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J K Baird

Publications and source records attributed to J K Baird.

At least 73 records · Page 4Linked to original sources
PubMed1986

Oxidative activity of hydroxylated primaquine analogs. Non-toxicity to glucose-6-phosphate dehydrogenase-deficient human red blood cells in vitro.

The individual effects of two putative metabolites of primaquine (5,6-dihydroxyprimaquine and 5,6-dihydroxy-8-aminoquinoline) on the hexose monophosphate shunt (HMS) and on the ATP-dependent proteolytic system which rapidly degrades oxidized erythrocyte protein were measured in intact red blood cells in vitro from two blood donors. In red cells treated with nitrite (1-40 mM) or phenylhydrazine (0.01-10 mM), proteolytic activity was detected only with concentrations (7.5 mM NaNO2 and 0.25 mM phenylhydrazine) causing greater than 15-fold elevation of HMS activity, and glucose-6-phosphate dehydrogenase (G6PD)-deficient (25% of normal activity) red cell suspensions thus treated showed approximately 30% greater proteolysis. G6PD-normal and deficient red cells treated with the primaquine analogs, however, did not experience proteolysis with concentrations (0.25 mM) in excess of those causing 17-fold elevation of HMS activity. Stimulation of the HMS by the primaquine analogs thus appears unrelated to an erythrotoxic oxidative stress. Methylene blue is known to cause an elevation of HMS activity through direct and diaphorase II-dependent oxidation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) which is independent of injurious oxidative stress. It was found that the putative primaquine metabolites also caused direct and diaphorase II-dependent oxidation of NADPH in dilute hemolysate, thus suggesting that the putative primaquine metabolites have a methylene blue-like redox disposition in red blood cells. Results obtained in this study suggest that the hemolytic toxicity of primaquine may be unrelated to processes which lead to oxidative deterioration of red cell protein.

Adenosine Triphosphate↗
PubMed1986

Effects of nine synthetic putative metabolites of primaquine on activity of the hexose monophosphate shunt in intact human red blood cells in vitro.

Suspensions of washed human red blood cells were treated with nine synthetic putative metabolic derivatives of primaquine (PQ'), and their individual effects on activity of the hexose monophosphate shunt (HMS) were quantitated by radiometric analysis of 14CO2 from [14C] glucose. The most potent HMS stimulant was 5-hydroxy-6-methoxy-8-aminoquinoline (5H6MQ), which caused 10-fold elevation of HMS activity at an estimated concentration of 0.004 mM. Ten millimolar primaquine (PQ) was required to achieve the same effect. Thus, 5H6MQ was approximately 2500-fold more reactive with the HMS than PQ. Other analogs achieved less than 0.4- to 154-fold increases in HMS reactivity. Patterns of effects on HMS activity indicated that 5-hydroxylation and/or N-dealkylation of PQ strongly enhanced HMS reactivity. In contrast, none of the putative metabolites of PQ activated the proteolytic system known to degrade oxidized protein in red cells, indicating that stimulation of the HMS by the PQ analogs was not related to an injurious oxidative stress. Red cells pretreated with 1.0 mM N-ethylmaleimide (NEM) or with 1.0% (w/v) sodium nitrite to cause glutathione sulfhydryl blockage and conversion of red cell hemoglobin to methemoglobin (metHb), respectively, also showed elevation of HMS activity when exposed to 5H6MQ. These observations suggested that 5H6MQ-induced elevation of HMS activity was at least partially independent of glutathione redox reactions, hydrogen peroxide accumulation and reaction with oxyhemoglobin. The relevance of these observations to proposed mechanisms of hemolytic toxicity of PQ is discussed.

Aminoquinolines↗
PubMed1986

North American brugian filariasis: report of nine infections of humans.

Nine people living in Rhode Island, New York, Pennsylvania, Florida, or California acquired autochthonous brugian filariasis. Each patient had an enlarged lymph node containing a single worm or, in one patient, a pair of worms. Most worms were in lymphatic vessels within the node, but two worms were in the substance of the node. Ten worms were studied, seven female and three male. Female worms contained paired uteri that occupied most of the body cavity of the worm, and male worms contained a single reproductive tract. No worms were gravid. The diameter of the worms was small, 30 micron to 75 micron. The usual diameter of female worms was 65 micron to 75 micron, and 45 micron to 50 micron for male worms. The morphologic features of these worms, their anatomical location, and their geographic distribution are all characteristic of infection with a North American Brugia species.

Adult↗
PubMed1986

Fatal human ascariasis following secondary massive infection.

More than 796 Ascaris lumbricoides worms weighing 550 g were recovered at autopsy from a 2-year-old black South African girl. Most of the worms were taken from necrotic small intestine, but worms were also in the stomach, esophagus, intrahepatic and extrahepatic bile ducts, and gallbladder. The worms had caused torsion and gangrene of the ileum, which was interpreted as the cause of death. Worms were formalin-fixed and individually weighed. There were 796 intact worms and 112 appreciably large (greater than 0.2 g) fragments of worms. Statistical analysis of the weights revealed 2 distinct populations of worms: 16 large worms (0.5-2.3 g) and 778 small worms (0.03-0.95 g). The difference in weight between these 2 groups of worms was significant (male and female worms treated separately; P less than 0.05 to P less than 0.001). These observations reveal that the patient acquired a massive and fatal infection with A. lumbricoides while hosting a relatively burden.

Ascariasis↗
PubMed1984

An in vitro micro-volume procedure for rapid measurement of erythrocytic hexose monophosphate shunt activity.

A radiometric micro-volume procedure for measurement of erythrocytic hexose monophosphate shunt (HMS) activity in intact cells in vitro is described. The procedure is rapid, allowing 200 individual HMS determinations in a single experiment of 5 hr duration. The procedure is reproducible, yielding HMS activity means insignificantly different (P greater than 0.05) between replicate experiments. A profile of sodium nitrite-induced HMS stimulation is reported: HMS was elevated 2-fold (P less than 0.001) between zero and 2.5 mM NaNO2; HMS elevation was more distinct (7-fold) between 2.5 and 5.0 mM NaNO2; maximum activity (22-fold) was observed between 10 and 20 mM NaNO2; greater than 20 mM NaNO2 caused significant (P less than 0.001) diminution of HMS; glucose carbon recycling through the HMS occurred only with greater than 2.5 mM NaNO2 where this process contributed less than or equal to 16% to total HMS activity.

Adult↗
PubMed1984

Methylene blue-mediated hexose monophosphate shunt stimulation in human red blood cells in vitro: independence from intracellular oxidative injury.

The red blood cell hexose monophosphate shunt (HMS) and proteolytic responses to several concentrations of Methylene Blue or sodium nitrite were measured. The results suggested two distinct mechanisms for activation of the HMS: (1) nitrite treatment increased HMS activity in response to oxidative challenge to red cell protein; (2) Methylene Blue treatment activated HMS without injurious oxidative challenge. Nitrite-treated cells actively degraded protein, whereas Methylene Blue-treated red cells did not activate proteolytic systems that degrade oxidized red cell protein. These observations are relevant to proposed in vitro systems for evaluation of drug hemolytic toxicity potential on the basis of HMS stimulation capacity.

Adult↗
PubMed1984

Effect of membrane filtration of antimalarial drug solutions on in vitro activity against Plasmodium falciparum.

Antimalarial activities of chloroquine, mefloquine, amodiaquine, and quinine in vitro against Plasmodium falciparum were diminished as a consequence of membrane filtration. Filtered drug solutions gave ID(50) values up to 25-fold greater than those of non-filtered (ethanol-sterilized) drug solutions. Loss of activity by filtration was overcome by increasing the drug concentration prior to filtration. Water solutions filtered through Millex-GS filter units consistently showed an absorbance maximum at 277 nm, accompanied by a lesser peak at 225 nm. Water filtrates from Nucleopore and Millex-GV filters showed no absorbance at 277 nm and only slight absorbance was evident for the Gelman filter unit. Activity losses were attributed to extractable contaminating moieties in the membrane filters and/or drug binding to the membrane filters.

Antimalarials↗
PubMed1977

Enhanced plasma persistence of therapeutic enzymes by coupling to soluble dextran.

Conjugation of carboxypeptidase G and arginase, two enzymes of therapeutic interest, to a soluble dextran significantly enhanced plasma persistence in normal and tumour-bearing mice. A prolonged decrease in arginine concentrations in plasma of tumour-bearing mice was demonstrated by using the dextran-linked arginase. Gel filtration of dextran-enzyme conjugate showed that enzyme activity co-chromatographed as a single peak with carbohydrate, and enzyme was shown to be covalently linked to the dextran.

Animals↗
PubMed1976

Variations in surface polymers of Streptococcus mutans.

The cell wall composition of strains of S mutans with respect to sugars and proteins appears to be correlated to the serological grouping although groups c and E are rather similar. There also appear to be similarities in the structure of the polysaccharide formed by the glycosyltransferases from organisms of serological groups b and d. However, the activity of these enzymes appears to be variable in these groups. The most noteworthy difference found was that between the three Ingbritt strains. All three strains gave identical results with regard to their cell wall composition, and presumably this would mean that they were identical serologically. However, Ingbritt LH differed considerably from both the others in the types of polysaccharide formed by their glycosyltransferases from sucrose. Ingbritt B was a reisolate from monkeys, whereas Ingbritt LH was maintained in laboratory culture, and this may explain the difference. Clearly, more work will be required to explain this difference and as c strains are commonly isolated from plaque, it would seem desirable to clear up this point.

Cell Wall↗