Mink plasmacytosis, caused by Aleutian Mink Disease Virus (AMDV), poses a threat to the development of the animal fur industry. Neutralizing antibodies against AMDV may result in a persistent infection rather than providing protection for minks. To date,no specific methods to prevent or cure this disease have been developed. In order to eliminate mink plasmacytosis, antibody detection technology has been used globally as a dominant approach to screen for AMDV-positive minks. This paper introduces the classical technology, counterimmunoelectrophoresis and emerging technology in terms of AMDV antibody detection,and provides a glimpse into the future development of these technologies.
Aleutian Mink Disease ; diagnosis ; immunology ; virology ; Aleutian Mink Disease Virus ; immunology ; isolation & purification ; Animals ; Antibodies, Viral ; immunology ; Immunoassay ; instrumentation ; methods ; Mink

Aleutian mink disease parvovirus (AMDV) causes a persistent infection associated with immune complex disease, hypergammaglobulinemia, and high levels of antiviral antibodies. Despite the presence of an antibody, the virus is not cleared in vivo. Pre-existing antibodies may enhance viral infections, by Fc-receptor-mediated antibody-dependent enhancement (ADE), but the mechanism that underlies ADE has not been fully defined. Three models have been proposed, including: (1) interactions between antibody and FcR, complement C3 fragment and CR, or between C1q and C1qR, which promotes viral attachment to cells; (2) suppression of IFN-gamma-mediated host-cell antiviral gene expression by the upregulation of negative regulators of pathogen pattern recognition; and (3) the promotion of early IL-10 secretion. In addition, the role of cytokine IL-6 in ADE mediated disease development is discussed, to facilitate a better understanding of the pathogenesis of AMDV infection, as well as give insights into rational vaccine design approaches.
Aleutian Mink Disease ; immunology ; virology ; Aleutian Mink Disease Virus ; genetics ; immunology ; Animals ; Antibodies, Viral ; immunology ; Antibody-Dependent Enhancement ; Mink ; immunology ; virology

To analyze the molecular mechanisms of cross-host transmission of the Aleutian mink disease vi rus (ADV), the hypervariable region fragment of the VP2 gene of the ADV in Jilin Province (China) was amplified. Sequencing analyses showed diversity at residue 174 by comparison with other VP2 genes in GenBank. The phylogenetic tree indicated that the ADV-JL strain had a close relationship with the highly pathogenic strain from Denmark: ADV-K. Results implied that residue 174 may be associated with ADV infectivity.
Aleutian Mink Disease ; virology ; Aleutian Mink Disease Virus ; chemistry ; classification ; genetics ; isolation & purification ; Amino Acid Sequence ; Animals ; Capsid Proteins ; chemistry ; genetics ; China ; Mink ; Molecular Sequence Data ; Phylogeny ; Sequence Alignment ; Sequence Analysis

There were 4 Acinetobacter lwoffii obtained from soil samples. The antimicrobial susceptibility of the strains to 16 antimicrobial agents was investigated using K-B method. Three isolates showed the multi-drug resistance. The presence of resistance genes and integrons was determined using PCR. The aadA1, aac(3')-IIc, aph(3')-VII, aac(6')-Ib, sul2, cat2, floR, and tet(K) genes were detected, respectively. Three class 1 integrons were obtained. The arr-3-aacA4 and blaPSE-1 gene cassette, which cause resistance to aminoglycoside and beta-lactamase antibiotics. Our results reported the detection of multi-drug resistant and carried resistant genes Acinetobacter lwoffii from soil. The findings suggested that we should pay close attention to the prevalence of multi-drug resistant bacterial species of environment.
Acinetobacter ; drug effects ; Animals ; Anti-Bacterial Agents ; pharmacology ; Drug Resistance, Multiple, Bacterial ; Housing, Animal ; Mink ; Soil Microbiology

Self-biting is a chronic disease, which cause wound to take effect on mink growth and pelt quality. In this study, we firstly adopted RAPD (random amplification polymorphism DNA) technique based on the reproducible 26 polymorphism primers screened from 100 random primers to analyze hereditary constitution of the samples from healthy minks and self-biting minks, respectively, at molecular level to aim to discuss the causes of self-biting. The results showed that 29 straps showed polymorphism among amplified 105 straps, of which the polymorphism rate is 27.62%. Between healthy and sick mink groups, the amplified DNA fragment through different primers indicated different distribution frequency. The similarity coefficient of mink groups is 0.8471 and genetic distance (variation) index is 0.1529. Through primer S356 (whose sequence is CTGCTTAGGG), we amplified different straps between healthy and sick mink. The amplified 1000 bp DNA fragment in the sick mink groups can preliminarily serve as molecular genetic label to distinguish from healthy and sick mink groups to gradually remove the mink individual of self-biting, achieve to purify mink groups and reduce economy loss of mink breeding industry. This work provide theoretical basis for further study on molecular breeding and disease prevention of mink.
Animals ; Base Sequence ; Genetic Diseases, Inborn ; etiology ; genetics ; veterinary ; Mink ; genetics ; Molecular Sequence Data ; Random Amplified Polymorphic DNA Technique

A chordoma is an uncommon tumor that originates from the remnants of the notochord and most commonly involves the cranial and caudal regions of the axial skeleton. Chordoma has been described in laboratory animals such as dogs, rats, minks, and ferrets. This report describes a case of a chordoma in the tail of a ferret. Grossly, a grayish-white, expansile, subcutaneous soft-tissue mass was observed in the tail. Histopathologically, the mass was a loosely placed, nodular, unencapsulated neoplasm within the dermis. In the mass, tumor lobules were intermingled with fibrous tissues. Fibrous tissues contained abundant extracellular basophilic material that was consistent with mucin. The tumor was composed of a close pack of adipocyte-like vacuolated cells (physaliferous cells). The cells were centrally or eccentrically located round nuclei and eosinophilic cytoplasm with large vacuoles. Immunohistologically, neoplastic cells were positive for vimentin and S-100 protein. Based on histopathologic findings and special staining characteristics, this case was diagnosed as chordoma.
Animals ; Animals, Laboratory ; Basophils ; Chordoma ; Cytoplasm ; Dermis ; Dogs ; Eosinophils ; Ferrets ; Mink ; Mucins ; Notochord ; Rats ; S100 Proteins ; Skeleton ; Tail ; Vacuoles ; Vimentin

OBJECTIVETo investigate whether the cellular gap junctional communication(GJIC) down-regulation in alveolar epithelial cells (CCL-64 cells) induced by silica-stimulated pulmonary alveolar macrophages (PAM) supernatant is related with the phosphorylation states of connexin 43(Cx43) protein.

METHODWestern-blot analysis was used to identify phosphorylated Cx43 species.

RESULTSWestern-blot analyses of SiO2- and phorbol 12-myristate 13-acetate(TPA)-treated CCL-64 cells showed the same phosphorylation states of Cx43 as the control group. There were no Cx43 protein in nucleus of CCL-64 cells.

CONCLUSIONThe inhibition on GJIC induced by SiO2 and TPA in CCL-64 cells may not be brought about by altering the phosphorylation states of Cx43.

Animals ; Cell Communication ; drug effects ; Cell Line ; Connexin 43 ; metabolism ; Gap Junctions ; drug effects ; Lung ; drug effects ; metabolism ; Mink ; Phosphorylation ; Silicon Dioxide ; toxicity ; Tetradecanoylphorbol Acetate ; pharmacology

AIMTo establish a new, reliable vomiting model in minks.

METHODSAdult male minks (Mustela vison) were randomly divided into groups (n = 6). Cisplatin, apomorphine, copper sulfate and X-radiation were used to establish vomiting model. Retching and vomiting were observed after the vomiting models were given anti-vomiting agents. After the behavioral experiment, assay of 5-HT in the ileum was performed by immunohistologic method.

RESULTSCisplatin 7.5 mg.kg-1 i.p., apomorphine 1.6 mg.kg-1 s.c. and copper sulfate 40 mg.kg-1 ig were shown to evoke vomiting. Retching and vomiting were significantly inhibited in ondansetron and metoclopramide pretreated minks (P < 0.05, P < 0.01).

CONCLUSIONAs a new vomiting model, minks may be of great value in studying vomiting mechanism and screening new antiemetic drugs.

Animals ; Antiemetics ; therapeutic use ; Apomorphine ; Cisplatin ; Copper Sulfate ; Disease Models, Animal ; Male ; Metoclopramide ; therapeutic use ; Mink ; Ondansetron ; therapeutic use ; Vomiting ; chemically induced ; drug therapy

OBJECTIVETo study the effect of supernatants from silicon dioxide(SiO2) stimulated pulmonary alveolar macrophages(PAM) on the localization of connexin 43(Cx43) so as to explore the inhibition level of SiO2 on alveolar epithelial cellular gap-junctional communication(GJIC).

METHODSThe supermatants from the primary cultured PAM were prepared, and then added 5% (v/v) SiO2 into 2% (v/v) NBS RPMI 1640 to stimulate the normal mink lung epithelial cell line CCL-64 for 24 hours. The localizations of Cx43 in CCL-64 were analyzed by indirect immunofluorescence histochemistry and laser confocal scanning microscopy(LCSM).

RESULTSThe normal cultured CCL-64 cells displayed bright membrane-associated Cx43 plaques labeling and formed dashes at regions of intercellular junction. Being exposed to supernatants from SiO2-stimulated PAM, the CCL-64 cells retained a relative low degree of Cx43 labeling at the cell periphery, localized in cytoplasm, and the individual spot, rather than plaques, were smaller compared to normal cultured cells. Along with the increase of the concentrations of SiO2, the cells displayed a different staining pattern, with clear cluster labeling aggregating towards the nucleus.

CONCLUSIONThe altered localization of the gap-junctional protein Cx43 in alveolar epithelial cells, mediated by SiO2, indicated that the internalization of Cx43 may contribute to the inhibition on GJIC in silica-induced lung epithelium injury.

Animals ; Cell Communication ; drug effects ; Cell Line ; Connexin 43 ; analysis ; Epithelial Cells ; chemistry ; drug effects ; Fluorescent Antibody Technique, Indirect ; Gap Junctions ; drug effects ; Microscopy, Confocal ; Mink ; Pulmonary Alveoli ; chemistry ; drug effects ; Silicon Dioxide ; toxicity

BACKGROUNDGingerol is the generic term for pungent constituents in ginger, which has been reported to be effective for inhibiting vomiting. We attempted to investigate the antiemetic effect of gingerol and its effective mechanism on substance P and NK(1) receptors in minks.

METHODSThe antiemetic effect of gingerol was investigated during a 6-hour observation on a vomiting model in minks induced by cisplatin, (7.5 mg/kg, intraperitoneal). The distribution of substance P and NK(1) receptors in the area postrema and ileum were measured by immunohistochemistry, and the expression of NK(1) receptor in the area postrema and ileum were measured by Western blotting.

RESULTSThe frequency of cisplatin induced retching and vomiting was significantly reduced by pretreatment with gingerol in a dose-dependent manner (P < 0.05). Substance P-immunoreactive was mainly situated in the mucosa and submucosa of the ileum as well as in the neurons of the area postrema. The immunoreactive production of NK(1) receptor was mainly situated in the muscular and submucosa of ileum and the neurons of area postrema, gingerol markedly suppressed the increased immunoreactivity of substance P and NK(1)1 receptor induced by cisplatin in a dose-dependent manner (P < 0.05), and exhibited effective inhibition on the increased expression levels of NK(1) receptor in both the ileum and area postrema dose-dependently (P < 0.05).

CONCLUSIONSGingerol has good activity against cisplatin-induced emesis in minks possibly by inhibiting central or peripheral increase of substance P and NK(1) receptors.

Animals ; Area Postrema ; metabolism ; Blotting, Western ; Catechols ; therapeutic use ; Disease Models, Animal ; Fatty Alcohols ; therapeutic use ; Ileum ; metabolism ; Immunohistochemistry ; Male ; Mink ; Receptors, Neurokinin-1 ; metabolism ; Substance P ; metabolism ; Vomiting ; chemically induced ; drug therapy