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Biomedical subjects

C D Anderson

Publications and source records attributed to C D Anderson.

At least 37 records · Page 2Linked to original sources
PubMed1989

Kinetic studies of Haemophilus influenzae 6-phosphogluconate dehydrogenase.

Haemophilus influenzae 6-phosphogluconate dehydrogenase (6-phospho-D-gluconate:NADP+ 2-oxidoreductase (decarboxylating), EC 1.1.1.44) was purified 308-fold to electrophoretic homogeneity with a 16% recovery through a five-step procedure involving salt fractionation and hydrophobic and affinity chromatography. The purified enzyme was demonstrated to be a dimer of Mr 70,000, and to catalyze a sequential reaction process. The enzyme was NADP-specific and kinetic parameters for the oxidation of 6-phosphogluconate were determined for NADP and four structural analogs of NADP. Coenzyme-competitive inhibition by adenosine derivatives was significantly enhanced by the presence of a 2'-phosphoryl group consistent with the observed coenzyme specificity of the enzyme. The purified enzyme was effectively inhibited by 3-aminopyridine adenine dinucleotide phosphate, but at concentrations higher than that observed to inhibit growth of the organism. Rates of inactivation of the enzyme by N-ethylmaleimide were suggestive of sulfhydryl involvement in the reaction catalyzed.

Adenine Nucleotides↗
PubMed1988

Long-lasting changes in regional brain amino acids and monoamines in recovered pyrithiamine treated rats.

Rats were subjected to a severe bout of thiamine deficiency induced by daily pyrithiamine + a thiamine deficient diet, reversed by thiamine administration and allowed to recover. Pyrithiamine treated animals demonstrated impaired retention of a 24 h recall of passive avoidance. Regional brain concentration of norepinephrine, dopamine, serotonin, 3,4-dihydroxyphenylacetic acid, 5-hydroxyindoleacetic acid, GABA, glutamate, aspartate, glutamine, and glycine were determined after 2 and 9 weeks of nutritional recovery. A significant increase in NE content of cerebellum from the pyrithiamine treated animals was observed at both 2 and 9 week recovery periods. The concentrations of serotonin and its metabolite were significantly elevated in midbrain-thalamus and striatum. Significant reductions of GABA and glutamate were also observed in midbrain-thalamus. Amino acid levels in all other brain areas were unchanged from pair-fed controls. These results suggest regionally specific, chronic alterations in GABA, glutamate, serotonin, and norepinephrine activity following recovery from an acute bout of pyrithiamine-induced thiamine deficiency. The absence of a permanent reduction of cortical norepinephrine similar to that observed in an earlier study is discussed.

Amino Acids↗
PubMed1988

Behavioral impairments, brain lesions and monoaminergic activity in the rat following recovery from a bout of thiamine deficiency.

Learning impairments were measured in rats following recovery from a subacute bout of thiamine deficiency. Behavioral training was carried out in an automated T-maze, beginning with paired run spatial delayed non-matching to sample (PR-1), then light-dark discrimination (LD), light-dark discrimination reversal (LD-R), spatial discrimination (SD), spatial discrimination-reversal (SD-R), and finally retraining on the original paired run task (PR-2). Comparable deficits were observed for PR-1 and PR-2, thus demonstrating long-lasting impairment on delayed non-matching to sample. Experimentals performed as well as controls on LD and LD-R. Two experimental animals were unable to perform above chance on the simple SD task. The remaining 15 experimental animals were equivalent to controls on several measures of SD and SD-R performance (errors to criterion, number of animals reaching criterion, correct responses in last 60 trials) although they were significantly worse than controls on both PR-1 and PR-2. Taken together, these results indicate an impairment of representational memory (PR-1, PR-2) with a spared capacity for dispositional memory (LD, LD-R, SD, SD-R) as defined by Thomas and Spafford (Behav. Neurosci., 1984, 98: 394-404). Histological analyses of left hemispheres revealed a high incidence (94%) of thalamic lesions, specifically within the intralaminar nuclei and ventral parts of the mediodorsal nucleus; and an absence of detectable changes in other structures, including the mammillary bodies, hippocampus, cortex, and locus coeruleus. In the right hemispheres, assays of monoamines and metabolites in 17 brain regions showed significant reduction only for norepinephrine in entorhinal cortex. All animals that were selectively impaired on the paired-run task had both the medial thalamic lesions and reduction in entorhinal norepinephrine.

Alcohol Amnestic Disorder↗
PubMed1988

Actinic damage in the skin of patients on haemodialysis for chronic renal failure.

Seventy-nine patients on long-term haemodialysis for chronic renal failure were interviewed and examined as to ethnic origin, actinic habits and the occurrence of blisters, skin fragility and slow healing of the skin of the dorsal part of the hands. On clinical examination, the 6 patients (7.5%) with blisters of the dorsal part of the hands had more damaged skin at that site than would be expected for their age. They also tended to be predominantly of English descent with blue eyes, poorer skin tanning ability and increased net exposure to sunlight. A skin imprint method for the grading of actinic damage showed a statistically significantly increased degree of actinic damage in the haemodialysis patients compared to a control group of healthy individuals matched for age and sex, the difference being more pronounced in the 35-64 year age group. Plasma and erythrocyte porphyrin levels were not related to the degree of actinic damage. It is suggested that reduction of the actinic load on the dermis by avoiding excessive exposure to sunlight might minimize the extent of skin changes in haemodialysis patients.

Adolescent↗
PubMed1987

Monoamines and metabolites in cortex and subcortical structures: normal regional distribution and the effects of thiamine deficiency in the rat.

The present study measured the concentration of monoamines, metabolites and estimates of turnover rate in eighteen separate brain regions from controls and a rat model of Korsakoff's disease induced by a two week bout of pyrithiamine and thiamine deficient diet (PTD). A behaviorally tested control (n = 12) and PTD (n = 17) group, and a non-behaviorally tested PTD group (n = 8) were sacrificed 7 months after recovery from treatment. The brains were dissected into nine cortical areas and nine subcortical regions. In behaviorally tested PTD animals, a significant reduction of NE was observed in entorhinal cortex. Diminished norepinephrine (NE) concentration was also observed in entorhinal, hippocampal, septal and olfactory areas of the non-behaviorally tested PTD group. Serotonin and 5-hydroxyindoleacetic acid (5-HIAA) levels were increased in several brain areas, particularly midbrain-thalamus, striatum, of both groups of recovered PTD animals. These findings are discussed with respect to results and hypotheses presented in our previous study of this animal model. Significant differences in monoamine, metabolite and turnover estimates were also observed among cortical areas of the control animals. Entorhinal cortex contained the highest concentration of NE and 5-hydroxytryptamine (5-HT), while DA was highest in somatosensory cortex. The distribution of 5-HT and 5-HIAA were more homogeneous and displayed a rostral-caudal decline in concentration.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

Potentiation of inflammatory reactions in guinea-pig skin by an angiotensin converting enzyme inhibitor (MK 422).

There have recently been reports of persistent cough and increased broncho-obstruction likely to have been induced by ACE inhibitors. In order to study the effect of MK 422 (the active parent diacid of enalapril) on the inflammatory response, ovalbumin-sensitized guinea-pigs were tested intradermally with ovalbumin, capsaicin and bradykinin. All inflammatory responses were enhanced by treatment with MK 422 for 2 days prior to testing as compared to the responses of control animals. Infiltration of neutrophils, eosinophils, basophils and monocytes was increased following ovalbumin challenge in the MK 422-treated animals. We suggest that skin reactions and airway symptoms noticed during ACE inhibitor therapy might have been due to induced or potentiated inflammatory reactions in the skin or in the bronchial wall.

Allergens↗
PubMed1987

Inhibitory effects of clonidine on allergic reactions in guinea-pig skin.

An experimental guinea-pig model was used to show that clonidine inhibited dose dependently the wheal and flare reaction to i.d. ovalbumin in sensitized animals. The effect of clonidine was counteracted by an alpha 2-adrenoceptor antagonist, yohimbine, but not by an alpha 1-adrenoceptor antagonist, prazosin. An H1-receptor antagonist, clemastine, initially reduced the wheal and flare reaction but did not influence the effect of clonidine. Cimetidine, an H2-receptor antagonist slightly reduced the effect of clonidine on the wheal and flare reaction. It is suggested that clonidine reduces the wheal and flare reaction by stimulating alpha 2-adrenoceptors, which inhibits the axon reflex of the response.

Animals↗
PubMed1987

Inactivation of human lactate dehydrogenase isozymes by sulfhydryl reagents.

Human lactate dehydrogenase isozymes, LDH-1 and LDH-5, were inactivated at 25 degrees C and pH 7.5 by N-alkylmaleimides of varying chain length, and by fluorescein mercuric acetate. Second-order rate constants for the inactivation of LDH-5 by N-alkylmaleimides increased with increasing chain length of the maleimide derivative while essentially no chain-length effect was observed in the inactivation of LDH-1. Both isozymes were effectively inactivated by low concentrations of fluorescein mercuric acetate, and in both cases saturation kinetics were observed. Dissociation constants obtained from double-reciprocal plotting methods indicated a twofold better binding of fluorescein mercuric acetate to LDH-1. Protection from fluorescein mercuric acetate by NAD was observed with both enzymes.

Fluoresceins↗
PubMed1987

Effects of some antihypertensive drugs on cutaneous blood flow and inflammatory skin responses following allergen challenge in guinea pigs.

The effects of the antihypertensive drugs clonidine, prazosin, and MK 422 (the active parent diacid of enalapril) were studied on the cutaneous blood flow and allergen evoked inflammatory skin reactions in ovalbumin sensitized guinea pigs. The hypotensive effect of the drugs did not significantly change the basal cutaneous blood flow at the time of allergen challenge. MK 422 (0.02 mg/kg) markedly enhanced the wheal and flare reaction following allergen challenge, whereas clonidine (0.005 and 0.05 mg/kg) inhibited the inflammatory response. Prazosin (0.03 mg/kg) did not significantly influence the wheal and flare reaction. Our results indicate that some antihypertensive drugs (clonidine) could be beneficial to antihypertensive patients with inflammatory diseases, while others (ACE-inhibitors) may enhance their inflammatory disorders.

Allergens↗
PubMed1987

Effects of clonidine on the dermal inflammatory cell response of experimental toxic and allergic contact reactions and intradermal hypersensitivity.

In previous studies, the alpha 2-adrenoceptor agonist clonidine has been shown to suppress the wheal and flare reaction in guinea pigs sensitized to ovalbumin. This phenomenon has been further studied with special reference to effects on the dermal inflammatory cell infiltrate and mast cells. Clonidine lessens the degranulation of mast cells seen in control untreated immediate hypersensitivity reactions. Less neutrophils and eosinophils arrive to the treated reactions. Basophils and mononuclear cells (chiefly lymphocytes) which characterize the late phase of the wheal and flare reaction were not influenced by clonidine. Clonidine had a possible minimal effect on allergic contact (delayed hypersensitivity) reactions. The toxic contact reaction to croton oil (nonspecific cutaneous inflammation) was not affected.

Animals↗
PubMed1987

Porphyrin studies in chronic renal failure patients on maintenance hemodialysis.

Porphyrin studies were performed on 85 chronic renal failure patients on maintenance hemodialysis. Free erythrocyte porphyrins were elevated in 70% of patients, and a significant positive correlation between erythrocyte porphyrin and serum aluminium was found. Although plasma porphyrins were elevated in 58% of our patients, the elevated heptacarboxylic fraction invariably seen in porphyria cutanea tarda (PCT) was not present in the hemodialyzed patients. Total urine and fecal porphyrins were low, due to a marked decrease in the coproporphyrin and dicarboxylic fractions, respectively. An unequivocal diagnosis of PCT was made in 1 hemodialysis patient whose biochemical findings included an extremely high total plasma porphyrin with a large heptacarboxyl-porphyrin fraction. We found no biochemical evidence for any trend towards PCT in the remaining hemodialysis patients. The porphyrin results on a subgroup of hemodialysis patients with blisters or a history of blisters on sun-exposed skin were similar to those of the hemodialysis patients without blisters.

Aluminum↗
PubMed1986

Learning impairments after 6-OHDA treatment: a comparison with the effects of thiamine deficiency.

Cortical norepinephrine, dopamine and 3,4-dihydroxyphenylacetic acid were reduced by injection of 6-hydroxydopamine (6-OHDA) jointly into the cisterna magna and the dorsal noradrenergic bundle. On subsequent behavioral testing, deficits were observed for spatial delayed alternation learning, but not for active or passive avoidance. Treatment with clonidine resulted in a significant improvement in spatial delayed alteration for experimental as compared to control animals. Injections of 6-OHDA into the cisterna magna alone had no significant effect on brain chemistry or behavioral measures. These results are similar to previous observations following a bout of thiamine deficiency, in which cortical catecholamines were depleted in animals that had exhibited deficits for spatial delayed alternation learning. We argue that the cortical catecholamine deficits observed in post-thiamine-deficient animals are sufficient to account for the delayed alternation deficits observed in this animal model of Korsakoff's psychosis.

Alcohol Amnestic Disorder↗
PubMed1985

Thiamine deficiency depletes cortical norepinephrine and impairs learning processes in the rat.

Several lines of evidence indicate that thiamine deficiency causes the Wernicke-Korsakoff syndrome, a human memory disorder. The present study examined behavioral deficits in rats after recovery from a bout of thiamine deficiency. Following behavioral testing, the brains were dissected into regions and assayed biochemically for levels of dopamine, norepinephrine, serotonin and the primary metabolites of these monoamines. Based on previous findings in this laboratory, we predicted that thiamine deficiency not only produces behavioral deficits but loss in catecholamines as well. Impairments were observed for a spatial delayed alternation task that had been learned prior to experimental treatment. In addition, experimental animals were impaired in their ability to acquire two novel tasks, active and passive shock avoidance, after recovery from the acute effects of thiamine deficiency. Comparable deficits were not observed for a number of reflex responses that were measured to assess the general neurological state of the animals. Biochemical analyses revealed that the concentration of norepinephrine was reduced significantly in cortex-hippocampus and olfactory bulb but not in other regions, while dopamine and serotonin levels were not altered in any brain region examined. These data demonstrate that a bout of thiamine deficiency can produce persistent deficits in brain norepinephrine and concomitant decrements in behavioral measures of learning and memory. These results are consistent with our hypothesis and evidence that noradrenergic deficits contribute to the amnesic symptoms of Korsakoff's psychosis.

Alcohol Amnestic Disorder↗