Circulating immune complexes in recurrent oral ulcers.
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Biomedical subjects
Publications and source records attributed to A Sun.
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Serum IgG, IgM, IgA, C3, C4 concentrations and circulating immune complexes (CIC) were measured in a series of 46 patients with oral lichen planus (LP). This investigation revealed a significant increase in the level of serum IgG in patients with oral LP as compared with 36 healthy subjects. In erosive LP, serum IgM was also elevated as compared with healthy subjects and patients with the non-erosive type. The results of this study did not support the suggestion that a humoral immunodeficiency underlies oral LP. Elevated serum level of IgM may be considered to represent secondary oral infection during mucosal erosion. The study also demonstrated a significant reduction in serum C4 in both variants of oral LP, but the C3 level was normal. A 3% polyethylene glycol precipitation (PEG-ppt) method was used, no significant amount of CIC could be detected in the patients. It is tempting to speculate that oral LP reflects an immunologic disorder in which serum IgG and C4 is disturbed. However, further investigation is needed to clarify the pathogenesis of oral LP.
This paper considers the feasibility of automatic screening procedures for detecting malaria parasites in blood smears prepared in the field. A simple programme for pattern recognition by computer has been developed for thin blood films that identifies parasites as densely stained particles within an erythrocyte. The parasites are detected correctly, but platelets falling accidentally within the outline of an erythrocyte and perhaps reticulocytes may be wrongly classified as parasites. The results indicate that automated detection of parasites is technically feasible but that the technique needs to be refined to reduce the incidence of false positives. A substantial increase in processing speed is required if the automatic procedure is to be economically feasible in screening programmes. The complexity of the equipment and the need for well prepared blood smears point to a possible use of the technique in laboratory checks but not under usual field conditions.
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Recent progress in cytogenetic and biochemical mutation assay technologies has enabled us to detect single gene alterations and gross chromosomal rearrangements, and it became clear that all cancer cells are genetically unstable. In order to detect the genome-wide instability of cancer cells, a new simple method, the DNA-instability test, was developed. The methods to detect genomic instability so far reported have only demonstrated the presence of qualitative and quantitative alterations in certain specific genomic loci. In contrast to these commonly used methods to reveal the genomic instability at certain specific DNA regions, the newly introduced DNA-instability test revealed the presence of physical DNA-instability in the entire DNA molecule of a cancer cell nucleus as revealed by increased liability to denature upon HCl hydrolysis or formamide exposure. When this test was applied to borderline malignancies, cancer clones were detected in all cases at an early-stage of cancer progression. We proposed a new concept of "procancer" clones to define those cancer clones with "functional atypia" showing positivities for various cancer markers, as well as DNA-instability testing, but showing no remarkable ordinary "morphological atypia" which is commonly used as the basis of histopathological diagnosis of malignancy.
Ischemic stroke is a major health care problem worldwide, and the mechanisms that lead to ischemic brain injury are not completely defined. In the past few years, the identification of many molecules that participate in neuronal death and particularly in apoptosis, has shed light on the development of neuroprotective therapy. Glycine site antagonism of N-methyl-D-aspartate (NMDA) receptors may offer an alternative means to a blockade of glutamate neurotoxicity, which lacks most side effects associated with competitive and noncompetitive NMDA receptor antagonists. Inflammatory processes executed by some proinflammatory molecules contribute to secondary brain injury. Neutral protease calpain is capable of degrading critical cytoskeletal and regulatory proteins, mainly causing postischemic neuronal necrosis. Caspases, a family of cysteine proteases, are at the heart of the apoptotic pathway. Severe DNA damage induced by oxidative stress or apoptotic stimuli activates poly(ADP-ribose) polymerase, causing a rapid depletion of nuclear NAD pools, cellular energy, and thiols. Inhibition of these inducible molecules is expected to achieve effective neuroprotection without serious side effects because the molecules seem relatively unimportant in normal neurotransmission. In the future, the efficacy of these novel strategies should be confirmed in larger study populations, individually and in combinations, before considering clinical application.
The method to reveal DNA-instability as demonstrated by immunohistochemical staining with anti-cytidine antibody after acid hydrolysis (DNA-instability test) was used as a marker of malignancy. The test was applied to paraffin-embedded sections taken from 15 urinary bladders, renal pelvic cavities, and ureters bearing multiple carcinoma in situ (CIS) and totally 31 papillary urothelial cancers. The serial sections of the same tissues were also subjected to immunohistochemical staining for PCNA, p53, DFF45, and VEGF. The DNA-instability test was positive in 100% cancer lesions irrespective of the grades, and apparently normal urothelium, and hyperplastic and dysplastic urothelial lesions also showed the areas with clones positively stained with DNA-instability testing, and the percent numbers of positive areas in them were 28.3%, 37.7%, and 61.5%, respectively. These clones, which were present in apparently normal urothelium and in hyperplastic and dysplastic urothelial lesions, showed higher percent values of PCNA-positive-cells, in comparison to the values estimated in the areas with negatively stained DNA-instability testing, and the former values were statistically not different from those in carcinoma lesions. Furthermore, the percent numbers of areas positive for p53, DFF45, and VEGF, with positive DNA-instability testing were also much higher than those with negative DNA-instability testing in apparently normal urothelium, and hyperplastic and dysplastic urothelial lesions, and the former values were again comparable to those in cancer lesions with no statistical differences. These clones were regarded as already being malignant and should be the direct precursors of progressed cancer lesions. They will make progression through two different pathways, one to papillary non-invasive G1 cancers by neovascularization induced by paracrine secretion of VEGF, and another to flat CIS G2 without secretion of VEGF; thus the clones should be regarded as non-papillary, non-invasive Gl TCC, or CIS G1. It should be always taken into account that the probability for apparently normal urothelium, and hyperplastic and dysplastic urothelial lesions to contain cancer clones, will be high already, especially in tumor-bearing bladders.