CPT tests in the neutral kaon system.
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Biomedical subjects
Publications and source records attributed to P Haas.
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DNA profiles (immunoprints) were generated for 120 patients suffering from early onset pauciarticular chronic arthritis (EOPA-JCA) and > 500 healthy controls utilizing highly polymorphic microsatellites in the vicinity of immunorelevant genes. Six T cell receptor (TCR) markers for the CD3D, TCRDVAJ, TEA, TCRBV6S1, BV6S3, BV6S7 and BV13S2 genes were analysed. Furthermore markers for the cell surface molecule CD40L, for cytokine genes (IL-1A, IL-2, IFN-alpha, FGF-alpha, TNF-alpha), the chromosomal region of the IRF2 and the cytokine receptor gene IL5RA were studied as well as two polymorphisms within the promotor region of the TNF-alpha gene. Coding region polymorphisms were evidenced indirectly by repeat length variation or they were predicted from the microsatellite distribution profiles and then confirmed by direct sequence analysis. Statistical evaluations were performed with respect to known predispositions, predominance of females (> 80%) and HLA-DR and -DQ haplotypes. Cell surface molecules (TCR, CD40L, IL5RA) as well as almost all cytokines (IL-1A, IFN alpha, FGFA, IRF2 region) were excluded as predisposing in our JCA panel. The TNF-alpha microsatellite alleles (GT)10-12 contribute considerably to manifestation of the disease, in HLA-DRB1*11(12) individuals (RR = 12.8). The TNF-alpha allele is not found in linkage disequilibrium with HLA-DRB1*11(12) and may be present on either chromosome 6. Thus, a novel susceptibility factor probably within the TNFA/TNFB gene region has been identified via linkage with the TNF-alpha microsatellite allele. Apparently complex compositions of the genetic background rather than single genes provide the precondition for manifestation of the autoimmune disease EOPA-JCA. Immunoprinting unravels the variability of the immunological genome via the semi-directed microsatellite approach efficiently.
Although the role of gonadal steroids in inducing the LH surge is undisputed, the mechanism(s) whereby steroids induce the release of the hypothalamic luteinizing hormone-releasing hormone (LHRH) remain(s) enigmatic. In this study we examined the issue of the presence of steroid receptors in LHRH neurons using a mammalian species that has a true luteal phase, namely, guinea pigs. Progestin receptors (PR) were localized in LHRH neurons of ovariectomized guinea pigs administered estradiol (10-20 micrograms estradiol benzoate) for 3-4 days, using several different immunocytochemical protocols. The subgroup of LHRH neurons containing PR, although small, was strategically positioned within the core of the total population of LHRH neurons. This central position was visualized in simultaneous views of three-dimensional computer reconstructions of the populations of LHRH/PR neurons and LHRH neurons. The subgroup of LHRH/PR neurons formed a thread permeating the population of LHRH neurons. We propose that in guinea pigs, LHRH neurons containing progestin receptors, are foci of activity, capable of activating a larger component of the LHRH population of cells in certain endocrine conditions, such as prior to the LH surge.
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Injuries to the popliteal artery or vein are rare complications of knee arthroscopy or osteosynthesis at the distal femur or the proximal tibia. We report a case of iatrogenic arteriovenous fistula after proximal tibial osteotomy for varus deformity. A 71-year-old woman complained of pain and swelling of the foot 9 weeks after a corrective barrel-vault osteotomy of the left tibia. Angiography demonstrated an arteriovenous fistula between the popliteal vessels due to osteotomy of the tibial head. The fistula was separated and popliteal vessels closed by continuous suture and a small saphenous vein patch.
Coeliac disease (CD) is associated with particular HLA genotypes. The susceptibility gene (or genes) has been mapped to the class II region, most probably to the DQ loci. Polymorphism of the upstream promoter region of the DQA1 gene (QAP) has been recently reported. At least ten variants or QAP alleles have been found, some of which are present in the cis-acting regulatory sequences. Allelic differences in DQ molecule expression may play a role in susceptibility to CD. We investigated the QAP polymorphism in 102 CD patients and 142 unrelated healthy controls of Czech origin using polymerase chain reaction amplification (PCR) of genomic DNA and oligonucleotide probes. We found a significant frequency increase of the alleles QAP 4.1 (RR = 10.3, p.c. = 10(-6) and QAP 2.1 (RR = 2.4, p.c. = 0.017) in patients over controls. An increased susceptibility is provided by the presence of both alleles, as is shown by the higher proportion of QAP 4.1, 2.1 heterozygotes among patients than expected from the Hardy-Weinberg equilibrium and by the comparison of the odds ratios for these alleles. There is a strong linkage disequilibrium between the QAP alleles and the DQA1, DQB1, and DRB1 loci. Two haplotypes carrying the QAP alleles whose frequency is increased are predominant in this group of CD patients: DQB1*0201, DQA1*0501, QAP4.1, DRB1*0301 and DQB1*0201, DQA1*0201, QAP 2.1, DRB1* 0701. Thus, the QAP variants are increased as part of these haplotypes and we cannot discriminate if they are responsible for the primary association.
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Even today, Virchow's triad is still a useful method for describing the circumstances under which thrombosis can occur. To investigate the underlying pathophysiological principles, however, the methods must differentiate more clearly. Only recently, the complicated interactions of blood coagulation and fibrinolysis have been described. Although detailed determinations of markers of activated coagulation and fibrinolysis can be performed, it has not been possible to achieve a reliable screening method to indicate the individual patient's risk. Alterations in the endothelial cells seem to play a key role in thrombogenesis. The clinician's interest in thrombosis research is based on several open or insufficiently answered questions, such as why thrombosis can occur in veins for away from the site of the operation, whether reliable and simple screening methods can be established in order to determine the patient's risk constellation, and how the methods of preventing thrombosis and administering therapy can be improved.
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The authors report the results of investigations in Nice from July, 16 to August, 3, 1991. The 2,098 phlebotomes captured represent three species: Phlebotomus perniciosus, Phlebotomus ariasi and Sergentomyia minuta. Two species: P. perniciosus and P. ariasi are infected with promastigotes. About 4% of dissected females are parasited. This is the first description in France of P. perniciosus infected.