Search

The fine structure of the epimerite and the protomerite of D. gigantea was investigated following the different stages of the evolution of the trophozoite. The first stage is mononucleate and very poor of cytoplasmic structures (Fig. 1). All following stages are polynucleate (Fig. 3). The septum between protomerite and deutomerite appears at the third stage (Fig. 22). The body of the gregarine is in all stages surrounded by a thick cell-wall constituted of three membranes. The limit between epimerite and protomerite is indicated by the existence of an osmiophilic basal ring just under the parasite's cell-wall. This basal ring has a transverse substructure with a periodical distance of 450 A (Fig. 12). The two inner membranes join together just beneath the basal ring, whereas the outer membrane continues and forms the single cell membrane of the epimerite (Fig.9). The epimerite displays a large number of microvillosities and evaginations of the membrane which increase considerably its surface (Figs. 11-14). The epimerite essentially contains ribosomes and mitochondria (Fig.6). The protomerite contains in addition to the usual cell organites cytoplasmic agglomerations consisting of endoplasmic reticulum, ribonucleoprotein and peripheric mitochondria. During evolution from stage IV to V, these agglomerations produce osmiophilic granula of different form and size, most of which are surrounded by an elementary membrane (Fig. 18). Beside these granula one can observe sometimes small spherical or lamellar structures (Fig. 21). Large bundles of microtubules run from the protomerite into the epimerite where they generally branch off and penetrate into the mitochondrial layer (Figs. 6, 19, 20). Between the parasite and the host-cell exists a space, the periparasitic space, without any cytoplasmic inclusions. The cell membrane of the host-cell has in the periparasitic space an outer cell-coat with a ripped pattern (Fig. 13). The microvillosities of the cell membrane disappear at this place. The host-cell cytoplasm displays a large number of microtubules and a fibrillar network (Figs. 13, 14). The importance of these structures for the relationship between parasite and host-cell is discussed.

Leimyosarcomas were induced in rabbit skeletal muscle by Ni3S2 implantation. Tumor myosin was isolated and compared with normal adult muscle myosin and cow uterine smooth muscle myosin. This study has shown that this leiomyosarcoma myosin precipitates as long fusiform filaments and possesses two light-chain of 25000 and 18000 daltons as does the once-fetal type. The biochemical findings demonstrate that tumoral stem myoblasts originate from retrodifferentiated muscle cells.

The binding of nickel to proteins in lung and in liver was investigated by analysis of 63Ni[II] incorporation into the nuclear, mitochondrial, microsomal and soluble fractions. Three different procedures were performed: (i) in vitro incorporation, (ii) a time course study of in vivo incorporation where the animals were sacrificed after 30 min, 1, 2 and 4 h after a single i.p. injection of 63NiCl2, (iii) in vivo incorporation after 7 successive i.p. injections of 63NiCl2 every 24 h and the animals were sacrificed 24 h after the last injection. In all cellular fractions (except the nuclear fractions) we could observe several nickel-binding proteins regardless of the type of incorporation performed. Most of these proteins were revealed after in vitro as well as in vivo incorporation, some of them, however, were labelled only after in vitro incorporation, others only after in vivo incorporation. Some proteins can only be revealed after successive injections. In addition, the 63Ni-labelled proteins are not all the same at the beginning of the incorporation (30 min) as after longer periods (1 and 2 h). The lung fractions (especially the mitochondrial fraction) were always more highly labelled than the liver fractions. These biochemical investigations not only confirm that the lung is a target organ for nickel-retention, but also demonstrate that Ni is preferentially bound to its mitochondrial and microsomal fractions. It is shown here that several cellular proteins are implicated in the transport and the metabolism of nickel in the cell.

The induction of rabbit rhabdomyosarcoma was obtained after intramuscular implantation of a large quantity of very pure nickel subsulphide, though until the present time the rabbit was considered refractory to Ni3S2 tumorigenesis. These tumors are similar to those induced in rats under the same conditions. Four different cell types were observed: small polygonal cells, small elongated cells, giant cells, and mature myofibers. Electron microscopy reveals a complete disorientation of myofibrils in mature myoblasts. Giant cells appear by pluripolar endomitosis and always contain myofibrillar structures, but M-lines and Z-lines are not present in these cells. Cylindrical laminated bodies were observed very often in all four cell types. They are formed of 4 nm fibrils arranged in crossed position in each lamella. Some of these paracrystalline structures were also observed in nuclei. The laminated bodies are considered to be abnormal formations of contractile proteins produced during tumoral myofibrillar differentiation.

Microtubules were prepared by in vitro polymerization-depolymerization cycles, 1.0 M NaCl which totally depolymerizes was then added to the preparation. After removal of NaCl new arrangements of tubulin were observed at 4 degrees C: simple and double rings as well as fibrils. At 37 degrees these structures disappeared and tubulin polymerized into microtubules. The highly microtubules contain tubulin, tubulin associated proteins of 300,000 and 330,000 molecular weight, minor proteins of low molecular weight and proteins similar to the Tau factors. This raises a question of the role played by low molecular weight polypeptides. Are they products of proteolysis of rather factors of polymerisation?

Possible correlations between allergic reactions and the significance of a dental prosthesis or restoration made from one or more of the metals nickel, cobalt and chromium are considered. Described clinical cases are reviewed. These allergic reactions may appear either locally as stomatitis or distantly in the form of general or local contact dermatitis.

The fundamental basis of allergy, particularly in relation to contact allergy, is described, together with the importance and frequency of sensitization to nickel, chromium and cobalt in both the consultant and general population. 139 published cases of allergy to dental restorations containing these metals are reviewed involving 92 female and 47 male patients, 115 of whom recovered when the restorations were removed. The most frequent symptoms were local (99/139), particularly gingivitis and stomatitis, while general or remote symptoms occurred in 33 cases. This probably underestimates the true prevalence of the condition, because a large number of reported cases have not been due to their "current appearance". The influence of the occupational environment of the patient is described with special reference to dental technicians. The persistence of contact allergy to metals for which no desensitization is possible is also emphasised. The discussion includes experimental investigations and an appraisal of other methods of revealing hypersensitivity. Finally, some simple recommendations for prevention are made which are of value to practitioners.