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Biomedical subjects

K M Johnson

Publications and source records attributed to K M Johnson.

At least 199 records · Page 11Linked to original sources
PubMed1983

Viral haemorrhagic fever surveillance in Kenya, 1980-1981.

Following two cases of Marburg virus disease in Kenya in 1980, viral haemorrhagic fever surveillance was undertaken in western Kenya. Over a 21-month period investigations, including virus isolation attempts, patient and contact serology, visits to areas where suspected cases occurred, interviewing family members and neighbours of suspected cases and following up any additional illnesses in these areas, were carried out. During the study two cases were found that were likely to have been Ebola haemorrhagic fever based on rising antibody titres or positive serology in contacts. Diagnoses of hepatitis A, hepatitis B, malaria, bacterial septicaemia or other causes were arrived at in 24 cases. No diagnosis could be made in 26 instances. 741 human sera were tested for antibodies against Marburg, Ebola, Congo haemorrhagic fever, Rift Valley fever or Lassa fever viruses by indirect fluorescence. Eight sera were positive for Ebola virus antibodies, all of which were from suspected cases or contacts of suspected cases. Two sera were antibody positive to Congo virus and one had antibodies against Rift Valley fever virus. No Marburg or Lassa virus antibodies were detected.

Adolescent↗
PubMed1983

Effects of phencyclidine on the release of radioactivity from rat striatal slices labeled with [3H]choline.

Phencyclidine (PCP) has been shown to antagonize the effects of acetylcholine (ACh) in a variety of systems and to inhibit the binding of muscarinic antagonists to brain membranes. Therefore, we have studied the effects of PCP on ACh release from rat striatal slices in order to characterize the effect of PCP in a central cholinergic system. After incubation with [3H]choline, striatal slices were superfused and the superfusate was assayed for radioactivity. The presence of PCP led to dose-related inhibition of K+-stimulated ACh release. This may be due to the reported ability of PCP to enhance dopamine release as both direct (pergolide) and indirect (amphetamine) dopamine agonists also inhibited striatal ACh release. Haloperidol blocked the inhibitory effects of PCP, amphetamine and pergolide on ACh release, supporting the notion that the decrease in ACh release produced by PCP is mediated indirectly via the release of dopamine onto cholinergic neurons.

Acetylcholine↗
PubMed1982

Acute and chronic phencyclidine administration effects on the conversion of 3H-tryptophan to 3H-serotonin in rat forebrain.

Acute administration of phencyclidine hydrochloride (PCP) resulted in a dose-responsive decrease in the conversion of 3H-tryptophan to 3H-serotonin (3H-5-HT) in rat forebrain. Subsequent experiments measured the effect of a subthreshold dose of PCP (4 mg/kg) daily for one, seven, or four-teen days on this index of 5-HT turnover. Although single administration again had no effect at this dose, repeated administration for seven days resulted in a 37% decrease in 5-HT turnover. However, after fourteen days of administration this index was not significantly different from saline controls The possible significance of these findings are discussed in relation to reported alterations in PCP-induced behaviors observed with chronic administration.

Animals↗
PubMed1982

Phencyclidine: behavioral and biochemical evidence against the anticholinergic hypothesis.

Phencyclidine (PCP) is known to have anticholinergic effects in various in vitro test systems and to inhibit the binding of muscarinic antagonists to rat brain membranes. In order to verify the anticholinergic properties of PCP, its interaction with oxotremorine (OXO), a muscarinic agonist, was studied in mice. OXO (1 mg/kg) in combination with PCP (10 mg/kg) was lethal in 100% of the mice studied. The lethality of this combination was completely reversed by 3.3 mg/kg methyl atropine bromide (MA), a quarternary muscarinic antagonist. Therefore, PCP appears to act as a muscarinic agonist in some peripheral systems. The central interactions between PCP and OXO were studied in mice in which the preipheral effects of OXO were blocked by MA. In a test of motor performance, OXO potentiated the effect of PCP at one dose only. Contrary to the effects of PCP in other behavioral measures, no evidence for an anticholinergic effect of PCP was observed. The in vivo anticholinergic potential of PCP was estimated by adding a brain extract from PCP-treated mice to brain muscarinic receptors in the presence of 3H-quinuclidinyl benzilate. These data suggested that PCP, after in vivo administration, does not attain a sufficient brain concentration to directly affect central muscarinic receptors. However, a direct action of PCP on peripheral muscarinic receptors was not discounted.

Animals↗
PubMed1982

Experimental infection of rhesus monkeys with Lassa virus and a closely related arenavirus, Mozambique virus.

As a model for the pathogenesis of Lassa fever in humans, nine rhesus monkeys were inoculated with Lassa virus. Three monkeys had had a previous asymptomatic experimental infection with Mozambique virus, a closely related arenavirus; these monkeys were protected from illness and viremia and manifested only mild pathologic lesions. The other animals developed severe disease and viremia. At necropsy, hepatocellular necrosis, interstitial pneumonia, a unique pulmonary arteritis, adrenal gland necrosis, encephalitis, and uveitis were prominent pathologic lesions which correlated with the organ titers of virus. One animal infected with Lassa virus developed prolonged viremia, a typical immune response, and sudden onset of lower limb paralysis after recovery; at necropsy chronic proliferative arteritis of the spinal cord, brain, and heart was evident. Similarities and differences in the pathologic lesions in this model and Lassa fever in humans indicate that care must be taken in interpreting the results of experiments concerning immune prophylaxis, pathogenesis, and treatment in rhesus monkeys.

Animals↗
PubMed1982

Antibody to Ebola virus in guinea pigs: Tandala, Zaire.

A case-control study was conducted to investigate the findings of antibody to Ebola virus in the serum of a guinea pig from Tandala, Zaire. Case households, defined by the possession of one or more guinea pigs, were compared to neighboring households without guinea pigs. Seven (5.1%) of 138 samples of human sera and 36 (26%) of 138 samples of guinea pig sera had antibody to Ebola virus. There was no clustering of seropositivity among humans or guinea pigs within households, nor was there any association between the ownership of guinea pigs and seropositivity among household members. These data suggest sporadic subclinical infection of guinea pigs and humans without a dominant role for person-to-person or guinea pig-to-guinea pig transmission.

Animals↗
PubMed1982

Isolation of Hantaan virus, the etiologic agent of Korean hemorrhagic fever, from wild urban rats.

Urban rats captured in Seoul and four nearby Korean cities were found to have immunofluorescent antibodies reactive with Hantaan virus, the etiologic agent of Korean hemorrhagic fever (KHF). Serum antibodies were detected in 13% from 477 Rattus norvegicus and 11% of 47 Rattus rattus. Hantaan viral antigen was found in pulmonary tissues of 42 animals, and Hantaan virus was recovered from 23 rats, all but two of which were R. norvegicus. Wistar rats were qualitatively much more sensitive than Apodemus agrarius rodents for isolation of virus from tissues of wild rats. Wistar rats inoculated with one of these strains had virus in lung and spleen for at least 75 days. These results document the existence of an urban cycle for Hantaan virus, which had been suspected on the basis of the occurrence of sporadic urban cases in humans of KHF, and suggest that Rattus-borne Hantaan virus may be widely distributed in urban centers.

Adult↗
PubMed1982

Laboratory-acquired infections with Hantaan virus, the etiologic agent of Korean hemorrhagic fever.

Clinically apparent infections with Hantaan virus, the etiologic agent of Korean hemorrhagic fever, occurred in nine persons exposed to the virus at the Korea University Virus Institute (Seoul) between 1971 and 1979. All were directly related to trapping of wild rodents or work with naturally or experimentally infected wild and laboratory rodents in a designated animal suite. All infections were acquired during the months of November-April, and none was associated with accidental parenteral inoculations. These facts suggested that aerosols produced by chronically infected rodents were the infectious vehicles and that limited air circulation and lowered humidity in the animal rooms during winter months increased the probability of viral transmission. Four persons, including two casual visitors, became ill within four months after the initiation of experimental studies of infections in Wistar rats with Hantaan virus, an occurrence suggesting that this rodent may be a highly infectious host for Hantaan virus.

Adolescent↗
PubMed1982

Paradoxes, double binds, and reflexive loops: an alternative theoretical perspective.

This article presents a new theory of reflexivity in systems of social meaning and action. It is argued that Russell's Theory of Logical Types, which formed the basis of the early work of the Palo Alto group, rests upon an inappropriate and largely outdated epistemology. The theory offered here rejects the assumption that reflexivity and paradox are coterminous. It is further argued that reflexivity is a natural and necessary feature of human systems of meaning. New analytic tools are offered for discerning problematic from nonproblematic reflexive loops. The new tools take the form of a symbol that can be used to represent the rules that organize reflexive relationships. The theory also contains a set of statements designed to delimit conditions under which problematic reflexive loops have ramifications for persons' mental health.

Communication↗
PubMed1982

Inactivation of Lassa, Marburg, and Ebola viruses by gamma irradiation.

Because of the cumbersome conditions experienced in a maximum containment laboratory, methods for inactivating highly pathogenic viruses were investigated. The infectivity of Lassa, Marburg, and Ebola viruses was inactivated without altering the immunological activity after radiation with Co60 gamma rays. At 4 degrees C, Lassa virus was the most difficult to inactivate with a rate of 5.3 X 10(-6) log 50% tissue culture infective dose per rad of CO60 radiation, as compared with 6.8 X 10(-6) log 50% tissue culture infective dose per rad for Ebola virus and 8.4 X 10(-6) log 50% tissue culture infective dose per rad for Marburg virus. Experimental inactivation curves, as well as curves giving the total radiation needed to inactivate a given concentration of any of the three viruses, are presented. We found this method of inactivation to be superior to UV light or beta-propiolactone inactivation and now routinely use it for preparation of material for protein-chemistry studies or for preparation of immunological reagents.

Arenaviridae↗
PubMed1982

Epidemiological significance of Venezuelan equine encephalomyelitis virus in vitro markers.

One hundred and fifty-eight strains of Venezuelan equine encephalomyelitis virus were typed antigenically and classified epidemiologically as either epizootic or enzootic. Plaque sizes for 148 of these strains were determined, and the pH requirements for hemagglutination (HA) of goose erythrocytes of 131 were studied. Only antigenic variant group IABC strains could be classified epidemiologically as epizootic. In vitro these strains were characterized by the formation of small plaques in Vero cells and a relatively narrow pH range for optimum HA reactivity. Experimental studies in horses confirmed the fact that only IABC strains have epizootic potential. We concluded that plaque size in Vero cell monolayers would be a useful method of screening VEE viruses for equine virulent strains. Indirect evidence suggested that small plaques resulted from sensitivity to an anionic substance present in the agar overlay medium.

Animals↗
PubMed1982

Similar dopamine-releasing effects of phencyclidine and nonamphetamine stimulants in striatal slices.

Phencyclidine (PCP) elicits some behavioral and biochemical effects in rodents which resemble the effects of other central nervous system stimulants. Because an indirect dopaminergic agonist role has been proposed for PCP, we have compared the dopamine (DA)-releasing properties of PCP, amphetamine and certain nonamphetamine stimulants (methylphenidate, nomifensine, amfonelic acid). Striatal slices from male albino Sprague-Dawley rats were incubated with [3H]DA (10 nM) and then superfused in microperfusion chambers with a modified Tyrode's buffer (pH 7.4). Drug effects on [3H]DA release during depolarizing (40 mM KCl) and nondepolarizing (basal) conditions were determined by comparison with drug-free DA release rates in each preparation. PCP (3-100 microM) and all central nervous system stimulants tested produced a concentration-dependent increase of basal [3H]DA release (potency order: amfonelic acid, amphetamine greater than nomifensine, methylphenidate greater than PCP). At higher concentrations, PCP and the nonamphetamine stimulants also enhanced stimulated [3H]DA release. The effect of PCP on basal release was unchanged by the removal of extracellular calcium, addition of tetrodotoxin (1 microM) or pretreatment of rats with reserpine. Nomifensine (1 microM) enhanced the DA releasing actions of PCP and other nonamphetamine stimulants, but antagonized the DA releasing action of amphetamine. PCP, at concentrations which did not affect basal DA release (less than 1 microM), also antagonized the action of amphetamine. From these results, it appears that PCP enhances DA release in a manner similar to the nonamphetamine class of central nervous system stimulants.

Animals↗
PubMed1982

The binding of staphylococcal protein A by the sera of different animal species.

The capacity of purified immunoglobulin or serum to bind (125I)-labeled staphylococcal protein A (SPA) was measured by means of an immunofiltration assay that facilitated the examination of large numbers of sera and required only a minute quantity of each. Sera from 80 species, including humans, laboratory animals, domestic animals, and a variety of African mammals were examined. A wide interspecies variation in the SPA-binding capacity of serum immunoglobulins was confirmed. Only small variations were observed among individuals within the same species with one notable exception. A greater than 10,000-fold variation in SPA-binding capacity was observed among sera from nine goats. Interspecies differences in serum SPA-binding capacity correlated well with taxonomic differences, and the serum SPA-binding capacity correlated well with taxonomic differences, and the serum SPA-binding capacities of African mammals corresponded closely to those of their more common relatives. The sensitivity of antibody detection by indirect (125I)SPA immunoassay was shown to be determined mostly by the SPA-binding capacity of the serum examined. The titer of antibody to influenza A/Texas/1/77(H3N2) virus in sera from several different species, when measured by (125I)SPA immunofiltration assay, was directly proportional to the SPA-binding capacity of the serum and was not proportional to the hemagglutination inhibition titer. An (125I)SPA immunofiltration assay for antibody to Lassa virus in the serum of Mastomys natalensis (which binds SPA only one-thousandth as well as human serum) was at least as sensitive as the standard fluorescent antibody assay.

Adult↗
PubMed1982

Pathologic and virologic study of fatal Lassa fever in man.

Postmortem examination of 21 virologically documented cases of Lassa fever, including 6 complete autopsies, was performed as part of a field study of community-acquired Lassa fever in Sierra Leone. The most consistently observed lesions were hepatocellular, adrenal, and splenic necrosis and adrenal cytoplasmic inclusions. Neither these lesions, nor other milder and less constantly observed lesions such as myocarditis, renal tubular injury, and interstitial pneumonia, appeared severe enough to explain the cause of death in Lassa fever. The central nervous system (CNS) contained no specific lesions. Viral titrations demonstrated high viral content in liver, lung, spleen, kidney, heart, placenta, and mammary gland. Clinical laboratory data included elevation of hepatic enzymes, creatine phosphokinase (CPK), and blood urea nitrogen (BUN). Because of the paucity of pathologic lesions in spite of widely disseminated viral infection, further investigation of humoral inflammatory mechanisms is indicated.

Adult↗