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Biomedical subjects

J Hamburger

Publications and source records attributed to J Hamburger.

At least 55 records · Page 3Linked to original sources
PubMed1989

Schistosoma mansoni antigens recognized in Biomphalaria glabrata hemolymph by monoclonal antibodies.

In order to identify and characterize Schistosoma mansoni antigens in Biomphalaria glabrata, we examined 19 murine monoclonal antibodies (Mabs) for specific binding to schistosome larvae. None of the murine Mabs induced by infection or by immunization with a crude cercarial antigen (CCA) served this purpose. Two Mabs out of 9 (KCSme22-3 and KCSme22-4) induced by soluble egg antigens reacted with CCA but not with normal snail (NSN) extract. We selected these 2 for studies on detection and characterization of schistosomal antigens in snails. When employed in an ELISA, they differentially detected schistosomal antigens in extracts and cell-free hemolymph (plasma) of infected snails. The selected Mabs bind to cercarial surface as demonstrated by the indirect fluorescent antibody technique (IFAT) with paraformaldehyde-fixed cercariae. The epitopes corresponding to the selected Mabs are periodate sensitive, suggesting the glycoprotein nature of the antigens recognized. Immunoblotting analysis employing the selected Mab revealed 1 antigen in CCA (Mr = 205 kDa) and 3 antigens in snail plasma (Mr = 220 kDa, 180 kDa, and 135 kDa). Schistosomal antigens were first detectable in the snails' plasma 2 weeks after snail infection, and their quantity increased afterwards.

Animals↗
PubMed1989

Identification of snails infected with schistosomes by ELISA employing monoclonal antibodies: Schistosoma mansoni in laboratory snails (Biomphalaria glabrata) and in field snails (Biomphalaria pfeifferi) from Kenya.

An enzyme-linked immunosorbent assay (ELISA) employing monoclonal antibodies was used for detecting Schistosoma mansoni antigens in hemolymph of laboratory snails (Biomphalaria glabrata) in Kenya. Infected laboratory snails shedding cercariae were differentially identified by ELISA from uninfected snails with 100% sensitivity and specificity. Prepatent infections were detected by ELISA from 2 weeks after exposure to miracidia. Thus, ELISA revealed infection 3 weeks before maximal patency was reached (5-6 weeks post-exposure). Infected field snails (B. pfeifferi) shedding cercariae were differentially identified by ELISA, with 100% sensitivity and specificity, from uninfected field snails and from snails naturally infected with other trematodes (echinostomes and strigeids). Prepatent infections with S. mansoni were readily identified by ELISA in field snails. A case is demonstrated where infection rate, as determined by shedding test alone, was 9.8%, whereas the combined figure of prepatent and patent infection rates was 22.9%

Animals↗
PubMed1987

The methylation state of the proviruses in avian sarcoma virus transformed chick and rat cells.

The endogenous viruses in the avian cells are not completely methylated, nor are the Schmidt-Ruppin RSV-D (SRD) proviruses in the infected cells completely unmethylated. Avian sarcoma proviruses integrated in rat transformed cloned cells are heavily methylated. In these cells, a region in the 3' end of the env gene is unmethylated in all the src-containing proviruses but not in the transformed defective (td) proviruses. A possible role for the hypomethylation of the 3' end of the env region is proposed.

Animals↗
PubMed1987

Genetic alterations of integrated avian sarcoma virus DNA sequences in transformed rat cells.

Clones and subclones of Schmidt-Ruppin-RSV-D-(SRD-) infected rat cells that were isolated in soft agar have shown differences in their morphology. Some of the subclones were round or spindle-shaped cells with lower anchorage dependence and high growth rate, while others were more fibroblast-like and failed to overgrow one another. In correlation to their morphology, subclones with high degree of phenotypic transformation contained amplified amounts of full length proviral DNA or proviral fragments. The amplification affected the proviral DNA elements together with host cellular DNA sequences. We have also shown a relationship between the copy number of the proviruses in the cells, the level of expression of viral RNA, and between those two parameters and the various degrees of phenotypic transformation.

Animals↗
PubMed1987

Histamine-producing cell-stimulating activity. A biological activity shared by interleukin 3 and granulocyte-macrophage colony-stimulating factor.

The histamine-producing cell-stimulating factor (HCSF) was first described as a lymphokine which is produced during secondary mixed leukocyte culture and which induces increased histamine synthesis by murine hematopoietic cells. It has been shown that it is different from interleukin 3 (IL 3), despite the fact that pure IL 3 expresses HCSF activity. Our results provide evidence that this factor (constitutively produced by the P388 D1 cell line) is identical with granulocyte-macrophage colony-stimulating factor (GM-CSF) i.e.: (a) physiochemical properties of HCSF and GM-CSF, such as molecular weight, isoelectric charge, hydrophobicity and behavior during affinity chromatography, are indistinguishable and both activities coelute during all biochemical purification procedures; (b) increased bone marrow cell histamine synthesis induced by P388 D1-derived HCSF is inhibited by anti-GM-CSF antiserum; (c) the GM-CSF cDNA probe hybridizes with a poly(A)+RNA from P388 D1 cells while no hybridizing signal was obtained with poly(A)+RNA from WEHI-3 and from P815 cells. On the other hand, the IL 3 cDNA probe hybridizes with a 1.0-kb poly(A)+RNA from WEHI-3 but not with those from P388 D1 and P815. Moreover, well known sources of GM-CSF, such as lung conditioned medium and semi-purified GM-CSF from phytohemagglutinin-induced supernatant of the murine T lymphoma LBRM-33-5 A4 (preparation devoid of IL 3), as well as recombinant murine GM-CSF, induce increased histamine synthesis by hematopoietic cells. All these results demonstrate that, in our culture conditions, the P388 D1 cell line spontaneously produces GM-CSF which is responsible for the P388 D1-induced HCS activity. Consequently, the latter is a property shared by the two distinct hematopoietic growth factors acting on the less committed cells, i.e. IL 3 and GM-CSF, whereas M-CSF or G-CSF are unable to induce histamine production. Interestingly, IL-4 which is known to support established mast cell line proliferation cannot induce HCS activity. In addition, none of the other cytokines tested, such as IL 1, IL 2, interferons or tumor necrosis factor can express HCS activity. This expression seems to be a specific property of IL 3 and GM-CSF.

Animals↗
PubMed1987

The medication of patients with oral lichen planus and the association of nonsteroidal anti-inflammatory drugs with erosive lesions.

While the cause of lichen planus remains unclear, a number of drugs are known to produce oral and cutaneous lesions that clinically and histologically resemble lichen planus. In this study, the medication taken by 225 consecutive patients with oral lichen planus was compared with the drug histories of 202 age- and gender-matched control patients who were treated at the same clinics. Fifty-three percent of the patients with lichen planus and 44% of the control patients were taking one or more drugs (p greater than 0.05). However, 17% of the patients with lichen planus were taking nonsteroidal anti-inflammatory drugs (NSAID) compared with 9% of the control patients (p less than 0.05). There were no significant differences in the use of antihypertensive, oral hypoglycemic, or psychotropic drugs between the two groups. Almost 30% of the patients with the more severe erosive form of lichen planus were taking NSAID while fewer than 9% of the patients without erosions were taking this type of medication indicating a relationship between NSAID and the more severe form of lichen planus (p less than 0.01). Withdrawal from NSAID resulted in resolution or marked clinical improvement in the 12 patients tested. These results indicate that oral lichen planus may be aggravated or precipitated by NSAID and that withdrawal from the drug may benefit some patients.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1986

Immunoglobulin-producing cells in labial salivary glands of patients with rheumatoid arthritis and systemic lupus erythematosus.

The distribution of immunoglobulin-producing cells within labial salivary glands from normal individuals (n = 7) and patients with rheumatoid arthritis (n = 10) and systemic lupus erythematosus (n = 9) was studied using morphometric and indirect immunoperoxidase methods. Cell counts revealed a significant increase in the density of IgG cells within glands from both patient groups compared with glands from normal individuals. No significant differences in the density of IgA- or IgM-producing cells between the 3 groups were observed although large individual variations were apparent. Histomorphometric studies showed an increase in the lymphoid compartment and a decrease in glandular elements within glands from the 2 patient groups. When data for all specimens were pooled a significant positive correlation was obtained between the percent area of stromal lymphoid tissue and density of IgG and IgM cells.

Adult↗
PubMed1986

[Insulin-dependent diabetes, an autoimmune disease].

In type I (insulin-dependent) diabetes evidence for an autoimmune process is now fully established. This is also true for a similar disease observed in the NOD mouse and the BB rat. In addition to circulating antipancreatic antibodies, we demonstrated T-lymphocyte mediated cellular immunity in both these diabetic animals and in the human. Immunological abnormalities precede the development of diabetes and may be responsible for beta cell alteration. Evidence for this interpretation appears stronger for cell-mediated than for humoral immunity. However, full demonstration and understanding of the relationship between anti-beta cell immunity and beta cell alteration still raise many unresolved problems.

Animals↗
PubMed1986

An immunohistochemical study of lymphocyte subsets and expression of glandular HLA-DR in labial salivary glands from patients with symptomatic xerostomia, rheumatoid arthritis and systemic lupus erythematosus.

Lymphocyte subsets, T+6 cells and glandular expression of HLA-DR within labial salivary glands from patients with symptomatic xerostomia (n = 9), RA (n = 24) and SLE (n = 25) were studied using an immunoperoxidase method and monoclonal antibodies. The results indicate that common immune cellular reactions are involved in glandular changes irrespective of patient group and that the appearance of T+6 cells and glandular expression of HLA-DR are unlikely to play a role in initiation of lymphoid infiltration.

Arthritis, Rheumatoid↗
PubMed1985

T6 antigen-positive cells in human labial salivary glands.

The distribution of T6-positive cells in glands from three healthy individuals and 18 patients suffering from various systemic disorders was studied using OKT 6 and NA1/34 monoclonal antibodies in an indirect immunoperoxidase method on frozen sections. Although no positive cells were seen in the glands of healthy controls, 10 of the 18 biopsies from the patient-group contained T6-positive cells which were mostly within glandular epithelium. The presence of T6-positive cells appeared to correlate with lymphoid infiltration of the glands. Only one of the 8 patient biopsies showing normal or minimally-altered structure contained T6-positive cells. Thus these cells are unlikely to play a role in the normal physiological function of labial salivary glands.

Adult↗
PubMed1985

Schistosoma mansoni: radiometric assay of lectin binding specificities of the major egg glycoprotein and its carbohydrate-rich fragment.

The binding by lectins of the Schistosoma mansoni major egg glycoprotein and of a carbohydrate-rich fragment which is serologically cross-reactive with it was studied. The major egg glycoprotein was purified from a crude soluble egg antigen by a succession of affinity chromatography procedures on concanavalin A-sepharose and by ion-exchange chromatography. The carbohydrate-rich fragment was isolated by ultrafiltration of the crude glycoprotein fraction initially obtained from the crude soluble egg antigens. The major egg glycoprotein and the carbohydrate-rich fragment contain 77 and 92.5% carbohydrate, respectively. When radioiodinated and run on SDS-polyacrylamide gel electrophoresis, each of them exhibited a single peak with respective Rf values of 0.33 and 1.0, and their respective molecular weights were 70K and 10-13K. The binding of the radioiodinated major egg glycoprotein and the carbohydrate-rich fragment by peanut agglutinin, Ricinus communis agglutinin-60, wheat germ agglutinin, and lotus agglutinin was studied by double diffusion in agar, and by a radiometric solid-phase assay in which the lectins were used to coat microtiter plates. The latter assay was employed to determine the specificity of the binding by inhibition with the specific sugars. Both the major egg glycoprotein and the carbohydrate-rich fragment bound specifically to concanavalin A columns as indicated by their isolation procedure. They also bound specifically to peanut agglutinin, R. communis agglutinin 60, and lotus agglutinin, while binding by wheat germ agglutinin appeared not to be specific.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylgalactosamine↗
PubMed1985

Lichen planus and liver disease: how strong is the association?

One hundred and thirteen patients with histologically confirmed oral lichen planus, from three stomatology clinics, were examined for evidence of liver disease. No patient had clinical evidence of liver disease. Nine patients (7.9%) had a raised serum concentration of a single enzyme; 6 patients had raised gamma-glutamyl transpeptidase, 2 had raised alkaline phosphatase, and 1 had raised aspartate transaminase levels. No patient had serum auto-antibodies suggestive of primary biliary cirrhosis or chronic active hepatitis. Most patients presenting with oral lichen planus are unlikely to have liver disease.

Adolescent↗
PubMed1985

Glycopeptides in soluble egg antigen of Schistosoma mansoni: isolation, characterization, and elucidation of their immunochemical and immunopathological relation to the major egg glycoprotein (MEG).

The major egg glycoprotein (MEG) of Schistosoma mansoni was purified by ion-exchange chromatography of glycoprotein fraction obtained from soluble egg antigen (SEA) by lectin affinity chromatography. Small carbohydrate-rich fragments (CRF) contained in the glycoprotein fraction of SEA were isolated by ultrafiltration followed by dialysis (10 to 13 kd). Comparison of MEG and CRF yielded the following results: purified MEG (70 kd) contains about 77% carbohydrate, and CRF contains 92.5% carbohydrate. When radioiodinated and run by SDS-PAGE, each yielded a single band with respective Rf values of around 0.33 and 1.0 CRF is capable of inhibiting, in a Farr-type RIA, the binding of 125I-MEG to serum from chronically infected mice. Furthermore, CRF and MEG exhibit a single and continuous line of radioimmunodiffusion. CRF, unlike SEA, SEA glycoproteins, or purified MEG, is incapable of eliciting delayed footpad swelling in egg-sensitized mice or of inducing granulomatous hypersensitivity, when given at amounts equivalent to or higher than MEG by protein or carbohydrate content. Thus, whereas SEA, SEA glycoproteins, or MEG elicited in a representative test net swelling of 0.28 mm, 0.34 mm, and 0.29 mm, respectively, CRF gave net swellings of 0.06 mm, similar to the control value (0.07 mm) in unsensitized mice. Also, mice sensitized to viable eggs, SEA, or purified MEG exhibited, after i.v. challenge with viable eggs, a mean area of granulomas in the lungs of 12,389 micron2, 16,412 micron2, and 12,354 micron2, respectively, as compared with 7940 micron2 in CRF-sensitized mice and 8428 micron2 in unsensitized control mice. Thus, CRF appears to contain fragments of MEG that are serologically active but immunopathologically inactive at the concentrations used.

Animals↗