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J Loewenstein

Publications and source records attributed to J Loewenstein.

11 recordsLinked to original sources

Analogical encoding facilitates knowledge transfer in negotiation.

Information learned in one situation often fails to transfer to a similarly structured situation. However, prior findings suggest that comparing two or more instances that embody the same principle can promote abstraction of a schema that can be transferred to new situations. In two lines of research, we examined the effects of analogical encoding on knowledge transfer in negotiation situations. In Experiment 1, undergraduates were more likely to propose optimal negotiation strategies and less likely to propose compromises (a suboptimal strategy) when they received analogy training. In Experiment 2, graduate management students who drew an analogy from two cases were nearly three times more likely to incorporate the strategy from the training cases into their negotiations than were students given the same cases separately. For both novices and experienced participants, the comparison process can be an efficient means of abstracting principles for later application.

Adult↗

Interleukin-6 in the fever and multiorgan crisis of pheochromocytoma.

A 31-y-old black man with neurofibromatosis, alcoholism and hypertension was admitted because of abdominal pain, hematemesis and cough. In the hospital he had prolonged fever and developed a multiorgan crisis. Despite thorough investigation, no infectious cause for fever was found. Urinary catecholamines and metabolites were markedly elevated. Computerized tomography revealed a mass abutting the left kidney. A diagnosis of pheochromocytoma was made, and as soon as treatment with phenoxybenzamine and propranolol was begun, the fever resolved. Serum interleukin-6 (IL-6) concentration was initially elevated, decreased after the start of adrenergic blockade, and gradually fell to an undetectable level after surgery. These observations suggest that interleukin-6 might have been causally related to the patient's fever and possibly the multiorgan crisis.

Adrenal Gland Neoplasms↗

Maintenance ECT: indications and outcome.

Maintenance electroconvulsive therapy (M-ECT) is used to prevent recurrence of depression. Indications regarding patient selection criteria and efficacy are uncertain, in part because data are lacking. Comparison of M-ECT patients (N = 21) with controls demonstrates that M-ECT is chosen for patients whose course is characterized by multiple hospitalizations and failure to adequately respond to other therapies. M-ECT patients were exposed, on average, to 10 different psychotropic medications, including five trials of tricyclic antidepressants. Greater than half of their cumulative hospitalizations were for ECT. Their rate of rehospitalization decreased by 67% after institution of prophylactic M-ECT, demonstrating treatment efficacy. A tendency toward relapse and rehospitalization remains when M-ECT patients are compared to controls.

Adult↗

Tumor necrosis factor as a mediator of Mycoplasma orale-induced tumor cell lysis by macrophages.

We and other investigators have previously demonstrated that mycoplasmas induce macrophage-mediated lysis of tumor cells, but the mechanism responsible for this process had, thus far, not been clarified. We now report that addition of either viable or heat-killed Mycoplasma orale to murine macrophages induces a cytolytic activity which, due to its neutralization by a specific antiserum against murine cloned recombinant tumor necrosis factor (rTNF), was identified as TNF-mediated. Both thioglycollate-elicited peritoneal macrophages and the normal macrophages cloned from our JBM phi 1.1 bone-marrow-derived cell line effectively produced TNF at levels similar to, or higher than, those obtained in the presence of high concentrations of lipopolysaccharide (LPS). Four other mycoplasma species demonstrated a varied capacity to induce TNF production by macrophages. Elevated TNF levels were also observed during macrophage-mediated cytolysis of murine A9 fibrosarcoma cells in the presence of either M. orale or LPS. Addition of the specific antiserum against rTNF at a concentration which neutralized all TNF activity in the co-cultures partially inhibited concomitant A9 cell killing. We can, therefore, conclude that M. orale induces TNF production which is, at least partially, responsible for subsequent tumor cell killing.

Animals↗

Production of a factor (CIF) from normal fibroblast cells inhibiting tumor necrosis factor/cachectin production.

Murine embryonic fibroblast cells produce a factor designated cytotoxin-inhibiting factor (CIF) which inhibits tumor necrosis factor (TNF) and interleukin 1 production as well as tumoricidal activity by lipopolysaccharide-activated macrophages. This study determines the physiologic conditions of CIF production in serum-free medium. CIF production was largely dependent upon the presence of lipopolysaccharide. A quantitative correlation between fibroblast cell number, lipopolysaccharide concentration, and incubation time was established. Evidence is presented that CIF inhibited the production or release of TNF. CIF did not destroy TNF after production and release nor did it sequester secreted TNF. The supernatant fluids which inhibited TNF production did not suppress the capability of resting macrophages to phagocytize opsonized sheep erythrocytes, suggesting that only functions expressed in the activated state are inhibited.

Animals↗

Establishment and characterization of murine bone marrow-derived spontaneously immortalized cell lines and clones expressing properties of normal macrophages.

Murine bone marrow (BM) cells were cultivated on bacteriological grade culture dishes (BCD) in liquid medium containing L-cell-conditioned medium (LCM). The first month of rapid exponential multiplication was always followed by an interim phase of slow growth, and then by continuous proliferation. These established lines were called Jerusalem bone marrow macrophages (JBM phi). One of these, which had been derived from a C3H/Crg1 female mouse and was designated JBM phi 1.1, was studied in more detail. Its cloning efficiency when grown in LCM-containing soft agar was 65%. Of several clones isolated, one, C1.26, was selected for further cultivation and propagated for about 600 days. Cells from all cultures were surface adherent with limited proliferative capacity on tissue culture plastic. The properties displayed by all cells in a culture or clone include a typical macrophage (M phi)-like morphology, effective ingestion of killed bacteria and zymosan, staining for nonspecific esterase, and expression of Fc receptors and of F4/80 surface antigen. Addition of lymphokine (LK) induced Ia antigen expression on a high percentage of the cells. The JBM phi 1.1 cells also secreted high levels of lysozyme, produced a zymosan-induced respiratory burst, and, upon addition of lipopolysaccharide (LPS), released interleukin-1 and tumor necrosis factor. Efficient tumoricidal activity could be induced by LK and LPS. No evidence for the production of colony-stimulating factors, even in the presence of LPS, could be found. The JBM phi 1.1 or C1.26 cells did not develop into tumors following subcutaneous injection in x-irradiated syngeneic or in nu/nu mice and were also incapable of growing in soft agar without LCM. All the properties studied were expressed at similar levels by the "young" BM-derived M phi during their first exponential growth phase, as well as by other JBM phi lines and clones. It is concluded that the established JBM phi lines consist of homogeneous cell populations which, according to all markers and functions studied, could be classified as non-activated, functional, and mature M phi, resembling in all aspects BM-derived M phi during their first few weeks of cultivation. This shows that cell lines expressing properties of normal M phi may develop spontaneously by continuous cultivation of BM cells in growth factor-containing liquid medium on BCD.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Correlation of macrophage-mediated tumor-cell lysis with the production of macrophage cytolytic factor (CF). Preliminary characterization of a factor inhibiting CF production.

Macrophage-mediated cytolysis of thymidine-prelabelled murine A9 fibrosarcoma cells was compared to the level of cytolytic factor (CF) present in the cultures by assaying supernatant aliquots on actinomycin (AcD)-treated A9 fibrosarcoma cells. A good correlation between the level of A9 killing and CF titer was observed when different concentrations of lipopolysaccharide (LPS) were added to various macrophage populations: murine peritoneal cells, short-term bone-marrow (BM)-derived macrophages and JBM phi macrophage lines. Optimal A9 killing and CF secretion, equivalent to the killing of about 1000 AcD-pretreated A9 cells by a single macrophage, were obtained following activation of JBM phi by LPS. CF production by BM-derived macrophages was enhanced in serum-free medium when compared to its release in the presence of fetal calf serum. The LPS-activated macrophages could be restimulated by the activating agent to produce CF following one week of propagation in the absence of LPS. On the other hand, CF activity was absent from the supernatants of activated macrophages co-cultured with normal embryonic fibroblasts, which are resistant to macrophage-mediated killing. This effect could be attributed to a factor, secreted by normal fibroblasts but not by A9 cells, which suppressed CF release from the activated macrophages. Our data strongly support earlier observations, suggesting that CF [which appears to resemble the tumor necrosis factor (TNF)] is responsible for LPS-induced macrophage-mediated tumor cell lysis. It is suggested that suppression of the latter process by the fibroblast-derived factor proceeds via inhibition of CF/TNF production from the macrophage.

Animals↗

Suppression of both macrophage-mediated tumor cell lysis and cytolytic factor production by a factor (CIF) derived from normal embryonic fibroblasts.

We had previously established a murine bone marrow-derived cell line, designated JBM phi 1.1, which displayed properties of normal macrophages, including the ability to perform macrophage-mediated cytolysis. It was also found that these cells could be induced by lipopolysaccharide (LPS) to produce reproducibly high levels of a cytolytic factor (CF) resembling tumor necrosis factor (TNF). This cell line was therefore selected for further studies on macrophage-mediated tumor cell lysis and CF production. Moreover, the CF production during incubation with LPS was higher in the absence of serum than in its presence, with a maximum at days 2-3 following the addition of LPS. A factor inhibitory to CF production (CIF) was detected in our laboratory in the supernatant of embryonic fibroblast cultures. We established the experimental conditions required for the optimal production and suppressive effect of CIF. High levels of CIF activity were obtained under conditions that promote fibroblast proliferation. Addition of embryonic fibroblast culture supernatant to the macrophages shortly before LPS suppressed both LPS-induced CF production and tumoricidal activity. CIF did not affect macrophage protein synthesis in the presence or absence of LPS. However, LPS-induced interleukin 1 release was partially (55%) suppressed by embryonic fibroblast culture supernatant. Our results show that CIF does not exert a general inactivating effect on the macrophages, although it may possibly affect other functions in addition to CF production and tumor cell lysis. The strong inhibition of both the latter properties further indicates that TNF-like CF is an important mediator in macrophage-mediated tumor cell lysis.

Animals↗

Studies on the mechanism of macrophage-mediated tumor cell lysis induced by Mycoplasma orale.

Following our previous demonstration that both viable and heat-killed Mycoplasma orale induce selective tumor cell killing by murine peritoneal macrophages, further investigations reported here showed that also macrophages from a continuously proliferating cell line established from long-term cultures of murine bone marrow explants can effectively be induced by the heat-killed mycoplasmas to express cytolysis. The use of single-cell suspensions of M. orale from a 0.45-micron filtrate or following either sonication or treatment with DNase did not significantly affect the level of cytolysis. Minute quantities of M. orale acted synergistically with ineffectively low levels of either lymphokines (LK) or lipopolysaccharide (LPS) to produce killing. The exceptional resistance of M109 lung adenocarcinoma cells to macrophage-mediated killing induced by LK and LPS, as previously reported by us, could not be overcome by the addition of M. orale. These data appear to indicate a mechanism of macrophage activation by M. orale similar to that caused by LPS.

Animals↗

Induction of macrophage-mediated cytolysis of neoplastic cells by mycoplasmas.

Unexpected cytolysis was encountered when nonactivated murine peritoneal macrophages were cultured with [3H]TdR-prelabeled syngeneic or allogeneic tumor cells at a 10:1 ratio. The level of specific cytolysis reached 70% within 48 hr of cocultivation. Similar killing was observed whether the macrophages were derived from untreated, thioglycollate-treated, or germ-free mice. Cytolytic activity was also demonstrated when bone marrow-derived or peritoneal macrophages from 9- and 5-day in vitro cultures, respectively, were employed rather than freshly harvested peritoneal macrophages. Thus, the macrophage-mediated killing was neither the result of in vivo preactivation nor a consequence of the presence of lymphocytes in the assay. Moreover, macrophages derived from different strains caused similar effects. Our study revealed that the neoplastic target cell cultures susceptible to cytolysis by nonactivated macrophages were contaminated with mycoplasma. A mycoplasma was isolated from the supernatant of a culture of the A9HT fibrosarcoma line, identified as Mycoplasma orale, and cultivated. Addition of viable mycoplasma from that isolate to mixed cultures of thioglycollate-elicited macrophages and [3H]TdR-prelabeled mycoplasma-free target cells resulted in specific cytolysis of transformed A9 cells, but not of normal mouse fibroblasts. The level of macrophage-dependent cytolysis correlated with the number of viable mycoplasma cells added and was higher than that attained by activation with LPS at optimal concentration. Similar specific cytolysis was observed with heat-killed mycoplasmas. Our results demonstrate that mycoplasmas may cause selective macrophage-mediated cytolysis of neoplastic but not of normal target cells, perhaps via activation of the macrophages. It is suggested that undetected infection of experimental systems by mycoplasmas may account for some reports on lysis of neoplastic cells by nonactivated macrophages.

Animals↗