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Biomedical subjects

F E Cox

Publications and source records attributed to F E Cox.

At least 37 records · Page 2Linked to original sources
PubMed1991

Nonspecific defence mechanism: the role of nitric oxide.

There is a marked contrast between the extraordinary complexity and specificity of the adaptive immune response and the limited number of effector mechanisms that it can direct. Recently, a great deal of interest has focused on the possible role of nitric oxide (NO) in one of these mechanisms. Here F.Y. Liew and Frank Cox examine the evidence supporting a role for NO in parasitic disease and suggest possible mechanism of NO-mediated parasite damage.

Amino Acid Oxidoreductases↗
PubMed1991

TNF-alpha reverses the disease-exacerbating effect of subcutaneous immunization against murine cutaneous leishmaniasis.

Earlier studies have demonstrated that mice injected subcutaneously or intramuscularly with leishmanial antigens develop significantly exacerbated disease compared with unimmunized controls when challenged with the cutaneous protozoan parasites Leishmania major. We report here that this disease enhancement can be prevented, and protective immunity induced, by the incorporation of recombinant tumour necrosis factor (TNF-alpha) in the immunizing inoculum. This effect of TNF-alpha is dose-dependent and is not evident when TNF-alpha and the antigens are injected into separate sites. Furthermore, TNF-alpha injected together with p183, a peptide known to preferentially stimulate Th2 cells and disease exacerbation in H-2d mice, activates spleen and lymph node cells secreting more interferon-gamma (IFN-gamma) and less interleukin-4 (IL-4) and induces a modest but significant degree of resistance against L. major infection in highly susceptible BALB/c mice.

Animals↗
PubMed1986

Cefuroxime versus ampicillin plus chloramphenicol in childhood bacterial meningitis: a multicenter randomized controlled trial.

In a multicenter randomized trial, 107 children with bacterial meningitis were initially given either cefuroxime or ampicillin plus chloramphenicol. Patients were alternately assigned to 7- or 10-day courses of the designated antimicrobial regimen. CSF isolates included Haemophilus influenzae type b (89, of which 25% were beta-lactamase positive), Streptococcus pneumoniae, and Neisseria meningitidis. Although mean CSF bactericidal titers against Haemophilus isolates were 1:6 in each treatment group, H. influenzae was cultured from CSF in four of 39 patients receiving cefuroxime, 24 to 48 hours after initiation of therapy, compared with none of 40 patients given ampicillin plus chloramphenicol (P = 0.11). Clinical cure rates were similar (95%); one death occurred in each group. One child given cefuroxime had persistent meningitis after 5 days of therapy, and mastoiditis with secondary bacteremia developed in one on day 10. Three patients had relapse or reinfection. One patient who received cefuroxime for 10 days had a relapse of epiglottitis 17 days later, and of the patients given ampicillin plus chloramphenicol, one had a relapse of meningitis 1 week after 7 days of therapy, and bacteremia developed in one 42 days after completion of 10 days of therapy. No increase in either in-hospital complications or relapses occurred with a 7-day treatment course. Proof of the equivalence of the antibiotic regimens and the efficacy of 7-day courses of treatment, as well as the consequences of delayed CSF sterilization, will require additional investigation.

Adolescent↗
PubMed1985

Interactions between Trypanosoma brucei and Babesia spp. and Plasmodium spp. in mice.

Swiss mice with chronic Trypanosoma brucei infections become refractory to subsequent infection with Babesia microti and B. rodhaini. Infection with B. microti 7 days after T. brucei resulted in an obvious inhibition of the babesia parasitaemias and this inhibition became more profound as the time interval between the infections increased, until at 17-20 days the parasitaemias were totally abolished. Even after intravenous injection of large numbers of parasites parasitaemias were inhibited. Similar inhibition was obtained in BALB/c mice but not in C57BL/6 mice. Mice with established T. brucei infections also showed reduced susceptibility to B. rodhaini. In mice similarly infected with T. brucei and the malaria parasites Plasmodium chabaudi chabaudi and P. c. adami the pre-patent periods were noticeably prolonged but the subsequent parasitaemias were unaffected. Infections with P. yoelii were unaffected. Trypanosoma brucei infections were not affected by the intracellular parasites. Among the mechanisms investigated to explain these findings were changes in red blood cell populations, cross-reacting antigens, the release of toxic factors and the generation of activated oxygen species. None of these could account for the inhibition observed.

Animals↗
PubMed1985

Specific suppressor T cells for delayed-type hypersensitivity in susceptible mice immunized against cutaneous leishmaniasis.

BALB/c mice injected intravenously with 10(6) or higher doses of formaldehyde-fixed promastigotes (ffp) of Leishmania major developed significantly lower levels of delayed-type hypersensitivity (DTH) compared with uninjected control mice when they were subsequently immunized intradermally with ffp. The suppression of DTH was antigen specific and was also inducible with lethally irradiated promastigotes or soluble parasite antigens. The suppressive effect was adoptively transferable with splenic T cells which express the Lyt-1+2+ and L3T4+ phenotypes. These specific suppressor T cells were active against both the inductive and expressive phases of DTH. They were sensitive to 200 rads of gamma-irradiation in vitro and appeared to manifest the suppressive activity via soluble factors. In spite of this profound suppression of DTH, BALB/c mice injected intravenously with 4 X 10(7) ffp were substantially protected against a challenge infection with L. major promastigotes. The possible relationship between the suppressor T cells for DTH and prophylactic immunization against fatal cutaneous leishmanial infection in susceptible BALB/c mice is discussed.

Animals↗
PubMed1984

A prospective study of maternal cytomegalovirus infection and its effect on the fetus.

In order to define the effects of maternal cytomegalovirus infection in pregnancy and to identify risk factors associated with delivery of a cytomegalovirus-infected infant, a cohort of 1089 adolescents were prospectively evaluated during pregnancy. One hundred twenty-four subjects (11.4%) manifested cytomegaloviruria during pregnancy. Primary cytomegalovirus infection, defined virologically and serologically, occurred in three subjects. Infants of 119 cytomegalovirus-excreting mothers were cultured at birth, with detection of 12 congenital infections (10%), including one infant delivered of a mother with a third-trimester primary infection. A high titer of urinary virus or a fourfold or greater increase in antibody during the third trimester was significantly associated with delivery of a congenitally infected infant. All maternal and infant infections were asymptomatic. None of the congenitally infected infants manifested adverse effects during the first year of life. Our data demonstrate that pregnant women with cytomegaloviruria are at increased risk of being delivered of congenitally infected infants, particularly if active infection occurs late in pregnancy. If the maternal infection represents reactivation, overall probability of a poor fetal outcome is low.

Adolescent↗
PubMed1984

The importance of parasite load in the killing of Plasmodium vinckei in mice treated with Corynebacterium parvum or alloxan monohydrate.

Mice pre-treated with Corynebacterium parvum and later challenged with Plasmodium vinckei become infected but do not die whereas control mice do. When pre-treated mice were challenged with 1, 10, 1 X 10(2), 1 X 10(4), 1 X 10(5) or 1 X 10(6) parasites, the pre-patent periods correlated directly with the number of parasites injected, but the subsequent parasitaemias reached similar levels. This suggests that parasite killing, resulting from pre-treatment with C. parvum, is not triggered until the parasite load has reached a particular threshold. The injection of alloxan monohydrate, which brings about the release of toxic oxygen intermediates thought to be involved in non-specific immunity, has little effect on P. vinckei infections until the parasitaemia is relatively high. This indicates that oxygen-mediated parasite killing also does not occur until the parasitaemia has reached a particular threshold. It is suggested that it is only at relatively high parasitaemias that the factors involved in parasite killing are able to enter the infected red blood cells.

Alloxan↗