Field clinic procedures for diagnosing Echinococcus granulosus in dogs

Echinococcus granulosus is the causative parasite of hydatid disease in humans and represents a significant public health problem within endemic foci in all major continents of the world. This report gives a detailed set of instructions whereby four trained individuals can examine 15–20 dogs per hour for the presence of this organism. The procedure permits the baseline determination of the prevalence of this parasite within any specific population of dogs and also allows the periodic examination of the same animals to determine if recommended preventive and control measures for hydatid disease are being followed by sheep and dog owners in any region where the parasite is known to occur.     

Mutants of avian myelocytomatosis virus with smaller gag gene-related proteins have an altered transforming ability

Avian myelocytomatosis virus strain MC29 is a replication-defective avian oncovirus which in newborn chickens causes myelocytomatosis and liver and kidney tumours. In vitro infection of bone marrow cells gives rise to colonies of transformed macrophage-like cells, and cloned viruses is also capable of transforming fibroblasts. The genome of MC29 contains cellular sequences which are closely related to those in other defective leukaemia viruses with similar transforming spectra. Consequently, these cellular sequences have been postulated to represent a new oncogene which has been designated mac, for macrophage transformation. MC29-transformed cells contain a gag gene-related protein of a 110,000 molecular weight (MW) (p110), which by tryptic peptide analysis has been shown to be a fusion product comprised of a gag gene-derived sequences and sequences which are presumed to be coded by the adjacent mac gene. These findings suggest that this protein may be implicated in transformation by MC29. We now describe three mutants of MC29 and synthesize smaller gag gene-related proteins. These mutants have an altered ability to transform bone marrow cells but not fibroblasts. This demonstrates for the first time a direct involvement of the p110 protein of MC29 in transformation.     

Mice heterozygous for mutation in Atm,the gene involved in ataxia-telangiectasia,have heightened susceptibility to cancer

Ataxia-telangiectasia is characterized by radiosensitivity, genome instability and predisposition to cancer. Heterozygous carriers of ATM, the gene defective in ataxia-telangiectasia, have a higher than normal risk of developing breast and other cancers. We demonstrate here that Atm 'knock-in' (Atm-Delta SRI) heterozygous mice harboring an in-frame deletion corresponding to the human 7636del9 mutation show an increased susceptibility to developing tumors. In contrast, no tumors are observed in Atm knockout (Atm(+/-)) heterozygous mice. In parallel, we report the appearance of tumors in 6 humans from 12 families who are heterozygous for the 7636del9 mutation. Expression of ATM cDNA containing the 7636del9 mutation had a dominant-negative effect in control cells, inhibiting radiation-induced ATM kinase activity in vivo and in vitro. This reduces the survival of these cells after radiation exposure and enhances the level of radiation-induced chromosomal aberrations. These results show for the first time that mouse carriers of a mutated Atm that are capable of expressing Atm have a higher risk of cancer. This finding provides further support for cancer predisposition in human ataxia-telangiectasia carriers.     

42K spaces in submandibular gland of early postnatal rats: effects of carbachol and transport inhibitors

Equivalent spaces of 42K were measured in fragments of the submandibular gland of 1-, 7-, 14- and 21-day-old and adult rats in the absence and presence of carbachol and the transport inhibitors ouabain and furosemide. The results indicate that the 42K space was increased by carbachol in an ouabain-sensitive manner at all ages studied and that part of the secretagogue-stimulated K uptake occurred by way of a furosemide-sensitive transport system in the latter part of the postnatal period and in the adult.     

42K spaces in submandibular gland of early postnatal rats: effects of carbachol and transport inhibitors

Summary Equivalent spaces of⁴²K were measured in fragments of the submandibular gland of 1-, 7-, 14- and 21-day-old and adult rats in the absence and presence of carbachol and the transport inhibitors ouabain and furosemide. The results indicate that the⁴²K space was increased by carbachol in an ouabain-sensitive manner at all ages studied and that part of the secretagogue-stimulated K uptake occurred by way of a furosemide-sensitive transport system in the latter part of the postnatal period and in the adult.     

Molecular basis of the copulatory plug polymorphism in Caenorhabditis elegans

Heritable variation is the raw material for evolutionary change, and understanding its genetic basis is one of the central problems in modern biology. We investigated the genetic basis of a classic phenotypic dimorphism in the nematode Caenorhabditis elegans. Males from many natural isolates deposit a copulatory plug after mating, whereas males from other natural isolates?including the standard wild-type strain (N2 Bristol) that is used in most research laboratories?do not deposit plugs. The copulatory plug is a gelatinous mass that covers the hermaphrodite vulva, and its deposition decreases the mating success of subsequent males. We show that the plugging polymorphism results from the insertion of a retrotransposon into an exon of a novel mucin-like gene, plg-1, whose product is a major structural component of the copulatory plug. The gene is expressed in a subset of secretory cells of the male somatic gonad, and its loss has no evident effects beyond the loss of male mate-guarding. Although C. elegans descends from an obligate-outcrossing, male?female ancestor, it occurs primarily as self-fertilizing hermaphrodites. The reduced selection on male?male competition associated with the origin of hermaphroditism may have permitted the global spread of a loss-of-function mutation with restricted pleiotropy.