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J J Taylor

Publications and source records attributed to J J Taylor.

At least 19 recordsLinked to original sources
PubMed2006

Pivotal advance: vasoactive intestinal peptide inhibits up-regulation of human monocyte TLR2 and TLR4 by LPS and differentiation of monocytes to macrophages.

Vasoactive intestinal peptide (VIP) is an immunoregulatory peptide, which inhibits LPS-induced cytokine secretion in myeloid cells and has beneficial effects in animal models of inflammatory diseases. We show for the first time that VIP decreases LPS-induced up-regulation of TLR2 and TLR4 by human monocytic THP1 cells and peripheral blood monocytes (PBM). VIP inhibited up-regulation of TLR4 expression in THP1 cells in response to LPS from Escherichia coli or the periodontal pathogen Porphyromonas gingivalis within 6 h poststimulation but had less of an effect on TLR2. After 24 h, P. gingivalis LPS-stimulated monocytic THP1 cells to differentiate into macrophages, which predominantly expressed TLR2, and E. coli LPS-stimulated THP1 differentiation to predominantly TLR4-expressing macrophages. VIP decreased monocyte differentiation to macrophages induced by LPS from either species and also reduced overall TLR2 and TLR4 expression in these cells. VIP had a similar effect on human PBM. The transcription factor PU.1 regulates TLR expression and has a central role in myeloid cell differentiation. VIP inhibited the nuclear translocation of PU.1 in LPS-stimulated THP-1 monocytes. VIP also inhibited the expression of the M-CSF receptor, which is regulated by PU.1. In summary, VIP inhibited LPS-induced differentiation of monocytes with a concomitant reduction in TLR2 and TLR4 expression. Although there was differential induction of TLR expression by LPS from P. gingivalis and E. coli, VIP inhibited the action of both of these LPS types on monocytes. The mechanism of action of VIP on monocyte differentiation may be via inhibition of the transcription factor PU.1.

Cell Differentiation↗
PubMed2006

The effect of cyclosporin on cell division and apoptosis in human oral keratinocytes.

BACKGROUND AND OBJECTIVE: Gingival overgrowth (GO) is a side-effect of cyclosporin A (CsA) therapy and is characterised by enlargement of the gingiva with epithelial thickening and overproduction of extracellular matrix components. The pathogenesis of the epithelial thickening in GO remains obscure. The objective of the present study was to investigate the effects of CsA on the growth of oral epithelial cells in vitro and to test the hypothesis that CsA influences apoptosis in these cells. MATERIAL AND METHODS: Cyclosporin was cocultured with an immortalized normal human oral keratinocyte cell line (HOK-16B), an epitheloid cervical carcinoma cell line (HeLa) and primary oral keratinocytes. Cell division was quantified using a CyQUANT kit. Apoptosis was induced using tumour necrosis factor-alpha (TNF-alpha) and assayed by analysis of caspase-3 activity. Expression of the anti-apoptotic protein, Bcl-2, was measured by western blotting. RESULTS: CsA exhibited a dose- and time-dependent inhibition of cell division in all three keratinocyte cell cultures. Significantly, HOK-16B cells treated with high doses of CsA (10 alphag/ml) did not recover their proliferative capacity 3 d after withdrawal of CsA, indicating that CsA-induced inhibition of growth is not temporary. Concentrations of CsA that inhibited cell division (1 microg/ml) did not have any effect on constitutive or TNF-alpha -induced apoptosis or Bcl-2 expression in HOK-16B cells. CONCLUSION: CsA inhibits oral epithelial cell division and this effect is not associated with changes in apoptosis in these cells. The action of CsA on oral epithelial cells may be associated with a long-lasting stress signal, which might account for some of the pathological effects of this drug.

Apoptosis↗
PubMed2005

A human oral keratinocyte cell line responds to human heat shock protein 60 through activation of ERK1/2 MAP kinases and up- regulation of IL-1beta.

Heat shock proteins (HSP) are released by cells in response to stress signals. It is hypothesized that pathogenic bacteria stimulate the cells in the periodontium to up-regulate the expression of HSP60, which would stimulate macrophages, and possibly other cells, to produce proinflammatory cytokines. We sought to determine whether oral keratinocytes responded to recombinant human HSP60 and to identify the signalling pathways involved. In addition, whether oral keratinocytes are a source of endogenous HSP60 was also investigated. RT-PCR revealed that rhHSP60 induced expression of the IL-1beta gene in the Human Oral Keratinocyte (HOK-16B) cell line and it was highest at the lowest concentration used (0.1 microg/ml). These responses were mediated via activation of p44/42 MAP-kinases and to a lesser extend the MAP-kinase SAP/JNK. Similar data was obtained from analysis of intracellular signalling pathways in HOK-16B cells by rhHSP70 and LPS (from both E. coli and the oral pathogen Porphyromonas gingivalis). However, there was little activation of p38 by rhHSP60. Blocking of the p44/42 pathway decreased HSP60-induced IL-1beta gene expression and protein secretion. In addition, we discovered that self-HSP60 proteins were constitutively secreted by HOK-16B cells. Secretion of self-HSP60 was up-regulated in cells treated with LPS from P. gingivalis, but down-regulated with LPS from E. coli. To summarize, oral keratinocytes respond to exogenous HSP60 by triggering expression of the inflammatory cytokine IL-1beta through activation of p44/42 MAP kinase. Oral keratinocytes are also a source for self-HSP60 and the secretion of this protein may be differentially modified by LPS from different bacterial species. These results highlight the importance of oral keratinocytes and HSPs in the development of an immune response against bacterial infection.

Blotting, Western↗
PubMed2005

VIP Inhibits Porphyromonas gingivalis LPS-induced immune responses in human monocytes.

Lipopolysaccharide (LPS) from the Gram-negative pathogen Porphyromonas gingivalis (Pg) stimulates cytokine secretion in immune cells, and thereby initiates the inflammation associated with periodontitis. Modulation of pro-inflammatory cytokine activity is a plausible therapeutic target in periodontal disease. Vasoactive intestinal peptide (VIP) has a role in immunoregulation, and has been identified as a molecule with therapeutically beneficial immunosuppressive effects in inflammatory and autoimmune conditions. We aimed to investigate the effect of VIP on immune responses induced by Pg LPS in vitro. VIP (10(-8) M) significantly (P < 0.05) inhibits TNF-alpha production by human monocytic THP1 cells stimulated with Pg LPS. In parallel, we showed that VIP inhibits nuclear translocation of NFkappaB and c-Jun in a time-dependent manner, but does not decrease the expression of CD14 receptors. This is the first report to show the potential of VIP as an immunomodulator of Pg-stimulated inflammatory pathways in human monocytes.

Cells, Cultured↗
PubMed2004

Prevalence of gingival overgrowth in transplant patients immunosuppressed with tacrolimus.

AIMS: The study aims to determine the prevalence and severity of gingival overgrowth in a group of adult organ transplant recipients immunosuppressed with tacrolimus in comparison with ciclosporin, and to examine various risk factors for the development of gingival overgrowth. METHODS: Forty patients taking tacrolimus were compared with 197 ciclosporin patients. Demographic, pharmacological and periodontal data were recorded for all patients. Comparison between the groups was made using independent sample t-tests, chi2 statistic or Mann-Whitney test. The effects of risk variables on overgrowth severity were examined using forward and backward stepwise regression analysis. RESULTS: Those taking tacrolimus had a significantly lower mean gingival overgrowth score (14.1%) compared with ciclosporin (22.4%). Fifteen percent of the tacrolimus group had clinically significant gingival overgrowth compared with 30% in the ciclosporin group (p=0.053). CONCLUSIONS: The prevalence and severity of gingival overgrowth is less in adult transplant patients taking tacrolimus compared with ciclosporin. Concomitant use of calcium channel blockers and previous medication with ciclosporin are significant risk factors for the presence and severity of gingival overgrowth. Patients who have alteration of their immunosuppressant from ciclosporin to tacrolimus may persist in demonstrating gingival overgrowth attributable to their ongoing therapy with calcium channel blockers.

Adolescent↗
PubMed2004

Plasma TGF-beta1 as a risk factor for gingival overgrowth.

BACKGROUND AND AIMS: Induction of the pro-fibrotic growth factor TGF-beta1 has been suggested as a possible mechanism through which immunosuppressant drugs may induce gingival overgrowth. This study aims to investigate plasma levels of TGF-beta1 and relate them to the development and severity of gingival overgrowth in immunosuppressed transplant patients. MATERIALS AND METHODS: One hundred and thirty-two ciclosporin-treated and 13 tacrolimus-treated transplant patients and 24 drug-free control subjects underwent a full periodontal examination including a determination of the presence and severity of gingival overgrowth. RESULTS: Plasma TGF-beta1 concentrations were determined by ELISA, and were found to be significantly elevated in samples from the transplant patients (mean=29.1 ng/ml) as compared with controls (mean=6.1 ng/ml, p<0.0001). There was no significant difference between the levels of plasma TGF-beta1 in the ciclosporin- and tacrolimus-treated patient groups. CONCLUSIONS: Furthermore, concomitant treatment with calcium channel blockers did not influence the levels of plasma TGF-beta1 in the patients group. The relationship between gingival overgrowth, independent periodontal variables and TGF-beta1 plasma concentrations was examined using univariate and multivariate regression analyses; low TGF-beta1 plasma concentrations were found to be a risk factor for gingival overgrowth in immunosuppressed patients concomitantly receiving a calcium channel blocker.

Age Factors↗
PubMed2002

Molecular mediators of Porphyromonas gingivalis-induced T-cell apoptosis.

Porphyromonas gingivalis produces virulence factors which can modify the molecular and cellular components of the host immune response. In the present work we investigated the role of specific virulence factors from P. gingivalis in the induction of apoptosis in Jurkat T cells. P. gingivalis culture supernatants mimicked the effect of butyric acid on T-cell apoptosis and this effect was associated with an increase in histone H4 acetylation. A role for proteases was excluded in experiments which demonstrated that neither protease inhibitors nor use of P. gingivalis mutants defective in protease synthesis had any effect on the stimulation of T-cell apoptosis in this system.

Acetylation↗
PubMed2000

Association of interleukin-1 gene polymorphisms with early-onset periodontitis.

BACKGROUND, AIMS: Early-onset periodontal diseases (EOP) are a group of inflammatory disorders characterised by a rapid rate of periodontal tissue destruction, in young individuals who are otherwise healthy. There is now substantial evidence to suggest that genetic factors play a rôle in the pathogenesis of EOP but the precise nature of these factors remains unclear. Polymorphisms in cytokine genes which may underpin inter-individual differences in cytokine synthesis and secretion have been associated with other diseases which have an inflammatory pathogenesis, including chronic adult periodontal disease (CAPD). METHOD: We therefore investigated the frequency of polymorphisms in the genes encoding interleukin-1 beta (IL-1 beta) and its receptor antagonist (IL-1RA) in 70 EOP patients, including a subgroup of 21 localised EOP (L-EOP) patients and 72 periodontally healthy controls. All subjects were of Caucasian heritage and systemically healthy. A single nucleotide polymorphism (SNP) in exon 5 of the IL-1 beta gene (IL-1 beta+ 3953) was analysed by amplifying the polymorphic region using PCR, followed by restriction digestion with Taq1 and gel electrophoresis. RESULTS: The frequency of IL-1 beta genotypes homozygous for allele 1 (corresponding to the presence of a restriction site) of the IL-1 beta+3953 SNP was found to be significantly increased in EOP patients (chi2 test, p = 0.025). Upon stratification for smoking status a significant difference was found in the IL-1 beta genotype distribution between EOP smokers compared to control smokers (F-exact test, p = 0.02), but not between EOP non-smokers and control non-smokers. The IL-1 beta 1/1 genotype occurred at a higher frequency in EOP smokers (odds ratio = 4.9) compared to control smokers. A variable number tandem repeat polymorphism (VNTR) in intron 2 of the IL-IRA gene was analysed by amplifying the polymorphic region using PCR and fragment size analysis by gel electrophoresis. There was no evidence for an association of an IL-1RA genotype with EOP. However the combination of IL-1 beta allele 1 and IL-IRA allele 1 (corresponding to 4 repeats) was associated with EOP (Clump, p = 0.01). CONCLUSIONS: These findings suggest that an IL-1 beta genotype in combination with smoking, and a combined IL-1 beta and IL-1RA genotype are risk factors for EOP and support a role for genetic and environmental factors in susceptibility to EOP.

Adolescent↗
PubMed2000

Dinucleotide repeat polymorphism in the interleukin-10 gene promoter (IL-10.G) and genetic susceptibility to early-onset periodontal disease.

Emerging evidence suggests that certain genetic polymorphisms are associated with various sub-groups of early-onset periodontal diseases (EOP). We determined the genotype with respect to a (CA)n dinucleotide repeat polymorphism in the promoter region of the interleukin-10 gene (IL-10.G) in 72 patients with EOP and in 73 healthy individuals in order to test for possible disease associations. Some differences between the frequency of individual IL.10.G alleles in the patients groups as compared to the healthy controls were detected. For example the frequency of the IL-10.G9 allele in a clinical sub-group of the EOP patients with localised disease (L-EOP, n = 21) was 64.3% as compared to 41.8% in the controls. However, statistical analysis (Monte Carlo simulation) revealed that the differences in IL-10.G allele distribution between the healthy controls and both the EOP group and the L-EOP group were not statistically significant. We conclude that this study provides no evidence for a role of IL-10.G alleles in genetic susceptibility to EOP.

Age of Onset↗
PubMed1999

Apoptosis in Porphyromonas gingivalis-specific T-cell lines.

Fluorescence-activated cell sorter analysis and transmission electron microscopy were used to determine the presence of apoptotic cells in Porphyromonas gingivalis-specific T-cell lines established from the peripheral blood of 10 P. gingivalis-infected individuals. P. gingivalis outer membrane antigens were presented to the T cells by autologous Epstein-Barr virus-transformed B cells for 6, 24, 48 and 72 h. Transmission electron microscopy demonstrated the presence of typical apoptotic cells in all cultures. Annexin V-positive cells were present at low concentrations at all 4 four periods. A mean of approximately 2-3% of the CD4 cells and 1-3.5% of the CD8 cells were annexin V-positive, with an increase to around 5.5% positive CD4 cells at 6 h in wells containing P. gingivalis compared with cultures not containing antigen. This difference was not, however, significant at the 0.05 level (P = 0.073). The mean (+/- standard error) CD4:CD8 ratios of the T-cell lines when first established using peripheral blood mononuclear cells as antigen-presenting cells was significantly higher (5.2 +/- 1.1) than when transformed B cells were used as antigen-presenting cell (1.2 +/- 0.5). While this study has shown apoptosis occurring in the T-cell lines, it has not shown definitively that the reversion in the CD4:CD8 ratio in the P. gingivalis-specific T cells following antigen presentation by autologous Epstein-Barr virus-transformed B cells is due to apoptosis of a CD4 population. Alternatively, the reversion in the CD4:CD8 ratio could be due to a selective proliferation of the CD8 population which, in turn, could be relevant to the immunopathology of periodontal disease induced by P. gingivalis.

Analysis of Variance↗
PubMed1999

Transformation of the collateral vascular bundles into amphivasal vascular bundles in an Arabidopsis mutant.

Arabidopsis inflorescence stems develop a vascular pattern similar to that found in most dicots. The arrangement of vascular tissues within the bundle is collateral, and vascular bundles in the stele are arranged in a ring. Although auxin has been shown to be an inducer of vascular differentiation, little is known about the molecular mechanisms controlling vascular pattern formation. By screening ethyl methanesufonate-mutagenized populations of Arabidopsis, we have isolated an avb1 (amphivasal vascular bundle) mutant with a novel vascular pattern. Unlike the collateral vascular bundles seen in the wild-type stems, the vascular bundles in the avb1 stems were similar to amphivasal bundles, i.e. the xylem completely surrounded the phloem. Furthermore, branching vascular bundles in the avb1 stems abnormally penetrated into the pith, which resulted in a disruption in the ring-like arrangement of vascular bundles in the stele. The avb1 mutation did not affect leaf venation pattern and root vascular organization. Auxin polar transport assay indicated that the avb1 mutation did not disrupt the auxin polar transport activity in inflorescence stems. The avb1 mutation also exhibited pleiotropic phenotypes, including curled stems and extra cauline branches. Genetic analysis indicated that the avb1 mutation was monogenic and partially dominant. The avb1 locus was mapped to a region between markers mi69 and ASB2, which is covered by a yeast artificial chromosome clone, CIC9E2, on chromosome 5. Isolation of the avb1 mutant provides a novel means to study the evolutionary mechanisms controlling the arrangement of vascular tissues within the bundle, as well as the mechanisms controlling the arrangement of vascular bundles in the stele.

Arabidopsis↗
PubMed1999

In vitro studies of lymphocyte apoptosis induced by the periodontal pathogen Porphyromonas gingivalis.

Apoptosis has a physiological role in lymphocyte development and function serving to remove self-reactive T-cells in the thymus as well as activated peripheral T-cells when they are no longer required in the immune response. Evidence from the study of several pathogenic bacteria indicate that induction of premature cell death by apoptosis may be an important pathogenic mechanism promoting infection, inflammation and concomitant disease. In this paper we demonstrate that cultures of the periodontal pathogen Porphyromonas gingivalis (P. gingivalis) promote lymphocyte apoptosis in peripheral blood mononuclear cells (PBMC). We have used assays designed to investigate the different molecular and cellular changes associated with apoptosis. Thus flow cytometry revealed that whole cultures of P. gingivalis promoted cell shrinkage in the lymphocyte fraction of PBMC and analysis of hypodiploidy confirmed that the cellular changes were associated with nuclear changes characteristic of apoptosis. We also found that apoptosis was promoted in PBMC exposed to both whole P. gingivalis cultures and culture supernatant but not washed bacterial cells; this indicates that molecule(s) secreted into the medium were responsible for this activity and not a factor intrinsic to the bacterial cell. Furthermore heat treatment has no effect on the ability of P. gingivalis cultures to induce lymphocyte apoptosis. In summary, a soluble heat stable component of the supernatant from P. gingivalis cultures promotes lymphocyte apoptosis. These data establish the principle that bacteria-induced apoptosis may be an important feature of the pathogenesis of periodontal disease.

Apoptosis↗
PubMed1999

Association of a vitamin D receptor gene polymorphism with localized early-onset periodontal diseases.

BACKGROUND: Early-onset periodontal diseases (EOP) are caused by interactions between host factors, specific microbial pathogens, and environmental factors. It is, therefore, of interest to investigate the nature of host factors as they may provide useful risk markers and reveal important information regarding the disease pathogenesis. Genetic polymorphisms in the vitamin D receptor (VDR) gene are associated with parameters of bone homeostasis and with diseases in which bone loss is a cardinal sign, in particular osteoporosis. Rapidly progressive bone loss is one feature of EOP. We, therefore, sought to determine whether EOP is associated with a polymorphism in the VDR gene. METHODS: A restriction fragment length polymorphism (RFLP) for Taq I in exon nine of the VDR gene was analyzed by PCR, followed by restriction digestion with Taq I and gel electrophoresis. We analyzed the genotypes of 69 EOP patients, including 20 patients with unequivocal evidence of localized disease (L-EOP), and 72 controls with no history of EOP. RESULTS: The genotype distribution in the L-EOP patient group was 7 (35%), 5 (25%) and 8 (40%) and in the control group 31 (43.1%), 36 (50.0%) and 5 (6.9%) for TT, Tt and tt respectively (where t and T represent the alleles with and without the Taq I RFLP respectively). Chi2 analysis indicated that the distribution of the genotypes between these two groups was highly significantly different (P = 0.001). Allele frequencies were 47.5% and 52.5% for T and t in the L-EOP group; 68.1% and 31.9% in the control group, showing a significant association between the prevalence of the less frequent allele (t) and L-EOP (P = 0.017). There was no significant difference in the genotype distribution or the allele frequencies between the control samples and the larger EOP patient group (n = 69) which included patients with generalized and localized disease. CONCLUSIONS: These data indicate that carriage of the less frequent allele of the Taq I RFLP (t) in the VDR gene significantly increases the risk of developing L-EOP. However, VDR genotype may not affect the incidence of all cases of EOP. These findings contribute to our understanding of the genetic basis for periodontal disease and may help define sub-groups of this disease which share common pathogenic factors.

Adolescent↗
PubMed1998

Longitudinal changes in TCRB variable gene expression and markers of gingival inflammation in experimental gingivitis.

The aim of this study was to gain information of the cellular and molecular events which occur during the development of experimental gingivitis and to determine whether such changes occur in the presence or absence of alveolar bone resorption. Clinical, radiographic, biochemical and immunological variables were monitored in a 3-week, single-centre, experimental gingivitis study of 10 healthy volunteers. Following screening and professional prophylaxis to achieve visibly healthy gingival status, subjects abstained from all oral hygiene practises in one maxillary (test) quadrant for a period of 21 days. At days 0 and 21, in test and (contralateral) control quadrants, % bleeding on controlled pressure probing (% BOP) was calculated, and radiographic alveolar bone status was assessed using bilateral standardised vertical bite-wing radiographs and digital subtraction radiography (DSR) analysis. In test quadrants, gingival crevicular fluid (GCF) was sampled from 4 sites per subject with Periopaper strips, and prostaglandin E2 (PGE2) levels measured using an enzyme immunoassay (EIA) kit. At days 0, 7 and 21, one interdental papilla was surgically excised from the test quadrant, and the expression of T cell receptor B variable (TCRBV) genes was investigated using a reverse transcription-polymerase chain reaction (RT-PCR) procedure. At days 0, 7 and 21, peripheral blood lymphocytes (PBL) were isolated and additionally investigated for TCRBV gene expression. Following 21 days of plaque accumulation in test quadrants, a statistically significant increase in % BOP scores confirmed the presence of gingival inflammation (p<0.001). DSR analysis revealed that there were no significant alveolar bone changes in either the test or control quadrants between days 0 and 21 (p>0.05). EIA analysis of GCF samples identified a significant decrease in mean GCF PGE2 concentrations from day 0 to day 21 (p<0.05). RT-PCR analysis indicated that genes from all 3 TCRBV families studied (TCRBV-2, -6, -8) were expressed in the PBL samples at all time points and in healthy gingival tissues at day 0. A restriction in the expression pattern of TCRBV genes similar to those which have previously been reported in chronic periodontitis was noted at gingivitis sites. It is possible that such an event may identify susceptibility to periodontal disease independently of other positive predictive markers such as GCF-PGE2.

Adolescent↗
PubMed1997

Disruption of interfascicular fiber differentiation in an Arabidopsis mutant.

Arabidopsis develops interfascicular fibers in stems for needed support of shoots. To study the molecular mechanisms controlling fiber differentiation, we isolated an interfascicular fiber mutant (ifl1) by screening ethyl methanesulfonate-mutagenized Arabidopsis populations. This mutant lacks normal interfascicular fibers in stems. Interestingly, some interfascicular cells were sclerified in the upper parts but not in the basal parts of the ifl1 stems. These sclerified cells were differentiated at a position different from that of interfascicular fibers in the wild type. Lack of interfascicular fibers correlated with a dramatic change of stem strength. Stems of the mutant could not stand erect and were easily broken by bending. Quantitative measurement showed that it took approximately six times less force to break basal stems of the mutant than of the wild type. In addition, noticeable morphological changes were associated with the mutant, including long stems, dark green leaves with delayed senescence, and reduced numbers of cauline leaves and branches. Genetic analysis showed that the ifl1 mutation was monogenic and recessive. The ifl1 locus was mapped to a region between the 17C2 and 7H9L markers on chromosome 5. Isolation of the ifl1 mutant provides a novel means to study the genetic control of fiber differentiation.

Arabidopsis↗
PubMed1997

Expression of T-cell receptor Vbeta2, 6 and 8 gene families in chronic adult periodontal disease.

Substantial evidence exists to suggest a role for T-cells in periodontal disease. As yet, however, the T-cell receptors remain to be characterised at the molecular level. The expression and the nucleotide sequence of genes from the T-cell receptor beta variable (TCRBV) gene families 2, 6 and 8 were analyzed in periodontal tissue from 24 patients with chronic adult periodontal disease (CAPD) and peripheral blood lymphocytes (PBL) of 16 of these patients. A restriction in the expression of these TCRBV gene families was detected in periodontal tissue from 14/24 patients with CAPD, and the pattern of gene expression was often different between individual patients; however there was no restriction in TCRBV gene expression in matched PBL samples from 8 of these 14 patients. Quantitative RT PCR analysis of samples from 5 CAPD patients who expressed all 3 TCRBV gene families in their periodontal tissues did not reveal any significant differences in the levels of gene expression in periodontal tissue and PBL. In contrast to the findings with some CAPD patients, genes from all 3 TCRBV families were always expressed in periodontal tissue and PBL from disease-free control subjects. PCR products from both the PBL and periodontal tissue of CAPD patients were cloned and sequenced; analysis of the nucleotide sequence revealed diversity with respect to the expression of TCRB joining (TCRBJ) and TCRB diversity (TCRBD) genes and the sequence of the junctional region in all samples analysed. In conclusion, in CAPD, the pattern of TCRBV gene expression in periodontal tissue is often but not always different from that in PBL and healthy periodontal tissue, which may indicate, in some cases, a local influence on particular T-cell subsets which is relevant to the pathogenesis of periodontal disease. However, the expressed TCRB genes are heterogeneous at the nucleotide level, emphasising the underlying complexity at the molecular level in the local T-cell response in CAPD.

Adult↗
PubMed1994

Diatoms and drowning--a cautionary case note.

A case is described in which, due to long-term repeated exposure to the same body of diatom-containing water, comparable diatom findings in the tissues and environmental samples were not acceptable as proof of drowning. A commonly overlooked pitfall limiting the value of acid-digestion in marine cases is emphasized.

Diatoms↗