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Biomedical subjects

C C Chan

Publications and source records attributed to C C Chan.

At least 343 records · Page 19Linked to original sources
PubMed1993

Burnisher's asthma--a case due to ammonia from silverware polishing.

A 39-year-old man with no past or family history of asthma developed asthmatic symptoms five months after working as a burnisher in a hotel. He polished brass or silverware using "brasso" or "silvo" respectively. He noticed symptoms only when using "silvo". Specific bronchial provocation testing (BPT) to "brasso" was negative. Specific BPT to "silvo" produced a dual asthmatic reaction. Ammonia was present in both polishes. The ammonia-in-air levels during polishing was 8-15 ppm with "silvo" and less than 1 ppm with "brasso". A specific BPT to 12 ppm of ammonia produced an immediate asthmatic reaction. Our opinion is that he had occupational asthma from the ammonia liberated while polishing silverware with "silvo". Ammonia has been reported to cause asthma. However, there have been no previous reports of occupational asthma among burnishers doing silver polishing.

Adult↗
PubMed1993

The paradoxical effect of tumor necrosis factor alpha (TNF-alpha) in endotoxin-induced uveitis.

PURPOSE: To investigate the role of TNF-alpha in endotoxin-induced uveitis (EIU) in mice. METHODS: To neutralize TNF-alpha activity, mice were pretreated with either repeated injections of this cytokine or a single injection of antibody against it. The mice were then injected intraperitoneally with 500 micrograms endotoxin, to induce lethal septic shock, or into the footpad with 200 micrograms to induce EIU. RESULTS: Although both pretreatments conferred protection against the systemic toxic effects of LPS, TNF-resistant mice and mice treated with anti-TNF-alpha antibody demonstrated an exacerbation of EIU when compared to control animals. CONCLUSIONS: Unlike its apparent participation in the systemic effect of endotoxin, TNF-alpha is not directly involved in the pathogenesis of EIU and may even protect against the inflammatory processes of this disease.

Acute Disease↗
PubMed1993

The role of mast cells in endotoxin-induced uveitis.

PURPOSE: To investigate the role of mast cells in the induction of endotoxin-induced uveitis (EIU). METHODS: We previously showed that the mean mast cell number in the anterior uvea was greatest for Lewis rats, lowest for Brown Norway (BN) rats, and intermediate for LBNF1 rats. In the current experiment, we assessed the time of onset and severity of EIU in these three rat strains. We then studied changes in mast cell numbers in the anterior uvea during the induction period of EIU. RESULTS: Time of onset and severity of EIU were related to the number of mast cells in the anterior uvea. EIU occurred earliest in the Lewis rats, and the maximum mean grade of ocular inflammation on a scale of 0 (no inflammation) to 4 (severe inflammation) +/- standard error of the mean was 3.87 +/- 0.13 for Lewis rats, 1.06 +/- 0.06 for BN rats, and 1.19 +/- 0.12 for LBNF1 rats. The difference between the mean grade of inflammation in the Lewis rats and the other two strains was highly statistically significant (P < .001). In the Lewis rats, mast cell numbers +/- SEM decreased from 68.9 +/- 10.8 at baseline to 49.6 +/- 5.9 4 hr after lipopolysaccharide (LPS) injection and to 27.6 +/- 8.4 8 hr after LPS injection, suggesting that mast cell degranulation occurs before the development of EIU. CONCLUSION: Mast cells in the anterior uvea appear to potentiate endotoxin-induced ocular inflammation.

Animals↗
PubMed1992

Genetic control of susceptibility to experimental autoimmune uveoretinitis in the mouse model. Concomitant regulation by MHC and non-MHC genes.

Experimental autoimmune uveoretinitis (EAU) in animals is a T cell-mediated autoimmune response directed against cells of the neural retina, in particular the photoreceptors. EAU can be induced in susceptible strains of mice by immunization with purified retinal Ag, and serves as a model for human uveitis. Because strong HLA associations have been noted in a number of human uveitic diseases, we investigated the role of MHC vs non-MHC genes in the control of susceptibility to ocular autoimmunity using the mouse EAU model. Selected strains representing most of the known independent H-2 haplotypes, as well as several H-2-recombinant and congenic strains, were immunized with interphotoreceptor retinoid-binding protein. Ocular pathology was induced in strains of the H-2k haplotype and their I-A-matched congenics, as well as in strains of the H-2r, H-2b, and H-2d haplotypes. In a series of experiments utilizing intra-H-2 recombinant strains, MHC control of susceptibility was tentatively mapped to the I-A subregion of the H-2k. Expression of the I-Ek gene product was not required for susceptibility to EAU, and in fact appeared to have an ameliorating effect on disease. Incidence and severity of disease obtained in strains sharing the same H-2 on a different background, or sharing the same background in the context of a different H-2, indicated that non-MHC genes contribute significantly to the regulation of EAU. Disease expression of susceptible H-2 haplotypes was highest in strains with B10 background (permissive) and ranged from intermediate to absent in strains with other (nonpermissive) backgrounds. The data suggest that although the ability to develop ocular pathology is dependent on the I-A subregion of the H-2, the final expression of disease in susceptible haplotypes is largely determined by background, non-MHC genes.

Animals↗
PubMed1992

Suppression of experimental autoimmune uveitis in mice by induction of anterior chamber-associated immune deviation with interphotoreceptor retinoid-binding protein.

Immunization with bovine interphotoreceptor retinoid-binding protein induces autoimmune uveitis in B10.A mice. We have examined whether this soluble retina-specific Ag can induce anterior chamber-associated immune deviation when injected into the anterior chamber (AC) of the eye, and whether this deviant immune response has any effect on uveitis is susceptible mice. The results of these experiments indicate that interphotoreceptor retinoid-binding protein (IRBP) injected intracamerally altered the subsequent immune response of B10.A mice such that a) they were not able to develop IRBP-specific delayed hypersensitivity, nor (b) were they able to express significant autoimmune uveitis following a uveitogenic regimen. Moreover, spleen cells from mice that received IRBP in the AC suppressed uveitis when adoptively transferred into naive recipients. The splenic suppressor cells were able to prevent autoimmune uveitis in recipient mice when administered after the uveitogenic regimen. Most important, IRBP-specific splenic cells from mice treated with IRBP in the AC when injected into mice with established uveitis caused an abrupt cessation of the intraocular inflammation. The ability of intracamerally-injected soluble Ag to induce suppressor T cells that act on the efferent limb of the immune response suggests that the anterior-chamber-associated immune deviation phenomenon may have physiologic relevance in terms of preservation of the integrity of ocular tissue and renders this approach particularly suitable for treating already established experimental autoimmune diseases of this type. These results are discussed in terms of other methods that have been devised experimentally to suppress and prevent autoimmune uveitis and encephalomyelitis.

Animals↗
PubMed1992

Expression of cell adhesion molecules in posterior uveitis.

Cells in the eye express surface molecules that direct leukocyte migration during ocular inflammation. We studied the expression of intercellular adhesion molecule-1, lymphocyte function-associated antigen-1, and endothelial leukocyte adhesion molecule-1 in six enucleated eyes from patients with uveitis and in seven normal control eyes. Lymphocyte function-associated antigen-1 was expressed on infiltrating lymphocytes and intercellular adhesion molecule-1 was expressed on endothelial cells of retinal and choroidal blood vessels and the retinal pigment epithelium in all uveitic eyes, but in none of the normal control eyes. Ocular inflammatory cells stained strongly positive for tumor necrosis factor alpha in all eyes with uveitis, but four of six uveitic eyes showed mild staining for tumor necrosis factor beta and interferon gamma. Cell adhesion molecules are expressed in eyes with posterior uveitis and may be regulated by cytokines such as tumor necrosis factor alpha.

Adult↗
PubMed1992

Control of experimental autoimmune uveoretinitis by low dose T cell vaccination.

Autoimmune T lymphocytes can be used under appropriate conditions to induce resistance to the specific autoimmune disease that they usually produce. This practice, termed T cell vaccination, was found to be effective with the injection of a low (subpathogenic) number of autoaggressive T line lymphocytes. We report here that T cell vaccination produced marked resistance to the expression of experimental autoimmune uveoretinitis (EAU) in Lewis rats. In addition, vaccination led to the appearance of lymphoid cells in the vaccinated rats that demonstrated proliferative responses against idiotypic and ergotypic specificities of the injected T cells. This is the first report demonstrating the effector T lymphocytes specific for ocular antigens may be used as agents to modulate immunopathogenic responses responsible for EAU.

Amino Acid Sequence↗
PubMed1992

Association between mast cells and the development of experimental autoimmune uveitis in different rat strains.

To study the role of anterior uveal mast cells in experimental autoimmune uveitis (EAU), the mast cells in the iris and ciliary body of Lewis rats, Brown Norway (BN) rats, and their F1 hybrids (LBNF1) were quantitated in normal rats and during the induction period of EAU. The mean baseline mast cell number was 68.9 +/- 10.8 per anterior uvea for Lewis rats, 0.3 +/- 0.2 for BN rats, and 4.6 +/- 0.6 for LBNF1 rats. Detectable mast cells in the anterior uvea of S-Ag-immunized Lewis rats decreased to 60% of control at 6 days postimmunization, recovered to 80% at 10 days, and dropped again to 16% at 13 days, with disease onset around 14 days. In Lewis rats that were adoptively transferred with a uveitogenic T-lymphocyte line, a profound drop in anterior uveal mast cell numbers occurred in the eyes with early signs of EAU, 3 days after the transfer. The decrease in detectable mast cells is consistent with mast cell degranulation. The data suggest that anterior mast cells participate in the immunopathogenesis of EAU and may influence the genetic susceptibility to EAU.

Animals↗
PubMed1992

Enhancement of S-antigen and its mRNA in the irides of uveitic patients.

S-antigen (S-Ag) and its mRNA were analysed by immunohistochemistry and in situ hybridization in 32 iridectomy specimens from 29 uveitic patients and 10 non-uveitic patients. S-Ag was detected in one iris and its mRNA was detected in 12 uveitic patients. Neither S-Ag nor its mRNA was found in the controls (P < 0.003). Ten of the 12 patients who had detectable S-Ag mRNA, while only four of the 17 patients who did not, had received corticosteroids for more than 3 years (P = 0.006). We also demonstrated S-Ag and its mRNA in bovine iris by immunoprecipitation and polymerase chain reaction. These results indicate that S-Ag and its mRNA accumulate in the irides of some uveitic patients. This accumulation may be the result of local immunoregulatory factors and an effect of corticosteroid treatment, and may modulate ocular inflammation.

Adrenal Cortex Hormones↗
PubMed1992

Immunocytochemical staining of vitreous cells. Indications, techniques, and results.

Diagnostic vitrectomy is often performed because of suspected infection or malignancy. Giemsa, Gram, and Papanicolaou stains are used routinely to identify the components in the vitreous. Immunocytochemical staining of cellular components of vitreous specimens has the potential to significantly increase the amount of useful information that can be gained from histopathologic study. Vitreous specimens from 14 patients undergoing diagnostic or therapeutic vitrectomy for infection, suspected primary intraocular lymphoma, or uveitis were examined by immunocytochemical staining using monoclonal antibodies specific for leukocyte subclass antigens and immunoglobulin. The three classes of disorders showed characteristic patterns of staining, which were useful in confirming microbiologic and clinical diagnoses. Infections showed more pronounced neutrophils and macrophages, primary intraocular lymphomas demonstrated light chain restriction of the malignant B lymphocytes, and uveitis was characterized by the predominance of T lymphocytes. The routine use of immunocytochemical staining is recommended to characterize cellular infiltrates and increase the diagnostic yield from vitrectomy specimens.

Antibodies, Monoclonal↗
PubMed1992

Pneumocystis carinii and Mycobacterium avium-intracellulare infection of the choroid.

It has been hypothesized that coinfection with mycobacteria occurs in patients with Pneumocystis carinii choroiditis, but cases demonstrating ocular infection by both organisms have not been reported. This study reports the case of a patient with P. carinii choroiditis who was treated with intravenous trimethoprim and sulfamethoxazole, followed by intravenous trimethoprim and dapsone. The choroidal lesions failed to resolve despite 6 weeks of treatment, and the patient died from massive pulmonary infection caused by P. carinii, Mycobacterium avium-intracellulare, and cytomegalovirus infections. Ocular histologic and electron microscopic examinations revealed choroidal infection by both P. carinii and M. avium-intracellulare. Serum levels of sulfamethoxazole were below the recommended therapeutic range for treating P. carinii infection during the first week of therapy, but adequate drug levels were subsequently obtained. Failure of choroidal lesions of P. carinii to resolve in some cases may suggest insufficient antimicrobial levels in the blood or raise the possibility of coexistent M. avium-intracellulare or other opportunistic infection.

AIDS-Related Opportunistic Infections↗
PubMed1992

Structure of the 5S rRNA genes in birch (Betula papyrifera) and alder (Alnus incana).

Hybridization of a 5S rDNA probe to Southern transfers of birch (Betula papyrifera) or alder (Alnus incana) DNA digested with BamH1 reveals similar triple-band "ladder-like" patterns. The sizes of sequenced 5S repeat units from both plants ranges only from 471 to 490 base pairs, suggesting that the complexity detected by Southern analysis is not due to different size classes of 5S repeats as found in other species. Within the intercistronic spacer region, conservation of large blocks of sequence between birch and alder 5S is observed implying a close evolutionary relationship between these two species. In both species, a duplication of part of the coding sequence including a restriction site for BamH1 introduces a second BamH1 site into the repeat unit. Differential methylation of the two BamHI restriction sites can account for the observed triple-band pattern.

Base Sequence↗
PubMed1992

Aberrant crypt foci and microadenoma as markers for colon cancer.

Foci of aberrant crypts similar to those seen in experimental animals exposed to colon carcinogens have been identified and quantified on the mucosal surface of fixed resections of human colon after methylene blue staining. Many of the foci in humans showed dysplasia on histologic examination and were considered to be microadenoma (MA). These lesions may be precursors for adenomatous polyps and colorectal cancer. Rats and mice initiated with azoxymethane, then fed diets containing sucrose or casein heated at 180 degrees C to stimulate normal cooking conditions, had three to five times more large MA after 100 days than controls. Thus, cooked sugar and protein contain promoters of the growth of colonic MA. 5-Hydroxymethylfuraldehyde was identified as a promoter in cooked sugar.

Adenoma↗
PubMed1992

Genetic factors in susceptibility and resistance to experimental autoimmune uveoretinitis.

Experimental autoimmune uveoretinitis (EAU) can be induced in susceptible stains of rats and mice by immunization with purified retinal antigens, and serves as a model for human uveitis. Because strong HLA associations have been noted in a number of human uveitic diseases, we investigated the role of major histocompatibility complex (MHC) vs. non-MHC genes in the control of susceptibility to ocular autoimmunity, using the mouse and the rat EAU models. It was shown that EAU expression in mice requires both a susceptible MHC haplotype and a "permissive" genetic background. MHC control of susceptibility was tentatively mapped to the I-A subregion in H-2k. I-Ek expression appeared to have an ameliorating effect on disease. Susceptible H-2 haplotypes exhibited highest disease scores on the B10 background, and disease was reduced, or even absent, on some other (nonpermissive) backgrounds. Factors which may determine "permissiveness" or "nonpermissiveness" of a particular genetic background, as studied in mice and rats, may include diverse genetic mechanisms spanning regulation of cytokines, hormones, vascular effects and the T cell repertoire. Taken together, the data suggest that, in individuals susceptible to uveitis by virtue of their MHC, the final expression of disease will be determined by the genetic background.

Animals↗
PubMed1992

Use of ACAID to suppress interphotoreceptor retinoid binding protein-induced experimental autoimmune uveitis.

Experimental Autoimmune Uveitis (EAU) was induced by immunization with bovine interphotoreceptor retinoid binding protein (IRBP) in B10.A mice. The experiments were performed to evaluate whether Anterior Chamber Associated Immune Deviation (ACAID) can be induced by IRBP when injected intracamerally. The results indicate that anterior chamber (AC) injection of IRBP impaired the development of IRBP-specific delayed hypersensitivity and prevented the expression of EAU following immunization with IRBP-CFA. Adoptive transfer of spleen cells obtained from mice that received IRBP into AC suppressed EAU, whether administered prior to or after the uveitogenic regimen. Most important, IRBP-specific suppressor cells from AC-IRBP treated mice when injected into IRBP-EAU mice suppressed and eliminated already established intraocular inflammation. IRBP-specific, ACAID-inducing suppressor T cells act on the efferent limb of the immune response, and represent ideal modalities for treating already established EAU.

Animals↗
PubMed1992

Developmental expression of S-antigen in fetal human and rat eye.

Development expression of S-antigen and its mRNA in human and rat fetal retina was studied by immunocytochemical and in situ hybridization techniques. Immunocytochemistry indicated that S-antigen was present after 4 months gestation in the fetal human retina. In the rat, S-antigen was detected in the retina only after birth. In situ hybridization studies indicated that the S-antigen mRNA was present at 13 weeks gestational age in the human and at 15 days in the rat embryo. S-antigen mRNA was expressed not only in the retina but also in ocular tissues of neural crest origin in the fetus.

Adult↗