African trypanosomes present several features of interest to cell biologists. These include: a repressible single mitochondrion with a large mass of mitochondrial DNA, the kinetoplast; a special organelle, the glycosome, which houses the enzymes of the glycolytic chain; a surface coat of variable glycoprotein which enables the parasite to evade the mammalian host's immune response; and a unique flagellum-to-host attachment mechanism associated with novel cytoskeletal elements. Trypanosome development during the life cycle involves cyclical activation and repression of genes controlling these activities. Understanding the complexity of parasite development in the tsetse fly vector is especially challenging but may help to suggest new methods for the control of trypanosomiasis.
In cultures of tsetse proboscis stages during the development of Trypanosoma congolense, attached epimastigote forms multiply and give rise to free nondividing metacyclic trypanosomes. Prevention of attachment by shaking the cultures or by providing a polypropylene substratum does not inhibit epimastigote division but does prevent the differentiation of metacyclics. We conclude that epimastigote attachment forms a necessary part of the program of metacyclic development.
Laminitis is a major cause of lameness in dairy cattle, and is
widely
attributed to a defect in the horny tissue that gives the hoof its mechanical
strength.
Defective horn is associated with, and may be preceded by, impaired keratin
deposition in the hoof epidermis. The cause of abnormal keratin deposition
is not
easily identified but, like epidermal keratinization in other tissues,
is likely to be
controlled by hormones and the paracrine action of locally produced growth
factors.
The hormonal regulation of keratin synthesis and cell proliferation in
the bovine hoof
was studied using tissue explants in organ culture. As the highest incidence
of
laminitis is in early lactation, the study focused on insulin, cortisol
and prolactin,
three hormones implicated in lactogenesis and galactopoiesis. Incubation
of tissue
explants for 24 h in medium containing insulin (10–5000 ng/ml)
stimulated protein
synthesis measured by incorporation of 35 S-labelled amino acids.
Histochemical
examination showed that insulin binding co-localized with the site of protein
synthesis. Insulin also stimulated DNA synthesis, an index of cell proliferation,
which was measured by incorporation of [3H]methyl
thymidine. Cortisol
(10–5000 ng/ml) decreased protein synthesis, whereas prolactin
(10–5000 ng/ml) had
no significant effect on protein or DNA synthesis. Epidermal growth factor
(10–200 ng/ml), a potent inhibitor of keratinization in other
tissues, stimulated
protein synthesis compared with untreated controls. Epidermal growth factor
binding was located microscopically to the germinal and differentiating
epidermal
layers. SDS-PAGE and fluorography showed that the population of proteins
synthesized in the presence of any hormone or growth factor combination
did not
differ from that in untreated controls and included the keratins involved
in horn
deposition. The results show that bovine hoof keratinization is under endocrine
and
growth factor control, and suggest that systemic changes in lactogenic
hormones
may act to inhibit keratin deposition.
Lameness is a major welfare concern in dairy cattle. Estimates of the annual
incidence of lameness range from 4 to 30%, and even in well managed herds as many
as 15% of animals can be affected (Esselmont, 1990). In addition to the cost in
animal suffering, lameness is accompanied by loss of production on a scale
comparable, in temperate countries, with that caused by mastitis. Lost production,
veterinary charges and milk discard costs coupled with reduced
fertility or premature
culling in turn make lameness a major economic factor in dairy farming. In the UK
alone, the estimated cost in lost production is
£44–£90 million per annum, equivalent
to £10–20 per cow (Booth, 1989; Esselmont, 1990).
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