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J H Jansen

Publications and source records attributed to J H Jansen.

67 records · Page 4Linked to original sources
PubMed1990

Hairy cell leukemia preferentially expresses the IgG3-subclass.

Surface IgG expression of 29 cases of hairy cell leukemia (HCL) was assessed using IgG-subclass-specific monoclonal and F(ab)'2 polyclonal antibodies. A marked preference for the IgG3 subclass was found, as 16 of 19 IgG-positive HCL's expressed IgG3. In 10 cases, IgG3 was concurrently expressed with other heavy chains. No preferential IgG3 expression was observed in 11 IgG-positive non-Hodgkin's lymphomas. The marked predominance of IgG3 in HCL suggests a deviation in heavy chain class switching that may be related to the characteristically very low expression of LFA-1 and ICAM-1 molecules on hairy cells, and hence a defect in T-cell hairy cell interaction.

Antigens, Differentiation↗
PubMed1990

Interleukin-4. A regulatory protein.

Since its discovery in 1982, numerous biological activities of interleukin-4 (IL-4) have been described. Like other cytokines, IL-4 is highly pleiotropic, both with respect to the number of different target cells that are responsive to it and with respect to the number of different biological responses it elicits. Interleukin-4 was initially described as a costimulant for the proliferation of B lymphocytes stimulated with anti-IgM antibody. Synonyms for this cytokine are B cell growth factor-1 (BCGF-1) and B cell stimulatory factor-1 (BSF-1). After cloning of both the murine and human IL-4, the use of recombinant IL-4 enabled detailed studies of its biological functions. Many cell types, mainly of hematological origin, express receptors for IL-4. Accordingly, effects of IL-4 have been described on B lymphocytes, T lymphocytes, NK cells, mononuclear phagocytes, mast cells, fibroblasts and hematopoietic progenitor cells. Currently, there are three major areas in which IL-4 appears to play an important role: 1) regulation of B cell growth and of antibody isotype expression. In this context, a possible role for IL-4 in allergic reactions is of special interest. 2) Stimulation of T cell growth and the generation of cytotoxic T lymphocytes. In addition to the suppressive effects on the induction of non HLA-restricted cellular cytotoxicity by natural killer- (NK) and lymphokine-activated killer (LAK) cells, this suggests a role for IL-4 in the regulation of cellular immune responses. 3) Regulation of the growth and differentiation of hematopoietic bone marrow stem cells. IL-4 itself does not induce proliferation of hematological progenitor cells but it can modulate the growth-factor dependent proliferation of these cells. In this review the biological functions of IL-4, reported until present, are discussed.

Animals↗
PubMed1990

Therapeutic effect of THA on hemicholinium-3-induced learning impairment is independent of serotonergic and noradrenergic systems.

Tetrahydroaminoacridine (THA: Tacrine) has previously been shown to reverse deficits in spatial discrimination learning induced by hemicholinium-3 (HC-3). In the present experiments the effects of prior depletion of serotonin (5-HT) or noradrenaline (NA) on this reversal were examined. In the first experiment 5-HT lesions were made by injecting 5,7-DHT (2 x 50 micrograms/5 microliters) into the lateral ventricles of rats pretreated with desmethylimipramine (DMI 25 mg/kg IP). A permanently indwelling guide tube was then implanted over the right lateral ventricle. Subsequent testing under drug-free conditions, revealed no effect of the lesion on the number of trials needed to attain criterion (nine consecutive correct choices) in two-platform spatial discrimination learning in a watermaze. Using a latin square design rats were then tested for the effects of HC-3 and THA. HC-3 (5 micrograms/5 microliters ICV) or placebo (CSF) were injected 60 min before the start of a 30-trial training session. THA (4.6, 10 mg/kg SC) or placebo were then injected 15 min before training. Choice accuracy but not choice latency was significantly impaired by HC-3 and the effect was reversed by THA in both sham operated and 5-HT lesioned rats. In the second experiment two injections of DSP-4 (50 mg/kg IP) were given, following cannulation, to deplete forebrain NA. The lesion had no effect on spatial learning under drug-free conditions and failed to block the THA-induced reversal of spatial discrimination learning deficits following HC-3. These results confirm that forebrain Ach depletion by HC-3 impairs spatial discrimination learning and that the deficit is reversed by THA.(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗
PubMed1990

Oxalate nephropathy in a Tibetan spaniel litter. A probable case of primary hyperoxaluria.

Severe oxalate nephropathy with end-stage kidney lesions was found in two pups of a litter of three Tibetan Spaniels. This histopathological finding strongly suggests a primary hyperoxaluria since there was no exposure to agents capable of producing secondary hyperoxaluria. Primary hyperoxaluria has not been reported as a spontaneous disease in the dog, although it is a well-known, but rare, inherited metabolic disease of man.

Animals↗
PubMed1989

Inhibition of human macrophage colony formation by interleukin 4.

We investigated the effects of human rIL-4 on in vitro hematopoiesis. A profound inhibition of macrophage colony formation by IL-4 was observed, whereas colony growth of other lineages was not affected. Inhibition of macrophage colony growth was not restricted to GM-CSF-induced colony growth but was also present in cultures stimulated with M-CSF. This inhibition was not only observed in cultures of light density bone marrow cells, but also in cultures of monocyte- and T lymphocyte-depleted bone marrow cells. Since a similar inhibition was observed in cultures of CD34+HLA-DR+-enriched bone marrow cells, a direct action of IL-4 on monocyte-committed progenitor cells is suggested.

Antigen-Presenting Cells↗
PubMed1989

Hemicholinium-3 impairs spatial learning and the deficit is reversed by cholinomimetics.

The effects of hemicholinium-3 (HC-3) on spatial discrimination learning were studied. Rats were equipped with indwelling cannulae in the right lateral ventricle and, following recovery, were trained on a two platform spatial discrimination task in a water maze. In this task a visible escape platform remains in a fixed position in the pool during a single training session, whilst the location of an identical "float" (which affords no escape) is randomly varied. For each session the location of the fixed escape platform was changed and the rats were retrained to criterion following pretreatment either with artificial cerebrospinal fluid (CSF) or HC-3 (2.5, 5.0 micrograms/rat/ICV) 1 h before training. Each rat received every treatment according to a latin square design. The results showed that spatial learning was dose dependently impaired by HC-3, choice accuracy being reduced to chance levels by the higher dose. There was no evidence of motoric difficulty, as choice latencies were not significantly increased. Experiments were then conducted to test for reversal of the deficit using a range of psychotropic drugs. Rats were treated with CSF or HC-3 (5 micrograms/rat ICV) 60 min prior to testing and test drugs were injected 15 min before testing. Some doses of physostigmine (46-460 micrograms/kg/SC) and tetrahydroaminoacridine (THA) (2.2-10 mg/kg/SC) reversed the spatial learning deficit. The muscarinic agonists arecoline (0.046-1 mg/kg/SC), aceclidine (1-10 mg/kg/SC), oxotremorine (30-100 micrograms/kg/SC) and RS-86 (0.46, 1.0 microgram/kg/SC) were also effective. Pilocarpine (0.22-2.2 mg/kg/SC) showed marginal activity and isoarecoline (4.6-10 mg/kg/SC) was inactive. Nicotine (0.32, 1, 3.2 mg/kg/SC) and piracetam (10, 30, 100 mg/kg IP) were also inactive. The alpha 2 agonist, clonidine (46, 100 micrograms/kg SC) and the antagonist idazoxan (32, 100 micrograms/kg SC) were also inactive. Learning deficits were not reversed by haloperidol (20, 60 micrograms/kg), amphetamine (0.1, 0.46 mg/kg), the selective 5-HT1A agonist 8-OH-DPAT (30, 100 micrograms/kg) or by the benzodiazapine antagonist ZK-93426 (1, 3.2, 10 mg/kg). The results show that forebrain Ach depletion by HC-3 impairs spatial discrimination learning and these deficits are reversed by cholinesterase inhibitors and some muscarinic receptor agonists. Some degree of pharmacological selectivity is indicated by the failure of a range of other drugs to reverse the impairments.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1989

Residual T lymphocytes, and not malignant B cells, proliferate upon mitogenic stimulation.

Malignant B cells, derived from hairy cell leukemia (HCL), non-Hodgkin's lymphoma (NHL) or prolymphocytic leukemia were stimulated with mitogens and interleukin 2 after careful depletion of contaminating T cells resulting in final residual percentages of less than 0.1. No proliferation was found as measured by 3H-thymidine incorporation. Subsequently, to the non-T B cell cultures very small amounts of autologous or allogeneic T cells were added, ending up in final concentrations of 0.1, 0.5, 1, or 2% T cells. It appeared that a marked proliferation occurred which had in various coculture combinations to be ascribed to the T cells alone. Moreover, most HCL and other B cell NHL additionally stimulated the T cells, resulting in a further increase in proliferation. We conclude that 3H-thymidine incorporation by malignant B cells such as HCL and B-NHL stimulated with mitogens and IL-2 will in most cases wrongly be attributed to proliferation by the B cells themselves, and instead has to be ascribed to contaminating T cells.

B-Lymphocytes↗
PubMed1988

Colony growth of normal and neoplastic cells in various concentrations of methylcellulose.

To assess the semisolid character of methylcellulose (MC) and its ability to prevent cell migration and aggregation in clonogenic assays, we studied the influence of various concentrations of MC (0.7%-1.26%) on colony growth of neoplastic cell lines, normal bone marrow cells, and hairy cell leukemia (HCL). All cell lines (K562, HL-60, JOK-1, Daudi, and BB3, an IgM-kappa B-cell line) showed a prominent decrease in colony numbers and remarkable changes in colony morphology at rising MC concentrations, whereas no such influence could be demonstrated for HCL, mixed lineage colony-forming units (CFU-GEMM), granulocyte-macrophage CFU (CFU-GM), erythroid burst-forming units (BFU-E), and erythroid CFU (CFU-E). Despite a decrease in colony numbers at high MC concentrations, some cell lines showed a sustained proliferation as measured by growth index calculations and bromodeoxyuridine (BrdUrd) incorporation. This indicates that at certain MC concentrations colony formation is not always a reflection of proliferation. BrdUrd incorporation yielded an extremely low proliferation capacity for HCL. It is likely that HCL cells, which strongly aggregate, formed pseudo-colonies in spite of high MC concentrations.

Bone Marrow Cells↗
PubMed1988

Selective behavioural impairment after acute intoxication with trimethyltin (TMT) in rats.

A series of experiments was conducted to characterize the long term behavioural consequences of acute intoxication with trimethyltin (TMT) (5,6,7, mg/kg p.o.). The acute toxicity syndrome, including weight loss, convulsions, irritability and hyper-reactivity was confirmed in treated rats. These symptoms subsided to reveal marked increases in locomotor activity in a novel environment but no lasting effects on consummatory behaviour or sensorimotor integration. Neither two-way active avoidance nor passive avoidance learning were impaired by doses of up to 7 mg/kg p.o. although intertrial activity was elevated in the shuttle box and extinction responding was increased. Place navigation in a water maze was impaired, particularly at the highest dose of TMT (7 mg/kg p.o.) and when a brief training phase (8 trials) was used. Finally, TMT lesioned rats were compared with controls on spatial and non-spatial discrimination tasks. Following 7 mg/kg p.o. TMT rats were highly impaired on the spatial discrimination but not the non-spatial discrimination despite the greater difficulty of the latter task. Histological studies confirmed the pathological effects of TMT in limbic structures, particularly the pyramidal cells of CA1 and CA4, and also revealed increased acetylcholinesterase activity within the molecular layer of the dentate gyrus. The selective, long term behavioural impairments caused by TMT are discussed in the light of their qualitative similarity to the effects of hippocampectomy or hippocampal denervation. TMT lesioned rats may provide a suitable functional model for the partial hippocampal and temporal lobe pathology characteristic of Alzheimer's disease.

Animals↗
PubMed1987

Time development of distribution and toxicity following single toxic APAP doses in male BOM:NMRI mice.

The time development of the biodistribution and the hepatotoxicity following peroral administration of 14C-acetaminophen (APAP 400 or 800 mg.kg-1; 1 microCi) was characterized in a trial procedure using male Bom:NMRI mice. APAP (400 mg.kg-1) caused a transitory hepatic glutathione (GSH) depletion while APAP 800 mg.kg-1 maximally depleted hepatic GSH throughout the 12 h trial period. A lag time between the initial GSH depletion and the ensuing hepatic necrosis was seen. From 8 h post dosing a decrease of 14C-APAP or its metabolites coincided with recovery of the hepatic GHS level and the regeneration of the hepatic cells caused by APAP 400 mg.kg-1. Hepatic glycogen depletion preceded centrilobular necrosis, and irrespective of APAP dose definite kidney damage was absent. Irrespective of APAP dose the biodistribution of 14C-APAP or its metabolites was predominantly in organs associated with metabolism and excretion. After APAP (800 mg.kg-1) significant amounts of 14C-APAP or its metabolites were present up to 24 h post dosing. The operative status of the hepatic GSH conjugative system has an important influence on the rate of elimination of toxic APAP doses. Hepatic cell necrosis with a possible effect on the circulation may play an important secondary role in the elimination of toxic APAP doses. Factors which may influence the status of the hepatic GSH conjugative system and toxicokinetics of perorally administered APAP doses are discussed.

Acetaminophen↗
PubMed1987

Blockade of spatial learning by the M1 muscarinic antagonist pirenzepine.

Two experiments were conducted to determine the effects of the M1 muscarinic receptor antagonist pirenzepine on place navigation in a water maze. In the first experiment rats were required to learn the location of a hidden platform following intracerebroventricular injections of equimolar doses of pirenzepine or scopolamine methylbromide. Both drugs dose-dependently impaired spatial learning according to both escape latency data and transfer test analysis. Pirenzepine was approximately 3 times less potent than scopolamine, a potency ratio which suggests M1 receptor mediation of the impairment. In the second experiment pirenzepine (1 approximately 92.3 micrograms/rat ICV) was injected prior to training on a simultaneous place discrimination task in the water maze. Impairments of choice accuracy were found with a dose of 20 micrograms/rat in the absence of any marked increases in either errors of omission or choice latency. These data suggest that M1 receptor blockade impairs processes which are involved in spatial learning.

Animals↗
PubMed1984

Participation in the first and second round of a mass-screening for colorectal cancer.

Using data from a survey of a sample of 239 people asked to participate in a community-based screening for colorectal cancer, factors associated with participation were identified. Central were variables about social participation and perceived threat of the disease. Of the variables that accounted for (non)participation in the first round only a few, such as perceived seriousness and active membership of clubs or associations, also accounted for participation in the second round of the screening. In conclusion it was argued that factors associated with participation in a first screening round cannot be used without adjustment to explain participation in a second round.

Adult↗