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Biomedical subjects

T Schulz

Publications and source records attributed to T Schulz.

At least 145 records · Page 8Linked to original sources
PubMed1988

Developmental ocular disease of raptors.

Sixteen raptors, including one eagle, two falcons, five hawks and eight owls, were found to have developmental ocular lesions. The most common lesion was microphthalmia. Other findings included cataract, microphakia, retinal dysplasia, malformation of the ciliary body, choroid and pecten, and lentoid formation. Specific causes for these lesions could not be determined. It is hypothesized that developmental ocular disease probably is more common than available reports indicate.

Animals↗
PubMed1987

Ion-exchange fast protein liquid chromatography; optimization of the purification of cytochrome P-450 from marmoset monkeys.

Fast protein liquid chromatography (FPLC) on Mono Q and Mono S ion-exchange columns was employed to purify marmoset monkey hepatic cytochrome P-450. Cholate-solubilized liver microsomes from untreated animals as well as from animals induced with phenobarbital, beta-naphthoflavone, 3-methylcholanthrene, and ethanol were used as starting materials. Since established purification schemes for extensively studied species, such as the rat, were found to be not directly applicable, a purification method was developed and optimized by studying the effects of varying detergent types, detergent concentrations, elution buffers, pH values, elution salts, and flow-rates on the resolution and recovery obtained in analytical chromatograms.

Animals↗
PubMed1987

[Detection of antibodies to HTLV-III: a comparison of various ELISA methods as screening tests and the Western Blot with immunofluorescence as confirmatory procedures].

386 sera were examined with three commercially available ELISAs for antibodies to HTLV-III. Western Blot and an indirect immunofluorescence assay were performed on sera showing a positive reaction in one or more ELISAs as confirmatory assay. 299 sera reacted negatively in all ELISAs, 48 were positive in all ELISAs and the confirmatory assays, whilst 33 ELISA positive sera reacted negatively in the confirmatory assays. In the case of 5 sera both Western Blot as well as the immunofluorescence assay had to be undertaken to obtain conclusive results.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Individually disparate anti-inflammatory in-vivo susceptibility to corticosteroids in renal transplant recipients.

We used the strength of suppression of the interleukin-1-induced peak CRP response (CRPmax) post-transplant as a measure for the individual steroid susceptibility in vivo. This suppressive effect proved to be fully reversible after abrogation of steroid therapy following graft removal. The standardized suppressive therapy immediately post-transplant led to extremely different results in individual patients ranging from no suppression (26.1% of the patients) to a strong or practically absolute suppression of CRP synthesis in 20.7% of the patients studied. This behaviour is also reflected in anti-rejection bolus therapy whereby the percentage of prednisolone resistant patients strongly correlated with increasing (unsuppressed) CRPmax values. From our data we conclude that the disparate anti-inflammatory susceptibility for corticosteroids seems to be an individual feature of patients under high-dose steroid treatment.

Azathioprine↗
PubMed1987

Immune status of drug abusers.

This study followed 184 drug abusers. Examined in all of them were urinary neopterin levels, HBV, SGOT, and Luestest. Seventy-three percent of IV drug addicts showed elevated neopterin levels reflecting activated cellular immunity. Statistically, no correlation of neopterin levels with, eg, excessive alcohol consumption, duration of drug abuse, or studied laboratory parameters was found. Individuals using cocaine revealed higher neopterin levels than those not doing so. Twenty-one of twenty-two patients with no parenteral drug use had normal neopterin excretion. In 34 drug detoxification patients, we examined in addition: T-lymphocyte subsets (T4/T8 ratio) and serum neopterin levels. Thirty-eight of ninety-four parenteral drug addicts presented with anti-LAV/HTLV-III antibodies (ELISA + Western blot + IFT). Our data demonstrate an activated cellular immune status in parenteral drug addicts that cannot be attributed to LAV/HTLV-III infection in all cases. The development of AIDS seems to depend not only on the exposure to LAV/HTLV-III but also on activated cellular immunity, which is easily assessed by neopterin measurement.

Antibodies, Viral↗
PubMed1987

Activated T cells in addition to LAV/HTLV-III infection: a necessary precondition for development of AIDS.

Urinary neopterin levels are raised with a high incidence in all risk groups for AIDS. Neopterin elevations reflect activated cellular immunity in risk group members, in some cases independently of LAV/HTLV-III infection. Moreover, we are able to show that in patients receiving multiple blood transfusions at least a transient challenge of cell-mediated immunity occurs, which is indicated in part by increasing neopterin levels. We conclude that neopterin levels are a reliable index for assessment of susceptibility for AIDS when infection with LAV/HTLV-III occurs. Activated status of cell-mediated immunity might predispose infected persons to an overwhelming infection and secondary spreading of LAV/HTLV-III, thus leading to the development of full-blown AIDS or ARC. As a consequence of these observations, T-cell-stimulatory actions and agents should intentionally be avoided. Treatment of AIDS patients with immunosuppressants should be examined. The success of therapeutic regimens should be monitored by measurement of neopterin levels.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Cell cycle control of activated, synchronized murine B lymphocytes--roles of macrophages and complement C3.

Three restriction points control the cell cycle of activated murine B lymphocytes in a synergistic way. The first is controlled by the occupancy of surface immunoglobulin either by antigen- or by immunoglobulin-specific antibodies. The second is controlled by the complement C3d receptor CR2 which can be occupied by cross-linked C3b or C3d to stimulate the entry into S phase, or by soluble C3d or a C3 alpha-chain peptide, binding to the CR2 receptor, which inhibit the entry into S phase. Macrophages produce so-called alpha factors which also control the B-cell cycle at the same point. Thus, it is suspected that macrophages produce components of the early pathway of complement activation which finally lead to cross-linking of CR2 receptors on B cells. The third restriction point is controlled by unknown receptors that recognize so-called beta factors produced by helper T lymphocytes.

Animals↗
PubMed1986

Receptors for the third component of complement: their association with maturation stage in non-Hodgkin lymphomas (NHL) and their possible implication with the development of follicular structures.

In the majority of 188 non-Hodgkin lymphomas (NHL) investigated in this study, we found a simultaneous expression of the receptors for c3b and c3d (CR1 & CR2; cccorr = 0.69, P less than 0.0005). An analysis of the different histological entities of the Kiel classification revealed that this coexpression was most pronounced for germinal centre-derived (cccorr = 0.63, P = 0.0004) and immunocytic NHL (cccorr = 0.86, P = 0.0024), whereas in chronic lymphocytic leukaemias there tended to be a more heterogeneous pattern of complement receptor (CR) expression (cccorr = 0.29, P greater than 0.10). In contrast to these NHL of mid B cell stage, most of the NHL of early (i.e. acute lymphocytic leukaemia, lymphoblastic NHL) and late B cell stage (i.e. hairy cell leukaemia, immunoblastic NHL, multiple myeloma) did not express either of these receptors. CR positive NHL often showed a follicular arrangement of the neoplastic cells and had higher numbers of T helper/inducer (T4) lymphocytes (PCR1 less than 0.00005, PCR2 less than 0.05). Some cases of mid B cell NHL and all cases of hairy cell leukaemia reacted with antibodies against CR3 (i.e. the ic3b receptor).

B-Lymphocytes↗
PubMed1985

The action of human C3 in soluble or cross-linked form with resting and activated murine B lymphocytes.

The third component of complement C3 has been implied in the stimulation of B lymphocytes to proliferation and maturation for Ig secretion. We have reinvestigated the extent of this activation with either activated or resting murine splenic lymphocytes in serum-substituted cultures. Human C3 was used in either soluble or cross-linked form. Soluble as well as Sepharose-bound or glutaraldehyde-cross-linked C3, over a range of concentrations, was inactive with resting splenic lymphocytes of (C57BL/6J X DBA/2)F1, C3H/HeJ and C57BL/6J nu/nu mice. However, lipopolysaccharide-activated spleen cells, enriched for B cell blasts, were stimulated by immobilized and cross-linked C3, while they did not respond to soluble C3. The extent of restimulation was comparable to that induced by lipopolysaccharide and resulted in both increased proliferation and maturation to Ig-secreting cells. The stimulation of the blast cells appears to be C3 specific, since it can be inhibited by free C3.

Animals↗
PubMed1984

Role of C3b receptors in the enhancement of interleukin-2-dependent T-cell proliferation.

The mechanism by which the complement system influences immune responses to T-cell-dependent antigens has not yet been clarified. That is why we studied the effect of the third complement component (C3) on different T-cell-dependent processes using well-defined mouse T-cell lines. While C3 did not influence the interleukin-2 (IL-2) production of the ST2/K-9 helper T-cells, the IL-2-dependent proliferation of the ST1 line was shown to be dose-dependently enhanced by C3. It is proved that neither the haemolytic activity of C3 nor the C3a fragment had any role in the process. The effect of C3 on the IL-2-dependent T-cell growth is even more enhanced (up to five-fold) when using polymerised C3. When the ST1 cell line is cultured in the presence of the cross-linked ligand, T-cells formed 80% less rosettes with red blood cells coated with antibody and mouse or human C3b. It is strongly suggested that C3--particularly when aggregated--exerts its enhancing effect on the growth of IL-2-dependent cell lines by binding to C3b receptors present on such T-cells.

Animals↗
PubMed1984

Physiological and pathological effects of activated complement.

In this short review of our present understanding of the complement system the emphasis is on a synopsis of the biological aspects of the various complement components, their fragments and complexes. For this reason we decided to refer to a number of reviews where certain aspects are dealt with extensively.

Anaphylatoxins↗
PubMed1983

Conditions for the enhancing effect of protease inhibitors on the concanavalin A induced thymidine response of murine lymphocytes.

Incorporation of [3H]-thymidine - [3H]-TdR - into concanavalin A (Con A) stimulated murine splenocytes and thymocytes was found to be enhanced by addition of certain concentrations of phenyl-methylsulfonylfluoride (PMSF), di-isopropylfluorophosphate (DFP), N-alpha-tosyl-L-lysyl-L-chloromethylketone (TLCK), and soybean trypsin inhibitor (SBTI). No enhancement could be observed when mononuclear cells of the peripheral blood were used, and a medium enhancement when thymocytes were applied. Furthermore, no enhancing effect of the protease inhibitors (PI) on the Con A response of murine splenocytes could be observed within the first 24 h of the culturing period. DFP, PMSF, and TLCK enhanced the Con A response to a similar degree, whereas SBTI was less effective. DFP and SBTI proved to be also effective when they were added after 15-24 h to the Con A cultures, if the cultures were harvested 48 h later. Removal of adherent and phagocytic spleen cells or reduction of the concentration of spleen cells shifted the effective DFP concentration to lower concentrations, whereas addition of adherent spleen cells caused a shift of the enhancing DFP amounts to higher concentrations. The data presented suggest that the enhancing effect of PI on the T cell response depends on the concentration of PI, the time of culturing and incubation, the PI used, the origin of the stimulated cells, and especially on the number of adherent and phagocytic cells. These findings might explain - at least in part - the different results on the effect of PI on the T cell response obtained in the past.

Animals↗