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Biomedical subjects

S K Martin

Publications and source records attributed to S K Martin.

53 records · Page 3Linked to original sources
PubMed1990

Intake and digestibility of low-quality native grass hay by beef cows supplemented with graded levels of soybean hulls.

Twelve Hereford cows and four mature, ruminally cannulated Hereford x Angus heifers were fed supplements providing either 0 (control), 1, 2, or 3 kg/d of soybean hulls and including 440 g of protein/d (cottonseed meal was used to equalize protein intake) to determine the effects of supplementation on intake and utilization of low-quality native grass hay. Cattle were housed in individual pens and fed coarsely chopped (5-cm screen) native grass hay harvested in mid-November (4.1% CP, 76.9% NDF). Hay OM intake peaked (quadratic, P = .04) at 10.1 kg/d with 1 kg of soybean hulls and decreased when 2 kg (9.8 kg/d) or 3 kg (9.1 kg/d) of soybean hulls were fed. Although hay intake decreased when soybean hulls replaced cottonseed meal, feeding 3 kg soybean hulls decreased hay OM intake by only .64 kg. Total OM digestibility increased linearly (P = .009) with added increments of soybean hulls (45.8%, 46.2%, 46.6% and 48.6% for 0 through 3 kg soybean hulls/d, respectively), indicating that hulls were more digestible than the hay. Digestibility of NDF was not affected (P = .14) by level of soybean hull supplementation, although ADF digestibility increased (linear, P = .03). Increases in OM intake and digestibility with soybean hulls combined to increase digestible OM intake (linear, P = .0001). Soybean hull supplementation increased ruminal VFA concentrations (linear, P = .04) and the molar proportion of propionate (linear, P = .006).(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗
PubMed1988

Ultrastructural study of the effects of chloroquine and verapamil on Plasmodium falciparum.

Verapamil, a calcium antagonist, has recently been shown to reverse chloroquine resistance in malarial parasites in vitro. We report the first ultrastructural morphological changes associated with this phenomenon using chloroquine-sensitive and -resistant clones of Plasmodium falciparum. While the administration of 6.3 x 10(-8) M chloroquine had little morphological effect on the chloroquine-resistant strain, the combination of chloroquine and verapamil resulted in typical chloroquine-related food vacuolar swelling with increased amounts of granular matrix. Secondary morphological changes included degeneration of nuclei, mitochondria, and other organelles. These effects appeared similar to those in the chloroquine-sensitive strain of P. falciparum treated with chloroquine alone or with the chloroquine/verapamil combination. Furthermore mild food vacuolar changes were seen in a small number of parasites (from both chloroquine-sensitive and -resistant groups) exposed to high concentrations (1 x 10(-4) M) of verapamil alone.

Animals↗
PubMed1987

Efflux of chloroquine from Plasmodium falciparum: mechanism of chloroquine resistance.

Chloroquine-resistant Plasmodium falciparum accumulate significantly less chloroquine than susceptible parasites, and this is thought to be the basis of their resistance. However, the reason for the lower accumulation of chloroquine was unknown. The resistant parasite has now been found to release chloroquine 40 to 50 times more rapidly than the susceptible parasite, although their initial rates of chloroquine accumulation are the same. Verapamil and two other calcium channel blockers, as well as vinblastine and daunomycin, each slowed the release and increased the accumulation of chloroquine by resistant (but not susceptible) Plasmodium falciparum. These results suggest that a higher rate of chloroquine release explains the lower chloroquine accumulation, and thus the resistance observed in resistant Plasmodium falciparum.

Animals↗
PubMed1987

Reversal of chloroquine resistance in Plasmodium falciparum by verapamil.

The parasite Plasmodium falciparum, like neoplastic cells, develops resistance to multiple structurally unrelated drugs. If the mechanisms by which P. falciparum and neoplastic cells become resistant are similar, then it may be possible to reverse the resistance in the two types of cells by the same pharmacological agents. Verapamil, a calcium channel blocker, completely reversed chloroquine resistance in two chloroquine-resistant P. falciparum clones from Southeast Asia and Brazil. Verapamil reversed chloroquine resistance at the same concentration (1 X 10(-6)M) as that at which it reversed resistance in multidrug-resistant cultured neoplastic cells. This same concentration of verapamil had no effect on chloroquine-sensitive parasites. Hence, chloroquine resistance in P. falciparum may fit the criteria for the multidrug-resistant phenotype.

Animals↗
PubMed1979

Severe malaria and glucose-6-phosphate-dehydrogenase deficiency: a reappraisal of the malaria/G-6-P.D. hypothesis.

Nigerian children with convulsions and Plasmodium falciparium parasitaemia above 100,000/microliter did not show a decreased frequency of glucose-6-phosphate-dehydrogenase (G.-6-P.D.) deficiency. A re-evaluation of earlier studies has led to the conclusion that clinical evidence of protection against falciparum malaria in G.-6-P.D.-deficient individuals is lacking. Evidence for the possible role of malaria in selecting for G.-6-P.D.-deficient genes consists solely of the geographical association of high frequencies of G.-6-P.D. deficiency with endemic malaria.

Child↗
PubMed1979

Frequency of blood group antigens in Nigerian children with falciparum malaria.

The frequencies of the following blood group antigens: A, B, O, M, N, S, s, U, Fya, FyB, Lea, Jsa and K have been determined in Nigerian children with severe falciparum malaria. The frequency distribution of M, N, S, s, U, Fya and Fyb were not significantly different in children with life-threatening falciparum malaria and controls. The frequencies of A, B, O, Lea, Jsa and K found in the children with severe malaria were similar to those previously reported for healthy adults in this population. The Duffy blood group antigens Fya and Fyb were virtually absent from both infected and control children. This finding is in variance with a Fya frequency of 23% reported by Worlledge et al. (1974) for healthy adults in this population.

ABO Blood-Group System↗
PubMed1978

Low erythrocyte pyridoxal-kinase activity in Blacks: Its possible relation to falciparum malaria.

The red-cell glucose-6-phosphate dehydrogenase (G.-6-P.D.) activity and red-cell pyridoxal-kinase (P.L.K.) activity of 27 Nigerian children with severe Plasmodium falciparum parasitaemia were compared with those of 26 healthy Nigerian children and 6 White adults. The mean P.L.K. activity of the malaria patients was similar to that of the Whites but significantly higher than that of the Nigerian controls. Correction for reduced mean red-cell age in patients was made by comparing the P.L.K.: G.-6-P.D. ratio for those subjects with stable G.-6-P.D. phenotypes. The mean P.L.K.:G.-6-P.D. ratio was the same for malaria patients and adult White but significantly higher than that for the Nigerian controls. These results suggest that the relatively high frequency of low red-cell P.L.K. activity among Blacks may have been selected for by falciparum malaria.

Adult↗
PubMedDate not supplied

Chloroquine resistant Plasmodium falciparum in indigenous residents of Cameroon.

Thirty-nine percent (36 of 92) of children in Limbe, Cameroon, treated with chloroquine (10 mg/kg body weight on days 1 and 2, and 5 mg/kg on day 3) for falciparum malaria failed to respond within 7 d of treatment. Twenty-two of these children with chloroquine-resistant malaria were successfully treated with Fansidar [one-half tablet (250 mg sulfadoxine and 25 mg pyrimethamine) per 10 kg body weight], while the other 14 children were cured with mefloquine (25 mg/kg body weight). In vitro, a combination of verapamil at 1.0 x 10(-6) M with chloroquine or desethylchloroquine reversed resistance to the antimalarial drug and its primary metabolite in each of the 2 isolates successfully adapted and maintained in continuous culture. Similar combinations had no effect on susceptibilities of a sensitive reference clone, D6, used as control. Both chloroquine-resistant isolates from Cameroon were significantly more susceptible to mefloquine and halofantrine in vitro than the chloroquine-sensitive reference clone. Clinical observation, and in vitro confirmation, of chloroquine-resistant falciparum malaria in these indigenous children from Cameroon, and the current socio-economic condition in West Africa, underscore the need for pragmatic health management policies for efficient use of alternative antimalarial drugs in controlling drug resistant Plasmodium falciparum in the region. This observation of reversal of chloroquine resistance in isolates of P. falciparum obtained from West Africa, and a previous report on clones obtained from south-east Asia and South America, suggest that the mechanism(s) of resistance to chloroquine may be identical in resistant parasites from the 3 continents.

Animals↗
PubMedDate not supplied

Plasmodium falciparum: modulation by calcium antagonists of resistance to chloroquine, desethylchloroquine, quinine, and quinidine in vitro.

Intrinsic interactions of calcium antagonists (broadly defined) and quinoline-containing antimalarial drugs were evaluated against chloroquine-sensitive and chloroquine-resistant clones of Plasmodium falciparum in vitro. Verapamil, D-600 (methoxyverapamil), Ro 11-2933/001 (tiapamil analogue), chlorpromazine, SKF 21133-A (chlorpromazine analogue), and diltiazem each potentiated the efficacy of the quinoline-containing antimalarials chloroquine, desethylchloroquine, and quinine with a chloroquine-resistant clone of P. falciparum, but did not affect the response of the quinoline-susceptible clone. Similar concentrations of either chlorpromazine or Ro 11-2933/001 lowered the IC50 of the resistant clone to approximately the same level as that observed for the sensitive clone for each of the quinolines tested. This reversal of resistance by many of the same calcium antagonists underscores the similarities in one mechanism of multi-drug resistance in neoplastic cells and quinoline-resistance in P. falciparum.

Animals↗
PubMedDate not supplied

Reversal of drug-resistant falciparum malaria by calcium antagonists: potential for host cell toxicity.

Agents capable of reversing multidrug resistance (mdr) in falciparum malaria were investigated for potentiation of chloroquine accumulation and toxicity in a cell culture system. Verapamil, its analog RO11-2933, and desipramine caused a dose-dependent increase in the accumulation of chloroquine (CQ) within human and mouse hepatocytes but not human lung cells. Only those cells in which drug accumulation was enhanced by reversing agents reacted positively for P-glycoprotein (PgP)--the putative mediator of the enhanced drug efflux characteristic of mdr. Clinically achievable concentrations of verapamil (0.4 microM) and desipramine (1 microM) increased CQ accumulation within primary mouse hepatocytes by more than 50%. A well-differentiated normal human cell line (Hep-G2) was killed in media containing a combination of supraphysiological concentrations of CQ and verapamil but survived the same concentrations of either drug alone. Reversing agents may block PgP-mediated drug export from normal tissues as well as from MDR cells. Iatrogenic toxicity resulting from this accumulation of potentially toxic drugs such as CQ within normal cells could complicate the reversal of mdr in vivo.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMedDate not supplied

Determination of methyl 2-benzimidazolecarbamate in bulk fruit juice concentrates by competitive-inhibition enzyme immunoassay.

A polyclonal enzyme immunoassay (EIA) was used to quantitate methyl 2-benzimidazolecarbamate (MBC or carbendazim), a degradation product of benomyl, in bulk fruit juice concentrates. These concentrates are used by industrial producers to prepare juice or juice concentrates sold in supermarkets. Total sample analysis time was less than 18 min without cleanup or 35 min with cleanup. As many as 8 samples can be analyzed simultaneously, with a limit of quantitation of 10 ppb. The assay's dynamic range ran from 0.5 to 20 ppb MBC but was best from 0.5 to 10 ppb. Intra-assay coefficients of variation (CVs) varied from 4.0 to 13% for standards and from 4.1 to 26% for samples. Interassay CVs varied from 4.5 to 47% for standards and 5.6 to 22% for samples. Average recovery of several juice concentrates spiked at 10 to 290 ppb was 97%. A total of 140 juice concentrates comprising 20 different kinds of juice were analyzed by 2 EIA methods and one liquid chromatographic (LC) procedure. MBC-positive samples gave the following correlation coefficients: 0.954 for EIA without cleanup vs LC, 0.956 for EIA with cleanup vs LC, and 0.978 for EIA with cleanup vs EIA without cleanup. MBC concentrations in MBC-positive juice samples ranged from 5 to 2960 ppb.

Benzimidazoles↗