Severe toxic laryngo-tracheo-bronchitis in a drunken man.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to A Ritter.
Explore the source record for details and available documents.
Dental hygienists perform tasks that are repetitive, strenuous, and can contribute to cumulative trauma disorders (CTDs) of the upper body. Besides prevalent disorders of the hand and wrist, such as carpal tunnel syndrome (CTS), there are many other upper extremity disorders, including thoracic outlet syndrome (TOS). If a dental hygienist can identify symptoms and seek treatment early, prognosis for recovery is greatly improved.
Explore the source record for details and available documents.
The described method permits the determination of the five most important metabolites of the pyrethroids permethrin, cypermethrin, deltamethrin, lambda-cyhalothrin, fenvalerate, phenothrin and beta-cyfluthrin in human urine in one run. The major urinary metabolites of these substances are cis-3-(2,2-dichlorovinyl)-2,2-dimethylcyclopropane-1-carboxylic acid (cis-Cl2CA), trans-3-(2,2-dichlorovinyl)-2,2-dimethylcyclopropane-1-carboxylic acid (trans-Cl2CA), cis-3-(2,2-dibromovinyl)-2,2-dimethylcyclopropane-1-carboxylic acid (Br2CA), fluoro-3-phenoxybenzoic acid (F-PBA) and 3-phenoxybenzoic acid (3-PBA). After acidic hydrolysis to release the conjugated carboxylic acid metabolites, the analytes were separated from the matrix by means of solid-phase extraction using a reversed-phase column. The components of the eluate were converted to their methyl esters and extracted in hexane. Separation and quantitative analysis of the pyrethroid metabolites was carried out by capillary gas chromatography and mass selective detection. 2-Phenoxybenzoic acid served as an internal standard. The detection limits lay between 0.3 and 0.5 microg per litre urine. The relative standard deviations of the within-series imprecision were between 1% and 6%. The relative recovery rates ranged between 90% and 98%. Using this method we determined the elimination of pyrethroid metabolites in 24-h urine samples from eight pest controllers after indoor application of permethrin. The detected concentrations ranged from 1 to 70 microg g(-1) creatinine.
Previous analyses of the Wechsler Memory Scale-Revised (WMS-R; Wechsler, 1987) have reported one-, two-, and three-factor solutions and raised questions about the validity of the visual memory subtests. These various findings may stem in part from different methods of analysis, and from the study of different participant samples. To address these issues, we analysed data from the WMS-R and a spatial maze test administered to 154 participants with a history of alcohol dependence. Results from confirmatory factor analysis supported the interpretation of three factors underlying the WMS-R subtests and the spatial maze score in this sample, namely, attention-concentration, immediate memory, and delayed recall. This result held despite the inclusion of the maze score which is a well-validated measure of visuo-spatial memory.
The uropathogenic Escherichia coli strain 536 (06:K15:H31) carries two large chromosomal pathogenicity islands (Pais). Both Pais are flanked by tRNA genes. Spontaneous deletion of Pai II results in truncation of the leuX tRNA5Leu gene. This tRNA is required for the expression of type 1 fimbriae (Fim) and other virulence factors. Transcription of fimA, encoding the major type 1 fimbrial subunit is controlled by an invertable DNA switch. The inversion is catalysed by two recombinases, FimB and FimE. FimB is able to turn the switch on, FimE only off. The fimB gene of strain 536 contains five TTG codons recognized by tRNA5Leu, fimE contains only two. It was proposed that turning on the fim switch requires efficient translation of FimB, in turn requiring tRNA5Leu. Strains in which the TTG codons in fimB were replaced with CTG codons at the wild-type locus were able to produce type 1 fimbriae in the absence of leuX. fimB transcription was influenced by the presence of leuX, but only slightly affected by the presence or absence of leuX codons in fimB. FimB translation was significantly higher from codon-replaced fimB genes than that of wild-type fimB genes in various strain backgrounds. The fim switch was shown to be switched off in leuX-derivatives of E. coli 536, but could be found in the on position when the codon-altered fimB gene was exchanged into the chromosome of these strains. From these data, it is apparent that tRNA5Leu is required for efficient translation of FimB, in turn, leading to type 1 fimbrial expression.
OBJECTIVE: The purpose of this project was to develop a computer model of cerebrovascular hemodynamics interacting with a pharmacokinetic drug model to examine the effects of various stimuli on cerebral blood flow and intracranial pressure during anesthesia. METHODS: The mathematical model of intracranial hemodynamics is a seven-compartment, constant-volume system. A series of resistance relate blood and cerebrospinal fluid fluxes to pressure gradients between compartments. Arterial, venous, and tissue compliance are also included. Autoregulation is modeled by transmural pressure-dependent, arterial-arteriolar resistance. The effect of a drug (thiopental) on cerebrovascular circulation was simulated by a variable arteriolar-capillary resistance. Thiopental concentration was predicted by a three-compartment, pharmacokinetic model. The effect site compartment was included to account for a disequilibrium between drug plasma and biophase concentrations. The model was validated by comparing simulation results with available experimental observations. The simulation program is written in VisSim dynamic simulation language for an IBM-compatible PC. RESULTS: The model developed was used to calculate the cerebral blood flow and intracranial pressure changes that occur during the induction phase of general anesthesia. Responses to laryngoscopy and intubation were predicted for simulated patients with elevated intracranial pressure and non-autoregulated cerebral circulation. Simulation shows that the induction dose of thiopental reduces intracranial pressure up to 15%. The duration of this effect is limited to less than 3 minutes by rapid redistribution of thiopental and cerebral autoregulation. Subsequent laryngoscopy causes acute intracranial hypertension, exceeding the initial intracranial pressure. Further simulation predicts that this untoward effect can be minimized by an additional dose of thiopental administered immediately prior to intubation. CONCLUSION: The presented simulation allows comparison of various drug administration schedules to control intracranial pressure and preserve cerebral blood flow during induction of anesthesia. The model developed can be extended to analyze more complex intraoperative events by adding new submodels.
The uropathogenic Escherichia coli strain 536 (O6:K15:H31) possesses pathogenicity islands which are incorporated into two tRNA genes, the selC and the leuX gene. The leuX gene influences the expression of different putative virulence factors. We demonstrate an effect of the leuX-specific tRNA on adherence and uropathogenicity.
Investigations of the regulation of the bacteriophage-encoded Shiga-like toxin II (SLT-II) in Escherichia coli demonstrated that bacteriophages exhibit a regulatory impact on toxin production by two mechanisms. Firstly, replication of the toxin-converting bacteriophages brings about an increase in toxin production due to concomitant multiplication of toxin gene copies. Secondly, an influence of a phage-encoded regulatory molecule was demonstrated by using low-copy-number plasmid pADR-28, carrying a translational gene fusion between the promoter and proximal portion of slt-IIA and the structural gene for bacterial alkaline phosphatase (phoA). PhoA activity, reflecting the slt-II promoter activity, was significantly enhanced in E. coli strains which and been lysogenized with an SLT-I or SLT-II-converting bacteriophage (H-19B or 933W, respectively) or bacteriophage lambda. Both mechanisms are dependent on bacteriophage induction and hence are recA dependent. Moreover, the study revealed that the DNA-binding protein H-NS has a regulatory impact on both bacteriophage-mediated SLT-II synthesis and the activity of the slt-II promoter of plasmid pADR-28. While a slight impact of growth temperature on SLT-II expression was observed, no impact of either osmolarity, pH, oxygen tension, acetates, iron level, or utilized carbon source could be demonstrated.
Explore the source record for details and available documents.
The uropathogenic Escherichia coli strain 536 (O6:K15:H31) carries two unstable DNA regions on its chromosome which were termed pathogenicity islands (Pais). Both pathogenicity islands, Pai I and Pai II, are incorporated into tRNA specific loci: Pai I is located in the tRNA gene for selenocysteine (selC), and Pai II is integrated in the leucine-specific tRNA locus leuX. Mutant strain 536-21 has lost the two pathogenicity islands together with the intact tRNA genes. While 536 is a virulent strain, 536-21 has lost a number of properties, including in vivo virulence. In previous publications we reported that the genes coding for two haemolysins (hly I, hly II) and P-related fimbria (prf) are located on the Pais. In this paper, we demonstrate that the expression of other gene products influencing metabolic properties in addition to in vivo virulence are strongly dependent on the intact tRNA loci selC and leuX. In order to determine the influence of the two tRNAs on the expression of these properties, the genes selC and leuX were cloned from the genome of strain 536 and then introduced into the mutant 536-21. Our results clearly show that the seleno-cysteine-specific tRNA (tRNA(Sec)) directly influences the ability of the bacteria to grow under anaerobic conditions, because selenocysteine is part of the enzyme formate dehydrogenase (FDH) which is involved in mixed acid fermentation. The rare leucine-specific tRNA5(Leu), encoded by leuX, influences a number if properties including type 1 fimbria production, flagellation and motility, production of enterobactin and serum resistance, and is also necessary for full in vivo virulence. While the tRNA(Sec) is directly involved in the production of FDHs, the leuX specific tRNA5(Leu) appears to influence the expression of various factors through specific transcriptional or translational control mechanisms.
The isolated spinal cord of the chick embryo generates episodes of rhythmic bursting in which sartorius (hip flexor) and femorotibialis (knee extensor) motoneurons exhibit characteristic patterns of activity. At the beginning of each cycle both sets of motoneurons discharge synchronously. Following this brief synchronous activation sartorius motoneurons stop firing at the time of peak femorotibialis activity, producing a period of alternation between the two sets of motoneurons. Intracellular recording from motoneurons has suggested that the pause is mediated by a synaptically induced shunt conductance. However, the pharmacological basis for this shunt and the nature of the excitatory drive to motoneurons is unknown. To address these questions we have investigated the pharmacology of the rhythmic, synaptic drive to lumbosacral motoneurons using local and bath application of several excitatory and inhibitory antagonists, and documenting their effects on motor output in E10-E12 chick embryos. Local application of bicuculline or picrotoxin over sartorius motoneurons abolished the pause in firing recorded from the sartorius muscle nerve. As a consequence, the pattern of sartorius and femorotibialis activity was similar and the motoneurons were coactive. The pause in sartorius firing was shortened following local application of the glycine antagonist strychnine the nicotinic, cholinergic antagonists mecamylamine, and dihydro-beta-erythroidine and several excitatory amino acid antagonists. Application of the GABA uptake inhibitor nipecotic acid depressed the slow potentials and discharge recorded from the sartorius muscle nerve. These findings suggest that the pause is determined primarily by synaptic inputs acting at motoneuron GABAA receptors with contributions from glycinergic, cholinergic, and glutamatergic inputs. The actions of locally applied GABA onto spinal neurons are consistent with these findings because the neurotransmitter depolarizes spinal neurons and reduces their input resistance. Local application of bicuculline, but not strychnine, onto segments containing femorotibialis motoneurons altered the amplitude and duration of femorotibialis discharge and changed the profile of the slow potentials recorded from the muscle nerve. This finding implicates GABAergic inputs in the regulation of femorotibialis discharge. The pause in sartorius firing was still present and a pause in firing appeared in each cycle of femorotibialis discharge following bath application of bicuculline or strychnine. The pause in both sets of motoneurons could be abolished by local application of the NMDA receptor antagonist AP-5 onto the motoneurons, but not by local application of bicuculline. This action of AP-5 was in contrast to its activity in normal Tyrode's solution where it shortened the pause slightly.(ABSTRACT TRUNCATED AT 400 WORDS)
Explore the source record for details and available documents.
Recombinant antigens from hepatitis E virus (HEV) open-reading frames 2 and 3 were expressed in Escherichia coli as cytidine monophosphate-2-keto-3-deoxyoctulosonic acid synthetase (CKS) fusion proteins, purified, and used to develop an EIA for the detection of antibodies. Serologic results were compared with those of previous assays by testing 102 samples from an HEV outbreak in Somalia. This CKS/HEV EIA detected anti-HEV in all 97 sera found reactive previously and in an additional 2 samples, which were shown to be true HEV-positive samples by supplemental peptide and Western blot tests. The CKS/HEV EIA and supplemental assays were then used to determine seroprevalence of HEV worldwide. HEV seroprevalence ranged from 1% to 25%, with higher rates found in Middle Eastern countries. Also, 7%-14% of acute cases of non-A, -B, or -C hepatitis were HEV-positive. Thus, this CKS/HEV EIA appears useful for detecting anti-HEV in various populations.
Uropathogenic Escherichia coli 536 (O6:K15:H31) carries two unstable DNA regions, which were shown to be responsible for virulence. These regions, on which the genes for hemolysin production (hly) and P-related fimbriae (prf) are located, are termed pathogenicity islands (PAI) I and II, and were mapped to positions 82 and 97, respectively, on the E. coli K-12 linkage map. Sequence analysis of the PAI region junction sites revealed sequences of the leuX and selC loci specific for leucine and selenocysteine tRNAs. The tRNA loci function as the targets for excision events. Northern (RNA) blot analysis revealed that the sites of excision are transcriptionally active in the wild-type strain and that no tRNA-specific transcripts were found in the deletion mutant. The analysis of deletion mutants revealed that the excision of these regions is specific and involves direct repeats of 16 and 18 nucleotides, respectively, on both sides of the deletions. By using DNA long-range mapping techniques, the size of PAI I, located at position 82, was calculated to be 70 kb, while PAI II, mapped at position 97, comprises 190 kb. The excision events described here reflect the dynamics of the E. coli chromosome.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The chromosomally encoded nonfimbrial adhesion I (NFA-I) from Escherichia coli urinary tract isolate 827 (O83:K1:H4) mediates agglutination of human erythrocytes. Subclones were constructed from an NFA-I-expressing recombinant E. coli K-12 clone, derived from a genomic library of E. coli 827. Minicell analysis and nucleotide sequencing revealed that proteins of 30.5, 9, 80, 15, and 19 kDa encoded on a stretch of approximately 6 kb are involved in the expression of NFA-I. NFA-I exhibits a polymeric structure, which disintegrates with elevated temperature into a 19-kDa monomer but with some relatively stable dimers. By using gold-conjugated monoclonal antibodies directed against NFA-I in electron microscopy, the adhesin could be localized on the outer surface of the recombinant E. coli K-12 bacteria. The nucleotide sequence of the nfaA gene encoding the monomeric structural subunit of the adhesin was determined. An open reading frame of 184 amino acids encoding the NfaA precursor, which is processed to the mature protein, was found; it consisted of 156 amino acids with a calculated molecular weight of 16,000. Peptide sequencing of the NFA-I subunit protein confirmed that this open reading frame corresponds to the NfaA coding locus. Furthermore, the nucleotide sequence of the open reading frame termed NfaE, located at the proximal part of the DNA stretch responsible for NFA-I expression, was elaborated. NfaE consists of 247 amino acids, including a presumptive 29-amino-acid signal peptide, leading to a molecular weight of 24,000 for the mature protein. The nfaE sequence shares homology with the 27-kDa CS3 protein, which is involved in the assembly of CS3 fibrillae, and might encode the 30.5-kDa protein, detected in minicells.