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Biomedical subjects

W Jordan

Publications and source records attributed to W Jordan.

At least 37 records · Page 2Linked to original sources
PubMed1988

Upper respiratory tract infection and serum antibody responses in nursing home patients.

Residents of a Veterans Administration nursing home care unit (NHCU) were observed for the development of upper respiratory tract infection (URI) during 12 consecutive months to determine the frequency of sporadic cases or outbreaks of URI and to characterize them clinically and by laboratory means. Fifty-nine episodes of URI occurred in 56 residents during the study period. Serologic testing or virus isolation proved or suggested an etiologic agent on 22 occasions. URI was more common in late Fall and Winter and was caused by various agents, including influenza, Mycoplasma pneumoniae, respiratory syncytial virus, and parainfluenza viruses. A minor outbreak of influenza B in February 1986 contrasted with previous cases of URI in that the patients had a higher mean temperature and abnormal breath sounds, and they were clinically sicker. This suggests that clinical and epidemiologic surveillance during the influenza season may allow the early recognition of influenza in elderly nursing home residents. Over a 4-year period 147 serum antibody responses after influenza infection or influenza vaccination were compiled. Antibody responses to individual influenza vaccine components were measured 75 to 90 days after vaccination. The geometric mean titer (GMT) and the percentage of samples with antibody levels greater than 1:40 were determined for each of the three antigenic subtypes on 3 consecutive years. The GMT to individual vaccine components was consistently greater than 1:40, except to influenza B/Singapore in 1984 and A/Chile and B/U.S.S.R. in 1985, when these subtypes were first included in the vaccine, suggesting the NHCU residents responded less vigorously to unfamiliar vaccine subtypes.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Evidence for a magnesium-insensitive membrane resistance increase during NMDA-induced depolarizations in rat neocortical neurons in vitro.

The responses of rat neocortical neurons in vitro to iontophoretically applied N-methyl-D-aspartate (NMDA) were investigated by means of intracellular recording in the presence and absence of extracellular magnesium ions (Mg2+). At Mg2+-concentrations of 1.3 mM the neurons responded with a depolarization accompanied by an increase in membrane resistance. Upon removal of Mg2+ the NMDA-induced depolarization was markedly potentiated. However, even in neurons recorded from slices which were incubated in a Mg2+-free solution for 3-7 h, the NMDA response was still associated with a resistance increase, suggesting that the voltage-dependence of the NMDA-activated conductance is not exclusively determined by Mg2+.

Animals↗
PubMed1987

Diversity of plasmids in Achromobacter xylosoxidans isolates responsible for a seemingly common-source nosocomial outbreak.

Achromobacter xylosoxidans, an uncommon yet highly resistant opportunistic pathogen, was isolated from nine hospitalized patients during an 8-month period. It had been isolated from only seven patients with either nonfatal infection or colonization from 1981 to 1984. From June 1985 to January 1986, A. xylosoxidans was isolated 18 times from seven different sites (sputum, 7 times; urine, 4 times; blood, 3 times; and lung, pleural fluid, wound tissue, and tracheal aspirate, 1 time each). Four patients died, including the three with bacteremia. All but two patients had nosocomial infections and either were on the same ward or were cared for by the same staff members. Eleven A. xylosoxidans strains yielded eight distinct plasmids (8, 21, 23, 26, 38, 50, 51, and 64 megadaltons). Whole-cell peptide patterns of 10 of these strains were determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Isolates from the same patient contained the same plasmids and had identical peptide patterns but differed from other strains in both parameters. Plasmids were absent from the two community-acquired isolates. Although nosocomial strains showed similar antibiotic resistance patterns (only moxalactam and ticarcillin-clavulanic acid were uniformly active) and cross-contamination was strongly suggested epidemiologically, results of plasmid and peptide analyses did not support the possibility of a single-strain outbreak.

Adult↗
PubMed1986

Corticosterone reduces the excitability of hippocampal pyramidal cells in vitro.

In the rat brain, the hippocampus (HC) is a major target area for corticosterone (CT). In this study, we investigated the effects of CT in the in vitro slice preparation of the rat HC. Population spikes (PS) evoked by stratum radiatum stimulation were recorded in CA1. Bath-applied CT (10(-7)-10(-5) M) induced a decrease in the PS amplitude. This effect occurred within 10-15 min after the onset of CT perfusion, reached a plateau after 20-40 min and was reversible after 20 min washout. Neither dexamethasone (10(-5) M) nor vehicle produced any significant change in PS amplitude. Paired-pulse stimulation showed that the degree of inhibition of the second PS produced by the conditioning stimulus was either unchanged or decreased by CT. In the latter case, CT also reduced the inhibitory effect of gamma-aminobutyric acid on PS and enhanced the excitatory action of the opioid peptide D-Ala2-D-Leu5-enkephalin. These results show that CT reduces the excitability of HC pyramidal cells with a time course which may be compatible with a genomic action of CT. The fact that paired-pulse inhibition was either not changed or reduced, suggests that the decrease in PS size by CT is not due to an indirect excitatory effect of CT on inhibitory interneurons. Instead, CT may hyperpolarize pyramidal cells thus lowering their excitability and depressing the interneurons involved in recurrent inhibition.

Animals↗
PubMed1986

The mitochondrial site of superoxide formation.

Ubiquinone and cytochrome b566 have both been postulated to cause mitochondrial O2 formation by autoxidation of their reduced forms. The present investigation was made to evaluate capabilities of the two candidates to transfer electrons to molecular oxygen out of sequence of the normal pathway of respiration. The results show that electron transfer from ubisemiquinone to oxygen depends on the availability of protons. In agreement with this finding autoxidation of redox cycling ubiquinone could not be observed due to its location in an aprotic environment of the mitochondrial membrane. However, O2 release from mitochondria was found to be related to the existence of low potential cytochrome b566. The transfer of this b type cytochrome to more positive values caused a concomitant decrease and finally inhibition of univalent electron transfer to oxygen out of sequence. Our findings suggest a role of cytochrome b 566 in mitochondrial O2 formation. A contribution by ubiquinone is unlikely as long as protons are deprived from penetrating into the domain where ubiquinone is operating.

Aerobiosis↗
PubMed1983

OH.-generation by adriamycin semiquinone and H2O2; an explanation for the cardiotoxicity of anthracycline antibiotics.

Anthracycline-induced cardiomyopathy is still a matter of discussion. The many mechanisms proposed cannot explain a selective sensitivity of the heart to these antitumor drugs. The present paper provides experimental evidence which shows that heart tissue has special biochemical conditions which favour an anthracycline-catalysed electron shuttle to H2O2. This results in the generation of highly reactive OH.-radicals, instead of O-.2-radicals, which are expected to be formed in tissues also supplemented with anthracycline-activating microsomal enzyme systems.

Animals↗
PubMed1982

Tolbutamide enhancement of ouabain cardiotoxicity in rabbits.

The amount of ouabain necessary to produce ventricular fibrillation (VF) was significantly decreased by 2-hour pretreatment with 50, 100 or 200 mg/kg tolbutamide in anesthetized rabbits. The two higher doses also decreased the dose of ouabain needed to produce ventricular ectopic (VE) beats. Only the 200 mg/kg dose decreased blood glucose. In unanesthetized rabbits, 30-min pretreatment with tolbutamide (200 mg/kg i.v.) significantly decreased the doses of ouabain that produced VE beats and VF. A similar effect was noted when the same dose (200 mg/kg) was given subcutaneously 30 min, 2 or 4 h before ouabain. In these experiments blood glucose decreased after 1 h. Pretreatment for 30 min with subcutaneous administration of 50, 100 or 200 mg/kg tolbutamide significantly reduced the doses of ouabain needed to produce VE beats and VF. Blood glucose was unaltered by any tolbutamide dose after 30 min. Insulin (1 unit) decreased blood glucose but did not alter the amount of ouabain that produced VE beats and VF. The mechanism for enhancement of ouabain cardiotoxicity by tolbutamide appears to be independent of alterations in blood glucose and may be related to some direct myocardial effect.

Anesthesia↗
PubMed1981

Reduction of chronic daunorubicin cardiotoxicity by ICRF-187 in rabbits.

To determine whether ICRF-187 (NSC-169780) would alter chronic daunorubicin (NSC-82151) cardiac toxicity, male New Zealand rabbits were given 3.2 mg/kg or daunorubicin iv alone or 30 minutes after 12.5 or 25.0 mg/kg of ICRF-187 ip at 3-week intervals. Control rabbits received either saline iv or ICRF-187 (12.5 or 25.0 mg/kg) ip on the same schedule. Three weeks after the fifth injection, the animals were sacrificed. The frequency and extent of cellular alterations were graded on a scale of 0 to 4. Lesions consisting mainly of vacuolization and myofibrillar loss were noted in the hearts of all 12 rabbits given daunorubicin alone. The severity ranged from 1 to 3 (average 1.8). In contrast, no abnormalities were noted in one of five (12.5 mg/kg) and three of seven (25.0 mg/kg) ICRF-treated rabbits. The remaining eight hearts from both pretreatment groups displayed animal alterations ranging from 0.5 to 1.0 (average 0.9). Thus, concurrent administration of the antineoplastic agent ICRF-187 may offer a means of reducing chronic daunorubicin cardiac toxicity.

Animals↗
PubMed1980

The metabolic fate of mitochondrial hydrogen peroxide.

1. Mitochondrial H2O2 formation is not in equilibrium with defence mechanisms that counteract an accumulation of H2O2 in rat-heart cells. 2. A model for the accumulation kinetics is proposed which is consistent with the data presented. 3. Four different pathways of H2O2 metabolism are described in rat-heart mitochondria. The major site for metabolic branching of H2O2 via different routes was found to be the mitochondrial catalase. 4. Glutathione (GSH) peroxidase accounts for only 15% of intramitochondrial H2O2 metabolism, while catalase-mediated destruction is four times more rapid. 5. Catalase activity is limited by its structural compartmentation in the matrix, while GSH peroxidase activity was found to be dependent on the availability of free GSH. 6. Catalase was shown to protect rat-heart mitochondria from upsetting redox states of GSH and pyridine nucleotides following H2O2 decomposition by GSH peroxidase. 7. Computer simulations of experimental data suggest the existence of a third sink for mitochondrial H2O2, possibly due to mitochondrial formation of OH . radicals; another fraction of the H2O2 matrix pool may cross the mitochondrial membrane and accumulate in the cytosol.

Animals↗
PubMed1978

Physical examinations in inner-city preschools.

This paper describes the physical examination program started in March 1974 and carried out by the Anacostia Headstart Program in Washington DC. Annual totals of 362, 274, and 458 preschool children were examined in 16 schools during the 1973-1974, 1974-1975, and 1975-1976 school years, respectively. For these years, 8, 9, and 12 percent, respectively, had heart murmurs. The rates for abdominal hernias were higher, 11, 17, and 16 percent, respectively. Eczema was also a common problem. Parents had easy access to counseling from health professionals who worked in the program.

Child Health Services↗
PubMed1975

Plasma concentration of alpha-methyldopa and sulphate conjugate after oral administration of methyldopa and intravenous administration of methyldopa and methyldopa hydrochloride ethyl ester.

The plasma concentrations of free alpha-methyldopa and methyldopa sulphate conjugate were measured in 7 hypertensive patients with normal renal function following alpha-methyldopa (1 g) orally. Five of these patients subsequently received alpha-methyldopa ethyl ester (250 mg) (methyldopate) intravenously and two further patients received 250 mg of alpha-methyldopa intravenously. After oral administration a large amount of total plasma alpha-methyldopa was present as sulphate conjugate. There were wide interindividual differences in the ratio of free: conjugated alpha-methyldopa in plasma (ratio at 4 hours ranged from 3.73-0.83) suggesting that individual differences in the extent of sulphate conjugation may occur. There was no close correlation between the degree of conjugation and the fall in arterial pressure. At all time intervals examined, plasma concentrations were higher following intravenous alpha-methyldopa than alpha-methyldopate. The plasma concentration of alpha-methyldopa (free and esterified) 60 minutes after i.v. alpha-methyldopate was 1.7+/-0.3 mug/ml while at the same time after the same dose of methyldopa by the same route the mean concentration was 5.9 mug/ml. Although small amounts of sulphate conjugate were detected after i.v. alpha-methyldopate, insignificant quantities of conjugate were found after i.v. alpha-methyldopa. The average fall in mean arterial pressure was 27 mm/Hg following i.v. alpha-methyldopa but only 2.7 mm Hg following alpha-methyldopate. These results suggest that sulphate conjugation of alpha-methyldopa occurs in the gastrointestinal tract during absorption. Hydrolysis of alpha-methyldopa ethyl ester does not appear to be instantaneous and pharmacokinetic differences between the ester and free alpha-methyldopa have been demonstrated.

Administration, Oral↗