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71.
J. R. NEEFE JR. H. BALNER A. D. BARNES C. FORD G. N. ROOENTINE JR. W. VAN VREESWIJK F. E. WARD 《Tissue antigens》1975,6(2):77-79
The Second International Nonhuman Primate Histocompatibility Workshop permitted comparison of rhesus monkey alloantisera developd in various laboratories on a single common panel of related and unrelated monkeys. Analysis of the data permits the conclusion that at least nine specificities are recognized by more than one laboratory, including six at the first locus and three at the second locus. 相似文献
72.
Linkage of the MHC to familial multiple sclerosis suggests genetic heterogeneity. The Multiple Sclerosis Genetics Group 总被引:5,自引:0,他引:5
Haines JL; Terwedow HA; Burgess K; Pericak-Vance MA; Rimmler JB; Martin ER; Oksenberg JR; Lincoln R; Zhang DY; Banatao DR; Gatto N; Goodkin DE; Hauser SL 《Human molecular genetics》1998,7(8):1229-1234
Multiple sclerosis (MS) is a demyelinating autoimmune disease of the
central nervous system. While its etiology is not well understood, genetic
factors are clearly involved. Until recently, most genetic studies in MS
have been association studies using the case-control design testing
specific candidate genes and studying only sporadic cases. The only
consistently replicated finding has been an association with the HLA-DR2
allele within the major histocompatibility complex (MHC) on chromosome 6.
Using the genetic linkage design, however, evidence for and against linkage
of the MHC to MS has been found, fostering suggestions that sporadic and
familial MS have different etiologies. Most recently, two of four genomic
screens demonstrated linkage to the MHC, although specific allelic
associations were not tested. Here, a dataset of 98 multiplex families was
studied to test for an association to the HLA-DR2 allele in familial MS and
to determine if genetic linkage to the MHC was due solely to such an
association. Three highly polymorphic markers (HLA-DR, D6S273 and TNFbeta)
in the MHC demonstrated strong genetic linkage (parametric lod scores of
4.60, 2.20 and 1.24, respectively) and a specific association with the
HLA-DR2 allele was confirmed (TDT; P < 0.001). Stratifying the results
by HLA-DR2 status showed that the linkage results were limited to families
segregating HLA-DR2 alleles. These results demonstrate that genetic linkage
to the MHC can be explained by the HLA-DR2 allelic association. They also
indicate that sporadic and familial MS share a common genetic
susceptibility. In addition, preliminary calculations suggest that the MHC
explains between 17 and 62% of the genetic etiology of MS. This
heterogeneity is also supported by the minority of families showing no
linkage or association with loci within the MHC.
相似文献
73.
The Gm-Pi linkage heterogeneity in view of Pi M subtypes 总被引:1,自引:3,他引:1
T. GEDDE-DAHL JR R. R. FRANTS† B. OLAISEN† A. W. ERIKSSON† E. VAN LOGHEM§ L. LAMM¶ 《Annals of human genetics》1981,45(2):143-153
In this study linkage between the loci for Gm (γ-type heavy-chain immunoglobulin markers) and Pi (α1 -antitrypsin/α1 -protease inhibitor) has been shown in families segregating for the Pi M subtypes (Ml, M2, M3 and Msal) as identified by separator isoelectric focusing. The estimate for the Gm-Pi (M-type) recombination is 0-29 (95% limits 0-24-O37) at a peak lod score of 4-31 and with no sex difference. This value is not significantly different from updated recombination frequency estimates for Gm-Pi in Pi MS (0-26) and Pi MZ, SZ and FZ families (0 21). The overall Gm-Pi recombination fraction estimate of 0 26 (95 % limits O23-0-30) at a peak lod score of 20-75 must now be considered as solid. There is a significant heterogeneity within the male Pi MZ families in that the new Finnish families show a higher recombination between Gm and Pi. There is also a possible segregation distortion (Z:M = 23:8). The heterogeneity is discussed in terms of haplotypes, the behaviour of which could be determined by linked genes or chromosomal rearrangements. The possibility that the α1 -antitrypsin level influences recombination frequency has not been ruled out, but cannot explain the heterogeneity within Pi MZ families. 相似文献
74.
The ramification of the portal vein at the porta hepatis was studied by anatomic dissection performed in 32 formalin fixed human livers. In all the specimens there were branches which ran towards the caudate lobe, arising from the portal vein and either from the left or the right portal branches. Tri-and quadrifurcation of the portal vein was observed. In 5 cases (16%) there were branches arising from left portal branch or portal vein and directed anteriorly to the quadrate lobe or to the region of the gall-bladder sulcus. These branches ranged from 1.0 to 6.0 mm in diameter. The portal caudate branches were divided into 3 groups.Group 1: Branches to the papillary process; 1 or 2 branches in 26 cases (82%), 3 or 5 branches in 3 cases (9%) and no branches in 3 cases (9%); 相似文献
75.
76.
77.
The Charcot-Mane-Tooth disease type 1A (CMTlA) phenotype is most often associated with a 1.5 megabase (mb), tandem duplication of chromosome 17 band p12 (17˜12). The prevailing hypothesis is that the demyelinating neuropathy results from a dosage effect of the peripheral myelin protein gene PMP22 which is included within this duplication. We present a patient with clinical and electrophysiological features ofCMTlA in whom an extra PMP22 gene resulted from a rare unbalanced translocation of 17p to the X chromosome. This finding further supports the hypothesis of gene dosage as the basis for CMTlA. More-over, this case highlights the importance of fluorescence in siiu hybridization (FISH) as an alternative molecular technique in the diagnosis of CMTlA. 相似文献
78.
Inhibition of the Mixed Lymphocyte Culture Response by Antibody Following Successful Human Renal Transplantation 总被引:7,自引:0,他引:7
Immunoglobulin G, appearing after several months in the serum of a recipient of a successful kidney transplant from a closely matched sibling donor, was demonstrated to progressively inhibit unidirectional mixed lymphocyte cultures when donor lymphocytes were used either in responding or stimulating cell populations. The active recipient IgG had no effect in cultures in which donor cells were not used, nor did IgG obtained from other individuals show nonspecific inhibitory effects on cultures containing donor cells. It is suggested that the MLC inhibitory immunoglobulin may serve an immunoregulatory function after renal transplantation. 相似文献
79.
Dexamethasone alters TNF-alpha expression in retinopathy 总被引:3,自引:0,他引:3
TNF-alpha has been found in the retina. Hyperoxia and hypoxia regulate TNF-alpha expression. TNF-alpha is an important factor in inflammation and angiogenesis. Dexamethasone inhibits TNF-alpha production. Changes in TNF-alpha expression in the retina may play an important role in the development of oxygen-induced retinopathy. Oxygen-induced retinopathy was produced in C57BL6 mice by exposure to 75% oxygen at Postnatal Day 7 (P7) for 5 days and the mice recovered in room air until Day 17 (P17). Dexamethasone was administered at 0.5 mg/kg/day once daily subcutaneously during the 5 days of oxygen exposure. TNF-alpha expression was evaluated at Day 7 prior to oxygen exposure, at Day 12 (P12) immediately upon removal from oxygen, and at Day 17, the time of maximal vasoproliferation by RT-PCR. TNF-alpha is developmentally regulated in the retinae of C57BL6 mice. From P7 to P12, there is a 3-fold increase in TNF-alpha expression and from P7 to P17 there is a 2.7-fold increase. There was 2.7-fold suppression in expression immediately following oxygen exposure at P12. The expression was dramatically increased at P17, the time of maximal vasoproliferation. Dexamethasone inhibited the expression of TNF-alpha at P17 by 6.4-fold. At this dose, it also suppressed the baseline TNF-alpha expression in the mouse model. In summary, TNF-alpha is altered in the development of oxygen-induced retinopathy in the mouse. It increased markedly during the vasoproliferative phase and was suppressed by dexamethasone. Modulation of TNF-alpha expression may provide a potential site of action for future therapeutic targets. 相似文献
80.
Anne?W.?Higgins Karen?M.?Gustashaw Huntington?F.?WillardEmail author 《Chromosome research》2005,13(8):745-762
The centromere is essential for the faithful distribution of a cell's genetic material to subsequent generations. Despite
intense scrutiny, the precise genetic and epigenetic basis for centromere function is still unknown. Here, we have used engineered
dicentric human chromosomes to investigate mammalian centromere structure and function. We describe three classes of dicentric
chromosomes isolated in different cell lines: functionally monocentric chromosomes, in which one of the two genetically identical
centromeres is consistently inactivated; functionally dicentric chromosomes, in which both centromeres are consistently active;
and dicentric chromosomes heterogeneous with respect to centromere activity. A study of serial single cell clones from heterogeneous
cell lines revealed that while centromere activity is usually clonal, the centromere state (i.e. functionally monocentric
or dicentric) in some lines can switch within a growing population of cells. Because pulsed field gel analysis indicated that
the DNA at the centromeres of these chromosomes did not change detectably, this switching of the centromere state is most
likely due to epigenetic changes. Inactivation of one of the two active centromeres in a functionally dicentric chromosome
was observed in a percentage of cells after treatment with Trichostatin A, an inhibitor of histone deacetylation. This study
provides evidence that the activity of human centromeres, while largely stable, can be subject to dynamic change, most likely
due to epigenetic modification. 相似文献