Biomedical subjects

M Mangkornkanok-Mark

Publications and source records attributed to M Mangkornkanok-Mark.

6 recordsLinked to original sources

PubMed1985

Immunologically oriented concept of the genesis of acquired immunodeficiency syndrome.

An immunologically oriented concept of the genesis of acquired immunodeficiency syndrome is presented in which the central event is the lack of cytotoxic T8 cells. An interlocking system wherein the T4 (helper) cells do not synthesize interleukin-2 to generate the cytotoxic cells due to the lack of functional thymosin as well as the lack of interleukin-1 from the macrophages is postulated. The transmissible agent which sets the cascade of immunologic imbalance into play replicates only in the thymic epithelium and subverts thymosin synthesis. The T8 cells in the syndrome are exclusively H2 positive and functionally suppressor. The macrophage which phagocytizes the effete thymic epithelium hematogenously spreads the transmissible agent to others. Kaposi's sarcoma is considered to be an integral component of the immunologic disarray in that angiogenesis is proposed to require two essential events - endothelial cell proliferation and movement of those cells. Under normal circumstances although the activated macrophage elaborates a monokine that has endothelial cell proliferative inducing capacity the cells are held in situ by a lymphokine that prevents movement. The lymphokine is considered to be IL-2. Eight predictions of the model which are experimentally testable are presented.

Acquired Immunodeficiency Syndrome↗

PubMed1984

Immunoperoxidase evaluation of lymph nodes from acquired immune deficiency patients.

Immunoperoxidase evaluation of cryostat sections from acquired immune deficiency syndrome (AIDS) or prodromal nodes indicated that the majority (75%) had T8 dominance as contrasted to reactive hyperplasia nodes of unknown origin which had 80% T4 dominance. The cells in the AIDS nodes in the interfollicular and medullary sinuses areas marked intensely for Ia as opposed to sparse scattering in the comparative group. Finally, the follicles in the study group as opposed to the comparative group demonstrated hypervariability both in size and shape as outlined by a thin mantle zone of BA-1 positive cells. On the basis of the above three immunological criteria it is considered as highly likely that an AIDS node can be distinguished as such as opposed to the conventional characterization of 'reactive hyperplasia'.

Acquired Immunodeficiency Syndrome↗

PubMed1982

Progressive cutaneous protothecosis.

The diagnosis of severe progressive cutaneous protothecosis in a 34-year-old woman was made by skin biopsy and culture. Analysis of host defense mechanisms revealed a persistent defect in the ability of the patient's PMN to kill the infecting organism. Specific IgG and IgE antibody was demonstrated. Serum levels of complement and immunoglobulins were normal or elevated. The patient was not anergic and peripheral blood lymphocytes responded to nonspecific mitogens. Treatment with amphotericin B and tetracycline resulted in resolution of skin lesions and negative cultures.

Adult↗

PubMed1981

Induction, immunochemical identity and immunofluorescence localization of an 80 000-molecular-weight peroxisome-proliferation-associated polypeptide (polypeptide PPA-80) and peroxisomal enoyl-CoA hydratase of mouse liver and renal cortex.

The hypolipidaemic drugs methyl clofenapate, BR-931, Wy-14643 and procetofen induced a marked proliferation of peroxisomes in the parenchymal cells of liver and the proximal-convoluted-tubular epithelium of mouse kidney. The proliferation of peroxisomes was associated with 6-12-fold increase in the peroxisomal palmitoyl-CoA oxidizing capacity of the mouse liver. Enhanced activity of the peroxisomal palmitoyl-CoA oxidation system was also found in the renal-cortical homogenates of hypolipidaemic-drug-treated mice. The activity of enoyl-CoA hydratase in the mouse liver increased 30-50-fold and in the kidney cortex 3-5-fold with hypolipidaemic-drug-induced peroxisome proliferation in these tissues, and over 95% of this induced activity was found to be heat-labile peroxisomal enzyme in both organs. Sodium dodecyl sulphate/polyacrylamide-gel-electrophoretic analysis of large-particle and microsomal fractions obtained from the liver and kidney cortex of mice treated with hypolipidaemic peroxisome proliferators demonstrated a substantial increase in the quantity of an 80000-mol.wt. peroxisome-proliferation-associated polypeptide (polypeptide PPA-80). The heat-labile peroxisomal enoyl-CoA hydratase was purified from the livers of mice treated with the hypolipidaemic drug methyl clofenapate; the antibodies raised against this electrophoretically homogeneous protein yielded a single immunoprecipitin band with purified mouse liver enoyl-CoA hydratase and with liver and kidney cortical extracts of normal and hypolipidaemic-drug-treated mice. These anti-(mouse liver enoyl-CoA hydratase) antibodies also cross-reacted with purified rat liver enoyl-CoA hydratase and with the polypeptide PPA-80 obtained from rat and mouse liver. Immunofluorescence studies with anti-(polypeptide PPA-80) and anti-(peroxisomal enoyl-CoA hydratase) provided visual evidence for the localization and induction of polypeptide PPA-80 and peroxisomal enoyl-CoA hydratase in the liver and kidney respectively of normal and hypolipidaemic-drug-treated mice. In the kidney, the distribution of these two proteins is identical and limited exclusively to the cytoplasm of proximal-convoluted-tubular epithelium. The immunofluorescence studies clearly complement the biochemical and ultrastructural observations of peroxisome induction in the liver and kidney cortex of mice fed on hypolipidaemic drugs. In addition, preliminary ultrastructural studies with the protein-A-gold-complex technique demonstrate that the heat-labile hepatic enoyl-CoA hydratase is localized in the peroxisome matrix.

Animals↗

PubMed1981

Immunologic studies of bovine aortic and cartilage proteoglycans.

Rabbit antisera prepared against bovine cartilage and aortic proteoglycan monomer (PGM) were employed to identify and localize the distribution and cross-species reactivities of these PGMs. A specific reaction to both cartilage and aortic PGM was obtained as revealed by rocket immunoelectrophoresis of the immunogens against the respective antisera, with no reaction against bovine serum albumin or human fibronectin. These antisera appear to demonstrate tissue specificity. Indirect immunofluorescence studies with antiserum to aortic PGM on bovine aorta tissue revealed intense localization of fluorescence in the intima and superficial media with staining alone collagen fibers, around smooth muscle cells, and on the surface of elastin. When antiserum to cartilage PGM was applied to bovine aorta, staining was much weaker and localized more in the interfibrillar matrix. On the other hand, when antiserum to aortic PGM was used to stain bovine nasal septum cartilage, fluorescent staining was restricted to the pericellular matrix, in contrast to the diffuse, intense staining of both pericellular and extraterritorial staining by antiserum to cartilage PGM. Absorption with eigher bovine aorta or cartilage PGM abolished antibody activity against the absorbing molecules only. The immunologic distinction between the pericellular and extraterritorial cartilage matrix was demonstrated further when both antisera were studied with guanidine chloride (GuHCl)-extracted bovine nasal septum cartilage, when they both demonstrated the same pericellular matrix staining. Despite the tissue specificity, these antisera are not completely species specific, since staining in a similar pattern was observed in both human and rat tissues.

Animals↗

PubMed1980

Detection of alpha-lactalbumin in breast lesions and relationship to estrogen receptors and serum prolactin.

Alpha-lactalbumin, the B protein of lactose synthetase secreted by the mammary epithelial cells, was isolated and purified from fresh human milk and injected into rabbits for antibody production. Indirect immunofluorescence (IIF) was done on various types of breast lesions to assess the relationship, if any, between histologic type and production of alpha-lactalbumin. Fifty percent of fibroadenomas and fibrocystic disease and 63% of infiltrating ductal carcinoma showed positive reaction. No false positives were found on IIF of alpha-lactalbumin of several tumors of nonmammary tissue. These findings suggest that IIF for alpha-lactalbumin may be helpful in ascertaining the site of origin of metastatic breast tumors. However, serum alpha-lactalbumin was detected by radioimmunoassay in only 10% of women with infiltrating ductal carcinoma, indicating that this may not be a useful marker for the presence of breast cancer at least by the method employed. This discrepancy between serum and tissue alpha-lactalbumin may be due to the short half-life of serum alpha-lactalbumin or to the lack of secretion of the protein into the blood. There was no apparent relationship between the presence of estrogen receptors or serum prolactin and alpha-lactalbumin in the 27 mammary carcinomas investigated.

Adenofibroma↗