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D W Cox

Publications and source records attributed to D W Cox.

At least 181 records · Page 10Linked to original sources
PubMed1980

Release of amino acids from chronic epileptic and subepileptic foci in vivo.

Perforated discs of cobalt or nickel were implanted onto the sensorimotor strip of the cerebral cortex of rats. Co discs gave rise to myoclonic contralateral limb-jerks in a manner similar to Co powder lesions. In contrast, Ni-implanted animals were never observed to show overt limb-jerks. On superfusion with an in vivo cannula system, both types of lesion released increased amounts of glutamate, valine and glycine as compared with unlesioned tissue. However, the enhancement of release from epileptogenic Co lesions was approximately 3-fold greater than that from non-epileptogenic lesions. In addition, epileptogenic lesions showed a marked reduction in glutamine release compared to controls, while non-epileptogenic lesions did not. The possible involvement of local disorders of the glutamate/glutamine system in the generation of cobalt focus hyperactivity is discussed.

Amino Acids↗
PubMed1980

Purification of rat ceruloplasmin. characterization and comparison with human ceruloplasmin.

Rat ceruloplasmin was purified by a three-step column chromatography procedure, utilizing DEAE-Sepharose, Sepharose CL-6B, and CM-Sephadex A50 columns. The molecular weight of rat ceruloplasmin determined by a molecular sieve column was 124,000 daltons. An optical density ratio (610 nm/280 nm) of 0.051 and a molar extinction coefficient of 8600 were obtained. A decrease in lysine in rat ceruloplasmin compared with human ceruloplasmin could account for its reduced anodal mobility. Other differences in the amino acid sequence of the rat ceruloplasmin included an increase in methionine and cystine/cysteine, and a decrease in histidine, tyrosine and tryptophan.

Amino Acids↗
PubMed1980

Association of severe rheumatoid arthritis with heterozygosity for alpha 1-antitrypsin deficiency.

Genetic types of alpha 1-antitrypsin (protease inhibitor types, or Pi types) were determined in 108 patients with rheumatoid arthritis. These patients were selected for severely destructive disease and had classical rheumatoid arthritis according to ARA criteria, were seropositive, and had joint erosions shown by X-ray. Heterozygotes for the deficiency Z allele (Pi types MZ, SZ, etc.) were found among 9.2% of patients and 3.5% of a control adult population. The increased frequency in patients was statistically significant. Heterozygotes were most frequent among female patients with an early onset of disease. Heterozygosity for alpha 1-antitrypsin deficiency may be a factor in familial recurrence of rheumatoid arthritis. Among 98 patients with juvenile rheumatoid arthritis not selected for severity, 4.1% were Z heterozygotes compared with 1.3% of control children, not a statistically significant difference. Reduced concentrations of alpha 1-antitrypsin in Z heterozygotes may be inadequate to inhibit the proteolytic enzymes released into the joints of adults with rheumatoid arthritis during phagocytosis of immune complexes. This may be a factor promoting severe joint destruction.

Adult↗
PubMed1980

Activation of prorenin by proteases from polymorphonuclear leukocytes.

Inactive renin (prorenin) can be activated by certain proteases in human blood, of which a possible source in vivo is polymorphonuclear leukocytes (PMNs). We extracted enzyme from PMNs using methods established for the recovery of neutral and acid protease fractions, and tested their effectiveness on plasma prorenin in vitro. Neutral protease preparations, possessing mainly chymotrypsin and elastase activity, produce no activation of prorenin. Exogenous pancreatic alpha-chymotrypsin does activate plasma prorenin, but less effectively than trypsin. From the quantity of PMNs extracted for neutral protease, and its failure to activate protenin, we deduce that this enzyme preparation, like exogenous chymotrypsin, is qualitatively unimportant. In contrast, the extracted PMN acid protease fraction, believed to be rich in cathepsin D, exhibited high prorenin activating ability, suggesting both quantitative and qualitative importance. The low pH requirement of this acid protease (near pH 4.0), together with its inactivity at neutral pH, argues against an important systemic role in the conversion of prorenin. However, it may contribute to systemic activation in partnership with other enzymes, or else play a specialized local role in situations where PMN concentration and activity increase, and the pH is on the acid side.

Chymotrypsin↗
PubMed1980

Functional assay of alpha 1-antitrypsin in obstructive lung disease.

A decreased concentration of alpha 1-antitrypsin is associated with a high risk for obstructive lung disease. We measured the elastase inhibitory capacity, the most important biologic measure of alpha 1-AT function, using a natural substrate. The gel plate assay that we developed uses a commercial gelatin film and is more sensitive, faster, and cheaper than similar elastin-elastase methods. In serum samples from 76 patients with emphysema, there was a high correlation between the immunologically measured alpha 1-AT and the elastase inhibitory capacity. There was no evidence for a functionally deficient alpha 1-AT in any of these patients.

Humans↗
PubMed1979

Peripheral sensory stimulation and the release of transmitter amino acids in vivo from specific regions of cerebral cortex.

The effects of sensory stimulation on the release of amino acids from sensorimotor and visual cortex have been studied using a superfusion technique. Electrical stimulation of the brachial plexus contralateral to the superfusion cannula increased significantly the release of glutamate and glutamine from the sensorimotor cortex of anaesthetized rats. No clear effect was observed with the other amino acids. Stimulation of the ipsilateral plexus had no effect on glutamate and glutamine release. In unanaesthetized animals stimulation of the contralateral brachial plexus raised the levels of all the amino acids in sensorimotor cortex superfusate. Weak photic stimulation of the eyes of dark-adapted rats increased glutamate release from the visual cortex but caused no significant change in the release of other amino acids. All evoked increases in amino acids release were reversible at the cessation of the stimuli.

Amino Acids↗
PubMed1979

Peripheral sensory stimulation and the release of transmitter amino acids in vivo from specific regions of cerebral cortex.

The effects of sensory stimulation on the release of amino acids from sensori-motor and visual cortices have been studied using a superfusion technique. Electrical stimulation of the brachial plexus contra-lateral to the superfusion cannula increased significantly the release of glutamate and glutamine from the sensori-motor cortex of anesthetized rats. No clear effect was observed with the other amino acids. Stimulation of the ipsi-lateral plexus had no effect on glutamate and glutamine release. In unanesthetized animals, stimulation of the contra-lateral brachial plexus raised the levels of all the amino acids in sensori-motor cortex superfusate. Weak photic stimulation of the eyes of dark-adapted rats increased glutamate release from the visual cortex but caused no significant change in the release of other amino acids. All evoked increases in amino acid release were reversible at the cessation of the stimuli.

Amino Acids↗
PubMed1978

Inheritance of apolipoprotein C-II deficiency with hypertriglyceridemia and pancreatitis.

A study of the relatives of a patient with apolipoprotein C-II deficiency showed that the defect is inherited as an autosomal recessive trait. The kindred studied originated from an isolated population in which considerable inbreeding has occurred for 140 years. Seven homozygotes had marked fasting chylomicronemia and triglyceridemia, and lacked detectable apolipoprotein C-II by several assay methods. Five homozygotes had experienced one to many attacks of pancreatitis from as early as six years of age. Obligate heterozygotes had apolipoprotein C-II concentrations about 30 to 50 per cent of normal values and had normal plasma triglyceride concentrations. This metabolic defect should be considered in patients with markedly elevated plasma triglycerides who have apparent lipoprotein lipase deficiency, and usually also have pancreatitis.

Adolescent↗
PubMed1978

Catabolic rate of alpha1-antitrypsin of of Pi types S, and MMalton and of asialylated M-protein in man.

1. Human alpha1-antitrypsin was isolated with preserved microheterogeneity from subjects of Pi types M, S and MMalton. The M-protein was partially (20%) and completely desialylated. The proteins were labelled with either 125I or 131I. 2. The disappearance rate of these alpha1-antitrypsins was studied after simultaneous injection of the two types of labelled protein into Pi M subjects. The fractional catabolic rates of S- and MMalton-protein were 0.36 and 0.34 day(-1) respectively compared with 0.28 day(-1) for M-protein. The ratio of extravascular to plasma pools was 1.4 for S- protein and 1.6 for MMalton-protein. The 20% desialylated M-protein showed an increase of about 100% in its fractional catabolic rate. The disappearance rate of completely desialylated alpha1-antitrypsin was extremely rapid. 3. The slightly higher fractional catabolic rate of S- than of M-protein can only partly explain the 40% lower plasma concentration in subjects of Pi type S. Similarly the slight increase in catabolic rate of Pi MMalton- protein is too small to explain why the alpha1-antitrypsin content of the blood in Pi MMalton subjects is only 15% of that normally found. A low hepatic secretion seems to be the major cause of the low alpha1-antitrypsin concentration found in subjects of types Pi S and MMalton, as in Pi type Z.

Adult↗
PubMed1978

Group-specific component, alpha1-antitrypsin and esterase D in Canadian Eskimos.

Three genetic markers - group-specific component (Gc), alpha1-antitrypsin, and esterase D - were examined in a population of Eskimos from Igloolik in the eastern Canadian Arctic. Gc and esterase D were found to be polymorphic. In addition to the common Gc types, an anodal variant called Gc Igloolik was found, probably identical to previously reported Gc Eskimo. Gene frequencies were Gc1: 0.6524, Gc2: 0.3373, GcIgl: 0.0104, for 338 Eskimos. Genetic types of alpha1-antitrypsin (Pi types) were mostly M, with two MS sibs who were half Caucasian, in 170 Eskimos. Frequencies of the esterase D allele in 336 Eskimos were EsD1: 0.7083, EsD2: 0.2917. The frequencies of Gc2 and EsD2 are both higher than are found in Caucasian populations.

Canada↗