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Biomedical subjects

M T Fox

Publications and source records attributed to M T Fox.

At least 37 records · Page 2Linked to original sources
PubMed1997

Comparison of flea control strategies using imidacloprid or lufenuron on cats in a controlled simulated home environment.

OBJECTIVE: To compare the effect of monthly treatments with imidacloprid (an adulticide) or lufenuron (an insect development inhibitor) for protecting cats against Ctenocephalides felis felis in a simulated home environment. ANIMALS: 3 matched groups of 4 cats each. PROCEDURE: A self-propagating flea life cycle continuously exposing cats to 'natural' infestation was established in 3 pens. Small artificial infestations were later superimposed to mimic the effect of a cat roaming outdoors and acquiring extraneous fleas. One pen housed an untreated control group, and the other 2 pens housed cats treated every 28th day with an imidacloprid spot-on formulation or lufenuron suspension, respectively. Flea counts were performed at 14-day intervals for 112 days. RESULTS: Flea numbers increased on control cats around day 42 when mean counts on cats in the imidacloprid and lufenuron groups decreased by 100 and 86.8 percent, respectively. Fleas were not found on any imidacloprid-treated cat, but lufenuron-treated cats were consistently parasitized. CONCLUSIONS: Imidacloprid administered at monthly intervals maintained flea burdens below the limit of detection, whereas clinically important flea populations developed in the lufenuron treatment pen. CLINICAL RELEVANCE: Results from this experimental model suggest that flea populations within a home may be controlled by carefully timed on-host treatments with potent long-acting insecticides such as imidacloprid.

Administration, Cutaneous↗
PubMed1996

A mechanism for action of extremely low frequency electromagnetic fields on biological systems.

This report outlines a simple mechanism, based on the Hall Effect, by which static and low frequency (50-60 Hz) pulsed electromagnetic fields (PEMFs) can modify cation flow across biological membranes and alter cell metabolism. We show that magnetic fields commonly found in the environment can be expected to cause biologically significant interactions between transported cations and basic domains of cation channel proteins. We calculate that these interactions generate forces of a magnitude similar to those created by normal transmembrane voltage changes known to gate cation channels. Thus PEMFs are shown to have the potential of regulating flow through cation channels, changing the steady state concentrations of cellular cations and thus the metabolic processes dependent on cation concentrations.

Animals↗
PubMed1996

Wildlife diseases.

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Animal Diseases↗
PubMed1995

Differentiation between human and animal strains of Cryptosporidium parvum using isoenzyme typing.

Isoenzyme typing was used to study a number of oocyst isolates of Cryptosporidium parvum from different geographical locations and of human or animal origin. All isolates showed identical enzyme motility when glucose phosphate isomerase (GPI; 23 isolates tested) or lactate dehydrogenases (LDH; 20 isolates tested) was assayed. However, two isoenzyme forms were observed with phosphoglucomutase (PGM; 9 animal isolates showed one form, while 8/9 human isolates showed a second form) and hexokinase (HK; 4 human isolates showed one form and 6 animal isolates showed a second form). Thus, PGM and HK each exhibit 2 isoenzymes corresponding to 2 parasite populations associated with separate hosts. The data from this study, plus supportive evidence obtained by different methods and by independent researchers, lend support to the hypothesis that separate cycles of transmission of C. parvum may exist within human and animal hosts.

Animals↗
PubMed1995

Deletions in one domain of the Friend virus-encoded membrane glycoprotein overcome host range restrictions for erythroleukemia.

Although the Friend virus-encoded membrane glycoprotein (gp55) activates erythropoietin receptors (EpoR) to cause erythroblastosis only in certain inbred strains of mice but not in other species, mutant viruses can overcome aspects of mouse resistance. Thus, mice homozygous for the resistance allele of the Fv-2 gene are unaffected by gp55 but are susceptible to mutant glycoproteins that have partial deletions in their ecotropic domains. These and other results have suggested that proteins coded for by polymorphic Fv-2 alleles might directly or indirectly interact with EpoR and that changes in gp55 can overcome this defense. A new viral mutant with an exceptionally large deletion in its ecotropic domain is now also shown to overcome Fv-2rr resistance. In all cases, the glycoproteins that activate EpoR are processed to cell surfaces as disulfide-bonded dimers. To initiate analysis of nonmurine resistances, we expressed human EpoR and mouse EpoR in the interleukin 3-dependent mouse cell line BaF3 and compared the abilities of Friend virus-encoded glycoproteins to convert these cells to growth factor independence. Human EpoR was activated in these cells by erythropoietin but was resistant to gp55. However, human EpoR was efficiently activated in these cells by the same viral mutants that overcome Fv-2rr resistance in mice. By construction and analysis of human-mouse EpoR chimeras, we obtained evidence that the cytosolic domain of human EpoR contributes to its resistance to gp55 and that this resistance is mediated by accessory cellular factors. Aspects of host resistance in both murine and nonmurine species are targeted specifically against the ecotropic domain of gp55.

Animals↗
PubMed1994

Rapid capping in alpha-spectrin-deficient MEL cells from mice afflicted with hereditary hemolytic anemia.

A spectrin-based membrane skeleton is important for the stability and organization of the erythrocyte. To study the role of spectrin in cells that possess complex cytoskeletons, we have generated alpha-spectrin-deficient erythroleukemia cell lines from sph/sph mice. These cells contain beta-spectrin, but lack alpha-spectrin as determined by immunoblot and Northern blot analyses. The effects of alpha-spectrin deficiency are apparent in the cells' irregular shape and fragility in culture. Capping of membrane glycoproteins by fluorescent lectin or antibodies occurs more rapidly in sph/sph than in wild-type erythroleukemia cells, and the caps appear more concentrated. The data support the idea that spectrin plays an important role in organizing membrane structure and limiting the lateral mobility of integral membrane glycoproteins in cells other than mature erythrocytes.

Animals↗
PubMed1993

Stathmin in mung bean leaves and rat brain.

Stathmin is a highly-conserved, cytosolic protein whose synthesis and phosphorylation is closely associated with growth and differentiation. Although conserved among vertebrates, stathmin has not been identified in plants. In the present study, anti-stathmin antibodies were generated against a synthetic peptide corresponding to amino-acid residues 32-44 of rat stathmin, and these antibodies were used to probe immunoblots of proteins from rat brain and mung bean. The antibodies recognized 12-kDa, 21-kDa and 22-kDa proteins in cytosolic fractions from mung bean leaves and a 12-kDa protein in cytosolic fractions from roots. The two larger proteins identified by the antibodies have apparent molecular weights and isoelectric points similar to those of rat brain stathmin. These results are the first to show that stathmin-like proteins are present in plants.

Amino Acid Sequence↗
PubMed1993

Twenty-four hour gastric pH monitoring and blood gastrin concentrations in fasted ponies.

Gastric pH varied widely among eight fasted ponies, of which seven exhibited discrete episodes of spontaneous alkalinisation (SA). SA occurred at all times of the study and no significant variation in the summary variables of pH (median pH, mean pH and percentage of readings exceeding pH 4.0) was noted among the periods 0 to eight, eight to 16 and 16 to 24 hours. The occurrence of SA has significant implications for the performance of acid secretory studies in the fasted pony. There was, however, no significant correlation between pH and plasma gastrin concentration measured using a commercially available radioimmunoassay kit validated for use in the horse. This implies a lack of dependency of the incidence of SA on plasma gastrin or, conversely, of plasma gastrin on the variable pH associated with SA.

Animals↗
PubMed1993

Gastrin and gastrin-related responses to infection with Ostertagia ostertagi in the calf.

The effects of a single challenge with 60,000 infective Ostertagia ostertagi larvae on blood and gastrointestinal mucosal gastrin concentrations, gastrin-producing G-cell numbers in the pyloric mucosa and growth of different parts of the gut were investigated in 16, two-and-a-half-month-old calves. Infected calves exhibited a rise in abomasal pH which was accompanied by a 145 per cent increase in wet weight of the fundic mucosa (P < 0.05) and a significant rise in blood total gastrin concentrations (P < 0.01). Circulating little gastrin (G-17) was unaffected. Pyloric mucosal total gastrin concentrations remained unaltered in the infected calves until day 28 when levels fell to 36.9 per cent of control group values (P < 0.01). Pyloric mucosal G-cell numbers declined during the experiment in the infected group. It is suggested that release of previously stored tissue gastrin and not a change in G-cell numbers contributes to the hypergastrinaemia associated with ostertagia infection in the calf.

Animals↗
PubMed1993

Pathophysiology of infection with Ostertagia ostertagi in cattle.

Infection with the abomasal nematode, Ostertagia ostertagi, is an important cause of impaired productivity in young cattle in temperate parts of the world. Such losses have been associated with marked changes in feed intake, gastrointestinal function, protein, energy and mineral metabolism, and in body composition. The reduction in feed intake is an important factor in the pathogenesis of infection and may account for a large part of the difference in weight gain between ad libitum fed control and infected calves. Despite the obvious importance of inappetance, only recently has an association been made between reduced intake, altered gut motility and elevated levels of certain gastrointestinal hormones, such as gastrin. It has been suggested that the elevated gastrin levels accompanying abomasal parasitism may impair reticulo-ruminal motility and slow down abomasal emptying, leading to a stasis of ingesta and a reduction in feed intake. The rise in blood gastrin levels may also be partly responsible for the marked hyperplasia of the fundic mucosa seen in abomasal infections. Pronounced changes in protein metabolism have also been associated with Ostertagia infection. Radioisotopic studies have demonstrated increased losses of albumin into the gastrointestinal tract which are accompanied by an increase in the rate of synthesis in the liver. Dietary protein breakdown in the abomasum is also likely to be impaired, although there is evidence of a compensatory increase in protein digestion in the lower gut of parasitised calves. Increased losses of albumin are not always accompanied by increases in faecal nitrogen, suggesting that albumin is broken down and recycled as ammonia. Radioisotopic studies in animals with intestinal nematode infections have demonstrated a marked reduction in muscle protein synthesis and an increase in protein synthesis in gastrointestinal tissue. Such changes in the balance of protein synthesis are likely to be brought about by alterations in the balance of certain metabolic hormones. Marked changes in energy metabolism also accompany Ostertagia infection. Parasitised calves exhibit a marked increase in non-esterified fatty acid levels, resulting from the mobilisation of adipose tissue, and a reduction in digestive efficiency of energy, probably associated with the increase in cycling of protein through the gastrointestinal tract and the compensatory increases in protein synthesis. Mineral metabolism may also be affected although relatively little work has been conducted in cattle. Changes in body composition reflect a reduction in deposition of muscle protein and fat, and an increase in bone content and water retention.

Animals↗
PubMed1993

A Friend virus mutant that overcomes Fv-2rr host resistance encodes a small glycoprotein that dimerizes, is processed to cell surfaces, and specifically activates erythropoietin receptors.

The env gene of Friend spleen focus-forming virus (SFFV) encodes a membrane glycoprotein (gp55) that is inefficiently (3 to 5%) processed from the rough endoplasmic reticulum to form a larger dimeric plasma membrane derivative (gp55p). Moreover, the SFFV env glycoprotein associates with erythropoietin receptors (EpoR) to cause proliferation of infected erythroblasts [J.-P. Li, A. D. D'Andrea, H. F. Lodish, and D. Baltimore, Nature (London) 343:762-764, 1990]. Interestingly, the mitogenic effect of SFFV is blocked in mice homozygous for the Fv-2r resistance gene, but mutant SFFVs can overcome this resistance. Recent evidence suggested that these mutants contain partial env deletions that truncate the membrane-proximal extracellular domain of the encoded glycoproteins (M. H. Majumdar, C.-L. Cho, M. T. Fox, K. L. Eckner, S. Kozak, D. Kabat, and R. W. Geib, J. Virol. 66:3652-3660, 1992). Mutant BB6, which encodes a gp42 glycoprotein that has a large deletion in this domain, causes erythroblastosis in DBA/2 (Fv-2s) as well as in congenic D2.R (Fv-2r) mice. Analogous to gp55, gp42 is processed inefficiently as a disulfide-bonded dimer to form cell surface gp42p. Retroviral vectors with SFFV and BB6 env genes have no effect on interleukin 3-dependent BaF3 hematopoietic cells, but they cause growth factor independency of BaF3/EpoR cells, a derivative that contains recombinant EpoR. After binding 125I-Epo to surface EpoR on these factor-independent cells and adding the covalent cross-linking reagent disuccinimidyl suberate, complexes that had immunological properties and sizes demonstrating that they consisted of 125I-Epo-gp55p and 125I-Epo-gp42p were isolated from cell lysates. Contrary to a previous report, SFFV or BB6 env glycoproteins did not promiscuously activate other members of the EpoR superfamily. Although the related env glycoproteins encoded by dualtropic murine leukemia viruses formed detectable complexes with EpoR, strong mitogenic signalling did not ensue. Our results indicate that the SFFV and BB6 env glycoproteins specifically activate EpoR; they help to define the glycoprotein properties important for its functions; and they strongly suggest that the Fv-2 leukemia control gene encodes an EpoR-associated regulatory factor.

Animals↗
PubMed1992

Co-exposure to gasoline vapor decreases benzene metabolism in Fischer-344 rats.

The metabolic interactions of benzene and gasoline vapor were investigated in male Fischer-344 rats. A closed chamber gas-uptake exposure system was used to obtain inhalation uptake curves for benzene alone and benzene in the presence of gasoline vapor. Exposure to benzene as a component of gasoline vapor resulted in a decrease of benzene metabolism. A physiologically based pharmacokinetic model of benzene metabolism was used to quantitatively determine the extent of the inhibitory effect of gasoline vapor on benzene metabolism. This observed inhibitory effect cannot be accounted for by the presence of toluene in gasoline vapor.

Animals↗
PubMed1992

Microheterogeneity in purified broad bean polyphenol oxidase.

Polyphenoloxidase was purified from chloroplasts of broad bean leaves (Vicia faba L.) to apparent homogeneity. The enzyme was composed of two proteins with an apparent mass of 65 and 68 kilodaltons after sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The isolated enzyme contained covalently attached carbohydrates and bound concanavalin A, Phaseolus vulgaris erythroagglutinin, and Ricinus communis agglutinin lectins. Under native isoelectric focusing, several charged isoforms were present in the pH range of 4 to 6. Many, if not all, of the isoforms separated by isoelectric focusing were glycosylated and bound concanavalin A. All these isoforms shared a 65 kilodalton protein in common, and some of the isoforms were associated with both a 65 and 68 kilodalton protein. Isoforms separated by isoelectric focusing in the presence of 9 molar urea followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed a similar pattern of proteins within a slightly higher pH range from 5 to 6.5.

Journal Article↗
PubMed1992

Mutations in the env gene of friend spleen focus-forming virus overcome Fv-2r-mediated resistance to Friend virus-induced erythroleukemia.

Although Fv-2r homozygous mice are resistant to leukemias induced either by an erythropoietin-encoding virus or by wild-type Friend virus (FV) (M. E. Hoatlin, S. L. Kozak, F. Lilly, A. Chakraborti, C. A. Kozak, and D. Kabat, Proc. Natl. Acad. Sci. USA 87:9985-9989, 1990), they are susceptible to some variants of FV (R. A. Steeves, E. A. Mirand, A. Bulba, and P. J. Trudel, Int. J. Cancer 5:349-356, 1970; R. W. Geib, M. B. Seaward, M. L. Stevens, C.-L. Cho, and M. Majumdar, Virus Res. 14:161-174, 1989). To localize the virus gene involved in influencing the host range, we cloned and sequenced the env gene of the BB6 variant of FV (Steeves et al., Int. J. Cancer 5:349-356, 1970). In comparison with the wild-type env gene, the BB6 variant contains a 159-bp deletion that eliminates the membrane-proximal portion of the extracellular domain and 58 point mutations resulting in 13 amino acid changes. Substitution of the variant env gene for the wild-type env gene resulted in a recombinant virus that produced a Friend virus-like disease in Fv-2r homozygotes. Our results identify the spleen focus-forming virus env gene as the viral gene involved in this virus-host interaction. Additionally, they suggest that the product of the Fv-2r gene modifies the interaction between the spleen focus-forming virus envelope protein and the erythropoietin receptor.

Amino Acid Sequence↗
PubMed1992

Prolactin-induced proliferation of the Nb2 T-lymphoma is associated with protein kinase-C-independent phosphorylation of stathmin.

Phosphorylation of stathmin, a 19-kDa protein found in many tissues, has been linked to cell differentiation and proliferation. This protein is present in lymphocytes, and both phosphorylation and expression of stathmin are regulated by lymphotropic agents. In this study an antibody specific for stathmin was used to examine phosphorylation in response to PRL. The results suggest that PRL stimulates stathmin phosphorylation in the Nb2 lymphoma and that phosphorylation correlates with PRL-induced cell proliferation. Stathmin expression does not change substantially as PRL-stimulated Nb2 cells move through the cell cycle and enter into the S-phase. Thus, stathmin phosphorylation, but not expression, is regulated by PRL. Activation of protein kinase-C (PKC) in Nb2 cells also induces phosphorylation of stathmin, but PKC does not appear to mediate phosphorylation in response to PRL. The pattern of phosphorylation in response to 12-O-tetradecanoylphorbol-13-acetate differs from that in response to PRL, and down-regulation of PKC does not inhibit PRL-induced phosphorylation or proliferation. In addition to stathmin, PRL increases phosphorylation of a group of stathmin-like proteins. Phosphorylation of these proteins also correlates well with PRL-induced proliferation. Taken together, the results suggest that phosphorylation of stathmin and stathmin-like proteins may mediate some actions of PRL in Nb2 cells. The results further suggest that activation of PKC is not an important early event in PRL-stimulated mitogenesis in Nb2 cells.

Cell Division↗
PubMed1991

Increases in p11 and annexin II proteins correlate with differentiation in the PC12 pheochromocytoma.

Regulation of p11 and annexin II by nerve growth factor, staurosporine, and epidermal growth factor was examined in PC12 rat adrenal pheochromocytoma cells using immunoblot analysis. Nerve growth factor, which is known to induce neurite outgrowth in PC12 cells, stimulated a five-fold increase in p11 and the higher levels of p11 were characteristic of PC12 cells exposed to nerve growth factor for up to ten days. Nerve growth factor induced an even greater increase (13.6-fold) in annexin II. Staurosporine, a protein kinase inhibitor that at high concentrations induces neurite formation, was as effective as nerve growth factor in increasing the intracellular levels of p11 and annexin II. Epidermal growth factor was less effective than nerve growth factor and staurosporine, producing only a two-fold increase in p11 and a three-fold increase in annexin II. The ineffectiveness of epidermal growth factor in increasing intracellular levels of p11 and annexin II is consistent with the fact that epidermal growth factor does not stimulate neurite outgrowth in PC12 cells. Evidence presented here suggests that p11 and/or annexin II may play a role in PC12 cell differentiation.

Adrenal Gland Neoplasms↗