. Arrest of the bactericidal action of nalidixic acid by the addition of dinitrophenol or chloramphenicol also inhibited DNA degradation. The acid-soluble products, which were excreted into the medium, have not been characterized completely, but probably were not phosphorylated.

Bacterial Proteins↗
PubMed1966

Bactericidal action of nalidixic acid on Bacillus subtilis.

Cook, Thomas M. (Sterling-Winthrop Research Institute, Rensselaer, N.Y.), Karen G. Brown, James V. Boyle, and William A. Goss. Bactericidal action of nalidixic acid on Bacillus subtilis. J. Bacteriol. 92:1510-1514. 1966.-Nalidixic acid at moderate concentrations exerts a bactericidal action upon the gram-positive bacterium Bacillus subtilis. The synthesis of deoxyribonucleic acid (DNA) in B. subtilis is selectively inhibited by nalidixic acid at concentrations approximating the minimal growth inhibitory concentration. Higher concentrations (25 mug/ml) result in a 30 to 35% degradation of DNA. After extended exposure to nalidixic acid, protein synthesis is also depressed. Cells of B. subtilis treated with nalidixic acid exhibit characteristic morphological abnormalities including cell elongation and development of gram-negative areas. From the results presented, it can be concluded that the mode of action of nalidixic acid upon susceptible bacteria is similar for both gram-positive and gram-negative species.

Anti-Bacterial Agents↗
PubMedDate not supplied

Headache-free controls? Evidence of headaches in individuals who deny having headaches during diagnostic screening.

In the course of two studies investigating whether individuals with recurrent tension headache differ from headache-free controls in the frequency and appraisal of stressful life events, subjects were asked to complete a headache diary for 1 week. Subjects in the headache-free control group were screened twice and reported having infrequent headaches (two or less per month). However, 13 of 38 control subjects reported multiple headache days on their headache diaries. These subjects also reported a greater frequency of stressful events and a greater stress impact score. These results suggest that a careful screening of control subjects may be necessary in studies that examine differences between subjects with recurrent headache and headache-free controls. There is also some evidence that the inclusion of these subjects in a control group may bias the sample, making it less likely to find between-group differences.

Adult↗
PubMedDate not supplied

International Training and Research in Central and Eastern Europe: The University of Iowa model.

In 1995, with support from the Fogarty International Center of the National Institutes of Health, The Center for International Rural and Environmental Health (CIREH) at The University of Iowa began developing the multi-level International Training and Research Program in Occupational and Environmental Health, focusing on countries in Central and Eastern Europe that were formerly under socialist control and have particular occupational and environmental health needs after decades of neglect and mismanagement. The purpose of the program is to prepare health science professionals to return to their home countries with new skills, added confidence, and leadership capabilities in public health to lead their colleagues and institutions in meeting the needs in their respective countries and establish active national and international networks and collaborations. By December 1998, 19 trainees had completed the five-month program and returned home to conduct workshops for others in their countries. Details of the program are presented.

Communism↗
PubMedDate not supplied

Sensory nerve recovery following median nerve provocation in carpal tunnel syndrome.

The purpose of this study was to evaluate the recovery of median nerve sensory nerve action potentials (SNAP) following median nerve provocation in hands with carpal tunnel syndrome (CTS). Repeated nerve conduction measurements were performed before and after wrist flexion combined with resisted finger flexion in 35 hands with a clinical diagnosis of CTS and in 25 asymptomatic control hands. Orthodromic sensory median nerve potentials were recorded over an 8 cm segment between the palm and wrist. Hands with CTS had significant reductions in nerve potential amplitude and latency following median nerve provocation. Hands with mild to moderate CTS, had the greatest reductions in nerve potential amplitude and the longest amplitude recovery times following median nerve provocation. Determination of changes in amplitude and amplitude recovery time of the median nerve SNAP following median nerve provocation has the potential to improve the accuracy of the electrophysiological diagnosis of CTS.

Action Potentials↗