Monocyte hemolytic activity as an immunologic indicator of allograft rejection in rat skin transplantation.
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Biomedical subjects
Publications and source records attributed to H Jiang.
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Limulus polyphemus C-reactive protein (CRP) (limulin) has approximately 30% amino acid sequence homology and shares at least one idiotypic determinant associated with ligand-binding activity with human CRP (hCRP); limulin also shares amino acid sequence homology and lectin activity with human serum amyloid P component (hSAP). In the present study panels of 14 anti-hCRP monoclonal antibodies (mAb) directed to distinct hCRP epitopes and 11 anti-hSAP mAb directed to distinct epitopes of hSAP were tested for reactivity with limulin and pentraxins of other species including rabbit CRP (raCRP), rat CRP and hamster female protein (FP) by ELISA and Western blot analyses. None of the anti-human pentraxin mAb showed strong cross-reactivity with limulin; only five mAb reacted with limulin at all, and cross-reactivities of these mAb with the other pentraxins, when present, also were weak. Cross-reactivity of limulin with hCRP and hSAP was similar, and in light of comparable amino acid sequence homology, suggests this molecule can be considered the limulus SAP as well as the limulus CRP. Several anti-hCRP mAb cross-reacted strongly with rabbit CRP and rat CRP; a few anti-hSAP cross-reacted strongly with FP; and weak cross-reactions were observed between hCRP and hSAP, but cross-reactivities between the pentraxins generally were limited and weak. A rabbit polyclonal antibody raised to highly conserved limulin peptide 141-156 and strongly reactive with limulin reacted weakly with hCRP and raCRP but failed to react with rat CRP, hSAP or FP. These studies emphasize a limited but distinct antigenic similarity between limulin, hCRP and other pentraxins, and identify mAb reactive with potential regions of shared structure and/or function between pentraxins of different species.
Both intact IgG and Fab fragments of a monoclonal antibody SZ-21, directed against platelet glycoprotein (GP) IIIa, inhibited binding of anti-PLA1 antibodies to PLA1-positive platelets in a dose dependent manner. Conversely, the binding capacity of the platelets for SZ-21 was decreased in the presence of anti-PLA1 antibodies. In Western blots, the determinant for SZ-21 was present on GPIIIa from either PLA1 or PLA2 homozygotes, but SZ-21 did not affect the interaction of anti-Yukb alloantibodies with their target antigen on GPIIIa. These results suggest that SZ-21 reacts with an epitope on the GPIIIa molecule very close to but not identical with that for anti-PLA1. The existence of PLA1-reactive alloantibodies in serum could be demonstrated by their competitive effect on the binding of SZ-21.
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This paper deals with the changes in contents and chemical composition in the volatile oil of Ephedra sinica before and after processing. The results indicate that after processing, the more the substances of low boiling point, the higher their contents and vice versa. The changes are particularly obvious in yellow-fried Ephedra sinica.
The protective effects of m-Nif 15, 30 and 50 micrograms.kg-1 and of Nif 30 micrograms.kg-1 on experimental myocardial infarction and metabolism in rabbits were evaluated. Blood samples were collected simultaneously from the femoral artery and the coronary sinus for examining lactate and potassium balance. In the normal group (n = 8) and the sham ligated group (n = 5), the lactate balance were +17 +/- 1.0 and + 13 +/- 1.1% respectively and the potassium balance were +2.1 +/- 0.08 and +2.4 +/- 0.08%, respectively. After occlusion of the LAD, the lactate and K+ balance reduced to -196 +/- 60.2 and -83.0 +/- 8.2% respectively, and m-Nif produced a dose dependent improvement of both balance. After giving m-Nif 15, 30 and 50 micrograms.kg-1 i.v., the lactate balance improved to -60 +/- 9, -48 +/- 6.7 and -24 +/- 1.8% and the K+ balance went up to -32.2 +/- 2.1, -17.6 +/- 0.1, -3.3 +/- 0.06, respectively. In the mean time, Nif 30 micrograms.kg-1 i.v. improved the lactate and K+ balances to -52 +/- 8.6% and -36.4 +/- 3.1%. In another experiment, propranolol 1 mg.kg-1 i.v. improved the lactate balance to -18 +/- 1.2% while the K+ balance increased to +2.0 +/- 0.05%. The area of the myocardial infarct was measured by nitroblue tetrazolium (N-BT) technique 24 h after LAD occlusion.2+ angina pectoris.
An experimental study was designed to evaluate the effect of direct current stimulation on the rate of epidermis proliferation using guinea pigs. In the study, two full thickness skin defects were made over the paravertebral region in each animal. The edges of wounds were transfixed. One of the wounds in each animal received the DC stimulation, and the other did not. The 44 animals were divided into four groups of eleven animals each, the stimulation strengths were 10 muADC, 30 muADC, 50 muADC, 0 muADC respectively. The results showed that the rate of epidermal cell proliferation and wound healing with the DC stimulation were faster, especially on the side of the negative electrode, and the rate of healing of the unstimulated wound in animals which received stimulation in the contralateral wound was faster than that of wounds of control animals.
A 35-year old female with an autoimmune disease complaining of recurrent hemoptysis and macrohematuria had received a renal transplantation from her mother. After transplantation, recurrence of pulmonary hemorrhage occurred twice. First recurrence followed the peritonitis with ileal perforation. Steroid pulse therapy had no effect on this recurrence, while double filtration plasmapheresis was effective. During this treatment, renal function was not failed. Second recurrence followed acute rejection that was cured with the OKT3-rescue therapy. DFPP therapy was effective on this episode. Pulmonary hemorrhage was caused by auto immune reaction and acute rejection caused by transplant immune reaction were recognized independently, and they needed different treatment. According to this clinical course, we consider the relation between auto immune reaction and transplant immune reaction was as follows. T cell activation caused by primary transplant immune reaction may have no direct influence on auto immune reaction. Peritonitis and rejection may induce auto immune reaction. We suppose that this auto immune reaction was caused by humoral factor, because auto immune reaction was controlled by DFPP.
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The availability of DNA structural probes that can be applied to living cells is essential for the analysis of biological functions of unusual DNA structures adopted in vivo. We have developed a chemical probe assay to detect and quantitate left-handed Z-DNA structures in recombinant plasmids in growing E. coli cells. Potassium permanganate selectively reacts with B-Z or Z-Z junction regions in supercoiled plasmids harbored in the cells. Restriction enzyme recognition sites located at these junctions are not cleaved by the corresponding endonuclease after modification with KMnO4. This inhibition of cleavage allows the determination of the relative amounts of B- and Z-forms of the cloned inserts inside the cell. We have successfully applied this method to monitor the extent of Z-DNA formation in E. coli as a function of the growth phase and mutated topoisomerase or gyrase activities. The assay can in principle be used for any unusual DNA structure that contains a restriction recognition site inside or near the structural alteration. It can be a useful tool to analyze in vivo correlations between DNA structure and gene regulatory events.
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Membrane class I MHC molecules of Con-A activated and lymphoma murine cells have been labeled by exchange of the cell's beta 2m with soluble fl-beta 2m. It has previously been shown that this method of labeling is specific and does not affect the biologic properties of class I MHC Ag. With this labeling it has been possible to demonstrate the constitutive endocytosis of class I MHC by fluorescence microscopy and by measuring the resistance to quenching by crystal violet of the internalized fl-beta 2m molecules. We could also follow the kinetics of beta 2m dissociation from the class I molecules at different pH. At pH 5.5, that is the average pH of endosomes, there is considerable dissociation within 15 to 20 min, that is the average recycling half time of class I MHC containing endosomes in activated T cells. Inasmuch as the process is reversible it is likely that, in the recycling endosomes of T cells, class I MHC molecules undergo conformational changes with beta 2m going off and on and with consequent changes of the peptide binding site. This process might be involved in Ag presentation, but, because it is apparently limited to T cells, it would play a role in the presentation of the cell's own TCR in idiotypic interactions between T cells.
A topical application of a chalcone derivative, 4,2',4'-trihydroxychalcone (isoliquiritigenin) inhibited epidermal ornithine decarboxylase (ODC) induction and ear edema formation, i.e. inflammation, caused by a topical application of 12-O-tetradecanoylphorbol-13-acetate (TPA) in CD-1 mice. In addition, isoliquiritigenin potently inhibited 7,12-dimethylbenz[alpha]anthracene (DMBA)-initiated and TPA-promoted skin papilloma formation. This inhibitory effect of isoliquiritigenin was not due to any damage inflicted on the initiated cells but due to its anti-tumor-promoting action. Isoliquiritigenin also inhibited epidermal ODC induction and skin tumor promotion caused by 7-bromomethylbenz[alpha]anthracene (BrMBA), a non-TPA type of tumor-promoting agent, in DMBA-initiated mice. Isoliquiritigenin inhibits neither 12-lipoxygenase nor cyclooxygenase in epidermal subcellular fractions. This compound, however, inhibited TPA-stimulated prostaglandin E2 (PGE2) production in intact epidermal cells. ODC induction caused by TPA was inhibited by a topical application of cyclooxygenase inhibitor, indomethacin. Inhibition of ODC induction by indomethacin was counteracted by a topical application of PGE2, while inhibition caused by isoliquiritigenin was not overcome by PGE2. The results suggest that a mechanism other than the inhibition of PGE2 production is involved in the anti-tumor-promoting action of isoliquiritigenin. Isoliquiritigenin failed to inhibit phospholipase A2 activity of platelet sonicates, but inhibited platelet 12-lipoxygenase and 5-lipoxygenase in polymorphonuclear leukocytes. Therefore, it might be possible that isoliquiritigenin exerts its anti-tumor-promoting action through the lipoxygenase inhibition by acting on cells other than the target epidermal cells. Our present results, in combination with our previous data, demonstrate that some chalcone derivatives and flavonoids which show a potent lipoxygenase inhibitory action act on a common step in the skin tumor promotion caused by two different types of tumor-promoting agents, i.e. TPA and BrMBA, and suggest that these compounds show promise as drugs to prevent tumor promotion.
A single topical application of 10 nmol TPA to mouse skin caused an increase in epidermal cholesterol sulfotransferase activity, a squamous differentiation associated enzyme. A topical application of indomethacin (1.2 mumol), a cyclooxygenase inhibitor, 10 min before TPA application markedly inhibited the above TPA action. Concurrent application of prostaglandin E2 (PGE2) with indomethacin reversed the inhibitory effect of indomethacin. PGF2 alpha, however, failed to reverse the inhibition caused by indomethacin. Both indomethacin and PGE2 alone did not change epidermal cholesterol sulfotransferase activity significantly. These results indicate that PGE2 plays a significant role in the mechanism of TPA-caused increase in cholesterol sulfotransferase activity in mouse epidermis.