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Biomedical subjects

J J Taljaard

Publications and source records attributed to J J Taljaard.

At least 37 records · Page 2Linked to original sources
PubMed1995

Activation of the subthalamic nucleus and pedunculopontine tegmentum: does it affect dopamine levels in the substantia nigra, nucleus accumbens and striatum?

Parkinson's disease is a neurodegenerative disorder, of which the most prominent morphological feature is the progressive loss of dopaminergic nigrostriatal neurons. Increased glutamatergic transmission in the basal ganglia has been implicated in the pathophysiology of Parkinson's disease (PD). This study investigated whether death of substantia nigra (SN) dopaminergic neurons could be caused by the hyperactivity of afferent pathways resulting in the release of a toxic dose of excitatory amino acids in the SN. Twice-daily unilateral stimulation of the subthalamic nucleus (STN) for 21 days, using two different pulse frequencies and current strengths, significantly increased amphetamine-induced rotation, whereas sham stimulated rats showed significantly reduced rotation. Striatal and SN dopamine (DA) levels were unaffected when compared to naïve and sham stimulated rats. However, levels of the DA metabolite, homovanillic acid (HVA), were significantly higher in the ipsilateral anterior striata of rats that had been stimulated at high frequency (100 Hz) and low current (100 microA) as compared to sham treated animals. Stimulation of the pedunculopontine tegmentum (PPT), using a single kainic acid injection, did not affect DA concentration in the ipsilateral striatum and nucleus accumbens when compared to sham-treated rats. DA levels in the contralateral striatum and nucleus accumbens of lesioned rats were significantly higher than ipsilateral levels. DOPAC/DA ratios were lower in the contralateral striatum and nucleus accumbens, suggesting decreased DA turnover. Glutamic acid decarboxylase activity was significantly higher in the ipsilateral than the contralateral SN. The physical manifestations of PD require a large reduction in caudate and putamen DA levels and no such depletion was measured in this study.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗
PubMed1995

Alpha 2-adrenoceptor mediated inhibition of [3H]dopamine release from nucleus accumbens slices and monoamine levels in a rat model for attention-deficit hyperactivity disorder.

The spontaneously hypertensive rat (SHR) has been proposed as an animal model for attention-deficit hyperactivity disorder (ADHD). The behavioural problems have been suggested to be secondary to altered reinforcement mechanisms in which nucleus accumbens dopaminergic activity plays an important role. Interaction between the noradrenergic and dopaminergic system in the nucleus accumbens has been implicated in the locomotor hyperactivity and impaired discriminative performance of SHR. The present study therefore investigated whether there was any change in the alpha 2-adrenoceptor mediated inhibition of dopamine release from nucleus accumbens slices of SHR in comparison with their normotensive Wistar-Kyoto (WKY) controls. The electrically stimulated release of [3H]dopamine (DA) from nucleus accumbens slices was decreased to a similar extent by UK14,304, an alpha 2-adrenoceptor agonist, in SHR and WKY. Basal norepinephrine (NE) levels were increased in locus coeruleus (LC) and A2 noradrenergic nuclei, but not in the A1 nucleus of SHR, while basal serotonin (5-HT) levels were increased in all these pons-medulla nuclei. These results suggest that a primarily dysfunctional LC and A2 nucleus does not have a secondary effect on dopaminergic transmission in the nucleus accumbens via alpha 2-adrenoceptor mediated inhibition of DA release. Basal monoamine levels in several brain areas of SHR were significantly different from that of WKY. DA, and 5-HT turnover were decreased in SHR versus WKY suggesting hypofunctional dopaminergic and serotonergic systems in some brain areas of SHR.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1995

Transferrin C2 and Alzheimer's disease: another piece of the puzzle found?

A significant increase in the occurrence of the transferrin C2 genetic subtype has been found in patients with Alzheimer's disease. This variant has previously been linked to diseases thought to be associated with free radical damage. We hypothesize that Alzheimer's disease is caused by free radical damage to membranes of endocytic vesicles due to defective binding of iron and aluminium by Tf C2. The aluminium binds to the membranes, creating pores, while the iron reacts with H2O2 and superoxide radicals produced by activated microglia (brain phagocytes), to produce hydroxyl radicals (oxidative toxins), which attack the fatty acids in the membranes through these pores. In order to treat the disease successfully, it would be necessary to alleviate the multiple deficiencies caused by these toxins by constantly providing the cells with antioxidants and other essential nutrients. In addition, a drug that would stimulate the regrowth of neurons is needed.

Aluminum↗
PubMed1995

Use of adenosine deaminase as a diagnostic tool for tuberculous pleurisy.

BACKGROUND: A statistical audit of adenosine deaminase (ADA) in pleural effusions was undertaken. METHODS: ADA analysis, cytological and microbiological examinations, and differential cell counts were performed on 462 pleural fluid samples. RESULTS: ADA activity in tuberculous effusions was higher than in any other diagnostic group. At a level of 50 U/l the sensitivity and specificity for the identification of tuberculosis was 90% and 89%, respectively. CONCLUSIONS: ADA activity remains a useful test in the evaluation of pleural effusions.

Adenosine Deaminase↗
PubMed1995

Pleural Mesocestoides and cardiac shock in an obese vervet monkey (Cercopithecus aethiops).

Only one case of infection by tetrathyridia larvae of the tapeworm genus Mesocestoides was detected in 416 necropsies of captive vervet monkeys (Cercopithecus aethiops). Two hundred nine larvae were distributed between both pleural cavities. Mass and size ranges of larvae were determined. A plasma cell reaction indicated a humoral immune response to parasite antigens, which may have contributed to acute, lethal cardiac shock. Coagulative myocytolysis was confirmed. The history of this case and associated circumstantial evidence and reports in the literature suggest that infection of primates by tetrathyridia probably occurs after capture rather than before.

Animals↗
PubMed1995

Comparative analysis of the biochemical parameters used to distinguish between pleural transudates and exudates.

UNLABELLED: The differentiation between exudates and transudates is the initial step in the analysis of pleural effusions as it often gives an indication of the underlying pathophysiologic process, the differential diagnosis, and the need for further investigations. Four classifications have been suggested in the literature: Light's criteria, serum-effusion albumin gradient, effusion cholesterol concentration, and pleural/serum bilirubin concentration. AIM OF STUDY: To compare the various biochemical parameters used to identify exudates. PATIENTS AND METHODS: A study was carried out from February 1993 to March 1994 at Tygerberg Hospital, South Africa. Five hundred pleural effusions and serum specimens were analyzed. After discharge, the hospital records of all patients were reviewed for a diagnosis. RESULTS: A reliable diagnosis could be made in 393 cases (270 exudates and 123 transudates). Using the criteria of Light and associates 93% of the effusions were correctly classified, yielding a sensitivity and specificity of 98% and 83%, respectively, to detect exudates. The serum-effusion albumin gradient at a cutoff level of 12 g/L yielded the following results: accuracy, 89%; sensitivity, 87%; and specificity, 92%. Using a cutoff level of 1.55 mmol/L, the effusion cholesterol concentration yielded results of 70%, 54%, and 92%, respectively. The results improved at lower cutoff levels for effusion cholesterol level. Use of the pleural/serum bilirubin ratio as a means for identifying exudates produced results of 75%, 81%, and 61%, respectively. CONCLUSION: The criteria of Light et al remain the best method for distinguishing exudates from transudates. The serum-effusion albumin gradient is useful when patients are receiving concurrent diuretic therapy.

Adolescent↗
PubMed1994

Lipid peroxidation and platelet membrane fluidity--implications for Alzheimer's disease?

In humans, the fluidity of cell membranes generally decreases with age. Unexpectedly, several laboratories have found increased fluidity of platelet membranes (mainly endoplasmic reticulum) in patients with Alzheimer's disease (AD) compared with controls. In the present study, free radical induced lipid peroxidation was found to increase the fluidity of platelet membranes. Hydroxyl radicals were generated in the presence of Fe2+ and EDTA at low concentrations of ascorbate. It is hypothesised that platelet membranes are unable to restore their microviscosity by incorporating cholesterol. There may be a link between the result obtained in this study, the recently discovered decreased cholesterol content of affected AD neuronal membranes, and the increased frequency of epsilon 4 apolipoprotein E (a cholesterol carrier) found in AD patients.

Alzheimer Disease↗
PubMed1994

Lack of effect of bilateral locus coeruleus lesion and antidepressant treatment on gamma-aminobutyric acidB receptors in the rat frontal cortex.

The aim of the present study was to investigate whether a disturbance of the central noradrenergic (NA) system could cause changes in gamma-aminobutyric acidB (GABAB) receptors in the rat frontal cortex. Manipulation of the NA projection to the frontal cortex was achieved by bilateral lesion of the locus coeruleus with 6-hydroxydopamine (6-OHDA) or chronic treatment with the NA reuptake blocker and antidepressant drug, desipramine. Precautions were taken to ensure that the GABAB receptor assay was performed optimally and was not confounded by the presence of endogenously generated GABA. The results show conclusively that manipulation of the NA projection did not result in any significant change in the number (Bmax) or affinity (Kd) of GABAB receptors in the frontal cortex. These results do not support the hypothesis that hypoactivity of the central NA system can lead to changes in cortical GABAB receptors and that antidepressant drugs act by increasing GABAB receptor binding in the frontal cortex.

Animals↗
PubMed1994

Evidence that lithium induces a glutamatergic: nitric oxide-mediated response in rat brain.

Studies have indicated the involvement of a glutamatergic mechanism in lithium (Li+) action. Glutamatergic agonists, such as kainic acid, are known to promote the synthesis of nitric oxide (NO) and to increase cGMP, while Li+ has displayed a similar, yet unexplained, ability to increase cGMP. NO synthesis is regarded as the principal prodromal event leading to the activation of the guanyl cyclase-cGMP transduction mechanism. In the present study, the involvement of the NO:cGMP pathway in the action of Li+ was examined, while the possibility of a glutamatergic mechanism in this response was also investigated. Parameters examined included cortical accumulation of cGMP and the stable oxidative metabolites of NO, viz. NO2- and NO3-, collectively expressed as NO2-. A significant positive correlation was observed in the in vivo cGMP and NO2- data throughout all the groups. Chronic treatment of rats with LiCl (0.3% m/m) engendered a significant increase in cGMP levels which was inhibited by the NO-synthase (NOS) inhibitor, N-nitro-L-arginine methyl ester (L-NAME). Acute administration of kainic acid resulted in an increased accumulation of NO2-, also prevented by concomitant L-NAME administration. In addition, a synergistic stimulatory response on cortical NO2- was observed in the combination of LiCl and kainic acid. Collectively, these data implicate an involvement of a glutamatergic-mediated NO:cGMP transduction mechanism in the action of Li+.

Animals↗
PubMed1994

Decreased hippocampal noradrenaline does not affect corticosterone release following electrical stimulation of CA1 pyramidal cells.

Bipolar electrodes were implanted into the CA1 pyramidal cells of the dorsal hippocampus and the effect of electrical stimulation of these cells on corticosterone secretion was investigated in freely moving rats. Histology showed that the electrodes were positioned in close proximity to the CA1 pyramidal cells. Rats that were subjected to high intensity electrical stimulation (1, 10, and 100 microA) behaved differently when compared to their sham stimulated controls. They were more active and displayed wet dog shakes. Plasma corticosterone levels increased dose-dependently in rats subjected to different electrical stimulation intensities. Although prior treatment (24 hours) of rats with DSP4 (60 mg/kg, i.p.) significantly reduced hippocampal noradrenaline content by 46%, it did not bring about any behavioural changes. DSP4 treatment also had no effect on electrically stimulated corticosterone release. These data suggested that stimulation of CA1 pyramidal cells may lead to increased corticosterone release and that a decrease in hippocampal noradrenaline concentration was unable to alter this corticosterone response.

Animals↗
PubMed1994

Evidence that noradrenergic neurons in the A1 and A2 nuclei are lesioned by low doses of 6-OHDA injected into the locus coeruleus.

In order to determine the specificity of a lesion aimed at the locus coeruleus (LC), various doses of 6-hydroxydopamine (6-OHDA), a neurotoxin which selectively lesions catecholaminergic neurons, were bilaterally infused into the LC. The noradrenaline (NA) concentration in the frontal cortex, hippocampus, hypothalamus, LC, A1 and A2 nuclei decreased with increasing doses of 6-OHDA. A 1 microgram dose of 6-OHDA injected bilaterally into the LC caused maximal depletion of the NA concentration in the frontal cortex, hippocampus and A1 and A2 nuclei. A dose of 2 micrograms 6-OHDA caused further depletion of the NA content of the hypothalamus and LC. These findings suggest that A1 and A2 neurons which project to the hypothalamus may have been lesioned or that the noradrenergic projection from the LC to the hypothalamus may be greater than was previously suspected. Alternatively, leakage of 6-OHDA into the cerebrospinal fluid may have occurred at the higher doses, thus directly exposing the hypothalamus to the toxic effects of 6-OHDA.

Animals↗
PubMed1993

Increased frequency of the transferrin C2 subtype in Alzheimer's disease.

Several genetic variants of transferrin can be separated by polyacrylamide gel isoelectric focusing. Studies by other workers have revealed that the genetic type Tf C2 has an increased frequency in certain malfunctions which are associated with the formation of free radicals, suggesting that the iron binding of Tf C2 promotes the formation of hydroxyl radicals. In our study population of 20 patients with Alzheimer's disease, 13 had the C2 genetic subtype. Since the frequency of C2 in the South African population is 0.136 (14%), this represents a significant increase (p < 0.005) in the appearance of this genetic subtype.

Aluminum↗
PubMed1993

The development of an enzyme-linked immunosorbent assay for the determination of cortisol binding globulin.

A simple, reliable and reproducible enzyme-linked immunosorbent assay (ELISA) using polyclonal antibodies for human cortisol binding globulin (CBG) has been developed. The sensitivity of the ELISA (1.20 fmol CBG/well) compared favourably with the sensitivity of other immunoassays. The excellent agreement (r = 0.98) seen between the present study and a binding assay indicates that the polyclonal antibodies used recognize only intact steroid-binding CBG. The intra- and inter-assay coefficient of variation (4.0% and 7.1% respectively) compared favourably with those reported by other authors.

Carrier Proteins↗
PubMed1993

Lecithin:cholesterol acyltransferase activity and high-density lipoprotein subfraction composition in type 1 diabetic patients with improving metabolic control.

On initial diagnosis or when metabolic control is poor, subjects with type 1 (insulin-dependent) diabetes mellitus often exhibit decreased high density lipoprotein (HDL) cholesterol levels, which have been associated in numerous studies in non-diabetic subjects with atherosclerosis and coronary artery disease. We measured the activities of plasma lecithin:cholesterol acyltransferase (LCAT), post-heparin lipoprotein lipase, and the composition of the HDL subfractions HDL2 and HDL3, in ten poorly controlled type 1 diabetic patients admitted to a metabolic ward (six women and four men, aged 18-37 years). The measurements were repeated after metabolic control had been optimised and again a week after discharge. The results were compared with those of ten healthy normolipidaemic subjects matched for age, sex and body mass. LCAT activity increased significantly (P < 0.05) with improved metabolic control in the diabetic patients, and showed positive within-person correlation with HDL2 cholesterol ester (r = 0.67; P < 0.01), HDL2 free cholesterol (r = 0.67; P < 0.01), phosphatidylcholine (r = 0.49; P < 0.05), total phospholipids (r = 0.50; P < 0.01) and apolipoprotein A-I (apo A-I: r = 0.72; P < 0.01). With improving metabolic control HDL2 lipid levels increased more than twofold and the compositional changes in HDL2 were reflected by an increased apo A-I:apo A-II ratio (P < 0.05) and a decreased triglyceride:apo A-I ratio (P < 0.05). Changes in HDL3 levels and composition were minor. The results of this study indicate that an increase in LCAT activity increases the concentration and changes the composition of HDL2 in type 1 diabetic patients with improved metabolic control.

Adolescent↗
PubMed1993

The stimulatory effect of chronic lithium treatment on basal thyrotropin secretion in rats: in vivo antagonism by methylparaben.

Chronic treatment of rats with lithium chloride was examined in order to determine its effects on hypothalamic monoamine and metabolite content, basal thyrotropin (TSH) secretion and thyroid function. The hypothalamic concentrations of noradrenaline (NA), dopamine (DA) and its metabolites, dihydroxyphenylacetic acid. (DOPAC) and homovanillic acid (HVA) in the lithium treated rats remained unaltered when compared to control levels. NA turnover and the NA metabolite, 3-methoxy-4-hydroxyphenylglycol (total MHPG), were significantly lower (p < 0.01), whereas both serotonin (5-HT) and its metabolite, 5-hydroxyindole-3-acetic acid (5-HIAA), were significantly higher (p < 0.01 and p < 0.02, respectively) in the lithium treated rat hypothalami than in controls. Chronic lithium treatment significantly elevated basal TSH levels (p < 0.05). This effect was antagonized by methyl p-hydroxybenzoate (methylparaben, p < 0.01), which did not itself affect basal TSH levels. Free serum T3 and T4 levels were not significantly affected by chronic lithium treatment, although T4 tended to be slightly lower than control levels. The monoamine changes observed in the hypothalamus of lithium treated rats did not appear to account for the elevated TSH levels observed in these rats since NA activity which is generally regarded as stimulatory was decreased and 5-HT which has an inhibitory effect on TSH secretion, was increased. The elevated TSH levels may have been due to a reduced negative feedback inhibition of TSH release by the mildly reduced circulating T4 levels caused by chronic lithium treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗