Showing papers on "Mink published in 1984"

A Mus dunni cell line that lacks sequences closely related to endogenous murine leukemia viruses and can be infected by ectropic, amphotropic, xenotropic, and mink cell focus-forming viruses.

Abstract: A Mus dunni cell line has been developed that is permissive for all four classes of murine leukemia viruses (MuLV): ecotropic, amphotropic, xenotropic, and mink cell focus-forming viruses. The M. dunni cells contain fewer MuLV-related sequences than do feral or domestic mouse, rat, or mink cells. Infection of the line by ecotropic MuLV induces a distinct cytopathic effect, and the cells can be readily transfected by MuLV DNA. The M. dunni line has been used to isolate an endogenous MuLV from the SC-1 feral mouse cell line.

Molecular analysis of the envelope gene and long terminal repeat of Friend mink cell focus-inducing virus: implications for the functions of these sequences.

Abstract: We sequenced the envelope (env) gene and 3' long terminal repeat of a Friend mink cell focus-inducing virus (F-MCFV). We also sequenced the gp70 coding regions for two cDNA clones of another F-MCFV. The deduced amino acid sequence of the env gene products of both F-MCFVs were compared to the corresponding sequences of other MCFVs and of ecotropic viruses. The env polypeptides of the different viruses showed long stretches of homology in the carboxy-terminal half of gp70 and in p15env ("constant region"). The amino-terminal half of gp70 was very similar in all MCFVs, but showed extensive variations relative to the ecotropic viruses ("differential region"). This differential region in all MCFVs is of endogeneous origin. We show evidence that this region carries determinants for ecotropic or polytropic host range. No indication could be found that the env gene products determine the histological type of disease caused by particular MCFVs. When the long terminal repeats of F-MCFV and Friend murine leukemia virus were compared with those of other viruses causing either lymphatic leukemia or erythroleukemia, several nucleotides were localized which might determine the histological type of disease caused by these viruses.

Spontaneous and induced leukemias of myeloid origin in recombinant inbred BXH mice

Abstract: BXH-2 recombinant inbred (RI) mice produce high titers of B-ecotropic murine leukemia virus beginning early in life and have a high incidence of non-T-cell leukemias that occur before 1 year of age. The leukemias that develop are in some cases associated with hind limb paralysis. In addition, a dualtropic mink cell focus-forming virus has been isolated from leukemic cells of BXH-2 mice. Immunological and cytochemical characterization of the BXH-2 leukemias showed that they are of the myeloid lineage. To assess the oncogenicity of the BXH-2 viruses, newborn mice of several BXH RI strains were inoculated at birth with biologically cloned B-ecotropic or mink cell focus-forming murine leukemia virus. These studies demonstrated that the B-ecotropic virus can induce myeloid leukemias in other BXH RI strains, whereas the dualtropic mink cell focus-forming isolates were nononcogenic in the strains tested. DNA-DNA reassociation analysis indicated that the organotropism of the B-ecotropic murine leukemia virus is confined to lymphoid tissues. Southern analysis of tumor DNAs showed that there was amplification of ecotropic virus-specific sequences in BXH-2 myeloid tumors and in all leukemias induced in other BXH RI strains by inoculation of the BXH-2 B-ecotropic virus. Although B-ecotropic virus is expressed in central nervous tissues of paralyzed BXH-2 mice, we were unable to induce the disorder in several BXH RI strains inoculated intracranially at birth with either the B-ecotropic or dualtropic virus. These results suggest that the paralysis that occurs in BXH-2 mice is due to the infiltration of leukemic cells into the central nervous system.

Generation of AKR mink cell focus-forming viruses: a conserved single-copy xenotrope-like provirus provides recombinant long terminal repeat sequences.

Abstract: AKV and AKR mink cell focus-forming virus-specific probes from the envelope and long terminal repeat (LTR) regions were prepared for study of the structure of recombinant proviruses in tumor tissues of AKR mice. The results showed that (i) all somatically acquired proviruses possessed, besides a recombinant gp70 gene, an altered U3 LTR; (ii) in a substantial portion of the somatically acquired AKR mink cell focus-forming proviruses, the LTR comprised sequences derived from the same xenotropic-like provirus; (iii) this U3 LTR donating parental provirus (Xeno-dL) was present only once per genome equivalent in several mouse strains; (iv) in the strains containing the Xeno-dL provirus, the provirus was present in the same chromosomal site; (v) restriction analysis of the Xeno-dL revealed that the mink cell focus-forming gp70 sequences were derived from a parental provirus, different from Xeno-dL. Therefore, at least two non-ecotropic parents participate in the generation of leukemogenic AKR mink cell focus-forming viruses: a xenotropic-like virus, Xeno-dL, donating U3 LTR sequences, and another xenotropic-like virus or viruses providing gp70 sequences.

Generation of mink cell focus-forming viruses by Friend murine leukemia virus: recombination with specific endogenous proviral sequences.

Abstract: A family of recombinant mink cell focus-forming viruses (MCF) was derived by inoculation of NFS mice with a Friend murine leukemia virus, and their genomes were analyzed by RNase T1-resistant oligonucleotide fingerprinting. The viruses were obtained from the thymuses and spleens of preleukemic and leukemic animals and were evaluated for dualtropism and oncogenicity. All these isolates induced cytopathic foci on mink cells but could be classified into two groups based on their relative infectivities for SC-1 (mouse) or mink (ATCC CCL64) cells. One group of Friend MCFs (F-MCFs) (group I) exhibited approximately equal infectivities for SC-1 and mink cells, whereas a second group (group II) infected mink cells 1,000- to 10,000-fold more efficiently than SC-1 cells. Structural analyses of the F-MCFs revealed that group I and group II viruses correlated with recombination of Friend murine leukemia virus with two distinct, but closely related, endogenous NFS proviral sequences. No correlation was found between the type of F-MCF and the tissue of origin or the disease state of the animal. Furthermore, none of the F-MCF isolates were found to be oncogenic in NFS/N or AKR/J mice. F-MCFs of both groups underwent extensive substitution of ecotropic sequences, involving much of the gag and env genes of group I F-MCFs and most of the gag, pol, and env genes of group II F-MCFs. All F-MCF isolates retained the 3' terminal U3 region of Friend murine leukemia virus. Comparison of the RNAs of the F-MCFs with RNAs of MCFs derived from NFS.Akv-1 or NFS.Akv-2 mice indicated that the F-MCFs were derived from NFS proviral sequences which are distinct from the sequences contained in NFS.Akv MCF isolates. This result suggested that recombination with particular endogenous proviral sequences to generate MCFs may be highly specific for a given murine leukemia virus.

The Dark Mink: A Model of Male Infertility*

Abstract: Breeding mink for a fine dark fur has coselected male infertility, which may be manifest at the onset of breeding (primary infertility) or after one or more fertile breeding seasons (secondary infertility). Mink with primary infertility have low LH and testosterone levels. However, they respond to exogenous GnRH with increases in LH production and in the number and size of LH and FSH positive gonadotropes in the anterior pituitary. Exogenous human CG also induces testosterone secretion. Thus, mink with primary infertility are probably defective in GnRH secretion, which is due either to abnormal hypothalamic function or its control mechanisms. Autoimmune orchitis with testicular immune complexes are frequent in mink with secondary infertility, suggesting an autoimmune etiology. In contrast, fertile dark mink and fertile mink with the opaline and pastel fur have normal serum LH and testosterone levels; their testes are also normal. In mink with secondary infertility, the frequency and degree of orchitis and...

Induction of winter fur growth in mink (Mustela vison) with melatonin.

Abstract: Adult and kit standard dark male and female mink were treated with 0, 5 or 10 mg melatonin, or a reduced photoperiod of 6 h light: 18 h dark (6L: 18D, initiated during the last week of June) to determine the effects of treatment on winter fur growth. Melatonin was administered in a Silastic implant inserted sc over the scapular region during the last week of June. Regardless of sex or age, mink treated with melatonin or a 6L: 18D photoperiod molted the summer pelage and grew the winter pelage earlier than controls (P less than .001). Winter pelage was fully prime by mid-October, 6 wk earlier than normal. Weight gain of mink, regardless of sex or age, was not affected by melatonin treatment. These findings indicate that photoperiodic effects on the growth of winter pelage in mink may be mediated through the pineal gland and its secretion of melatonin.

Royal pastel mink respond variously to inoculation with Aleutian disease virus of low virulence.

Abstract: Information was sought on the varied responses of royal pastel mink (a non-Aleutian genotype) to Aleutian disease virus of low virulence. Thus, of 20 yearling female pastel mink inoculated subcutaneously with a large amount of the Pullman strain of Aleutian disease virus, only 3 succumbed to the disease. Of the other 17 mink, 3 had neither viremia nor a rise in level of serum gamma globulin during the 24 weeks after inoculation. The other 14 mink were viremic for variable periods during the first 12 weeks. In only five mink was the viremia accompanied by elevated levels of serum gamma globulin, usually from week 8 on. Of the 16 subclinically infected mink that did not succumb to intercurrent disease and otherwise remained healthy, 9 were examined at 19 to 31 months for persisting virus. In only one mink, small amounts were detected in the mesenteric lymph node and spleen nearly 28 months after inoculation. The other seven mink that survived the infection were not protected when challenged 31 months later with a small amount of the highly virulent Utah-1 strain. Even though still poorly understood, these varied responses of the royal pastel mink to infection with Aleutian disease virus of low virulence have important pathogenetic and epidemiological implications.

Effects of chronic dietary hexachlorobenzene exposure on the reproductive performance and survivability of mink and European ferrets

Abstract: Feeding adult mink and European ferrets diets that contained 1, 5, or 25 mg/kg added hexachlorobenzene (HCB) resulted in reduced reproductive performance as indicated by decreased litter size, increased percentage of stillbirths, increased kit mortality, and decreased early kit growth. Diets treated with 125 or 625 mg/kg HCB were lethal to the adults of both species. In general, the mink were more sensitive to the toxic effects of HCB than were ferrets.

Characterization of antigenic variation among mink enteritis virus isolates.

Abstract: Three antigenic forms of natural field isolates of mink enteritis virus were revealed with a panel of monoclonal antibodies generated against the closely studied feline panleukopenia virus and canine parvovirus-2 virus. Two types (types 2 and 3) were shown to be closely related by agar-gel precipitin tests and by restriction enzyme mapping. However, types 2 and 3 differed from the type 1 isolates in the same tests. In cross-protection studies, inactivated viral vaccines made from any one of the 3 variant types of mink enteritis virus protected mink against challenge exposure by the homologous, as well as the heterologous, antigenic types.

Aleutian disease virus, a parvovirus, is proteolytically degraded during in vivo infection in mink.

Abstract: The polypeptides of the highly virulent mink-passaged Utah I and the nonvirulent cell culture-adapted ADV-G strain of Aleutian disease virus (ADV) were compared. When CRFK cells infected with either Utah I or ADV-G were analyzed by immunoprecipitation, both viruses induced proteins with molecular weights characteristic of the ADV-G 85,000 ( 85k )- and 75k-dalton structural proteins (p85 and p75) as well as the 71k -dalton nonvirion protein p71 . However, when Utah I, Pullman ADV, and DK ADV (a Danish isolate of ADV) were purified from infected mink, only polypeptides with molecular weights between 27k and 30k could be identified. In addition, trypsin treatment of ADV-G degraded p85 and p75 to smaller antigenic proteins with molecular weights of 24k and 27k, similar to those found for the virulent in vivo viruses. The effect of proteolytic treatment of ADV was then studied in detail. Purification of Utah I ADV from mink organs in the presence of protease inhibitor did not prevent the appearance of the low-molecular-weight proteins and ADV-G proteins were not degraded upon purification from a homogenate of normal mink organs, suggesting that artifactual proteolysis was not occurring. When a serum pool from terminally diseased mink was analyzed by radioimmunoassay for antibody reactivity against trypsinized and nontrypsinized ADV-G, five times higher reactivity was found for the trypsinized ADV-G than for the nontrypsinized ADV-G, an effect which could not be elicited by chymotrypsin or V8 protease treatment, implying that in vivo-produced ADV was being modulated in vivo by trypsin or a trypsin-like enzyme. Trypsinization was shown not to cause a change in ADV virion density, but to decrease the in vitro infectivity of ADV-G for CRFK cells. These studies suggested that during infection of mink ADV proteins are degraded to highly antigenic smaller polypeptides.

Free and integrated recombinant murine leukemia virus DNAs appear in preleukemic thymuses of AKR/J mice.

Abstract: We studied the appearance and structure of murine leukemia viral genomes in preleukemic AKR/J mice by Southern hybridization. Up to an average of one to two copies per thymocyte of unintegrated murine leukemia virus DNA appears in the thymuses of preleukemic mice beginning at 4 to 5 months of age and disappears in leukemic thymuses. The free viral genomes are absent in the spleens, livers, and brains of preleukemic mice. Using a series of ecotropic and nonecotropic murine leukemia virus hybridization probes, we showed that the unintegrated viral genomes are structurally analogous to those of recombinant mink cell focus-forming viruses that appear as proviruses in leukemic AKR thymocytes, suggesting that these free viral DNAs are the direct precursors to the leukemia-specific proviruses. The mosaic of ecotropic and nonecotropic sequences within these unintegrated viral DNAs varies from one preleukemic thymus to another but often appears structurally homogeneous within individual thymuses, indicating that often each thymus was being infected by a unique mink cell focus-forming virus. Analysis of high-molecular-weight DNA shows that recombinant proviruses reside in the chromosomal DNA of thymocytes within the preleukemic thymus, with the number rising to an average of several copies per thymocyte, but we do not detect any preferred integration sites. These results suggest that, in general, before the development of thymic leukemias in AKR mice there is a massive infection by a unique mink cell focus-forming virus which then integrates into many different sites of individual thymocytes, one of which grows out to become a tumor.

Relationship between serum testosterone concentrations and fertility in male mink (Mustela vison).

Abstract: During 7 successive months in 1982 and 1983 blood and semen samples were taken from male mink. The patterns of testosterone development in sterile and fertile males were readily distinguishable from each other. Testosterone concentrations showed a clear correlation (r = 0.73) with sperm quality of mink males. High testosterone levels (16.0-24.5 ng/ml) in early February were associated with defective sperm quality in March and low testosterone levels (2.0-13.3 ng/ml) with good sperm quality.

Analysis of the quantity of antiviral antibodies from mink infected with different Aleutian disease virus strains.

Abstract: Mink persistently infected with Aleutian disease virus (ADV) develop hypergammaglobulinaemia and immune complex disease. Radiolabelled antibodies from mink infected with ADV-G, DK, Pullman , and Utah I strains of ADV were reacted against all four ADV strains in radioimmunoassay (RIA). The amount of anti-ADV antibody in two equally hypergammaglobulinaemic serum pools varied from 13% (anti- Pullman ) to 57% (anti-Utah I). Serum pools from two other sources (anti-DK and anti-ADV-G), although less hypergammaglobulinaemic , had 5% and 13%, respectively, indicating that 43-95% of the Ig in the sera of mink with AD was not specific antibody to ADV structural antigens. The possibility of a general polyclonal activation of the humoral immune system is being discussed. Comparison of plateau RIA binding levels for the four serum pools against the four viral antigens suggested three patterns of reactivity: DK and Utah I reacted similarly, but Pullman and ADV-G reacted serologically different.

Much of the increased IgG in Aleutian disease of mink is viral antibody.

Abstract: Aleutian disease (AD) is caused by a persistent infection of mink with an autonomous parvovirus. Chronically infected mink develop widespread plasmacytosis, a marked elevation of their serum IgG, and immune complex disease. A substantial fraction of the IgG in the serum of mink with Aleutian disease may be specifically absorbed by monolayer cell cultures infected with Aleutian disease virus. The maximum percentage of absorption of IgG found was 81% in a mink with 5.4 g/dl of IgG. Mink with the monoclonal gammopathy of Aleutian disease had a particularly large percentage of the IgG absorbed. The percentage of IgG absorbed from serums of mink with Aleutian disease is directly proportional to the serum IgG level and to the Aleutian disease viral antibody titer. The amount of IgG which can be absorbed by infected cell monolayers increases during the course of experimental infection, and the absorption is immunologically specific. Thus, it appears that much of the hypergammaglobulinemia in mink with Aleutian disease represents virus-specific antibody.

Vitamin E requirement of mink with special reference to tocopherol composition in plasma, liver, and adipose tissue.

Abstract: Tissue responses of 4 different tocopherols found in a basal diet (BD) and the effect of 2 physiologic levels of dl-alpha-tocopheryl acetate (25 and 150 mg/kg) on tissue tocopherol content were studied in the mink. The BD contained a total of 7.1 mg vitamin E/kg, with alpha-, beta-, gamma-, and delta-tocopherol in a ratio of 1:0.07:0.55:0.10, respectively. The corresponding ratios in the tissues were: liver, 1:0.04:0.12:0; plasma, 1:0:0.13:0; and adipose tissue, 1:0:0.19:0. After mink were fed diets containing vitamin E, alpha- and gamma-tocopherol were distributed in similar proportions in plasma and liver, but gamma-tocopherol was in a slightly higher proportion in adipose tissue. Addition of 25 or 150 mg/kg of alpha-tocopheryl acetate to the BD decreased the gamma-tocopherol levels in all 3 tissues; this was considered to be a dilution effect of other tocopherols in BD with added alpha-tocopheryl acetate. The beta-tocopherol content in the liver remained unchanged, irrespective of the dietary amount of alpha-tocopheryl acetate. Plasma alpha-tocopherol had a linear relationship to log dietary dose, with an apparent half-saturation of the vitamin E binding capacity at 13 mg vitamin E/kg diet. At the given dietary levels, liver and adipose continued to accumulate alpha-tocopherol. The correlation between total plasma lipids and plasma alpha-tocopherol was significant (P less than 0.001) only in the group fed the BD. Vitamin E analysis of plasma could be used as a routine method for controlling the vitamin E status of mink.(ABSTRACT TRUNCATED AT 250 WORDS)

A note on prey remains collected from the dens of feral mink (Mustela vison) in a coastal habitat

Abstract: Les terriers examines se trouvaient a 4 km de la cote dans les Dumfries et dans la region de Galloway, Ecosse

Immunoglobulin classes of Aleutian disease virus antibody.

Abstract: Aleutian disease virus (ADV) persistently infects mink and causes marked hypergammaglobulinemia. Immunoglobulin class-specific antisera were used to define the total immunoglobulin of each class by radial immunodiffusion and the immunoglobulin class of ADV-specific antibody by immunofluorescence in experimentally and naturally infected mink. Electrophoretic gamma globulin closely reflects the immunoglobulin G (IgG) level in mink, and the majority of the increased immunoglobulin and ADV antibody in infected mink is IgG. IgM becomes elevated within 6 days after infection, reaches peak levels by 15 to 18 days, and returns to normal by 60 days after infection. The first ADV antibody demonstrable is IgM, and most mink have virus-specific IgM antibody for at least 85 days postinfection. Serum IgA levels in normal mink are not normally distributed, and ADV infection causes a marked elevation of IgA. Low levels of ADV-specific IgA antibody can be shown throughout the course of infection. Failure of large amounts of virus-specific IgG antibody to inhibit the reaction of virus-specific IgM and IgA antibodies suggests that the various classes of antibodies are directed against spatially different antigenic determinants. The IgM and IgA were shown not to be rheumatoid factors.

Aleutian Disease Virus in B and T Lymphocytes from Blood and Spleen and in Bone Marrow Cells from Naturally Infected Mink

Abstract: In the nuclei of 4% of peripheral blood or spleen mononuclear cells (MNC), Aleutian disease virus (ADV)-specific antigens were found by a direct immunofluorescence test. The MNC were further fractionated by nylon wool, affinity chromatography using Staphylococcus aureus protein, or Percoll gradient techniques. ADV and specific antigens were detected in MNC fractions enriched in either the B or T lymphocytes. In the bone marrow, up to 40% antigen-positive cells were demonstrated over a period of 15 months. These findings were confirmed by the detection of infectious virus in the MNC of blood and spleen and in bone marrow cells. Adherent cells from mink and control cells from ADV-negative ferrets were negative in both tests. These findings indicate that ADV exhibits a lymphotropism and can persist in the B- and T-cell fractions from ADV-infected mink over a long period of time. Furthermore, co-cultivation of mink MNC and bone marrow cells with the CCC clone 81 cells was shown to be a reproducible method for the detection of ADV in persistently infected mink.

Effects of dietary hexachlorobenzene exposure on regional brain biogenic amine concentrations in mink and European ferrets.

Abstract: In the initial trial, adult mink and ferrets were administered hexachlorobenzene (HCB) via the feed at concentrations of 1, 5, or 25 ppm for 47 wk. Animals receiving 125 and 625 ppm HCB in the diet died before termination of the experiment, with female ferrets at the 125 ppm level displaying abnormal aggressiveness and hyperexcitability just prior to death. Hypothalamic serotonin (5-HT) was significantly elevated at all dose levels in mink, and cerebellar 5-HT was significantly elevated at 1 ppm in the ferret. Regional brain biogenic amine concentrations were also determined in the offspring of the female mink that were administered 1 and 5 ppm HCB. Hypothalamic dopamine (DA) concentrations were significantly depressed by 1 and 5 ppm in these kits. In a second study, adult male and female ferrets were administered 250 or 500 ppm HCB via the diet for 7 wk. Two animals at the 250-ppm level and 3 animals at the 500-ppm level died before termination of the experiment without showing behavioral changes. Of the remaining animals, 3 ferrets at 250 ppm and 1 ferret at 500 ppm showed slight aggressiveness and hyperexcitability during the last week of the experiment. Concentrations of 5-HT were significantly elevated at 500 ppm in the cerebral hemispheres and at 250 ppm in the midbrain of male ferrets, while in the females, 5-HT was elevated in the cerebral hemispheres at 250 ppm and in the hypothalamus at both 250 and 500 ppm. Norepinephrine (NE) concentrations were significantly elevated in the cerebellum of males exposed to 250 and 500 ppm, as were NE concentrations in the midbrain. HCB at 500 ppm caused a significant increase in medullary NE, while 250 ppm caused an increase in hypothalamic NE in males. The only change in regional brain dopamine (DA) concentrations occurred at 500 ppm HCB in the midbrain of males, where there was a significant elevation of this neurotransmitter.

Mink with Aleutian disease have high-affinity antiviral antibodies.

Abstract: Mink persistently infected with Aleutian disease virus (ADV) develop plasmacytosis (hypergammaglobulinaemia) and immune complex disease. Mink of different colour phases were infected with different strains of ADV and bled at different times after infection. The average antibody affinities (Kav) were measured in the sera and found to fall in the range of 2 X 10(9) - 2 X 10(10) M-1, thus indicating good-quality antibodies. In sera of non-Aleutian genotype mink a decline in Kav during development of plasmacytosis was observed. Moreover, the antibody heterogeneity (alpha values) tended to decrease during the disease progress. In contrast, the Kav values in sera of infected Aleutian genotype mink remained relatively high after hypergammaglobulinaemia developed, and the antibody heterogeneity for certain of the mink sera indicated restricted heterogeneity (high alpha values). In agreement with the clonal selection theory, low virus burden (for instance, during infection with a low-virulence ADV strain) generated relatively higher affinity antibodies than a high virus burden for instance, the highly virulent Utah I strain of ADV). Furthermore, antibodies present in low concentration were of higher affinity than antibodies present in high concentrations. The relatively high affinity antibodies found in this study indicate that if the immune complex disease seen in AD is caused by virus-anti-virus antibodies, good-quality antibodies are likely to be responsible for the pathological findings.

Cotransfer and phenotypic stabilisation of syntenic and asyntenic mink genes into mouse cells by chromosome-mediated gene transfer.

Abstract: By means of metaphase chromosomes, the genes for mink thymidine kinase (TK) and hypoxanthine-phosphoribosyltransferase (HPRT) were transferred to mutant mouse cells, LMTK-, A9 (HPRT-) and teratocarcinoma cells, PCC4-aza 1 (HPRT-). Eighteen colonies were isolated from LMTK- (series A), 9 from A9 (series B) and none from PCC4-aza 1. The transformed clones contained mink TK or HPRT. Analysis of syntenic markers in series B demonstrated that one clone contained mink glucose-6-phosphate dehydrogenase (G6PD) and the other alpha-galactosidase; in series A, nine clones contained mink galactokinase (GALK) and six mink aldolase C (ALDC). Analysis of 12 asyntenic markers located in ten mink chromosomes showed the presence of only aconitase-1 (ACON1) (the marker of mink chromosome 12) in three clones of series A. The clones lost mink ACON1 between the fifth to tenth passages. Cytogenetic analysis established the presence of a fragment of mink chromosome 8 in eight clones of series A, but not in series B. The clones of series A lost mink TK together with mink GALK and ALDC during back-selection; in B, back-selection retained mink G6PD. No stable TK+ phenotype was detected in clones with a visible fragment of mink chromosome 8. Stability analysis demonstrated that about half of the clones of series B have stable HPRT+ phenotype whereas only three clones of series A have stable TK+ phenotype. It is suggested that the recipient cells, LMTK- and A9, differ in their competence for genetic transformation and integration of foreign genes.

Immunoenzyme Western blotting analysis of antibody specificity in Aleutian disease of mink, a parvovirus infection.

Abstract: Aleutian disease virus (ADV), an autonomous parvovirus, persistently infects mink and induces very high levels of virus-specific antibody. All strains of ADV infect all mink, but only highly virulent strains cause progressive disease in non-Aleutian mink. The development of antibody to individual ADV proteins was evaluated by Western blotting by using the sera of 22 uninfected mink and 163 naturally or experimentally infected mink. ADV has virion proteins of 86,000 and 78,000 daltons that are closely related. A new, possibly nonvirion protein of 143,000 daltons was observed, as well as a known nonvirion protein of 71,000 daltons. Sera from mink experimentally or naturally infected with ADV of high or low virulence generally reacted about equally with all four proteins. The only exceptions noted were that 8 of 15 sera of mink infected transplacentally preferentially reacted with the two virion proteins and sera from mink with the monoclonal gammopathy of Aleutian disease reacted preferentially with either virion (10 of 12) or nonvirion (2 of 12) proteins.

Effects of Lactic Acid Bacteria as Feed Additive on Reproductive Performance and Early Kit Growth Rate in Mink and Blue Foxes

Abstract: In two experiments with female mink the effect of commercial lactic acid bacteria (LAB) preparations or an antibiotic (Tylan; Elanco) added to the standard mink diet in the late gestation period (one experiment) and in the lactation period were investigated with respect to reproductive results and kit performance. Microbial analyses of the experimental rations were carried out and the pH-development was followed at different feed storage conditions. Digestibility trials were conducted with kits reared in the second experiment. One LAB preparation was tested in field experiments with mink females (three farms) and with blue fox females (one farm) in late gestation and during lactation. The microbial analyses and the pH-development in stored feed implied that compounded mink diets have a considerable natural LAB flora. The added LAB survived in the feed and from at least two of the preparations LAB multiplied after a several hours' lag phase when stored at +24°C. A tendency for improved reproductiv...

Mercury and selenium in wild mink (Mustela vision) from Norway

Abstract: Levels of mercury, methylmercuri and selenium were determined in liver samples from wild mink (Mustela vision) caught in the Norwegian countries of Rogaland (38 samples), Sogn og Fjordane (15 samples) and Hedmark (18 samples). The average mercury levels from these counties were 2.6, 3.1 and 2.1 micrograms Hg/g wet weight, respectively. No significant differences in mercury levels were found. The methyl mercury levels (MeHg) were determined in 30 samples. A very strong positive correlation between total mercury (Hg) and methyl mercury (r = 0.91, P less than 0.001) was found. The average methyl mercury level was 35 per cent of total mercury. This indicates that wild mink has the ability to demethylate mercury. The selenium levels were determined in 35 samples. A strong positive correlation between the levels of total mercury and selenium (r = 0.87, P less than 0.001) was found. There was no correlation between age or nutritional condition and mercury level. In the present study mink was examined to see of it could be recommended as an indicator species for monitoring the local environment for mercury contamination. No definite answer to this question could be found. The study did reveal, however, that in all the counties studied there are individuals that are considerably contaminated with mercury.