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Biomedical subjects

M Johnson

Publications and source records attributed to M Johnson.

At least 649 records · Page 36Linked to original sources
PubMed1988

Antibody response to xenogeneic proteins in burned patients receiving cultured keratinocyte grafts.

Cultured keratinocytes (CK) have been used to resurface large burn wounds with some success. These CK are grown in the presence of fetal bovine serum (FBS) and mouse fibroblasts (MF). Serum from ten patients who received CK grafts as part of burn wound coverage was studied by ELISA technique for antibody to these xenogeneic antigens. All patients had some amount of antibody to FBS but no detectable antibody to MF. The amount of antibody to FBS varied between patients and with respect to time after graft application. Generally, the levels of antibody to FBS were moderate by 30 days, declined, and then rose slowly by 5 to 6 months. The majority of antibody to FBS was against bovine serum albumin (BSA), demonstrated by Western blot technique. The presence of such antibody to FBS might produce clinical problems of graft rejection, anaphylaxis, and serum sickness in patients receiving CK grown in FBS supplemental medium. Further investigation will need to determine the likelihood and potential severity of such clinical problems.

Adult↗
PubMed1988

Inhibition of bone marrow myelopoiesis and erythropoiesis in vitro by anti-retroviral nucleoside derivatives.

We have studied the in vitro effects of nucleoside inhibitors of reverse transcriptase on bone marrow myeloid and erythroid progenitor development. Both 3'-azido-3'-deoxythymidine (AZT) and 2',3'-dideoxycytidine (DDC) potently inhibited in vitro haematopoiesis, while 2',3'-dideoxyadenosine (DDA) was less inhibitory in this culture system. Studies of candidate antiretroviral agents in bone marrow culture may predict clinical toxicity as well as lead to strategies for combination therapy which minimize impairment of haematopoiesis.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Endogenous opioids inhibit oxytocin release during nicotine-stimulated secretion of vasopressin in man.

The effects of the opioid antagonist naloxone on the vasopressin (AVP) and oxytocin (OT) responses to nicotine were studied in male non-smokers (21-30 years old). Either saline (n = 6) or naloxone (4 mg bolus + 6 mg/h, n = 6) was infused i.v. during the study. After 60 min infusion the subjects smoked one high-nicotine content cigarette. Naloxone infusion for 60 min did not alter basal plasma AVP or OT levels. Smoking led to a significant rise in plasma vasopressin in both saline and naloxone-infused subjects (P less than 0.05). There was no significant difference in the plasma AVP response to smoking between the two groups. Saline-infused subjects did not show any change in plasma OT in response to smoking. Naloxone infusion was associated with a significant rise in OT from 1.3 +/- 0.1 pmol/l to 4.3 +/- 2.4 pmol/l 5 min after smoking (P less than 0.05). We conclude that there is endogenous opioid-mediated inhibition of OT which prevents its release when AVP is secreted in response to nicotine in man.

Adult↗
PubMed1988

An evaluation of reinforcement of genetic counselling on the consultand.

This project studied the effect of reinforcement of genetic counselling in the home, on consultand recall of information discussed in the clinic. Acceptable recall was observed in 84% of 227 patients scored for recall of rate of recurrence, understanding of the nature of the disease at special risk and of its mechanism of origin. Our results show no significant difference in the frequency of acceptable recall after reinforcement of genetic counselling compared with an absence of reinforcement. The consultands' understanding was substantially affected by the type of genetic mechanism involved.

Aftercare↗
PubMed1988

Single dose, oral antibiotic cover for transurethral prostatectomy.

A double-blind, randomised, placebo-controlled study was carried out to determine the incidence and significance of bacteriuria in 110 patients undergoing transurethral resection of the prostate (TURP) and to assess the effect of a single pre-operative dose of Ciprofloxacin, a 4-quinolone antibiotic. Fifteen (68%) of the 22 patients in the placebo group with a positive post-operative urine culture subsequently developed a clinically apparent urinary tract infection (UTI) or received antibiotics in view of a positive urine culture. Adequate prostatic concentrations of Ciprofloxacin were achieved in all who received the drug. A significant reduction in the number of positive post-operative urine cultures and urinary tract infections requiring antibiotic therapy was achieved in this group. Six patients (5.5%) developed clinical evidence of septicaemia, 5 of whom were in the placebo group. No organisms resistant to Ciprofloxacin were encountered. Prior to surgery, 19% of all patients were found to have previously unsuspected bacteriuria. Ciprofloxacin tended to reduce the chances of this group developing a UTI or requiring antibiotics. Further, there was a highly significant reduction in post-operative infective complications in those with sterile urine at the time of resection who had received the drug. This study suggests that antibiotic cover for TURP is of clinical benefit. Ciprofloxacin may prove suited to this purpose, although further experience with the drug is still required.

Administration, Oral↗
PubMed1988

Muscarinic cholinergic receptor subtypes in hippocampus in human cognitive disorders.

Total muscarinic receptor levels, the levels of the subtypes exhibiting high and low affinity for pirenzepine, and the high- and low-affinity agonist states of the receptor were investigated in hippocampal tissue obtained at autopsy from mentally normal individuals and the following pathological groups: Alzheimer's disease, Parkinson's disease, Down's syndrome, alcoholic dementia, Huntington's chorea, and motor-neurone disease. A moderate decrease in the density of both high-affinity pirenzepine and high-affinity agonist subtypes was found in Alzheimer's disease, whereas a trend towards an increase in the overall muscarinic receptor density was apparent in the parkinsonian patients without dementia, mainly due to an increase in the low-affinity agonist state; the differences between the Alzheimer's disease and nondemented parkinsonian cases were highly significant. As previously reported, the levels of both choline acetyltransferase and acetylcholinesterase were markedly reduced in both Alzheimer's disease and Parkinson's disease--with a greater loss of both enzymes in the demented subgroup of parkinsonian patients. Activities of the cholinergic enzymes were also extensively reduced in Down's syndrome, accompanied by a loss of high-affinity pirenzepine binding. There were no significant receptor or enzyme alterations in the other groups studied. These observations suggest that in the human brain, extensive degeneration of cholinergic axons to the hippocampus, as indicated by a loss of cholinergic enzymes, is not necessarily accompanied by extensive muscarinic receptor abnormalities (as might be expected if a major subpopulation were presynaptic). Moreover, the opposite changes in muscarinic binding in Parkinson's and Alzheimer's diseases may be related to the greater severity of dementia in the latter disease.

Acetylcholinesterase↗
PubMed1988

Facilitated calcium mobilization and inositol phosphate production in the priming effect of LH-releasing hormone in the rat.

The ability of LHRH to induce Ca2+ mobilization and production of inositol phosphates in rat anterior pituitary tissue in vitro was investigated in relation to the self-priming effect of LHRH. Prior exposure to LHRH (which caused a characteristic potentiation of subsequent secretory responses) specifically enhanced LHRH-induced inositol phosphate production and mobilization of intracellular Ca2+ stores. LHRH-induced influx of Ca2+ through dihydropyridine-sensitive Ca2+ channels was unaltered, as was ligand binding to LHRH receptors. These data suggest that a novel facilitation of signalling may occur in the phospho-inositide-Ca2+ mobilization response mechanism during LHRH priming, and that this may represent an important means of regulating cellular responsiveness in gonadotrophs.

Animals↗
PubMed1988

Recurrent tuberculosis: why do patients develop disease again? A United States Public Health Service cooperative survey.

In October 1983, a retrospective survey was initiated to determine if patients reported to the Centers for Disease Control as having recurrent tuberculosis truly had recurrent disease and, if so, why they had developed tuberculosis again. Twenty-three health jurisdictions provided information on 800 patients diagnosed as having recurrent tuberculosis during 1981 and 1982. We found that 199 (25 per cent) of the cases did not meet the criteria for recurrent disease. Of the remaining 601 recurrent cases, 20 per cent had no chemotherapy prescribed for their previous episodes of tuberculosis, 20 per cent were prescribed inadequate or inappropriate therapy, and 33 per cent were not compliant with their prescribed therapy regimens. Patients who, during their original episode of tuberculosis, received the major portion of their medical care from physicians in private practice were more compliant than those treated by other health care providers. However, those same patients were more likely to have received inappropriate therapy than patients treated by other providers. Better patient and physician education, closer monitoring, and greater use of preventive therapy and directly observed therapy are necessary to resolve these problems.

Adolescent↗
PubMed1988

Effects of 3,4-methylenedioxyamphetamine and 3,4-methylenedioxymethamphetamine isomers on central serotonergic, dopaminergic and nigral neurotensin systems of the rat.

This study demonstrates that the isomers of 3,4-methylenedioxyamphetamine (MDA) and 3,4-methylenedioxymethamphetamine (MDMA) are different in their ability to induce changes in serotonergic parameters and nigral concentrations of neurotensin-like immunoreactivity. With five successive doses (3.5 mg/kg) the d-MDA isomer was more potent than the l-MDA in its ability to decrease the concentrations of serotonin in the frontal cortex and hippocampus. The same difference occurred in the ability to decrease the hippocampal activity of tryptophan hydroxylase as well as the hippocampal and neostriatal 5-hydroxyindoleacetic acid concentrations. However, both isomers of MDMA were equipotent in their ability to decrease serotonergic parameters in the brain areas examined. When the doses were increased to 5 and 10 mg/kg, both isomers of MDA were equipotent in their effects on the serotonin system, whereas the l-MDMA was significantly less potent than its d isomeric counterpart in causing a decrease in serotonergic parameters of the different brain areas. In contrast, treatments with any of the isomers appeared to have a minimal impact on neostriatal dopaminergic parameters. However, treatment with MDA or MDMA caused increases in the nigral concentrations of neurotensin, with the d isomer of both compounds having substantially greater effects on this neuropeptide system. These increases are suspected to result from drug-released dopamine. This study demonstrates that at selected doses, the d isomers of MDA and MDMA are more potent than their l forms in affecting neurochemical systems, whereas high doses of either isomer of MDA share a common ability to induce changes in the serotonergic system that are likely associated with neuronal damage.

3,4-Methylenedioxyamphetamine↗
PubMed1988

Role of endogenous dopamine in the central serotonergic deficits induced by 3,4-methylenedioxymethamphetamine.

Similar to other amphetamine analogs 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy"), a currently popular illicit drug, has been characterized recently as a serotonergic neurotoxin due to its ability to cause long-lasting deficits in markers of central serotonergic function in animals. Because the serotonergic toxicity associated with the MDMA analog methamphetamine has been linked previously to endogenous dopamine and because MDMA, like methamphetamine, elicits pronounced dopamine release in vitro, we have examined the role of endogenous dopamine in both the immediate (3 hr) and longer-term (3 days) central serotonergic deficits induced by systemic MDMA administration to rats. Depletion of central dopamine content with alpha-methyl-p-tyrosine or reserpine, or selective destruction of nigrostriatal dopamine projections with bilateral 6-hydroxydopamine-induced substantia nigral lesions, partially blocked the immediate MDMA-induced reduction in rat striatal tryptophan hydroxylase (TPH) activity. In addition, the longer-term TPH deficits caused by a high single dose of MDMA were completely prevented by prior alpha-methyl-p-tyrosine or reserpine, and attenuated significantly by inhibition of dopamine uptake with the selective dopamine-uptake blocker GBR 12909. These results implicate endogenous drug-released dopamine as a partial mediator of the initial decrease in TPH activity caused by MDMA and as an important prerequisite to the development of long-term MDMA-induced neurotoxicity. Potential mechanisms of dopamine-mediated toxicity are discussed.

3,4-Methylenedioxyamphetamine↗
PubMed1988

HIV and the nervous system.

Neurological manifestations are common in HIV-infected individuals. Autopsy data suggest that the brain may be affected in as many as 80 per cent of cases. While opportunistic infections represent a major cause of neurological morbidity and mortality, there is growing evidence that HIV is itself neurotropic and can directly affect the nervous system.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Closed head injury in acute traumatic spinal cord injury: incidence and risk factors.

Investigators estimate that 15% to 50% of all patients with spinal cord injury (SCI) also incur a closed head injury (CHI), but studies have been hampered by design flaws, including retrospective assessment and inconsistent definition of CHI. We conducted a prospective study of combined CHI and SCI among 82 SCI patients consecutively admitted at two hospitals within 24 hours of injury. The purpose of the study was to determine the incidence and duration of loss of consciousness and posttraumatic amnesia (PTA), and to establish the risk factors for combined CHI and SCI. The overall incidence of CHI as defined by the presence of PTA of any duration was 49%. There was a significantly increased risk of CHI for patients involved in traffic accidents (risk ratio = 3.7; 95% confidence interval 1.8 to 7.2). There was no increased risk associated with level of injury (quadriplegic vs paraplegic; risk ratio = 1.2; 95% confidence interval = 0.8 to 1.8). All SCI patients, regardless of level of injury, deserve systematic evaluations for CHI in their acute care evaluations.

Adult↗
PubMed1988

Hydrogen peroxide removal by the calf aqueous outflow pathway.

Previous studies have shown that aqueous humor of calf and human eyes contains about 25 microM hydrogen peroxide. We have studied the removal of hydrogen peroxide by the outflow pathway of intact, freshly enucleated, calf eyes. Eyes were immersed under silicone oil that had a density greater than water and medium containing various agents was perfused into the anterior chamber. Medium passing through the trabecular meshwork and out the cut ends of the aqueous veins was trapped by the silicone oil and harvested. By measuring the concentration of hydrogen peroxide in the anterior chamber and in the emerging medium, we were able to study the rate of removal by the outflow structures and the effect of inhibitors on this rate. At 1 mM hydrogen peroxide, the amount emerging was undetectable by our methods. At 10 mM, the results were inconsistent, suggesting that tissue damage may have been occurring. At 5 mM, the concentration in the emerging medium was reduced 150-1000-fold, depending on time and conditions. This rate of removal could be reduced by 3-aminotriazole, reaching a maximum inhibition of about 50% at 80 mM. Addition of 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU) to further inhibit removal did not yield reliable results unless the concentration of H2O2 was lowered below 5 mM. Using loss of lactate dehydrogenase activity as a measure of cell damage, we found a 30% drop in activity after perfusing with BCNU, diamide, and 3-aminotriazole, followed by 3 hr with 10 mM hydrogen peroxide.(ABSTRACT TRUNCATED AT 250 WORDS)

Amitrole↗
PubMed1987

Effects of N-ethyl-3,4-methylenedioxyamphetamine (MDE) on central serotonergic and dopaminergic systems of the rat.

The influence of N-ethyl-3,4-methylenedioxyamphetamine (MDE) on the central serotonergic and dopaminergic systems of the rat after a single or multiple injections was studied. MDE (10 mg/kg) produced a significant decrease in the concentration of 5-hydroxytryptamine (5-HT) 1 hr later in the frontal cortex and the hippocampus without affecting the concentration of 5-hydroxyindoleacetic acid (5-HIAA) or tryptophan hydroxylase (TPH) activity. Hypothalamic and neostriatal concentrations of 5-HT, 5-HIAA, dopamine (DA), dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) remained unaffected, as well as the neostriatal TPH and tyrosine hydroxylase (TH) activities. However, 3 hr after the MDE injection, the serotonergic variables including TPH activity were decreased in most of the brain areas examined. The dopaminergic system remained unaffected, except for a significant reduction in neostriatal DOPAC concentrations. The changes in transmitter concentrations after a single injection were dose dependent; the maximum depletion in TPH activity was reached with a 10 mg/kg dose. The administration of multiple doses of MDE caused greater decreases in TPH activity and 5-HT concentrations 3 hr after the treatment than did a single injection; in addition, a partial recovery from multiple administrations occurred by 18 hr. The effects of MDE on DA and its metabolites were transient, and neostriatal TH activity was not altered. This study demonstrates that MDE primarily affects the central serotonergic system, as reported for its congeners 3,4-methylenedioxyamphetamine and 3,4-methylenedioxymethamphetamine. It does, however, produce less neurotoxicity as judged by its lower potency on the dopaminergic and the serotonergic systems as well as the recovery occurring in these systems.

3,4-Dihydroxyphenylacetic Acid↗