Biomedical subjects
Publications and source records attributed to M Bennett.
Cavernous lymphangioma is a benign congenital lesion that usually appears in childhood. It rarely presents in the adult but may be diagnosed at this late stage due to the slow growing nature of the tumour. It is rarely found in the salivary glands and when it does occur, the gland is usually incorporated by lymphangioma of surrounding tissue. We present and discuss the case of a cavernous lymphangioma in the parotid gland of an adult male.
The felid herpesvirus 1 (FHV-1) genes encoding the two ribonucleotide reductase (RR) subunits (RR1, large subunit and RR2, small subunit) were cloned and their nucleotide (nt) sequence determined. The RR1 open reading frame (ORF) is 2358 nts long and is predicted to encode a protein of 786 amino acids (aa). In common with herpesviruses in the Varicellovirus genus of the alphaherpesvirus subfamily, FHV-1 RR1 lacks the N-terminal serine threonine protein kinase region present in herpes simplex virus (HSV)-1 and -2. FHV-1 RR1 has a predicted aa identity of 47-64% with other alphaherpesvirus RR1 peptides, falling to 26-29% for gammaherpesviruses. The RR2 ORF is 996 nts long, predicted to encode a protein of 332 aa and has aa identities of 64-70% with alphaherpesviruses and 38-39% with gammaherpesviruses. Molecular phylogenetic analysis groups FHV-1 with equid herpesviruses 1 and 4 (EHV 1 and 4), pseudorabies virus (PRV) and bovid herpesvirus 1 (BHV 1) within the genus Varicellovirus.
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Protein production encoded by the avirulence gene avrPphB from Pseudomonas syringae pv. phaseolicola was examined. Incorporation of [35S]-labeled methionine into the AvrPphB protein indicated processing of the full-length peptide in Escherichia coli to give a major 28-kDa product. The 28-kDa native peptide was isolated from E. coli following over-expression of avrPphB and found not to elicit the hypersensitive response (HR) after infiltration into bean leaves. Antiserum raised to the 28-kDa peptide allowed expression of avrPphB and processing of AvrPphB protein to be examined in P. syringae pv. phaseolicola; immunoreactive peptides of both 35 and 28-kDa were detected in races 3 and 4 (which contain avrPphB) only after induction in minimal medium + 10 mM sucrose. Antiserum raised to a synthetic peptide, derived from the sequence of the 62 amino acids found to be cleaved from the full-length AvrPphB protein, revealed the accumulation of peptides corresponding to the smaller cleavage products, in both E. coli and P. syringae pv. phaseolicola. Biochemical localization experiments showed that all AvrPphB peptides were cytoplasmic in P. syringae pv. phaseolicola. No AvrPphB peptides were produced in a hrpL mutant unless expression of the gene was directed by a strong vector promoter; induction kinetics similar to wild type were observed in a hrpY- strain, although it also failed to cause a confluent HR. Growth of P. syringae pv. phaseolicola under inducing conditions removed the requirement for rifampicin-sensitive mRNA synthesis by bacteria to allow HR development (the induction time) in bean and lettuce leaves. Constitutive expression of hrpL reduced but did not remove the induction time. Expression of the hrp gene cluster of P. syringae pv. phaseolicola from plasmid pPPY430 in E. coli enabled phenotypic expression of avrPphE (also carried by pPPY430) and avrPphB (if over-expressed from pPPY3031). Despite constitutive expression of the hrp and avr genes in E. coli, a protein synthesis dependent induction time was still required for development of the HR in bean genotypes with matching resistance genes. The significance of processing for the function of AvrPphB peptides and the delivery of elicitors of the HR are discussed.
Natural killer (NK) cells of inbred mice reject allogeneic bone-marrow cells, and NK cells of F1 hybrid mice can reject parental bone-marrow cells (hybrid resistance). In some cases these patterns of rejection can be mimicked in vitro by utilizing IL-2 cultured NK effector cells and allogeneic or parental T-lymphoblasts as target cells. Lysis of allogeneic and parental targets in vitro can be explained on the basis of the missing self hypothesis. Subsets of NK cells that bear non-overlapping MHC class I inhibitory receptors belonging to the Ly49 family lyse allogeneic targets because they do not express self class I molecules of the NK cell donor. Parental strain targets are lysed because they do not express all of the self class I antigens of the F1 hybrid, and hence fail to deliver inhibitory signals to all subsets of F1 NK cells. The expression of Ly49 receptors on NK cells is regulated by host MHC to ensure maximal sensitivity to alterations in self class I molecules and to prevent autoreactivity. In many instances, however, the rejection of allogeneic bone marrow cells in vivo cannot be readily explained by the missing self hypothesis. In these instances, it appears that rejection is initiated by class I MHC receptors on NK cells that recognize allogeneic class I molecules as non-self, and activate rather than inhibit NK cell function.
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T cells present in bone marrow cell (BMC) grafts promote engraftment in histoincompatible hosts, but they or other T cells may also initiate lethal graft-vs.-host disease (GVHD). The purpose of this study was to determine whether T cells from donors tolerant of host alloantigens were able to prevent natural killer (NK) cell-mediated rejection of BMC grafts without causing GVHD. Previous studies have shown that H2d C.B-17 SCID BMC grafts were rejected by (BALB/c x B6)F1 (CB6F1,H2d/b) host NK cells, and that this rejection was reversed by adding H2d T cells to the donor inoculum. T cells tolerant of H2d/b alloantigens were produced by irradiating (3 Gy) BALB/c newborn mice, and infusing CB6F1 BMCs. Tolerance was assessed by donor (H2b+) cell chimerism, acceptance of CB6F1 skin grafts, the inability of adoptively transferred lymphocytes to initiate GVHD in irradiated CB6F1 mice, and the inability of spleen or thymus cells to generate cytolytic T lymphocytes against H2b target cells in vitro. Whole or H2-Kb-depleted BMCs isolated from tolerant donors were able to proliferate in both BALB/c and H2b/d (C57BL/6 x DBA/2)F1 hosts as determined by incorporation of a radiolabelled DNA precursor in the spleen. Furthermore, thymocytes from tolerant donors were able to prevent rejection of H2d SCID BMCs. Because the percentage of donor F1 cells was so high in these chimeras, we generated BALB/c to CB6F1 SCID BMC chimeras; the percentage of BALB/c cells was approximately 100%, the BMCs grew well in irradiated CB6F1 hosts, and their lymph node cells failed to cause a graft-vs.-host (GVH) reaction in CB6F1 hosts. Thus, GVHD may be prevented without inhibiting the ability of donor T cells to promote engraftment. Perhaps separate T cells, or separate functions of a common T cell subset, induce GVHD and enhance engraftment of stem cells.
NK cells require an intact bone marrow microenvironment to acquire lytic function. In mice rendered osteopetrotic by 17beta-estradiol treatment, NK1.1 positive cells are arrested in a nonlytic state. Culture with as little as 2 ng/ml of murine IL-15 (mIL-15), a cytokine produced by macrophages and stromal cells, causes these immature NK1.1+ cells to acquire lytic activity. By contrast, approximately 10- to 50-fold greater amount of mIL-2 was required to induce similar level of cytotoxicity. After culture with mIL-15, the relatively low expression of B220, CD11b, and Ly-49 molecules on immature NK1.1+ cells was increased to levels comparable to those of mature splenic NK1.1+ cells. mIL-15 also caused a greater expansion of NK1.1+CD3- cells as compared with NK1.1+CD3+ cells. We conclude that IL-15 is a specific maturation factor for NK cells and that it can mimic the marrow microenvironment in vitro.
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Several fox vaccination campaigns against rabies have been undertaken in Belgium by using a vaccinia-rabies recombinant virus distributed in baits in the field. However, foxes and other wild animals that may ingest the baits could be infected at the same time by another orthopoxvirus, such as cowpox virus, which circulates in wildlife. Recombination between the two viruses could therefore occur. A serological survey for antibodies to orthopoxvirus, and particularly to cowpox virus, was undertaken in foxes and in several other wild species. Antibodies were detected only in two rodent species, in 16 of 25 bank voles (64 per cent) and in two of 29 woodmice (7 per cent). The risk of virus recombination in wildlife can therefore be considered to be extremely low.
Natural killer cells are bone marrow-derived lymphocytes capable of lysing a variety of target cells without prior exposure. While the biological activities and function of mature NK cells have been extensively investigated, the differentiation of NK cells from primitive hematopoietic stem cells is poorly understood. Recently, we have reported on the identification of a highly enriched bone marrow population capable of repopulating recipient mice with mature NK cells. In this review, we will summarize our findings and those of others in an attempt to clarify the current status of murine natural killer cell differentiation.
Six monoclonal antibodies raised against feline calicivirus (FCV) strain F9 were used in an enzyme-linked immuno-flow-assay (ELIFA) to analyse 55 isolates of FCV. Forty seven field isolates were obtained from cats with acute oral/respiratory disease, chronic oral lesions, and from cats showing vaccine reactions, i.e. clinical signs of FCV infection shortly after vaccination. Eight reference strains including F9 and three vaccine strains based on F9 were also examined. All of the strains of F9, derived from various sources, reacted with all six of the monoclonal antibodies, whereas some of the field isolates did not react with any. In general, the field isolates showed a spectrum of reactivities and selected isolates could be distinguished. However, there were no clear cut differences between the clinical groups. Overall, the oral/respiratory group showed less reactivity with the monoclonals, suggesting they were less related to F9. Although the other groups appeared to be more closely related to F9, none of the isolates tested reacted with all six monoclonal antibodies.
Compromise of the spinal canal and its neural elements is a well-recognized pathological entity affecting the lumbar or cervical spine. Thoracic stenosis in the absence of a generalized rheumatological, orthopedic, or metabolic disorder is rare. The authors report a case of progressive thoracic myelopathy leading to paraplegia following severe thoracic spinal stenosis secondary to post-traumatic hypertrophy of thoracic laminae and ossification of the ligamentum flavum and posterior longitudinal ligament.
We address the mechanism of hybrid resistance (HR) in vitro using NK effector cells and target lymphoblasts from H-2b, H-2d, and H-2b/d mice. The 5E6 (Ly49C)+ subset of F1 NK cells lyse BALB/c (H-2d) but not B6 (H-2b) targets unless either anti-5E6 or anti-H-2Kb MAbs are present. H-2Dd transgenic B6 (D8) targets are not susceptible to F1 Ly49A+ effectors. Furthermore, 5E6+ Ly49A+ F1 effectors lyse B6 and BALB/c targets only in the presence of anti-5E6 and anti-Ly49A MAbs, respectively. Thus, recognition of H-2Kb by 5E6 and H-2Dd by Ly49A transduce independent inhibitory signals. Moreover, anti-5E6 MAbs enable 5E6+ BALB/c NK cells to lyse (BALB/c x B6)F1 targets. These data support the "missing self" and not the "hemopoietic histocompatibility antigen" hypothesis for HR. In addition, 5E6+ NK cells from BALB/c and BALB.B, but not B6 or (BALB/c x B6)F1, mice receive negative signals from both H-2d and Kb class I antigens. Thus, allelic differences in 5E6 (C57BL versus BALB) may regulate recognition events by NK cells.
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The effects of two types of training on 4-year-old children's understanding of the distinction between experienced positive affect and neutral or negative display were examined. One type of training provided first-hand experience of possible discrepancies between facial expression and actual affect. The other training focused on the sorts of motives that might prompt the concealment of positive affect. Compared with a control group, both experimental groups showed modest gains.