PubMed Health⌕ Search

Biomedical subjects

L C Andersson

Publications and source records attributed to L C Andersson.

At least 145 records · Page 8Linked to original sources

Cytotoxicity of latex urinary catheters.

After an epidemic of severe urethral strictures in cardiac surgery patients, all brand latex catheters marketed in Finland were investigated for cellular toxicity with eluates made from the catheters. Four of the seven brands, including the one involved in the stricture cases, showed marked cytotoxicity and inhibited almost all cell growth in various human cell cultures when a 30% catheter eluate was used. DNA histograms of cells cultured with toxic catheter eluate showed inhibition of DNA synthesis. Silicone catheters did not influence cell growth, which correlates with the finding that no new stricture cases were seen after the latex catheters were replaced with silicone ones. Attention is paid to the facts that international standards regarding urethral catheter toxicity are lacking and that catheter quality control is insufficient.

Adult↗

Identification of non-T non-B lymphocyte leukaemia patients with favourable prognosis by cell surface glycoprotein analysis.

Leukaemic cells from 15 children with ALL were isolated and their surface glycoproteins labelled with 3H after treatment with neuraminidase and galactose oxidase followed by NaB3H4. The labelled glycoproteins were separated by polyacrylamide slab gel electrophoresis and visualized by fluorography. The cells could be classified into four groups: 1) Surface glycoprotein pattern resembling that of normal T lymphocyte (one patient); 2) Surface glycoprotein pattern showing some T cell characteristics (5 patients); 3) Surface glycoprotein profile with strongly labelled glycoproteins of apparent molecular weight of 120 000 and 130 000, and frequently a glycoprotein with an apparent molecular weight of 210 000 and visible HLA-coded glycoproteins (6 patients); 4) Surface glycoprotein pattern not resembling those of the other groups (3 patients). Follow-up showed that patients in group 3 have remained in their initial remission (5/6) for the complete study period of 5-6 yr, whereas all patients in the other groups have relapsed and/or died. We conclude that the surface glycoprotein analysis enables the identification of patients with non-T non-B ALL with favourable prognosis.

Actuarial Analysis↗

Malignant transformation in human colorectal mucosa as monitored by distribution of laminin, a basement membrane glycoprotein.

The distribution of laminin, a basement membrane glycoprotein, was studied by indirect immunofluorescence technique using rabbit anti-laminin serum in fifty-seven samples of normal, hyperplastic, adenomatous and carcinomatous colorectal tissue. As judged by the expression of laminin normal, hyperplastic and adenomatous colorectal mucosa were characterized by a continuous, linear basement membrane. A thick band-like basement membrane was seen under the surface epithelium and at the mouths of the crypts in normal and hyperplastic mucosa. The adenomatous epithelium was uniformly characterized by a thin, linear basement membrane. In contrast, marked alterations were constantly observed in colorectal carcinomas and their metastases, which showed a discontinuous, linear or patchy basement membrane. Our study suggests that the expression of laminin is related to cellular differentiation, and the thickness of the laminin-positive basement membrane parallels with the epithelial maturation of normal and hyperplastic colorectal mucosa and with the failure of the epithelial differentiation in adenomas. In colorectal carcinomas and their metastases the distribution of laminin is constantly altered and the severity of the alterations correlates with the histological grade of these tumours.

Adenocarcinoma↗

Late expression of M and N antigens on glycophorin A during erythroid differentiation.

The M/N blood groups are carried by the major human red cell sialoglycoprotein, glycophorin A. O-glyosidic carbohydrate is needed for the activity, but the M/N specificity is due to amino acid replacements in the NH2-terminal portion of the molecule. We have used monoclonal antibodies specific for M and N blood groups to study their expression during normal erythropoiesis. Here we report that the M/N blood group activities are very weakly or not at all expressed before the polychromatic normoblast stage. Using polyclonal anti-glycophorin A antiserum, it was shown that glycophorin A molecules are already abundantly present on the earliest morphologically recognizable erythroid precursor, the proerythroblast. These findings can be explained by our previous observation that the O-glycosylation of glycophorin A gradually increases during erythroid maturation.

Antibodies, Monoclonal↗

The oestrogen antagonists, tamoxifen and FC-1157a, display oestrogen like effects on human lymphocyte functions in vitro.

We studied the in vitro effects of two anti-oestrogens (tamoxifen and FC-1157a) on human lymphocyte functions in pokeweed mitogen (PWM) stimulated cultures. Addition of 1-100 nmol/l of tamoxifen or FC-1157a to PWM cultures significantly increased the number of immunoglobulin secreting cells. This concentration of tamoxifen did not affect the proliferative response. Further experiments with fractionated lymphocyte subpopulations showed that the anti-oestrogens displayed their enhancing effect by inhibiting the suppressive function of T8+ cells. The anti-oestrogens had no significant effect on the T-independent activation of B cells with Epstein-Barr virus. We conclude that the anti-oestrogens display an effect on the functions of human lymphocytes similar to that previously reported for oestradiol (Paavonen, Andersson & Adlercreutz, 1981).

Antibody-Producing Cells↗

Changes in cell surface glycoproteins and antigens during differentiation of the human myeloid leukemia cell lines ML-1, ML-2, and HL-60.

Two recently derived human myeloid leukemia cell lines, ML-1 and ML-2, were induced to differentiate by treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) or with retinoic acid for 5 to 12 days. They were then compared with similarly treated promyelocytic HL-60 cells. TPA-treated ML-1 and ML-2 cells became firmly surface adhesive with a fibroblastoid morphology, while TPA-treated HL-60 cells adhered as rounded macrophages. In contrast, retinoic acid induced only slight morphological changes in all three cell lines. The differentiation-related alterations of the surface membrane glycoproteins were followed by polyacrylamide gel electrophoresis after surface labeling by the periodate-NaB3H4 or galactose oxidase-NaB3H4 methods. The expression of surface membrane differentiation antigens was analyzed with a panel of monoclonal antibodies against myeloid, myelomonocytic, monocytic, and granulocytic determinants using FACS IV flow cytometry. The acquisition of surface adhesiveness by TPA-treated ML-1 and ML-2 cells coincided with the appearance of membrane surface proteins of varying molecular weights, ranging between 90,000 and 155,000, which were not labeled in untreated ML-1 and ML-2 cells. These findings and the results obtained by monoclonal antibody staining and FACS analysis indicate that treatment of the myeloid lines ML-1, ML-2, and HL-60 by TPA induced the expression of antigenic and membrane molecular features compatible with a monocytic-macrophage phenotype, while treatment by retinoic acid induced granulocytic differentiation. The ML-1 and ML-2 cells offer interesting models for studies on the membrane molecular events occurring when nonadherent, monocytic cells become surface adherent.

Antigens, Surface↗

A human neuroblastoma cell line with an altered ornithine decarboxylase.

A human neuroblastoma cell line (Paju) was resistant to 10 mM difluoromethylornithine, a concentration at which the growth of all mammalian cells normally stops. Ornithine decarboxylase from Paju was very resistant to inhibition by difluoromethylornithine in vitro (Ki = 10 microM compared to 0.5 microM for mouse kidney ornithine decarboxylase). After purification, apparently homogeneous Paju ornithine decarboxylase was inactivated with [3H]difluoromethylornithine and analyzed by polyacrylamide gel electrophoresis. Under denaturing conditions it was found to have an altered molecular structure, i.e. two nonidentical subunits of Mr = 55,000 and 60,000. Another unusual feature of Paju ornithine decarboxylase was its long half-life in vivo (T 1/2 = 8 h compared with 36 min in human HL-60 promyelocytic leukemia cells). The disappearance of immunoreactive protein was only slightly slower than the loss of catalytic activity. The long half-life of Paju ornithine decarboxylase was not shared by adenosylmethionine decarboxylase. Despite the altered structure of Paju ornithine decarboxylase, it was recognized by a specific antisera raised in rabbit against mouse kidney ornithine decarboxylase. The Paju karyotype did not contain double minute chromosomes or any large homogeneously staining region such as that seen in a mouse lymphoma cell mutant that is resistant to difluoromethylornithine and overproduces ornithine decarboxylase (McConlogue, L., and Coffino, P. (1983) J. Biol. Chem. 258, 12083-12086).

Cell Line↗

Direct mitogenic effect of ionophore A23187 on isolated human T helper lymphocytes.

The Ca2+ ionophore A23187 induces only a weak mitogenic response in cultures of unfractionated mononuclear leukocytes from human blood. When a comitogen, 12-O-tetradecanoyl-phorbol-13-acetate, which by itself is nonmitogenic, is added, a greatly increased cell proliferation is obtained. Highly purified T lymphocytes respond by proliferation to A23187 alone. Studies on functional subsets of T cells, fractionated by using the monoclonal antibodies OKT4/OKT8, revealed that A23187 is a strong mitogen for pure T helper cells (T4+). This suggests that increased cytosolic Ca2+ directly triggers a proliferative response in T helper cells with no apparent need for accessory cells.

Calcimycin↗

Acquired pure red-cell aplasia: a consequence of increased natural killer cell activity?

A 19-year-old man with severe pure red-cell aplasia is described. An unusually high proportion of this patient's lymphocytes were large granular lymphocytes (LGL), both in the blood (40%) and in the bone marrow (50%). His blood leukocytes displayed a strongly elevated natural killer (NK) cell activity in vitro against the erythroblastic leukemia line K562. The patient's non-T blood lymphocytes inhibited in vitro erythroid colony formation (BFU-E and CFU-E) but not the granulocyte-monocyte colony growth (CFU-GM) from autologous and allogeneic bone marrow. Neither T-cell-mediated cytotoxicity nor circulating antibodies against erythroid precursors could be demonstrated. The patient's haemoglobin values returned to normal levels after three weeks of glucocorticoid treatment and have since then remained stable with continued prednisone administration. Attempts to reduce the prednisone dose to less than 10 mg/day have led to relapses. It is tempting to suggest that the patient's disease might be caused by hyperactivity of cytotoxic non-T (NK) cells specific for K562 cells and early erythroid precursors.

Anemia, Aplastic↗

Skeletal changes in childhood acute lymphoblastic leukemia: correlation with the presence of the cALL antigen.

We studied the occurrence of the radiolucent metaphyseal bands in pretreatment skeletal X-rays and the phenotype of leukemic cell in 66 children with non-T, non-B ALL. A striking correlation was found between the expression of the CALLA on the leukemic cell and the occurrence of the early metaphyseal bands. We speculate that the bands might reflect an ongoing anti-leukemic reaction which may have been in progress before the disease became clinically manifest and which is associated with relatively favorable prognosis after even a modest chemotherapy.

Adolescent↗

Antibodies against human neuroblastoma cells in the sera of patients with myasthenia gravis.

The autoimmune nature of acquired myasthenia gravis is well documented. Although anti-acetylcholine receptor antibodies are pathognomonic for this disease, their significance in the immunopathogenesis of myasthenia gravis may differ among patients. The presence of antibodies against human neuroblastoma cells in myasthenic sera was studied using the 125I-labelled protein-A radioimmunoassay and indirect immunofluorescence. For comparison sera of patients with other neurological diseases were examined. Significant levels of antibodies against neuroblastoma cells were found in the sera of over 60% of myasthenia gravis patients and in some patients of the other disease groups, but mainly in lower titers. Our findings suggests a more generalized neuroimmunological abnormality in some myasthenia gravis patients.

Adolescent↗

Differentiation of human erythroid cells is associated with increased O-glycosylation of the major sialoglycoprotein, glycophorin A.

Glycophorin A, the major human erythrocyte sialoglycoprotein, is found exclusively on cells of the erythroid lineage. The amino acid sequence is known, and glycophorin A isolated from mature erythrocytes contains a single N-glycosidic and 15 O-glycosidic oligosaccharides. Monoclonal antibodies against erythrocyte glycophorin A reacted weakly with erythroid precursors while a monospecific rabbit antiserum reacted strongly with immature and mature red cells. Glycophorin A was isolated from cells representing various stages of erythropoiesis in normal bone marrow, from blood cells of neonates with erythroblastosis fetalis, and from the erythroleukemic cell lines K562 and HEL before and after induced differentiation. Analysis of the oligosaccharides showed less O-glycosylation of glycophorin A in erythroid precursors. The degree of glycosylation increased concomitantly with differentiation.

Bone Marrow Cells↗

Expression of differentiation antigens in benign sweat gland tumours.

Fifty benign sweat gland tumours were studied for the expression of carcinoembryonic antigen (CEA) and apocrine epithelial antigen (AEA), using immunohistochemical methods. CEA was found in thirty-two and AEA in thirty-three neoplasms. Both antigens were located in the epithelium of the luminal structures and in the intraluminar material and CEA was occasionally found also in proliferating cells. Co-expression of CEA and AEA occurred frequently in cases of syringoma, syringocystadenoma papilliferum, hidradenoma papilliferum, eccrine spiradenoma and clear cell hidradenoma. AEA was seen also in tumours showing eccrine differentiation, even though it is not present in normal eccrine sweat ducts.

Antigens, Neoplasm↗

Sera from multiparous women contain antibodies mediating cytotoxicity against breast carcinoma cells.

We have searched for immunological mechanisms contributing to the epidemiologically established phenomenon of lower incidence of breast carcinoma among multiparous women and women with pregnancy at early age. Sera collected from 55 clinically healthy multiparous women were tested for the ability to mediate cytotoxicity in an antibody-dependent cell-mediated (ADCC) assay with normal blood leucocytes against three different mammary carcinoma cell lines (MDA-MB 157, MDA-MB 231, and MDA-MB 436). Sera from 12 women (22%) mediated significant cytolysis against all three cell lines. Three additional sera were positive against MDA-MB 231 and 10 more against MDA-MB 436 (total 42%). Cross-adsorptions revealed that the ADCC-active sera contained antibodies that recognized the same antigen(s) on the different mammary carcinoma-derived cell lines. The sera from multiparous women contained no detectable ADCC-active antibodies against a colon carcinoma cell line (SW 1116) or a neuroblastoma cell line (SH-SY5Y). ADCC-active antibodies were found neither in sera from 35 nulliparous women nor in sera from 20 men. The ADCC-active antibodies against mammary carcinoma cells could not be removed by adsorption with lymphoblastoid cells established from the respective husbands of the multiparous women. This observation and the fact that the mammary carcinoma cell lines were established from different patients argue against an impact of HLA-related antigens. The ADCC-active antibodies reported here might result from autoimmunization against some proliferation/differentiation antigen(s) of breast epithelium which is (are) expressed during pregnancy and lactation.

Antibody-Dependent Cell Cytotoxicity↗

Antiserum against formalin-fixed human milk fat globule glycoprotein for immunohistochemistry of normal and malignant apocrine epithelium.

A rabbit antiserum was raised against formalin-fixed glycoprotein isolated by lectin affinity chromatography from human milk fat globules. After adsorption with erythrocytes and normal blood leukocytes the antiserum detected in immunoblotting of fresh mammary carcinoma tissue a major component of 75 000 dalton apparent molecular weight. The antiserum specifically decorated normal and malignant apocrine epithelium in sections of formalin-fixed tissues. The usefulness of such antisera for routine immunohistochemical diagnosis of metastatic carcinomas is demonstrated.

Antigens↗

Basement membrane and apocrine epithelial antigens in differential diagnosis between tubular carcinoma and sclerosing adenosis of the breast.

The distributions of defined basement membrane proteins in nine pure tubular carcinomas, 10 cases of sclerosing adenosis, and 15 ductal adenocarcinomas were compared. Sections of formalin fixed, paraffin embedded specimens were pretreated with pepsin and then immunostained for laminin, type IV collagen, and basement membrane proteoglycan, components specific for basement membranes. In sclerosing adenosis the tubules were surrounded by a continuous intact basement membrane composed of laminin, type IV collagen, and basement membrane proteoglycan, while the epithelium in the tubular carcinomas was negative for these proteins. The tumours were also analysed for the distribution of the apocrine epithelial antigen (AEA). In contrast to the benign lesions the tubular carcinomas expressed the AEA in a distinct non-polar fashion throughout the cell surface. In normal ducts and in adenosis the AEA was confined exclusively to the luminal surface. These studies suggest that there is a disturbance of cell polarity in tubular carcinomas. It is concluded that a combined analysis of basement membrane proteins and luminal surface antigens is a reliable and convenient way to differentiate between tubular carcinoma and sclerosing adenosis of the breast.

Adenocarcinoma↗