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At least 325 records · Page 18Linked to original sources
PubMed1978

[The influence of MIF (melanocyte-stimulating hormone-release inhibiting factor) on psychomotor function and mood in parkinsonian patients. Preliminary report (author's transl)].

In 12 parkinsonian patients aged from 40--76 years the L-dopa-potentiating effect of MIF was investigated using a doubleblind crossover design. MIF was given i.v. in a dose of 200 mg. The following psychological tests were carried out 4 times after the injection of MIF at hourly intervals: Purdue pegboard, Minnesota-Rate of manipulation test, 2-key-tapping, simple and complex reaction time and a state of well-being scale. The results revealed a marked effect on finger dexterity, drive and complex reaction time. That means MIF does not only lead to an improvement of psychomotor performance but also of cognitive functions. In contrast thereto the influence on the state of well-being was less impressive.

Adult↗
PubMed1982

MIF-1 facilitates passive avoidance retention.

MIF-1 (Pro-Leu-Gly-NH2) is an endogenous substance which seems to be involved in the regulation of some central nervous system functions. It was recently shown to affect learning and memory processes. In order to further clarify the role of MIF in these processes we used two different passive avoidance tests: one-trial step down (SD) and shock suppressed drinking (SSD). Z-Pro-Leu-Gly-NH2 was administered on the training day ip either 15 minutes before trial or immediately after. The doses used were as follows: SD--1.0 mg/kg, SSD--0.05 mg/kg (in the group injected before trial) and 1.0 mg/kg--SD and SSD, in the groups injected post-trial. Only the immediate post-training injection of peptide resulted in significant prolongation of the step-down latencies on the retention-day. Similarly, in the SSD procedure only post-training MIF markedly attenuated water intake on the day after training. In a separate experiment we have found that in the dose of 1.0 mg/kg, but not 0.1 mg/kg, MIF significantly inhibited water intake. These results suggest that this naturally occurring peptide can contribute to the processes of memory consolidation and water intake.

Animals↗
PubMed1981

Immunological aspects of Theileria annulata infection calves. 2. Production of macrophage migration inhibition factor (MIF) by sensitized lymphocytes from Theileria annulata-infected calves.

Peripheral blood lymphocytes (PBLs) from calves infected experimentally with a stabilate of Theileria annulate, produced a factor which inhibited the migration of macrophages. This was first demonstrated against schizont antigen in some animals on day 8 post infection while in the others on day 12. The highest activity of the macrophage migration inhibition factor (MIF) was recorded on day 12 in some of the infected animals and on day 16 in the others, whereas on day 30 or more MIF was demonstrable. The MIF was also demonstrated against piroplasm antigen. 64 days after the first infection, the recovered calves were challenged with the homologous strain. It was found that PBLs from all challenged calves were able to produce MIF against both, schizont and piroplasm antigen. These results indicate occurrence of sensitized lymphocytes as effector cells of cell-mediated immunity to T. annulata infection.

Animals↗
PubMed1980

Role of sialic acid in the macrophage glycolipid receptor for MIF.

Acidic glycolipids from guinea pig macrophages enhance the response of macrophages to migration inhibitory factor (MIF), suggesting a role of glycolipid receptors for this lymphocyte mediator. Neuraminidase treatment of these glycolipids results in the loss of their biologic activity. This activity remains intact after incubation of the glycolipids with beta-galactosidase. In order to investigate whether sialic acid is essential for the macrophage's response to MIF, macrophages were incubated with neuraminidase. Neuraminidase treatment of peritoneal exudate cells results in the abrogation of macrophage responsiveness to MIF. Other exoglycosidases such as beta-galactosidase and beta-glucosidase had no effect upon the macrophage response. The effect of neuraminidase was found to be reversible within 18 hr. These experiments suggest that macrophage glycolipids containing sialic acid are components of the macrophage receptor for MIF.

Animals↗
PubMed1998

Tyr-W-MIF-1 attenuates down-regulation of opiate receptors in SH-SY5Y human neuroblastoma cells.

Down-regulation of opiate receptors is demonstrated more easily in vitro than in vivo. The possible role of endogenous opiate-modulating peptides in preventing such down-regulation was investigated by addition of Tyr-W-MIF-1 to an in vitro preparation, the human neuroblastoma cell line SH-SY5Y, in which down-regulation of opiate receptors has been demonstrated previously. Although both morphine and Met-enkephalin down-regulated mu and delta receptors after chronic (24 h) exposure in serum-free medium, Tyr-W-MIF-1, at doses of up to 100 microM, did not affect receptor number when administered alone. This lack of effect could not be attributed to degradation of the peptide during chronic treatment because high-performance liquid chromatography showed that 79% of the peptide remained intact after a 24-h incubation. When coadministered with 3 microM morphine, Tyr-W-MIF-1 dose-dependently attenuated morphine-induced down-regulation of both mu and delta receptors. Down-regulation of mu receptors by the selective agonist PL017 was also attenuated by Tyr-W-MIF-1, but down-regulation of delta receptors by the selective agonist DPDPE was not. These studies indicate that endogenous opiate modulators may play a role in opiate tolerance at the level of receptor down-regulation.

Culture Media↗
PubMed1994

MIF proteins are not glutathione transferase homologs.

Although macrophage migration inhibitory factor (MIF) proteins conjugate glutathione, sequence analysis does not support their homology to other glutathione transferases. Glutathione transferases are not detected with MIF proteins in searches of protein sequence databases, and MIF proteins do not share significant sequence similarity with glutathione transferases. Homology cannot be demonstrated by multiple sequence alignment or evolutionary tree construction; such methods assume that the proteins being analyzed are homologous.

Animals↗
PubMed1996

NMR characterization of structure, backbone dynamics, and glutathione binding of the human macrophage migration inhibitory factor (MIF).

Human macrophage migration inhibitory factor is a 114 amino acid protein that belongs to the family of immunologic cytokines. Assignments of 1H, 15N, and 13C resonances have enabled the determination of the secondary structure of the protein, which consists of two alpha-helices (residues 18-31 and 89-72) and a central four-stranded beta-sheet. In the beta-sheet, two parallel beta-sheets are connected in an antiparallel sense. From the total of three cysteines present in the primary structure of MIF, none was found to form disulfide bridges. 1H-15N heteronuclear T1, T2, and steady-state NOE measurements indicate that the backbone of MIF exists in a rigid structure of limited conformational flexibility (on the nanosecond to picosecond time scale). Several residues located in the loop regions and at the N termini of two helices exhibit internal motions on the 1-3 ns time scale. The capacity to bind glutathione was investigated by titration of a uniform 15N-labeled sample and led us to conclude that MIF has, at best, very low affinity for glutathione.

Amino Acid Sequence↗
PubMed2000

Tumor growth-promoting properties of macrophage migration inhibitory factor (MIF).

First identified nearly 40 years ago, macrophage migration inhibitory factor (MIF) is a potent pro-inflammatory cytokine and is an essential component of immune and inflammatory responses. Recent studies suggest that MIF may also contribute to multiple aspects of tumor progression and neoplasia. This review will attempt to summarize these findings focusing on MIF's ability to modulate cell proliferation, tumor angiogenesis and tumor suppressor activity.

Animals↗
PubMed1977

On the optimal dosage of Pro-Leu-Gly-NH2 (MIF) in neuropharmacological tests and clinical use.

Pro-Leu-Gly-NH2 (MIF) inhibits the tremor induced by oxotremorine. Objective measurement of this tremor permits the drawing of a dose-effect curve. The inhibitory effect of the peptide increases linearly with increasing doses until an optimum is reached (between 30 and 40 mg/kg i.p.). At still higher doses the peptide is inactive. The same phenomenon is observed with analogues of MIF. This finding may have important bearings on the interpretation of clinical and experimental data obtained with MIF.

Animals↗
PubMed1980

Some cellular immune reactions in infants. MIF, E-rosette formation and changes in nucleolar morphology.

The cellular immune response (MIF, E-rosette formation and changes in nucleolar morphology of lymphocytes) was followed as related to age and antigenic stimulation. MIF in healthy infants increased from the 2nd to the 12th week of life as compared with the first week, probably due to BCG vaccination. The total and active E-rosette formation did not change during the whole period of investigation. Ring-shaped nucleoli increased gradually from the second week of life. Active nucleoli increased up to the 4th week, i.e. after BCG vaccination and then slowly decreased. Micronucleoli being high in the first week, decreased during 24 weeks of life. After artificial colonization of the intestine the production of MIF was slightly lower in colonized infants than in controls from the 2nd to the 12th week. The other parameters followed were not influenced by colonization.

BCG Vaccine↗
PubMed1993

Tyr-MIF-1 precipitates abstinence syndrome in morphine-dependent rats.

The endogenous neuropeptide Tyr-MIF-1 (Tyr-Pro-Leu-Gly-amide) has been shown to counteract various opiate actions. In the current study, third ventricular injection of 35 micrograms Tyr-MIF-1 protected by the enzyme inhibitor bestatin precipitated an abstinence syndrome in morphine-dependent rats, but not in opiate-naive rats. The results raise the possibility that Tyr-MIF-1 might participate in opiate dependence and opiate abstinence syndrome.

Animals↗
PubMed1993

Purification of macrophage migration inhibitory factor (MIF) from bovine brain cytosol.

Two isoforms of the macrophage migration inhibitory factor (MIF) have been isolated to homogeneity from bovine brain cytosol. In agreement with the cDNA sequence of their human counterpart, they both have an apparent molecular weight of 12 kDa and are characterized by the following N-terminal amino acid sequence NH2-PMFVVNTNVPRASVPDGLLSELTQQLAQATGKPPQYIAV-. CD spectra revealed that bovine MIF contains 42% (+/- 3%) alpha-helix and 21% (+/- 3%) beta-structure. CD-constrained prediction of the secondary structure assigned MIF to the alpha/beta-class of proteins.

Amino Acid Sequence↗
PubMed1976

An evaluation of the methods available for analysing results from migration inhibitory factor (MIF) test.

In order to illustrate the potential dangers in using some of the methods available for calculating migration inhibitory factor (MIF) activity, selected results have been analysed in a number of different ways. The weights corresponding to the migration areas were used in a single ratio expression and then in a double ratio formula to calculate migration inhibition. Conclusions from these results were made using both the arbitrary 20% inhibition to indicate MIF activity and a statistically-derived minimum percentage inhibition needed to demonstrate a significant effect. The procedure was then repeated using the square root of the weight equivalents of the migration areas. A double ratio expression was preferable to the single ratio formula as the former considered the information from all the control cultures. The degree of inhibition needed to demonstrate MIF activity varied between tests and for accurate interpretation of the results it was necessary to use a statistically derived minimum value for inhibition in each experiment. Use of the square root of the weight equivalents of migration areas in the double ratio method gave conclusions analogous to those using the actual weights. Use of the square root transformation narrowed the difference between sample means and caused a corresponding reduction in within-sample variability.

Animals↗
PubMed1977

The statistical distribution of macrophage migration distance and its application to MIF test.

The measurement of the distance of macrophage migration is very simple and reasonable as a technique in MIF assay. By the use of this technique, a large scale model experiment was performed and its data were analysed statistically. As the result of analysis, Student's t-test for significance of the difference between control and test readings of migration distance at low activity level in the MIF test was justified, and it was proved that it is applicable to the routine MIF test. In addition to this, the measurement of migration distance was compared with that of migration area.

Animals↗
PubMed1978

A new assay for rapid measurement of MIF levels by 3H-labelled cells in liquid scintillation counting vials: statistical implications for the measurement of migration inhibition.

A new quantitative assay for migration inhibitory factor (MIF) employs 3H-labelled cultured mouse or human lymphoid cells migrating from capillary tubes. Capillaries filled with labelled cells are placed in liquid scintillation counting vials, along with the MIF-containing sample and are removed at the end of a five-hour incubation period. The residual, labelled cells which have migrated out of the tubes are solubilized and counted in a liquid scintillation counter. While cultured lymphoblast cells are routinely used in the assay, the method was checked against mouse and guinea pig peritoneal exudate cells in both the labelled cell technique and the conventional chamber assay. The assay is technically simple to perform and a useful tool for laboratory research purposes because of the short span of time needed to obtain the results. These advantages indicate a potential for automation and use of this assay in a clinical immunology laboratory. Statistical analysis of data from both assays demonstrated that the relative variation among replicates is lower in the labelled cell assay. The new assay also measured a significant difference between controls and MIF-containing samples when the migration index (MI) was greater than 80%. Criteria for significant inhibition of migration are discussed in regard to the use of analysis of variance (ANOVA) and other statistical procedures, and the inadequacy of a single measure, such as the MI, is discussed.

Animals↗
PubMed1977

Studies of cellular sensitization to myelin antigens in multiple sclerosis. Dissociation of MIF and LBT production in response to a peptide encephalitogenic in rhesus monkeys.

The macrophage migration inhibitory factor (MIF) assay and the lymphoblastic transformation (LBT) technique were utilized simultaneously to measure immune responses to peptide Y, the 17 amino acid C-terminal fragment of basic myelin protein, in patients with multiple sclerosis (MS). Ten normals and 67 MS patients from the Montreal Neurological Hospital and affiliated institutions were examined. A prospective attempt was made to correlate the measured responses with phasic clinical activity of the disease. The LBT results indicate some degree of cellular sensitization to peptide Y which parallels the clinical course of the illness, and resembles earlier positive findings obtained with the whole basic myelin protein molecule. These findings, however, are in contrast to a negative MIF response to the Y peptide used in the present study and further contrast the positive MIF results obtained earlier using the whole protein. It is not evident from the results of the present study whether sensitization may be of any pathogenetic significance, but the findings show that differing portions of the basic myelin protein molecule may selectively stimulate specific lymphokine elaboration by sensitized lymphocytes.

Acute Disease↗
PubMed1989

Chronic, but not acute, administration of morphine alters antiopiate (Tyr-MIF-1) binding sites in rat brain.

Opiate addiction could involve a change in the binding of endogenous antiopiates. A candidate for such a role is Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2), a brain peptide that can antagonize exogenous and endogenous opiates and bind to opiate receptors. Its primary action, however, may be through its own binding site in brain, which we now report is altered by chronic administration of morphine. Rats given morphine pellets had reduced binding of both iodinated and tritiated Tyr-MIF-1 on day 5, when substantial tolerance is evident. In contrast, mu and delta opiate receptors were increased. Acute injection of an analgesic dose of morphine did not reduce Tyr-MIF-1 binding, indicating that chronic administration is required for the change. These findings open new approaches to the study of addiction by focusing on antiopiate activity.

Animals↗
PubMed1991

Cimetidine does not change the effect of Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2) on the opiate form of footshock-induced analgesia.

It has been demonstrated that cimetidine blocks the effect of naloxone on footshock-induced analgesia. To study the effect of cimetidine on the antiopiate properties of an endogenous peptide Tyr-MIF-1, the opiate form of intermittent footshock-induced analgesia was elicited in the rat. The nociceptive responses were determined using the hot-plate test (52.5 degrees C). Intraperitoneal pretreatment with cimetidine (100 mg/kg) or chlorpheniramine maleate (20 mg/kg) did not affect the footshock-induced analgesia, and did not change the antagonizing effect of Tyr-MIF-1 (0.2 mg/kg) on this model of antinociception. It is concluded that cimetidine and chlorpheniramine maleate do not change the antagonizing effect of Tyr-MIF-1 on the opiate form of intermittent footshock-induced analgesia.

Amino Acid Sequence↗