Biomedical subjects

H R Miller

Publications and source records attributed to H R Miller.

At least 37 records · Page 2Linked to original sources

PubMed1997

Sheep mast cell proteinase-1: characterization as a member of a new class of dual-specific ruminant chymases.

Sheep mast cell proteinase 1 (SMCP-1), which is abundantly expressed in gastrointestinal but not skin mast cells, was isolated and its substrate specificity was investigated. Peptide substrates, including angiotensin I, substance P, bradykinin and oxidized insulin B chain were hydrolysed at P1 Phe, Leu or Tyr residues, conforming to the known chymotrypsin-like properties of the enzyme. However, SMCP-1 was found to hydrolyse some chromogenic substrates with P1 Lys and Arg residues. The enzyme also demonstrated trypsin-like activity against protein substrates, cleaving BSA at Lys114-Leu115, Lys238-Val239, Lys260-Tyr261 and Lys376-His377. Bovine fibrinogen beta-chain was cleaved at Lys28-Lys29. To ensure homogeneity of the enzyme, the ratio of chymotrypsin-like to trypsin-like activity was observed; it was found to be constant during purification and between different preparations of SMCP-1. Treatment of SMCP-1 with a range of inhibitors decreased chymotrypsin-like and trypsin-like activities by similar extents, supporting the assertion that both activities are the property of a single enzyme. In terms of activity, and by N-terminal amino acid sequencing, SMCP-1 strongly resembles the similarly dual-specific bovine duodenal proteinase, duodenase. It is proposed that SMCP-1 and duodenase represent a new class of ruminant chymases with unusual dual specificities.

Amino Acid Sequence↗

PubMed1997

Mast cell specific proteases in rat brain: changes in rats with experimental allergic encephalomyelitis.

Mast cell populations were identified within brain parenchyma by their specific proteases, using antibodies for immunohistochemistry and ELISAs, and riboprobes were developed for in situ hybridisation. Connective tissue mast cells expressing rat mast cell protease I (RMCPI) mRNA and immunoreactivity were observed in thalamus and showed no degranulation at 3, 8 and 13 days after induction of experimental allergic encephalomyelitis (EAE). Mucosal-like mast cells were clearly demonstrated in control rats by measuring RMCPII and by visualising cells expressing RMCPII mRNA and immunoreactivity. At day 13, but not 3 and 8 post immunisation, the number of RMCPII-expressing cells markedly increased in the EAE-induced group, mainly within brainstem and spinal cord close to inflammed blood vessels. The markers of histaminergic neurons were marginally affected 13 days after immunisation and the increase of [3H] histamine synthesis elicited by the H3-receptor antagonist, thioperamide, was not modified in any region of the brain. It is concluded that the cerebral RMCPII-expressing mast cells could play a role during EAE.

Animals↗

PubMed1997

Functional relationships between sensory nerve fibers and mast cells of dura mater in normal and inflammatory conditions.

In this study, we have characterized the phenotype of mast cells in rat dura mater and their topological and functional relationships with C-fibers in normal and inflammatory conditions. Three mast cell populations with different size, morphology and localization were characterized by their content of specific neutral serine proteases. They showed immunoreactivity corresponding to rat mast cell protease I, rat mast cell protease II, or both proteases. Using confocal microscopy, all three mast cell types were observed in close apposition (distance less than 100 nm) to calcitonin gene-related peptide- and substance P-immunoreactive nerve fibers in both controls and rats infected with the nematode Nippostrongylus brasiliensis. After nematode infection or neonatal treatment with capsaicin, a large increase in the number of rat mast cell protease II-immunoreactive mast cells was found within dura mater segments (+1478% and +596%, respectively), without concomitant changes of rat mast cell protease I- or rat mast cell protease I/II-immunoreactive mast cells. Under both these conditions, the increase in mast cell number was accompanied by a significant increase in rat mast cell protease II level within tissue extracts (+281% after nematode infection and +36% after capsaicin treatment). The functional interaction of mast cells with sensory nerve fibers in the dura mater was assessed by evaluating [3H]histamine synthesis after administration of L-[3H]histidine, an index of mast cell activity. The H3 receptor agonist (R)-alpha-methylhistamine (15 mg/kg, i.p.) had no effect, but administration of the H3 receptor antagonist, thioperamide (10 mg/kg, i.p.), resulted in a significant increase of [3H]histamine synthesis (+62%). This effect was reduced in neonatal capsaicin-treated rats, but not completely suppressed (+35%), very likely because of partial denervation, as assessed by monitoring calcitonin gene-related peptide immunoreactivity. It is concluded that, in the dura mater, as in peripheral tissues, sensory nerve fibers and mast cells actively synthesizing and releasing histamine form a short inhibitory feedback loop involving prejunctional H3 receptors that could regulate the release of pro-inflammatory mediators, thus limiting the extent of inflammatory reactions.

Animals↗

PubMed1997

Constitutive expression of mouse mast cell protease-1 in normal BALB/c mice and its up-regulation during intestinal nematode infection.

Rodent intestinal mucosal mast cells (IMMC) store and secrete soluble granule serine proteases, the beta-chymases, which may promote epithelial permeability during intestinal hypersensitivity reactions. The beta-chymase mouse mast cell protease-1 (mMCP-1) is generally considered to be expressed late in the in vitro differentiation of mast cells. The purpose of this study was to determine the kinetics of mMCP-1 transcription and expression in vivo during nematode-induced IMMC hyperplasia. Concentrations of mMCP-1 in blood and jejunum of BALB/c mice were quantified by enzyme-linked immunosorbent assay before and at various stages after infection with the intestinal nematode Nippostronglyus brasilliensis. Mature mMCP-1 enzyme was detected in jejunal homogenate (194 ng/mg soluble protein) and in blood (8.3 ng/ml serum) from normal uninfected BALB/c mice. Maximal IMMC hyperplasia occurred 7-14 days post infection and was significantly correlated with increased levels of mMCP-1 in jejunum (r = 0.58, P < 0.001) and with raised concentrations of mMCP-1 in serum (r = 0.66, P < 0.001). Transcription of the mMCP-1 gene was detected by RNA blotting in normal, uninfected jejunum, but transcription was up-regulated after infection with maximal transcription occurring on days 7 and 14. In conclusion, mMCP-1 transcription, storage and secretion occur constitutively in normal BALB/c jejunum but this basal secretion is up-regulated during nematode infection, suggesting both a physiological and pathological function for this protease.

Animals↗

PubMed1997

Mast cell heterogeneity in the gastrointestinal tract: variable expression of mouse mast cell protease-1 (mMCP-1) in intraepithelial mucosal mast cells in nematode-infected and normal BALB/c mice.

Soluble granule chymases in rodent intestinal mucosal mast cells (IMMCs) may play an important role in altering epithelial permeability during immediate hypersensitivity reactions. Using a monoclonal antibody against the chymase mouse mast cell protease-1 (mMCP-1), we have shown that it is constitutively expressed in < or = 20% of esterase-positive (esterase+) IMMCs but not in esterase+ gastric mucosal mast cells (GMMCs) in normal BALB/c mice. Intestinal infection with mouse- or rat-adapted strains of Nippostrongylus brasiliensis resulted in IMMC hyperplasia with 100% of esterase+ IMMCs expressing mMCP-1. In contrast, there was a variable response in terms of numbers of GMMCs and of the proportion expressing mMCP-1. Esterase+ mast cells in the gastric submucosa, muscularis, ear pinna, lung parenchyma, major airway submucosa, and peritoneal cavity did not express mMCP-1. The few airway esterase+ mast cells expressing mMCP-1 were, like the great majority of IMMCs and GMMCs, located intraepithelially. In conclusion, mMCP-1 is predominantly expressed by intraepithelial mucosal mast cells but not in all sites; the immunological stimulus associated with intestinal nematodiasis substantially up-regulates mMCP-1 expression by mast cells in the jejunum but not in the stomach; IMMCs and GMMCs in BALB/c mice are phenotypically and possibly functionally distinct.

Animals↗

PubMed1996

Trypsin stimulates proteinase-activated receptor-2-dependent and -independent activation of mitogen-activated protein kinases.

We have examined protease-mediated activation of the mitogen-activated protein (MAP) kinase cascade in rat aortic smooth-muscle cells and bovine pulmonary arterial fibroblasts. Exposure of smooth-muscle cells to trypsin evoked rapid and transient activation of c-Raf-1, MAP kinase kinase 1 and 2 and MAP kinase that was sensitive to inhibition by soybean trypsin inhibitor. The actions of trypsin were closely mimicked by the proteinase-activated receptor 2 (PAR-2)-activating peptide sequence SLIGRL but not LSIGRL. Peak MAP kinase activation in response to both trypsin and SLIGRL was also dependent on concentration, with EC50 values of 12.1 +/- 3.4 nM and 62.5 +/- 4.5 microM respectively. Under conditions where MAP kinase activation by SLIGRL was completely desensitized by prior exposure of smooth-muscle cells to the peptide, trypsin-stimulated MAP kinase activity was markedly attenuated (78.9 +/- 15.1% desensitization), whereas the response to thrombin was only marginally affected (16.6 +/- 12.1% desensitization). Trypsin and SLIGRL also weakly stimulated the activation of the MAP kinase homologue p38 in smooth-muscle cells without any detectable activation of c-Jun N-terminal kinase. Strong activation of the MAP kinase cascade and modest activation of p38 by trypsin were also observed in fibroblasts, although in this cell type these effects were not mimicked by SLIGRL nor by the thrombin receptor-activating peptide SFLLRNPNDKYEPF. Reverse transcriptase-PCR analysis confirmed the presence of PAR-2 mRNA in smooth-muscle cells but not fibroblasts. Our results suggest that in vascular smooth-muscle cells, trypsin stimulates the activation of the MAP kinase cascade relatively selectively, in a manner consistent with an interaction with the recently described PAR-2. Activation of MAP kinase by trypsin in vascular fibroblasts, however, seems to be independent of PAR-2 and occurs by an undefined mechanism possibly involving novel receptor species.

Animals↗

PubMed1996

Rat cerebral mast cells undergo phenotypic changes during development.

The evolution of rat cerebral mast cell phenotype during development was studied using antibodies against the granule chymases, rat mast cell protease I (RMCP-I) and rat mast cell protease II (RMCP-II) and their gene transcripts, as markers for serosal and mucosal mast cells, respectively. In situ hybridization using specific oligoprobes for RMCP-II permitted visualization of RMCP-II mRNA-containing cells as early as day 15 of embryonic development (E15). From E19 to day 4 postpartum (D4) their number increased whilst they migrated from the pia mater to the choroid fissure; at D8 cells expressing RMCP-II gene transcripts were no longer observed. The 3'-end untranslated nucleotide sequence of the RMCP-I cDNA was established in order to design selective cDNA probes for Northern blot analysis of both enzymes. Northern blot analysis revealed a strong expression of RMCP-I and RMCP-II mRNAs at D2. At D4, RMCP-I mRNA expression was still high, whereas that of RMCP-II was decreased. In adult brain, mRNA expression for both proteases was low, but detectable. Quantification of both proteases by ELISA showed that, from E19 to D4, levels of RMCP-II were maximal at E19 and remained constant until D4, whereas RMCP-I increased as a function of age. Thereafter, levels of both proteases decreased progressively, but were still present in the adult brain, with RMCP-II being uniformly distributed and RMCP-I concentrated in the thalamus. Immunohistochemical staining showed RMCP-II-immunoreactive cells within the pia mater at E19; on D2 and D4, cells with both RMCP-I and RMCP-II immunoreactivities were found within the choroid fissure and from D8, only RMCP-I-immunoreactive mast cells were observed. In the thalamus of adult rats, the latter had a perivascular localization. This study shows that in the adult, both types of mast cells are present, although in small numbers, except for RMCP-I-immunoreactive mast cells which are abundant in the thalamus. The changes in the number and phenotype of cerebral mast cells may result from the influence of a number of growth factors during development.

Amino Acid Sequence↗

PubMed1996

Characterization of whole-cell currents in mucosal and connective tissue rat mast cells using amphotericin-B-perforated patches and temperature control.

Rat mucosal type mast cells are thought to possess only a K+-selective inwardly rectifying (IRK) current in the resting state. We used rat-bone-marrow-derived mast cells (BMMCs) as a model of mucosal mast cells and recorded whole-cell membrane currents from cells perforated with amphotericin B. Under these conditions, both inwardly rectifying (IR) and outwardly rectifying (OR) currents were observed. The reversal potential and conductance of the IR current depended on the extracellular K+ concentration, indicating that the channel was K+ selective. The OR current was not affected by changes in extracellular K+ concentration, but lowering extracellular Cl- concentration reduced the conductance and shifted the reversal potential in a positive direction. The OR current was not affected by K+ channel blockers, but was reversibly blocked by the chloride channel blocker 4,4'-diisothiocyanato-2,2'-stilbenedisulphonate (DIDS), again indicating a Cl- conductance. The IRK current was also detected in the majority of cells using the conventional whole-cell recording configuration at room temperature. In contrast, the ORCl current was only observed in 7% of recordings made at room temperature with the conventional whole-cell voltage-clamp mode, but was detected in 66% of cells if the bath temperature was increased and the integrity of the cell's cytoplasm was preserved by using the perforated-patch technique. Under similar conditions, the ORCl current was also present in rat peritoneal mast cells, a connective tissue phenotype previously thought to have no whole-cell currents in the resting state. The role of this current and factors affecting its activation are discussed.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1996

Canine leucocyte histamine release: response to antigen and to anti-IgE.

Histamine release from canine leucocyte-enriched peripheral blood preparations was measured in atopic, non-atopic and artificially sensitised dogs after immunological challenge with D. farinae antigen and anti-IgE. Total cell histamine and spontaneous histamine release was also measured. The total cell histamine content of equal leucocyte preparations was not statistically significant between the atopic and non-atopic groups. At all dilutions of antigen a higher amount of histamine was released from the leucocytes of atopic dogs than was seen in the non-atopic group. No histamine release in response to D. farinae was seen in the sensitised dogs although a statistically significant increase in serum D. farinae-specific IgE could be demonstrated after sensitisation (P < 0.03). Histamine release in response to anti-IgE was significantly greater in the atopic dogs than the non-atopic dogs (P < 0.004) and the sensitised dogs (P < 0.003). There was no statistically significant difference in total serum IgE between the groups. The authors conclude that the leucocytes of atopic dogs have a greater tendency to release histamine than those of normal and artificially sensitised dogs and that this is independent of the concentration of total serum IgE or antigen-specific IgE. They suggest that there may be immunoregulatory abnormalities in atopic dogs intrinsic to the atopic state as is described in man.

Allergens↗

PubMed1996

Early pulmonary cell response during experimental maedi-visna virus infection.

A model of experimental infection with EV1, a British isolate of maedi-visna virus (MVV), has been developed. Twelve male Texel sheep were allocated to three groups and inoculated by the respiratory route with different inocula. Six of the animals received 10(7.2) tissue culture infective dose (TCID50) of MVV EV1 strain. Two sheep were inoculated with the same dose of heat inactivated MVV EV1 strain. An additional group of four sheep was sham-inoculated with identically prepared virus-free culture media. Experimental infection was followed for 16 weeks. Prior to inoculation, routine haematology, bronchoalveolar lavage (BAL) and flow cytometric analysis of bronchoalveolar lavage fluid (BALF) lymphocytes were performed in all animals to provide baseline parameters. Flow cytometric analysis of BALF lymphocytes and differential BALF cell counts were performed. Precipitating antibodies to MVV developed in all MVV-inoculated animals during the first 4 weeks post-inoculation, while the rest remained seronegative to MVV. MVV-infected animals had significantly decreased (P < 0.05) percentages of macrophages and significantly increased (P < 0.05) percentages of lymphocytes in BALF 4 weeks post-inoculation. Phenotypic changes in BALF T lymphocytes from MVV-inoculated animals, compared with the other two groups, showed significantly decreased (P < 0.05) percentages of CD4+ and gamma delta + T lymphocytes, significantly increased (P < 0.05) percentages of CD8+ lymphocytes and significant inversion (P < 0.05) of the CD4+/CD8+ ratio at different sampling times, but between 2 and 12 weeks post-inoculation. These findings indicate that during experimental MVV-infection an early, short-term cellular reaction occurs in the lung, that is characterised by T lymphocyte phenotypic changes that are very similar, if not identical, to those observed in natural MVV infection.

Animals↗

PubMed1996

Mucosal mast cells and the allergic response against nematode parasites.

IgE-mediated Type-I allergic reactions at nematode-infected mucosal surfaces are considered to have a direct protective function. The contribution of mucosal mast cells (MMC) to these mucosal allergic responses is reviewed. In addition to the T helper 2 cell-mediated regulation of MMC hyperplasia during nematode infection the kit ligand, stem cell factor (SCF), plays a key role in the early development of the MMC response. Studies in the mouse suggest that MMC protect against certain nematodes which enter the mucosa but not against lumen dwelling nematodes. The protective roles of MMC in other species, including sheep, are less certain and there is some evidence that MMC might enhance parasite fecundity. The measurement of MMC-specific granule chymases released systemically, and into the gut lumen, permits precise monitoring of mast cell activation and suggests that the secreted chymases may target epithelial junctional complex proteins, thereby causing increased mucosal permeability. The abundant intraepithelial MMC found in parasitised mucosa may, therefore, serve as epithelial gatekeepers permitting the translocation of plasma proteins onto the mucosal surface.

Animals↗

PubMed1996

Stem cell factor enhances immunoglobulin E-dependent mediator release from cultured rat bone marrow-derived mast cells: activation of previously unresponsive cells demonstrated by a novel ELISPOT assay.

Mucosal mast cells (MMC) are important effector cells in the immune response against gastrointestinal nematodes. We used cultured rat bone marrow-derived mast cells (BMMC) as an in vitro model of MMC to study the effects of the multifunctional cytokine stem cell factor (SCF) on immunoglobulin E (IgE)-dependent secretion of granule mediators. SCF (< or = 1000 ng/ml) was not a direct secretagogue for these cells, but it significantly enhanced IgE-mediated secretion of the granule constituents rat mast cell protease-II (RMCP-II) and beta-hexosaminidase from mature BMMC in a dose-dependent manner (> 10 ng/ml). Maximum up-regulation of secretion occurred after cells were pretreated with SCF (50 ng/ml) for 5 minutes before challenge with anti-IgE, but the effect then declined and was absent in cells incubated with the cytokine for 3 to 24 h. In a novel ELISPOT assay developed to identify individual BMMC secreting RMCP-II, the proportion of mature BMMC responding to anti-IgE was significantly increased by treatment with SCF. To investigate this effect further, the percentage release of RMCP-II and beta-hexosaminidase from populations of mature BMMC was directly compared to the proportion of individual cells releasing RMCP-II as detected by ELISPOT. The release of both mediators was enhanced by SCF, and the increased percentage release reflected both an increased proportion of secreting cells, and enhanced mediator release from individual cells. These results suggest that SCF can enhance IgE-dependent mediator release from BMMC not only by augmenting the secretory response from individual cells, but also by activating previously unresponsive cells.

Animals↗

PubMed1996

Rat bone marrow-derived mast cells co-cultured with 3T3 fibroblasts in the absence of T-cell derived cytokines require stem cell factor for their survival and maintain their mucosal mast cell-like phenotype.

When cultured without fibroblasts, rat bone marrow-derived mast cells (BMMC) contain abundant rat mast cell proteinase type II (RMCP-II), and exhibit survival and proliferation when maintained in mesenteric lymph node conditioned medium (CM). When BMMC were co-cultured with 3T3 fibroblasts in the absence of CM, BMMC numbers increased for 7 days and the BMMC survived for up to 23 days. There was a gradual loss of stored RMCP-II in BMMC that were co-cultured with 3T3 cells, but the fibroblast microenvironment did not induce a detectable increase in the low levels of the connective tissue mast cell (CTMC)-associated proteinase, RMCP-I, in the BMMC. Nor did 3T3 cell co-culture induce significant heparin synthesis in BMMC as judged by the cells' reactivity with the fluorescent heparin-binding dye, berberine sulphate. These results suggest that rat BMMC, unlike murine BMMC, do not have the potential to develop multiple CTMC-like characteristics upon co-culture with 3T3 cells. However, when BMMC and fibroblast co-cultures were treated with an antibody to recombinant rat stem cell factor (rrSCF), mast cell survival was completely abrogated. This result suggests that endogenous, fibroblast-derived SCF is essential for the maintenance of rat BMMC viability in the absence of CM. On the other hand, prior treatment of the fibroblasts with the anti-rrSCF antibody did not affect the adherence of BMMC to the monolayer, implying that (an) other molecule(s) is(are) involved in the attachment process. The demonstration that rat BMMC survival on fibroblasts in vitro is dependent upon SCF may indicate an important mechanism by which tissue mucosal cells can be maintained in vivo in the absence of T-cell derived factors.

Animals↗

PubMed1995

Release of the mucosal mast cell granule chymase, rat mast cell protease-II, during anaphylaxis is associated with the rapid development of paracellular permeability to macromolecules in rat jejunum.

The soluble granule chymase, rat mast cell protease-II (RMCP-II), is abundantly expressed in intestinal mucosal mast cells (MMC) but its function is not known. One hypothesis is that RMCP-II degrades the epithelial basement membrane and promotes the loss of enterocytes typically associated with type I hypersensitivity reactions in the rat. To test this hypothesis more directly, ex vivo perfusion of the cranial mesenteric artery and jejunal lumen was used to monitor the anaphylactic release of RMCP-II and its effects on mucosal permeability and epithelial integrity. Within 2 min of intravascular challenge with soluble adult Nippostrongylus brasiliensis worm antigen there was a 1,000-fold (P < 0.02) increase in the concentration of RMCP-II in the vascular perfusate from the jejunum of Nippostrongylus-sensitized rats but not the controls. Similarly, translocation of RMCP-II into the gut lumen increased 10-fold (P < 0.02) after 2 min only in worm antigen-challenged immune rats. Using an identical protocol, but incorporating Evans blue-labeled human serum albumin (EB-HSA) in the vascular perfusate, the timing of the release of RMCP-II into the two compartments was very similar to the first experiment and furthermore the translocation of EB-HSA increased 18-fold (P < 0.05) after 4 min in sensitized rats challenged with worm antigen. To examine the effects of RMCP-II more directly 1 mg of the highly purified chymase was introduced into the cranial mesenteric artery in ex vivo perfused normal rats. A significant (P < 0.05) 70-fold increase in concentration of RMCP-II in jejunal perfusate occurred after 6 min. In a repeat dose-response experiment, infusion of 0.375, 0.75, or 1.5 mg of RMCP-II, together with EB-HSA, established that the cumulative amounts of RMCP-II and EB-HSA translocated from the vasculature to the gut lumen in each perfusion (during the 10-min period of RMCP-II infusion) were significantly correlated. Analysis of intestinal perfusates by SDS-PAGE and by Western blotting using monoclonal anti-RMCP-II antibody confirmed that there was a concomitant translocation of both the protease and EB-HSA into the gut lumen. Histological evaluation of the mucosa failed to reveal any significant morphological change in any of the experiments. The rapid development of macromolecular leak, its association with the translocation of RMCP-II, and the absence of gross epithelial lesions, suggest for the first time that a mast cell granule chymase increases epithelial permeability via a paracellular route and implies that the substrate may be a protein, or proteins, in the epithelial junctional complex.

Anaphylaxis↗

PubMed1995

Stem cell factor contributes to intestinal mucosal mast cell hyperplasia in rats infected with Nippostrongylus brasiliensis or Trichinella spiralis, but anti-stem cell factor treatment decreases parasite egg production during N brasiliensis infection.

We assessed the effects of the c-kit ligand, stem cell factor (SCF), in the jejunal mucosal mast cell hyperplasia that occurs during infection with the intestinal nematodes, Nippostrongylus brasiliensis or Trichinella spiralis in rats. Compared with vehicle-treated rats, rats treated with SCF (25 micrograms/kg/d, intravenous [i.v.] for 14 days) during N brasiliensis infection exhibited significantly higher levels of the rat mucosal mast cell (MMC)-associated protease, rat mast cell protease II (RMCP II) in the jejunum and serum on day 8 of infection, but not on days 10 or 15 of infection. By contrast, in comparison to rats treated with normal sheep IgG, rats treated with a polyclonal sheep antirat SCF antibody exhibited markedly decreased numbers of jejunal MMCs, levels of jejunal RMCP II, and serum concentrations of RMCP II during infection with either nematode, particularly at the earlier intervals of infection (< or = day 10). Taken together, these findings indicate that SCF importantly contributes to MMC hyperplasia and/or survival during N brasiliensis or T spiralis infection in rats, but that levels of endogenous SCF are adequate to sustain near maximal MMC hyperplasia during infection with these nematodes. Notably, treatment of rats with SCF somewhat increased, and treatment with anti-SCF significantly decreased, parasite egg production during N brasiliensis infection. This finding raises the interesting possibility that certain activities of intestinal MMCs may contribute to parasite fecundity during infection with this nematode.

Analysis of Variance↗

PubMed1995

Development of a three-scale MMPI: the MMPI-TRI.

A 60-item short form of the MMPI with very high content validity and items that appear on both the MMPI and MMPI-2 was developed and named the MMPI-TRI. It contains three 20-item scales--the Subjective Distress, Acting-Out, and Psychosis scales. These three scales have excellent internal consistency and sufficient independence from each other. An anxiety and depression group of patients, prison inmate group, and a schizophrenic and other psychotic group had the highest mean scores on Subjective Distress, Acting-Out, and Psychosis, respectively. Correlations with the 13 regular scales of the MMPI and MMPI-2, their content and supplementary scales, and four other psychometric instruments provided very strong evidence for validity. Norms are provided.

Acting Out↗

PubMed1995

What's in a name? The MMPI-2 PTSD scales.

The MMPI-2 post-traumatic stress disorder scales (PK and PS) were examined with a sample of 96 outpatient anxiety disorder and 97 outpatient traffic accident subjects. PK and PS correlated .96 and showed highly similar correlations with MMPI-2 validity, clinical, content and supplementary scales for both groups, which indicated that these scales are indices of MMPI first-factor variance. This was supported by separate principal components analyses for each group, in which PK and PS contributed the most variance to the first component. Although the groups showed different MMPI-2 mean profiles, neither PK nor PS contributed to discriminant function classification of group members. It is suggested that PK and PS are indices of general emotional distress and maladjustment; implications for their use in diagnosing post-traumatic stress disorder were discussed.

Accidents, Traffic↗

PubMed1995

A study on lymphocyte activation in maedi-visna virus induced pneumonia.

The stage of activation of bronchoalveolar lavage fluid (BALF) lymphocytes and peripheral blood lymphocytes (PBL) from maedi-visna virus (MVV) infected (n = 7) and control (n = 7) sheep was investigated by assessing four parameters of lymphocyte activation; lymphocyte size and complexity, loss of CD5+ T cells, expression of cell surface interleukin-2 receptor (IL-2R) and expression of DR and DQ MHC Class II molecules. BALF lymphocytes from MVV-infected animals had a significant loss of CD5+ lymphocytes (P < 0.05) and upregulation of DR and DQ MHC Class II molecules compared with controls, consistent with BALF lymphocyte activation. No changes in cell size and complexity or expression of IL-2R were observed. No evidence of PBL activation was detected. These findings suggest an impaired BALF lymphocyte activation during MVV infection.

Animals↗