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Biomedical subjects

D E Taylor

Publications and source records attributed to D E Taylor.

At least 55 records · Page 3Linked to original sources
PubMed1998

The release of iron from different asbestos structures by hydrogen peroxide with concomitant O2 generation.

Treatment of aqueous suspensions of different asbestos fibers (amosite, anthophyllite, chrysotile, and crocidolite) at 0-4 degrees C and pH 7.2 with H2O2 results in the consumption of H2O2 with concomitant release of iron and production of O2. During incubations, [H2O2] decreased in proportion to the mass of the suspended fiber, the duration of incubation, and the initial [H2O2]. The consumption of H2O2, production of O2 and release of iron all vary synergistically with the structure of the asbestos fiber. Release of silicon during the incubation was small relative to the decrement in [H2O2], reflecting a lack of dissolution of the fiber. The data are consistent with a redox process for the release of surface bound iron and it is significant that iron release occurs in the absence of a Fe(II) or Fe(III) chelator. The implications of iron release from the asbestos surface may be important in inflammatory disorders in which both silicate bound iron and H2O2 accumulate.

Asbestos↗
PubMed1998

Selenium metabolism in Escherichia coli.

Escherichia coli will reduce selenite (SeO3(2-)) and selenate (SeO4(2-)) to elemental selenium Se0. Selenium will also become incorporated into proteins as part of the amino acids selenocysteine or selenomethionine. The reaction of selenite with glutathione produces selenodiglutathione (GS-Se-GS). Selenodiglutathione and its subsequent reduction to glutathioselenol (GS-SeH) are likely the key intermediates in the possible metabolic fates of selenium. This review presents the possible pathways involving selenium in E. coli. Identification of intermediates and potential processes from uptake of the toxic oxyanions through to their detoxification will assist us in understanding the complexities of metalloid oxyanion metabolism in these bacteria.

Escherichia coli↗
PubMed1998

Glucosylated N-acetyllactosamine O-antigen chain in the lipopolysaccharide from Helicobacter pylori strain UA861.

The O-antigen chain from the lipopolysaccharide of Helicobacter pylori strain UA861 was determined to be composed of an elongated type 2 N -acetyllactosamine backbone, -[-->3)-beta-D-Gal-(1-->4)-beta-D-GlcNAc-(1-]n-->, with approximately half of the GlcNAc units carrying a terminal alpha-d-Glc residue at the O -6 position. The O-chain of H.pylori UA861 was terminated by a N -acetyllactosamine [beta-D-Gal-(1-->4)-beta-D-GlcNAc] (LacNAc) epitope and did not express terminal Lewis X or Lewis Y blood-group determinants as previously found in other H.pylori strains. The absence of terminal Lewis X and Lewis Y blood-group epitopes and the replacement of Fuc by Glc as a side chain in the O-chain of H.pylori UA861 represents yet another type of lipopolysaccharide structure from H.pylori species. These structural differences in H.pylori lipopolysaccharide molecules carry implications with regard to possible different pathogenic events between strains and respective hosts.

Amino Sugars↗
PubMed1998

Helicobacter pylori--molecular genetics and diagnostic typing.

The genome of H. pylori is 1.68-1.73 Mb in size and contains a relatively low GC content (an average of 32.5 mol%). Physical and genetic maps of five H. pylori strains (NCTC 11637, NCTC 11638, NCTC 11639, UA 802 and UA 861) have been constructed and the complete genome sequence of strain 26695 has been determined. At least 50 genes, some of which play important roles in the physiology and pathogenicity of the bacterium, have been cloned. Marked genomic sequence variability has evolved from stain to strain demonstrated by random arrangement of 17 known genes on the chromosome and frequent mutations within individual genes. Based on such variability, sensitive and efficient molecular tying techniques such ribotyping, AR-PCR, PCR-RFLP, PCR-DNA sequencing and PFGE-RFLP have been developed and widely applied in both epidemiological and clinical studies of this pathogen. Subtypes of vacA (encoding a vacuolating cytotoxin) and the intermediate forms of a pathogenicity island (the cag region) have been identified in different H. pylori strains and these individual vacA subtypes are associated with specific clinical manifestations of H. pylori infection. Further studies on relationships between the genetic diversity and pathogenicity of H. pylori strains would lead to the development of novel and efficient therapeutic strategies for eradication of this microorganism.

Bacterial Typing Techniques↗
PubMed1998

The lung and Waldenström's macroglobulinemia.

We encountered a 47-year-old woman with Waldenström's macroglobulinemia (WM) manifested as lung involvement and endobronchial disease, without many of the other features common to the disease. In addition to the unusual aspects of this case, we review the clinical features of other reported cases of pulmonary involvement in WM.

Biopsy↗
PubMed1998

Host mutations (miaA and rpsL) reduce tetracycline resistance mediated by Tet(O) and Tet(M).

The effects of mutations in host genes on tetracycline resistance mediated by the Tet(O) and Tet(M) ribosomal protection proteins, which originated in Campylobacter spp. and Streptococcus spp., respectively, were investigated by using mutants of Salmonella typhimurium and Escherichia coli. The miaA, miaB, and miaAB double mutants of S. typhimurium specify enzymes for tRNA modification at the adenosine at position 37, adjacent to the anticodon in tRNA. In S. typhimurium, this involves biosynthesis of N6-(4-hydroxyisopentenyl)-2-methylthio-adenosine (ms2io6A). The miaA mutation reduced the level of tetracycline resistance mediated by both Tet(O) and Tet(M), but the latter showed a greater effect, which was ascribed to the isopentenyl (i6) group or to a combination of the methylthioadenosine (ms2) and i6 groups but not to the ms2 group alone (specified by miaB). In addition, mutations in E. coli rpsL genes, generating both streptomycin-resistant and streptomycin-dependent strains, were also shown to reduce the level of tetracycline resistance mediated by Tet(O) and Tet(M). The single-site amino acid substitutions present in the rpsL mutations were pleiotropic in their effects on tetracycline MICs. These mutants affect translational accuracy and kinetics and suggest that Tet(O) and Tet(M) binding to the ribosome may be reduced or slowed in the E. coli rpsL mutants in which the S12 protein is altered. Data from both the miaA and rpsL mutant studies indicate a possible link between stability of the aminoacyl-tRNA in the ribosomal acceptor site and tetracycline resistance mediated by the ribosomal protection proteins.

Anti-Bacterial Agents↗
PubMed1998

Site-specific mutations in the 23S rRNA gene of Helicobacter pylori confer two types of resistance to macrolide-lincosamide-streptogramin B antibiotics.

Clarithromycin resistance in Helicobacter pylori is mainly due to A-to-G mutations within the peptidyltransferase region of the 23S rRNA. In the present study, cross-resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics (MLS phenotypes) has been investigated for several clinical isolates of H. pylori. Two major types of MLS resistance were identified and correlated with specific point mutations in the 23S rRNA gene. The A2142G mutation was linked with high-level cross-resistance to all MLS antibiotics (type I), and the A2143G mutation gave rise to an intermediate level of resistance to clarithromycin and clindamycin but no resistance to streptogramin B (type II). In addition, streptogramin A and streptogramin B were demonstrated to have a synergistic effect on both MLS-sensitive and MLS-resistant H. pylori strains. To further understand the mechanism of MLS resistance in H. pylori, we performed in vitro site-directed mutagenesis (substitution of G, C, or T for A at either position 2142 or 2143 of the 23S rRNA gene). The site-directed point mutations were introduced into a clarithromycin-susceptible strain, H. pylori UA802, by natural transformation followed by characterization of their effects on MLS resistance in an isogenic background. Strains with A-to-G and A-to-C mutations at the same position within the 23S rRNA gene had similar levels of clarithromycin resistance, and this level of resistance was higher than that for strains with the A-to-T mutation. Mutations at position 2142 conferred a higher level of clarithromycin resistance than mutations at position 2143. All mutations at position 2142 conferred cross-resistance to all MLS antibiotics, which corresponds to the type I MLS phenotype, whereas mutations at position 2143 were associated with a type II MLS phenotype with no resistance to streptogramin B. To explain that A-to-G transitions were predominantly observed in clarithromycin-resistant clinical isolates, we propose a possible mechanism by which A-to-G mutations are preferentially produced in H. pylori.

Anti-Bacterial Agents↗
PubMed1998

Genotypic characterization of clarithromycin-resistant and -susceptible Helicobacter pylori strains from the same patient demonstrates existence of two unrelated isolates.

Clarithromycin-susceptible and clarithromycin-resistant Helicobacter pylori isolates from the same patient were investigated for the mode of development and mechanism of clarithromycin resistance. The clarithromycin-resistant strain UA1182 harbors homozygous A-to-G mutations at position 2143 in both copies of the 23S rRNA gene and has a phenotype of resistance to clarithromycin and clindamycin but no significant resistance to streptogramin B. Pulsed-field gel electrophoresis patterns of NruI- and NotI-digested genomic DNA from the Clas and Clar isolates demonstrated that they are genetically distinct, suggesting that the development of clarithromycin resistance is not from the mutation of the existing Clas strain but from a completely new strain.

Anti-Bacterial Agents↗
PubMed1998

Mitochondrial respiration after sepsis and prolonged hypoxia.

Recently, marked oxygen dependence of respiration by isolated mitochondria after exposure to prolonged hypoxia has been described. Because mitochondrial oxygen-dependent respiration could significantly influence oxygen consumption during critical illness, we sought to confirm the oxygen-dependent behavior of mitochondria. We hypothesized that mitochondria isolated during sepsis would exhibit increased oxygen dependence. We isolated rat liver mitochondria 16 h after cecal ligation and puncture and found a 30-40% greater oxygen uptake compared with control rats under state 3 conditions. Mitochondria incubated in deoxygenated buffer were studied for oxygen dependence at 10-min intervals for 90 min. Mitochondrial respiration after reoxygenation was stable over a 60-min period of hypoxia for control rats and decreased slightly for septic rats (10-15%). State 3 respiration was 10% lower when mitochondria were reoxygenated at low (15-25 Torr) versus high (90-100 Torr) and low (10-15 Torr) versus intermediate (40-45 Torr) oxygen tension. Oxygen consumption with ascorbate+N, N, N', N'-tetramethyl-p-phenylenediamine was 20% lower at low versus high oxygen tension. No increase in oxygen dependence was observed during 1 h of hypoxic incubation. Our data indicate only a modest oxygen dependence of respiration between 10 and 100 Torr, which is similar for septic and control mitochondria. Additionally, oxygen dependence did not increase significantly during a 1-h hypoxic exposure for well-coupled mitochondrial preparations.

Animals↗
PubMed1998

Ribosomal protection from tetracycline mediated by Tet(O): Tet(O) interaction with ribosomes is GTP-dependent.

Tet(O) mediates tetracycline resistance by protecting the ribosome from inhibition. A recombinant Tet(O) protein with a histidine tag was purified and its activity in protein synthesis characterized. Tetracycline inhibited the rate of poly(Phe) synthesis, producing short peptide chains. Tet(O)-His was able to restore the elongation rate and processivity. 70S ribosomes bound tetracycline with high affinity. Tet(O)-His in the presence of GTP, but not GDP or GMP, reduced the affinity of the ribosomes for tetracycline. Non-hydrolyzable GTP analogs in the presence of the factor were also able to interfere with tetracycline binding. Ribosomes increased the affinity of Tet(O)-His for GTPgammaS. Tet(O), 70S ribosomes and GTPgammaS formed a complex that could be isolated by gel filtration. The GTP conformer is the active form of Tet(O) that interacts with the ribosome. GTP binding is necessary for Tet(O) activity.

Bacterial Proteins↗
PubMed1998

Effects of cold and compression dressings on early postoperative outcomes for the arthroscopic anterior cruciate ligament reconstruction patient.

Efforts to minimize the morbidity of anterior cruciate ligament (ACL) reconstruction include the use of cryotherapy and/or compressive dressings in the immediate postoperative period. We undertook the present study to determine if the alleged benefits of the Cryo/Cuff, which combines these modalities, are more attributable to its compressive effect rather than cold application. Seventy-eight patients admitted for primary endoscopic ACL reconstruction using a bone-patella tendon-bone autograft were randomized to receive Cryo/Cuff compressive dressings postoperatively. Forty subjects (Group 1) had the cuff applied with continuous circulating ice water using the Autochill device, while 38 others (Group 2) received the cuff with room temperature water. Cases were performed as inpatients and all subjects were administered intravenous morphine postoperatively via a patient-controlled infusion pump for the first 24 postoperative hours. At baseline, the groups were well matched in age, sex, duration of symptoms, operative time, and associated meniscal surgery. No significant difference between groups was detected with respect to length of hospitalization, Hemovac knee drainage, oral and intravenous narcotic requirement, or subjective pain as measured by a visual analog scale. No apparent complications related to the use of the Cryo/Cuff dressings were noted. The clinical effect of the Cryo/Cuff in this study was not influenced by the use of continuous ice water vs. room temperature water. Further study should focus on variations in compression to evaluate the clinical impact of this device.

Adult↗
PubMed1998

Revving the motor of multiple organ dysfunction syndrome. Gut dysfunction in ARDS and multiorgan failure.

Despite its initial description as primarily a pulmonary disorder, the acute respiratory distress syndrome (ARDS) has been recognized as one component of a systemic disorder associated with microvascular permeability and widespread organ involvement that often afflicts the gastrointestinal tract. Although a healthy gut is an important defense for the body, its unique vascular anatomy and its predisposition toward ischemia and mucosal hypoxia put the gastrointestinal tract at high risk of injury during the course of the systemic inflammatory response syndrome. Once the mucosa is damaged and host defenses break down translocation of bacteria and bacterial toxins is likely to contribute to the inflammation associated with sepsis and ARDS. Gastric tonometry offers a potentially useful mechanism to monitor regional perfusion and oxidative metabolism in the splanchnic vascular bed. Many studies have shown that tonometry can assist the clinician on prognostic assessment of patients. Several studies also have demonstrated improved patient outcome when therapies aimed to protect the GI tract are aggressively pursued with tonometric guidance.

Carbon Dioxide↗
PubMed1997

Cloning and functional characterization of Helicobacter pylori fumarate reductase operon comprising three structural genes coding for subunits C, A and B.

In this study, we cloned and sequenced the Helicobacter pylori genes encoding fumarate reductase (FRD). H. pylori frdA, frdB and frdC specify polypeptides of 715, 245 and 254 aa, respectively. The deduced aa sequences of FrdA and FrdB are highly homologous to those of the corresponding subunits of Wolinella succinogenes FRD and also exhibit a significant sequence identity with other bacterial FRD and succinate dehydrogenase subunits A and B. However, H. pylori FrdC shares a striking degree of sequence identity only with W. succinogenes FrdC, which is a cytochrome b with two haem groups. The products encoded by H. pylori frdA, frdB and frdC were overproduced in maxicells and H. pylori FrdA was characterized using an anti-E. coli FrdA serum. H. pylori FRD activity, which was measured as fumarate-dependent benzyl viologen oxidation, is membrane-associated. Inactivation of frdA led to the loss of such activity and the mutant H. pylori cells were delayed (approx. 10-20 h behind their parent cells) in entering the mid-log phase, suggesting that FRD-driven metabolism plays an active but non-essential role for growth of H. pylori cells in vitro. H. pylori FRD contains three subunits, of which FrdA and FrdB appear to form the catalytic dimer, whereas FrdC serves as a membrane anchor.

Amino Acid Sequence↗
PubMed1997

Oxidative metabolism in rat hepatocytes and mitochondria during sepsis.

We hypothesized that cellular oxygen consumption is abnormal during sepsis as a result of increased oxidative stress and selective mitochondrial damage. In a rat model of sepsis (cecal ligation and puncture), we studied the respiratory characteristics of isolated hepatocytes and liver mitochondria 16 h after onset of septic injury. Endogenous respiration by isolated cells was decreased during sepsis, while cyanide-resistant (nonmitochondrial) respiration was unaffected. Maximal oxygen consumption in ADP-supplemented, permeabilized hepatocytes was decreased with succinate as the substrate, but not with malate + glutamate or TMPD + ascorbate. In contrast, maximum oxygen consumption (State 3) by isolated liver mitochondria increased up to 35% during sepsis using either succinate or malate + glutamate as substrate. The electrophoretic features and mobility of nondenatured mitochondrial respiratory complexes were similar in control and septic hepatocytes, with the exception of decreased Complex V protein in sepsis. Structural evaluation of mitochondria in fixed liver slices by electron microscopy showed mitochondrial swelling in most of the septic animals. Measurements of oxidative stress during sepsis suggested an increase in hydroxylation of salicylate by isolated hepatocytes, and mitochondrial protein carbonyl content was increased significantly. Induction of iNOS in hepatocytes after 16 h of sepsis was variable, and little release of the oxidation products of NO. was detected. These findings are interpreted to mean that hepatocytes contain a mixed population of injured and hyperfunctional mitochondria during sepsis.

Animals↗
PubMed1997

Cloning and heterologous expression of an alpha1,3-fucosyltransferase gene from the gastric pathogen Helicobacter pylori.

Helicobacter pylori is an important human pathogen which causes both gastric and duodenal ulcers and is also associated with gastric cancer and lymphoma. This microorganism has been shown to express cell surface glycoconjugates including Lewis X (Lex) and Lewis Y. These bacterial oligosaccharides are structurally similar to tumor-associated carbohydrate antigens found in mammals. In this study, we report the cloning of a novel alpha1,3-fucosyltransferase gene (HpfucT) involved in the biosynthesis of Lex within H. pylori. The deduced amino acid sequence of HpfucT consists of 478 residues with the calculated molecular mass of 56,194 daltons, which is approximately 100 amino acids longer than known mammalian alpha1,3/1,4-fucosyltransferases. The approximately 52-kDa protein encoded by HpfucT was expressed in Escherichia coli CSRDE3 cells and gave rise to alpha1,3-fucosyltransferase activity but neither alpha1,4-fucosyltransferase nor alpha1,2-fucosyltransferase activity as characterized by radiochemical assays and capillary zone electrophoresis. Truncation of the C-terminal 100 amino acids of HpFuc-T abolished the enzyme activity. An approximately 72-amino acid region of HpFuc-T exhibits significant sequence identity (40-45%) with the highly conserved C-terminal catalytic domain among known mammalian and chicken alpha1,3-fucosyltransferases. These lines of evidence indicate that the HpFuc-T represents the bacterial alpha1,3-fucosyltransferase. In addition, several structural features unique to HpFuc-T, including 10 direct repeats of seven amino acids and the lack of the transmembrane segment typical for known eukaryotic alpha1,3-fucosyltransferases, were revealed. Notably, the repeat region contains a leucine zipper motif previously demonstrated to be responsible for dimerization of various basic region-leucine zipper proteins, suggesting that the HpFuc-T protein could form dimers.

Amino Acid Sequence↗
PubMed1997

Acrolein-induced cell death in human alveolar macrophages.

Acrolein is an environmental air pollutant that is known to suppress respiratory host defense against infections. The mechanism of the decrease in host defense is not yet clear. In this study, the effects of acrolein on human alveolar macrophages and their function were examined. Acrolein caused dose-dependent cytotoxicity to alveolar macrophages as demonstrated by the induction of apoptosis and necrosis. In addition, at lower doses, acrolein caused induction of heme oxygenase 1 protein; however, stress protein 72 (SP72) was not induced. These findings demonstrated that acrolein caused a dose-dependent selective induction of a stress response, apoptosis, and necrosis in human alveolar macrophages. Macrophage function was assessed by release of cytokines in response to endotoxin stimulation. Acrolein caused a dose-dependent inhibition of release of IL-1beta, TNF-alpha, and IL-12. The inhibition of cytokine release and cytotoxicity to alveolar macrophages may in part be responsible for acrolein-induced immunosuppression of the lung.

Acrolein↗
PubMed1997

Measurement of gastric mucosal carbon dioxide tension by saline and air tonometry.

PURPOSE: This study compares the balloon air tonometry method of measuring gastric mucosal CO2 to standard saline tonometry. Also, this study investigates the effect of histamine-2 receptor blockade on the precision of tonometric measures of gastric mucosal PCO2 (PtCO2). MATERIALS AND METHODS: We obtained hourly measurements of PtCO2 from two gastric tonometers inserted orally in 19 healthy volunteers. One tonometer measured PtCO2 by the intermittent saline method, whereas the other measured PtCO2 using a newer continuous air method. Subjects received intravenous 5% dextrose during the first 6 hours of the experiment followed by a continuous infusion of a solution of ranitidine in 5% dextrose for another 6 hours. The ranitidine infusion was titrated to maintain gastric fluid pH > or = 4. RESULTS: Comparison of air to saline tonometry yielded a bias of -1.3 mm Hg with a limit of agreement of 6.6 mm Hg under optimal conditions of optimal gastric fluid pH (gastric fluid pH > or = 5.0). Measures of PtCO2 were lower with ranitidine for either group, 45.3 +/- 1.3 mm Hg versus 39.7 +/- 0.5 mm Hg for saline (P < .01) and 45.9 +/- 1.0 versus 41.3 +/- 0.5 for air (P < .01). The mean PCO2 gap (PtCO2-P(arterial)CO2) at gastric fluid pH > or = 5.0 was 1.4 mm Hg, with a standard deviation of 2.7 mm Hg. A span of three standard deviations yields a normal limit for PCO2 gap of 9.5 mm Hg. CONCLUSION: Measures of PtCO2 with the air tonometer method are similar to those obtained with saline tonometry. The reliability of PtCO2 measurements with either method improved with the use of ranitidine to maintain gastric fluid pH > or = 5.

Adult↗