Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autonomic neuropathy is one of the complications of diabetes, and several lines of evidence, supporting that sympathetic neural dysfunction may play the major role in the orthostatic hypotension (OH) of diabetic patients have been presented. In this paper the responses of plasma norepinephrine (PNE), plasma renin activity (PRA) and plasma aldosterone (PAC) to upright standing were studied in 17 diabetic patients without OH, 25 diabetics with OH and 17 age-matched, non-diabetic normotensives (controls). All were kept on a 200mEq sodium diet. Assay procedure for PNE was high-performance liquid chromatography with trihydroxyindol method and fluorimetric detection using dihydroxybenzylamine as internal standard. Intra- and inter-assay coefficient variations by this method were 3.4 and 5.8% respectively. PRA and PAC were determined by radioimmunoassay. Total blood volume was examined by the plasma tracer method using 131I-HSA and expressed in percent normal. Mean PNE level in the non-diabetic controls was 217 pg/ml in recumbency and increased to a level of 551 at 15 minutes on standing. The PNE responses to standing in the diabetic subjects without OH (defined as group I) were not significantly different from those in the controls. In the diabetics with OH, 14 cases, with the PNE increments less than 1SD below the mean in the controls, were defined as group III, and discriminated from other 11 subjects with OH (group II). PNE levels in group III were significantly lower than in the controls at both recumbency and upright posture. PRA was significantly elevated by standing in the controls and the diabetics except for group II. PRA in all the diabetic groups was significantly lower than in the controls, at both recumbent and upright. The mean values of PAC in the diabetics but group II at supine were significantly lower than those of the control group. PAC levels increased after standing contemporaneously with PRA, though significant rise in group II was shown without PRA response. Total blood volume was significantly (p less than 0.025) decreased in only group II. The results suggest: 1) PNE was normal in the diabetic patients without OH, 2) there are at least two types of OH in diabetes mellitus: one is hypoadrenergic and the other hypovolemic, 3) adrenergic neuropathy may be a cause of low PRA in diabetics with OH but another factor may also be involved in both with and without OH, 4) low PRA is a main factor of low PAC in diabetics (group I and III), but the dissociation between PRA and PAC responses to orthostasis is present in some cases (group II), which reflects disturbances in other regulatory mechanisms of aldosterone secretion.
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PMID:[The responses of norepinephrine, renin and aldosterone to standing in diabetic patients with orthostatic hypotension]. 675 61

To investigate the role of T cells in drug allergy, we stimulated PBMC from penicillin-allergic patients with reactive penicillin G itself or penicillin G coupled with human serum albumin (BPO-HSA). T cell clones specific for penicillin G or BPO-HSA were established and their phenotype and reactivity to both forms of the beta-lactam were analyzed. T cell clones stimulated by penicillin G were CD4 and CD8 positive, whereas BPO-HSA stimulated the growth of CD4+ T cells. The penicillin G-specific clones were HLA class I or class II restricted and processing was not required as fixed APC could still present penicillin G. In contrast, BPO-HSA has to undergo processing to stimulate BPO-HSA-specific T cell clones. In addition to classical APC, activated MHC class II expressing T cells could also restimulate the penicillin G-specific clones, indicating that various cell types might serve as APC. Penicillin G and BPO-HSA-specific T cell clones produced a heterogeneous cytokine pattern as most clones produced high amounts of IL-2, IFN-gamma, TFN-alpha, and rather variable levels of IL-4 and IL-5. Since no Ag processing was required, penicillin G may stimulate T cells by binding directly to MHC molecules on the cell surface or to their embedded peptide. Alternatively, it may bind to soluble proteins like HSA, which are processed and subsequently presented in an immunogenic form. These different modes of presentation, which elicit a variety of immunological reactivities, may explain the great heterogeneity of the clinical pictures seen in penicillin allergy.
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PMID:Heterogeneous T cell responses to beta-lactam-modified self-structures are observed in penicillin-allergic individuals. 765 Mar 95

Dominant second signals for T cell activation can be generated through interactions between CD28 and CTLA-4 on T cells with their co-stimulatory ligands B7-1 and B7-2 on APC. Nevertheless, some B7-negative cell lines appear capable of providing second signals to T cells, illustrating that B7-independent co-stimulatory pathways may exist. One such cell line, the peptide-transporter defective T lymphoma RMA-S, was investigated in the present study, to determine the origin of the co-stimulatory effects it provides. RMA-S can support clonal expansion of purified CD4 or CD8 T cells from unprimed mice activated with concanavalin A (ConA) or immobilized anti-CD3. Nevertheless, RMA-S does not express B7-1 or B7-2, nor does it express other known co-stimulatory molecules, i.e. CD40, gp39, CD70 and HSA. Also, co-stimulation provided by RMA-S could not be blocked by antibodies or fusion proteins specific for these co-stimulatory molecules, excluding their participation. However, RMA-S' co-stimulatory activity is dependent on adhesive interactions. RMA-S is incapable of IL-2 production in the presence of ConA or anti-CD3, but T cells co-stimulated by RMA-S produce IL-2 and IFN-gamma upon anti-CD3- or ConA-induced activation. Furthermore, co-stimulation of antigen-specific T cell proliferation of both class I- and class II-restricted T cell clones can be provided by RMA-S, and RMA-S can preclude induction of anergy by 1-ethyl-3-(3-dimethyl amino propyl)carboiimide-fixed APC in a class II-restricted T cell clone. The results suggest that potent co-stimulatory pathways can be induced by cellular interactions between a T lymphoma, RMA-S and T cells, not involving gp39, CD40, CD70, HSA, B7-1 (CD80) or B7-2 (CD86). Characterization of the molecules involved is in progress.
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PMID:A T cell lymphoma can provide potent co-stimulatory effects to T cells that are not mediated by B7-1, B7-2, CD40, HSA or CD70. 858 81

The distal end of human Chromosome (HSA) 21 from PDXK to the telomere shows perfect conserved linkage with mouse Chromosome (MMU) 10. This region is bounded on the proximal side by a segment of homology to HSA22q11.2, and on the distal side by a region of homology with HSA19p13.1. A high-resolution PAC-based physical map is described that spans 2.8 Mb, including the entire 2.1 Mb from Pdxk to Prmt2 corresponding to HSA21. Thirty-four expressed sequences are mapped, three of which were not mapped previously in any species and nine more that are mapped in mouse for the first time. These genes confirm and extend the conserved linkage between MMU10 and HSA21. The ordered PACs and dense STS map provide a clone resource for biological experiments, for rapid and accurate mapping, and for genomic sequencing. The new genes identified here may be involved in Down syndrome (DS) or in several genetic diseases that map to this conserved region of HSA21.
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PMID:Perfect conserved linkage across the entire mouse chromosome 10 region homologous to human chromosome 21. 1061 44

The proliferative and interleukin (IL)-10 responses to Lacto-n-fucopentaose III (LNFPIII) that contains Lewis(x)(Le(x))-trisaccharide was assessed in PBMC from humans infected with Schistosoma mansoni. All patient groups with low, medium, and high egg counts in their feces responded to polyvalent LNFPIII-HSA (where HSA = human serum albumin) conjugate. PBMC of all subjects showed a significant proliferative response to this sugar conjugate. However, the levels of interleukin (IL)-10 induced by LNFPIII-HSA were higher in groups with low and medium egg counts than those with high egg. Soluble egg antigens (SEA) also induced IL-10 production by PBMC from infected patients. Interestingly, the SEA-induced IL-10 production was remarkably inhibited by pretreatment of PBMC with free ligands of LNFPIII (monovalent form). These LNFPIII-pretreated PBMC displayed appreciable increase in the level of proliferation to SEA stimulation. We propose that the observed bystander immune potentiation rendered by free LNFPIII is due to the reduced IL-10 level which, presumably, up-regulate expression of co-stimulatory molecules on APC. The ensemble of results indicates that the Le(x)-containing LNFPIII is a potent immunoreactive epitope in SEA that negatively influences PBMC response against this parasite antigens via IL-10.
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PMID:Lewis(x)-containing oligosaccharide attenuates schistosome egg antigen-induced immune depression in human schistosomiasis. 1068 12

Seven of nine pericentric inversions that distinguish human (HSA) and chimpanzee karyotypes are chimpanzee-specific. In this study we investigated whether the two extant chimpanzee species, Pan troglodytes (common chimpanzee) and Pan paniscus (bonobo), share exactly the same pericentric inversions. The methods applied were FISH with breakpoint-spanning BAC/PAC clones and PCR analyses of the breakpoint junction sequences. Our findings for the homologues to HSA 4, 5, 9, 12, 16, and 17 confirm for the first time at the sequence level that these pericentric inversions have identical breakpoints in the common chimpanzee and the bonobo. Therefore, these inversions predate the separation of the two chimpanzee species 0.86-2 Mya. Further, the inversions distinguishing human and chimpanzee karyotypes may be regarded as early acquisitions, such that they are likely to have been present at the time of human/chimpanzee divergence. According to the chromosomal speciation theory the inversions themselves could have promoted human speciation.
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PMID:The chimpanzee-specific pericentric inversions that distinguish humans and chimpanzees have identical breakpoints in Pan troglodytes and Pan paniscus. 1632 4