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41.
Transplacental Neospora caninum infection in cats 总被引:1,自引:0,他引:1
Transplacental transmission of Neospora caninum was studied in 2 pregnant cats (queens). Queen 1 was inoculated subcutaneously with 2 x 10(6) cell culture-derived N. caninum tachyzoites on day 47 of gestation. She gave birth to a full-term kitten on the 17th day after inoculation. The kitten died the second day after birth due to generalized N. caninum infection. The mother cat was killed on the third day after parturition and was found to have a macerated kitten in the uterus. Severe placentitis, metritis, hepatitis, and nephritis due to N. caninum were seen in tissues from the queen. Queen 2 was fed N. caninum tissue cysts and mated 111 days later. She gave birth to 3 healthy full-term kittens. The kittens were necropsied at 2, 22, and 30 days of age. Neospora caninum was recovered from the organs and was seen in histologic sections in 1 of the 3 kittens. Results indicate that N. caninum can be transplacentally transmitted in cats during acute and chronic stages of infection. Neospora caninum-specific IgG antibodies were demonstrated in the sera of inoculated cats and nursing kittens. 相似文献
42.
A cotton rat was inoculated orally with oocysts of Caryospora bigenetica from the feces of a rattlesnake. Sixteen days later the rat was euthanized, and portions of the scrotum, foot pad and muzzle were processed for histological sections and transmission electron microscopy. Sporozoites within caryocysts had typical coccidian features such as an anterior and posterior refractile body, centrally located nucleus, micronemes, rhoptries, a conoid, a micropore near the anterior refractile body, a posterior pore, amylopectin granules, lipid bodies, a Golgi-like body, a mitochondrion and subpellicular microtubules. The infected host cell was spherical and surrounded by a fibrous wall-like covering, 0.35-1.00 microns thick. This outer covering, when viewed in stained histological sections, was periodic acid-Schiff (PAS)-positive. 相似文献
43.
44.
Claudia Gaspar Iscia Lopes-Cendes Anita L. DeStefano Patrícia Maciel Isabel Silveira Paula Coutinho Patrick MacLeod Jorge Sequeiros Lindsay A. Farrer G. A. Rouleau 《Human genetics》1996,98(5):620-624
Machado-Joseph disease (MJD) is an autosomal dominant spinocerebellar degeneration originally described in families of Portuguese-Azorean
ancestry. The hypothesis that its present world distribution could result from the spread of an original founder mutation
has been raised. To test this possibility we have conducted a linkage disequilibrium study of markers segregating with the
MJD1 locus in a total of 64 unrelated families of different geographical origins. Significant association was detected between
the MJD1 locus and marker alleles at loci D14S280, D14S1050 and D14S81. All affected individuals, except one Chinese family, had allele
3 (237 bp) at D14S280. This finding is consistent with a founder effect in our MJD population. However, distinct haplotypes
were observed in patients originating from the two Azorean islands showing the highest disease prevalence; therefore, the
possible existence of more than one founder mutation can not be excluded with the markers currently available.
Received: 27 February 1996 / Revised: 4 June 1996 相似文献
45.
Locus Heterogeneity for Waardenburg Syndrome is Predictive of Clinical Subtypes 总被引:5,自引:4,他引:1 下载免费PDF全文
Lindsay A. Farrer Kathleen S. Arnos James H. Asher Clinton T. Baldwin Scott R. Diehl Thomas B. Friedman Jacquie Greenberg Kenneth M. Grundfast Christopher Hoth Anil K. Lalwani Barbara Landa Kate Leverton Aubrey Milunsky Robert Morell Walter E. Nance Valerie Newton Rajkumar Ramesar Valluri S. Rao Jennifer E. Reynolds Theresa B. San Agustin Edward R. Wilcox Ingrid Winship Andrew P. Read 《American journal of human genetics》1994,55(4):728-737
Waardenburg syndrome (WS) is a dominantly inherited and clinically variable syndrome of deafness, pigmentary changes, and distinctive facial features. Clinically, WS type I (WS1) is differentiated from WS type II (WS2) by the high frequency of dystopia canthorum in the family. In some families, WS is caused by mutations in the PAX3 gene on chromosome 2q. We have typed microsatellite markers within and flanking PAX3 in 41 WS1 kindreds and 26 WS2 kindreds in order to estimate the proportion of families with probable mutations in PAX3 and to study the relationship between phenotypic and genotypic heterogeneity. Evaluation of heterogeneity in location scores obtained by multilocus analysis indicated that WS is linked to PAX3 in 60% of all WS families and in 100% of WS1 families. None of the WS2 families were linked. In those families in which equivocal lod scores (between −2 and +1) were found, PAX3 mutations have been identified in 5 of the 15 WS1 families but in none of the 4 WS2 families. Although preliminary studies do not suggest any association between the phenotype and the molecular pathology in 20 families with known PAX3 mutations and in four patients with chromosomal abnormalities in the vicinity of PAX3, the presence of dystopia in multiple family members is a reliable indicator for identifying families likely to have a defect in PAX3. 相似文献
46.
Garry Lindsay Allan Jim Camakaris George J. F. Legge 《Biological trace element research》1994,40(2):103-126
A scanning proton microprobe has been used for the elemental microanalysis of individual fibroblast cells. Both normal fibroblasts and fibroblasts cultured from patients with Menkes' disease, an X-linked genetic disorder known to be associated with defective copper metabolism, were examined by the probe. The cells were cultured on a thin ultra-clean nylon foil and retained on that surface for analysis. The focused high-energy proton beam was used to irradiate selected individual cells and elemental information was derived from X-ray and backscattered proton data. The sensitivity of the scanning proton microprobe to trace concentrations of heavy elements has allowed this elemental information to be used to identify individual cells as being either normal or a Menkes' mutant. The cell identification was based on the application of discriminate analysis to a data set formed from the ratios of copper to each of the macroelements present in the cell. This method of cell identification offers the promise of rapid diagnosis of Menkes' disease. 相似文献
47.
The action ofClostridium perfringens cytotoxic enterotoxins may be activated/exacerbated both in vivo and in vitro by the addition of an activator molecule present in a brush border membrane fraction isolated from young rabbits. Increased concentrations of the activator could be induced by immunologically stimulating rabbits with Ribi adjuvant. Comparative studies suggested that the activator was interferon-gamma (IFN-). In vitro IFN- sensitized cell lines apparently by enhancement of cell permeability, which allowed a more rapid uptake of the toxins, resulting in cell death at lower toxin concentrations. Viral and/or bacterial infections are inducers of IFNs. We propose that some immunologically immature infants are predisposed to infection. In the weeks prior to death, these infants may suffer from an infection that induces the synthesis of IFNs, sensitizing the infant to a more virulent infection and possible sudden death.Florida Agricultural Experiment Station Journal Series No. R-02380 相似文献
48.
cDNA cloning and expression of a potato (Solanum tuberosum) invertase 总被引:10,自引:0,他引:10
Peter E. Hedley Gordon C. Machray Howard V. Davies Lindsay Burch Robbie Waugh 《Plant molecular biology》1993,22(5):917-922
A cDNA clone encoding an invertase isoenzyme has been isolated from a potato leaf cDNA library. The deduced amino acid sequence shows significant similarities to previously characterised invertases. The highest degree of overall similarity, including the signal peptide sequence, is to carrot cell wall invertase, suggesting that the potato gene encodes an apoplastic enzyme. Expression of the gene, as determined by RT-PCR, is detected in stem and leaf tissue, and at lower levels in tuber, but is absent from roots. 相似文献
49.
8-Hydroxydeoxyguanosine (8-OHdG) is now widely used as a sensitive marker of oxidative damage to DNA. When human granulocytes are stimulated with TPA, they release a large quantity of reactive oxygen species (superoxide, hydrogen peroxide) which might be expected to generate hydroxyl radicals (OH-) which in turn could produce 8-OHdG in the DNA. There had been considerable debate as to whether OH -is detectable in stimulated granulocytes; most workers now agree that none can be detected, unless exogenous iron is added. An earlier report had described that 8-OHdG (a marker of OH -) was increased in the DNA of TPA-stimulated, compared to control, granulocytes. We have repeated this experiment and have been unable to reproduce this Finding. We conclude that the amount of 8-OHdG produced in the DNA of TPA-stimulated human ganulocytes is indistinguishable from that seen in control (unstimulated) cells (less than one 8- OHdG/105 dG). 相似文献
50.
Tihomir Paul Obrenovitch Jutta Urenjak Douglas Arthur Richards † Yukihiko Ueda Gerald Curzon † Lindsay Symon 《Journal of neurochemistry》1993,61(1):178-186
Abstract: Changes in the extracellular levels of excitatory and inhibitory amino acid transmitters were studied in the rat striatum during penumbral ischaemia using intracerebral microdialysis. Effects of penumbral forebrain ischaemia were compared with those of ischaemia with sustained anoxic depolarisation and K+ (100 m M ). Comparisons were also made between different groups of animals at 2 and 24 h after dialysis probe implantation. The K+ stimulus did not provoke any release of excitatory amino acids in the 24-h group, probably reflecting a decrease of functional synapses adjacent to the probe. During 30 min of penumbral ischaemia, excitatory amino acids did not reach critical concentrations in the extracellular fluid, and increases in levels of inhibitory/modulatory amino acids were similar. On the other hand, severe transient ischaemia resulted in massive synchronous release of many neuroactive excitatory and inhibitory compounds, in both the 2- and 24-h groups. These and other data suggest that changes during severe ischaemia may arise from both neurotransmitter and metabolic pools. It is concluded that is- chaemic damage in the penumbra may not be related to extracellular neuroactive amino acid changes generated within this region. 相似文献