PubMed Health⌕ Search

Biomedical subjects

D H Duckworth

Publications and source records attributed to D H Duckworth.

At least 19 recordsLinked to original sources
PubMed1992

Arteriovenous differences for glutamine in the equine gastrointestinal tract.

Glutamine has been shown to be an important metabolic substrate of enterocytes in many animals, including cats, dogs, hamsters, human beings, monkeys, rabbits, rats, and sheep. To determine whether glutamine is important in the metabolism of cells of the equine gastrointestinal tract, we examined transintestinal differences in glutamine concentrations in the arterial and venous circulation, and measured activity of the major glutamine catabolizing enzyme, glutaminase. Arteriovenous differences provide an index of the amount of a given substrate removed by the tissue across which the measurements are made, and commonly are expressed as a percentage of substrate removed, or percent extraction. Arteriovenous differences for glutamine were determined in 7 anesthetized adult horses (weight, 450 to 500 kg) before and after an i.v. glutamine infusion. The mean baseline arterial glutamine concentration (+/- SEM) was 572 +/- 24 microM; this concentration quadrupled (to 2,167 +/- 135 microM, P less than 0.01) 1 minute after i.v. bolus infusion of a 17.5-g glutamine load. Baseline extraction by the portal-drained viscera was 7.5 +/- 1.5%; this value increased to 18 +/- 2% at 1 minute (P less than 0.01) and had returned to baseline values 60 minutes later. Arteriovenous differences were greatest across the jejunum (11.8 +/- 1.8% in the baseline period vs 33.1 +/- 3.1% at 1 minute, P less than 0.001), with smaller differences across the colon, suggesting that the jejunum was the more avid utilizer of glutamine. Glutaminase activity was 4.38 +/- 0.16 and 4.00 +/- 0.60 mumol/mg of protein/h under standard conditions in jejunal and ileal mucosa, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Managing psychological trauma in the police service: from the Bradford fire to the Hillsborough crush disaster.

Particularly since the Bradford football stadium fire of May 1985, the UK Police Service has been developing increasingly sophisticated procedures for managing post-traumatic stress reactions in its officers. Coupled with the growth of dedicated occupational health units within the Police Service, this suggests that physicians working within police forces will have an increasingly important role to play in the management of such problems. A brief account is given of the confidential screening and counselling service for police officers that was instituted after the Bradford fire, and a corresponding description is given of the more elaborate procedures implemented after the Hillsborough football stadium crush disaster of April 1989. In conclusion, the possible scope for preventive management of Post-traumatic stress disorder (PTSD) is highlighted.

Crowding↗
PubMed1988

ColIb plasmid genes that inhibit the replication of T5 and T7 bacteriophage.

The colicin Ib (ColIb) plasmid genes that inhibit the replication of the T5-like and T7 bacteriophage have been cloned on an approximately 7200-bp ClaI fragment and their sites relative to each other and to the colicin immunity (imm) gene have been mapped. The inhibition of wild-type T7 by the clone is shown to be caused by the same gene or genes (pic) that cause the inhibition of T7 kinase-negative mutants and is a different gene than the one that causes inhibition of T5 (ibf or abi). The pic gene does not hybridize to the pif genes of the F plasmid that also cause the replication of T7 to be inhibited. The abi gene and the pic gene map very closely together but are under the control of different promoters. The abi gene has a maximum size of 900 bp and lies approximately 3000 bp away from the immunity gene, distal to the colicin gene. A site which maps in or near the gene binds very tightly to Escherichia coli RNA polymerase. The pic gene or genes lie between the abi gene and the imm gene and are contiguous with abi. Promoters for pic have been mapped and hypotheses to explain the inhibition of T7 by a cloned gene but not the whole ColIb plasmid are presented.

Bacteriocin Plasmids↗
PubMed1986

The relationship of the delta transfer factor and KColIb to the ColIb plasmid.

The structures of the colicin Ib plasmid (ColIb), the delta transfer factor and a plasmid determining kanamycin resistance and colicin Ib production called KColIb, were compared. Radiolabelled mini-ColIb plasmids and isolated DNA fragments of ColIb were used as probes for nitrocellulose blots of digests of the other two large plasmids. The structure of delta was consistent with it having one large deletion of about 10 MDa in the SB fragment and two insertions of approximately 6 MDa and 12 MDa in the SB and SA fragments of the ColIb plasmid. It was hypothesized that KColIb had six small insertions in SA, SB, SE and near the junction of the SB and SD fragments. However, ColIb, KColIb and delta were homologous for at least 70% of their lengths. The highly conserved regions in the three plasmids were the regions that corresponded to fragments SA, SC and SD of ColIb. In addition, delta and KColIb differed from ColIb at similar sites. The possible evolution of these plasmids is discussed.

Bacteriocin Plasmids↗
PubMed1983

Inhibition of T7 bacteriophage replication by a colicin Ib plasmid gene.

Clones containing fragments of the colicin Ib (ColIb) plasmid inserted into pBR322 have been found that inhibit the replication of T7 bacteriophage. Cells containing the whole ColIb plasmid grow T7 normally but cannot grow T7 protein kinase-negative mutants of T7. The cloned fragments inhibit not only the T7 protein kinaseless mutants but wild-type T7 as well. However, the whole plasmid can suppress the wild-type T7 inhibition caused by the cloned inhibiting genes. These results are consistent with a model in which a ColIb gene (pic) exists which can inhibit replication of T7 phage. A second gene (rpi) can repress the function of pic provided the rpi product is phosphorylated.

Base Sequence↗
PubMed1983

Construction and analysis of miniplasmids of the colicin Ib plasmid.

Miniplasmids of the colicin Ib (ColIb) plasmid have been isolated from two Tn5-induced mutants of ColIb and their structure determined. These have then been used to order the sequence of restriction endonuclease fragments of the whole plasmid. In addition, the sites of the colicin, colicin immunity, and abortive infection gene have been determined in relation to the restriction sites. By comparison of the miniplasmids with other "I" incompatibility group plasmids, the probable location of the incompatibility gene and the origin of replication have been confirmed.

Base Sequence↗
PubMed1983

Location of the abi, col and imm genes on pHU011, a colicin Ib plasmid derivative.

A cleavage site map of pHU011, a derivative of the colicin Ib plasmid containing the complete SalI-B fragment ligated to pBR322, has been determined. Sites of cleavage by PstI were determined using the Smith and Birnstiel [Nucl. Acids Res. 3 (1976) 2387-2398] method of mapping, whereas those for XbaI, XhoI, and HindIII were determined by double digestions or digestion of isolated fragments. In addition, the sites of the abi gene, which causes the abortive infection by T5 bacteriophage, and of the colicin (col) gene have been determined. The results indicate that these genes are not contiguous.

Bacteriocin Plasmids↗
PubMed1981

Colicin activity and abortive infection of T5 bacteriophage in Escherichia coli (ColIb).

We performed three types of experiments to test the hypothesis that abortive infection of T5 bacteriophage in Escherichia coli (ColIb+) is due to internally released colicin. (i) We measured the sensitivity of cells to colicin under a variety of conditions and then looked at the plating efficiency of T5 in ColIb+ cells under these same conditions. Cells grown at 42 degrees C or with hexanol had a reduced sensitivity to externally added colicin and an increased efficiency for T5 when the ColIb plasmid was present in the infected cells. Phage growth was far from normal, however. (ii) We measured the colicin sensitivity of a mutant bacterium that grew T5 normally even in the presence of the ColIb plasmid and measured the plating efficiency of T5 on another mutant that was colicin tolerant. Here again, the correlation between colicin activity and inhibition of phage replication was not complete. (iii) We looked for colicin-negative plasmid mutants and tested the ability of cells containing these plasmids to support the growth of T5. These experiments used Tn5, a kanamycin resistance transposon, as the mutagen. All possible combinations of colicin production and phage inhibition were found, including mutants that produced no colicin but still inhibited phage production.

Bacteriocin Plasmids↗
PubMed1980

Fluorescence changes of a membrane-bound dye during bacteriophage T5 infection of Escherichia coli.

The fluorescence intensity of membrane-bound N-phenyl-1-naphthylamine increases dramatically when T5 bacteriophage infect colicin Ib plasmid-containing hosts. This dramatic increase is not seen during normal infections or in infections wherein either the plasmid or the phage contain mutations which allow productive infection to occur. Two smaller increases in fluorescence intensity are seen, however, in all T5 infections in which the characteristic two-step injection of DNA can proceed.

Bacteriocin Plasmids↗
PubMed1979

Amino acid and sugar transport in Escherichia coli (ColIb) during abortive infection by bacteriophage T5.

T5 bacteriophage cannot replicate in Escherichia coli containing the colicinogenic factor ColIb. We show that active transport of proline and glutamine begins to decline at about 10 min after infection, the same time at which macromolecular synthesis stops during abortive infection. Uptake of alpha-methylglucoside is stimulated, however, and this change is evident even by 5 min after infection. These changes in membrane function do not occur during infections that are productive because of mutations on the plasmid or phage. The results suggest that the abortive infection is caused by membrane depolarization.

Amino Acids↗
PubMed1979

Are class I (pre-early) proteins of bacteriophage T5 sufficient to induce abortive infection of ColIb+ Escherichia coli?

When T5 bacteriophage infect a colicin Ib-containing host, a variety of membrane changes and inhibition of macromolecular synthesis occur. This work shows that all these changes also occur when a mutant of T5 that can only inject 8% of its DNA is used. This indicates that all the information necessary for the abortive infection is present on this 8% (first-step-transfer) DNA.

Colicins↗
PubMed1977

Membrane damage in abortive infections of colicin Ib-containing Escherichia coli by bacteriophage T5.

Strains of Escherichia coli K-12 containing the colicin Ib (Col Ib) factor did not produce progeny phage when infected by T5 bacteriophage. The cells were killed but did not lyse. If sodium dodecyl sulfate (SDS) was added to T5-infected E. coli (Col Ib), lysis occurred prematurely, but no phage were produced. SDS had no effect on infected cells that did not contain the Col Ib factor or on uninfected cells with or without the Col Ib factor. Cells that contained a mutant Col Ib factor that allowed phage production were not prematurely lysed after infection in the presence of SDS. When the Col Ib-containing cells were infected, protein and RNA synthesis stopped at about 10 min postinfection, and the cells released abnormal amounts of 32P-containing material, ATP, and beta-galactosidase into the medium. They also became inhibited in their ability to accumulate thiomethyl-beta-D-galactopyranoside and to utilize glycerol. Two alternative hypotheses are presented to explain these results.

Adenosine Triphosphate↗