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Biomedical subjects

J Hamburger

Publications and source records attributed to J Hamburger.

At least 19 recordsLinked to original sources
PubMed1992

Identification of schistosome-infected snails by detecting schistosomal antigens and DNA sequences.

Cercarial shedding tests do not provide species identification of the schistosomes concerned and cannot detect prepatent schistosomal infections. We have demonstrated that both immunodetection by ELISA of schistosomal antigens in snail hemolymph, and dot hybridization of snail extracts by a DNA probe representing highly repeated sequences, proved suitable for detecting infected snails during prepatency as well as patency. A group-specific monoclonal antibody was found to be suitable for detecting Schistosoma mansoni infection in Biomphalaria sp., but not for positive identification of S. haematobium in Bulinus sp. Comparative evaluation of the diagnostic qualities, and technical aspects and cost of these tests, point to the superiority of the immunodetection approach for large scale detection of snails prepatently infected with S. mansoni. This approach is potentially useful for providing extended information on schistosome-snail epidemiology that may facilitate rapid evaluation of the danger of post-control reinfection, and help make decisions on the time and place of supplementary control measures. In this context the potential usefulness of the immunodetection or DNA probing approach for facilitating catalytic model representation of schistosome-snail epidemiology warrants further evaluation. Specific identification of S. haematobium in Bulinus by either of these approaches may be possible depending on the development of suitable antibodies or DNA probes.

Animals↗
PubMed1991

Detection of Epstein-Barr virus antigens and DNA in major and minor salivary glands using immunocytochemistry and polymerase chain reaction: possible relationship with Sjogren's syndrome.

This study has investigated the presence of Epstein-Barr virus (EBV) in parotid (n = 12), submandibular (n = 15), and minor salivary glands (n = 25) using immunohistochemical methods for detection of EBV-encoded antigens and the polymerase chain reaction (PCR) for detection of viral DNA. Major salivary glands were from patients without connective tissue disease. Labial glands were from patients with primary Sjogren's syndrome (n = 10), rheumatoid arthritis (n = 8), or from normal individuals (n = 7). None of the glands exhibited specific reactivity for lytic (EA-D, EA-R, VCA) or latent (EBNA-2, LMP) viral antigens. Antibodies to EA-D, when used at 20-50 times their optimal concentration, gave lumenal staining of ducts and acini of all the specimens tested (n = 14), irrespective of the presence (n = 8) or absence (n = 6) of EBV-DNA by PCR. Ductal immunoreactivity for the EBV/C3d (CR2, CD21) receptor was found in 40 per cent of specimens. PCR detected EBV-DNA in 64 per cent submandibular, 46 per cent parotid, and 80 per cent of minor glands. There were no significant differences in the detection of EBV-DNA between specimen/patient groups. Only type A EBV was detected by strain typing PCR. These results indicate that EBV (type A), undetected immunocytochemically, is commonly present at low copy numbers within salivary glands irrespective of a clinical diagnosis of Sjogren's syndrome.

Adult↗
PubMed1991

Primed and naive helper T cells in labial glands from patients with Sjogren's syndrome.

This study has investigated the presence and distribution of B cells, T cells and T-cell subsets within labial glands of patients with primary Sjogren's syndrome (n = 9) and secondary Sjogren's syndrome associated with rheumatoid arthritis (n = 8) using a sequential double immunoperoxidase technique and true colour image analysis. The composition of the inflammatory infiltrates was similar in glands from both patient groups. B cells were normally present within large foci with few detected in diffuse infiltrates such that the ratio of T:B cells in foci (2.4:1) was significantly lower than in diffuse infiltrates (7.3:1; P less than 0.001). In all infiltrates helper T cells (CD8-, CD3+) predominated over suppressor/cytotoxic cells (CD8+, CD3+; 2.7:1). Analysis of primed (CD45RA-, CD45RO+) and naive (CD45RA+, CD45RO-) CD8- T cells showed that the ratio of the primed to naive subset was significantly higher in focal (4.2:1) compared to diffuse (1.5:1; P less than 0.001) areas of lymphoid infiltration. These results indicate that the focal lymphocytic infiltrates characteristic of Sjogren's syndrome contain B cells associated with a T-cell population consisting predominantly of primed CD8- helper T cells. This latter population may be responsible for upregulating glandular B-cell activity in Sjogren's syndrome.

Antigens, CD↗
PubMed1991

Expression of rheumatoid factor associated cross-reactive idiotopes by glandular B cells in Sjögren's syndrome.

B cell expression of the germline gene-encoded, kappa IIIb-associated, rheumatoid factor (RF) cross-reactive idiotope (CRI) 17-109 and three VHI associated RF CRIs (G6, G8, H1) was investigated immunocytochemically in labial salivary glands from nine patients with primary and six with secondary Sjögren's syndrome, and in inflamed submandibular salivary glands from 10 patients with no history of connective tissue disease. Expression of CRIs by B cell infiltrates in labial glands from patients with primary and secondary Sjögren's syndrome were similar. Lymphoid infiltrates of labial glands from Sjögren's syndrome patients contained a higher proportion of kappa III+ cells reactive for the kappa IIIb-associated 17-109 idiotope (P less than 0.01) and larger G6 (P less than 0.02) and H1 (P less than 0.01) positive B cell populations than those within inflamed submandibular salivary glands. Furthermore, in labial glands there was a significant correlation between numbers of 17-109 and G6 idiotope reactive cells (r = 0.61; P less than 0.02), reflecting the known association between these H and L chain CRIs in RF IgM paraproteins. These results indicate that B cells bearing both VKIII and VHI-associated CRI are increased in the glandular infiltrates in Sjögren's syndrome and support the idea that this condition is associated with proliferation of immature B cell clones retaining germ-line V genes.

B-Lymphocytes↗
PubMed1990

Unique sequences in the env gene of avian hemangioma retrovirus are responsible for cytotoxicity and endothelial cell perturbation.

An avian retrovirus isolated from spontaneous cavernous hemangiomas of layer hens codes for an env protein that induces a cytopathic effect on a wide variety of cultured avian and mammalian cells and also causes thrombogenicity of endothelial cells. Sequence analysis of the avian hemangioma inducing virus revealed unique elements in both its env gene and its LTR. We propose that these elements are responsible for the biological and pathogenic characteristics of the virus.

Amino Acid Sequence↗
PubMed1990

Persistent Schistosoma mansoni infection in Yemeni immigrants to Israel.

Following sporadic reports on persistent Schistosoma mansoni (S.m) infections in Israelis of Yemeni origin, we systematically surveyed a group of 129 individuals who immigrated to Israel 38 years ago. Physical examination was uneventful in all members of the study group. A single stool examination revealed S.m eggs in 15 of 129 subjects (12%). Specific anti-S.m. IgE was detected in the sera of 48 individuals (37%). Among the 15 egg-positives, 14 had specific IgE (sensitivity 93.3%), but only 80 of the 114 egg-negatives were also negative for specific IgE (specificity 70%). This specific IgE positivity among egg-negatives in the study group (34/114) and its complete absence from two control groups, one of them comprising Yemenites born in Israel, suggest either an S.m infection with low egg output stemming from a low worm burden or low fecundity of senescent worms, or occult infections. Since the S.m infections could not have been contracted in Israel, our findings point to inordinately persistent infections in the members of our study group, and incidentally also to the diagnostic usefulness of specific IgE testing in such cases.

Adult↗
PubMed1989

Cytocidal effect caused by the envelope glycoprotein of a newly isolated avian hemangioma-inducing retrovirus.

We isolated a field strain of avian hemangioma retrovirus (AHV) which induces a cytopathic effect (CPE) on cultured avian and mammalian cells shortly after infection. The kinetics of cell killing were dependent on the multiplicity of infection. The CPE on avian and mammalian cells was independent of virus replication, because UV-irradiated virus led to cell death as well. Biochemical and genetic experiments indicated that AHV env gene products were responsible for the CPE. Partially purified AHV envelope glycoproteins (gp85), but not those of the Rous sarcoma virus Prague C strain, induced a CPE. Rous-associated virus type 1, in which the env region was replaced by the AHV gp85 region, induced a CPE on avian and mammalian cultured cells. Therefore, we suggest that CPE is induced by AHV via interaction between viral gp85 and the cell membrane. This mode of CPE is unique among avian sarcoma-leukemia viruses.

Alpharetrovirus↗
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↗