Expression of the activation antigen CD27 in rheumatoid arthritis

Differentiation of CD4+ T-cells is reflected by the change from the CD45RA+CD27+ phenotype via CD45RO+CD27+ to the CD45RO+CD27- phenotype. To provide insight into the migration and activation of T-cells at the site of inflammation in rheumatoid arthritis (RA), CD27 expression by T-cells in peripheral blood (PB), synovial fluid (SF), and synovial tissue (ST) as well as the levels of the soluble form of CD27 (sCD27) in plasma and SF were studied in patients with RA. Since CD4+CD27+ T-cells are involved in providing helper activity for B-cells, we also investigated the levels of rheumatoid factors in serum and SF in relation to CD27 expression. The mean level of sCD27, which is produced by CD27+ cells, and the mean percentage of CD27 T-cells within the CD4+CD45RA- subset were higher in SF than in PB. SF sCD27 levels were higher in the patients with RA than in the patients with osteoarthritis, who served as controls. In ST infiltration by CD4+CD45RO+CD27+ T-cells, could be demonstrated in the rheumatoid perivascular lymphocytic aggregates with a relative increase in the percentage of CD27- T-cells in the diffuse lymphocytic infiltrate. The sCD27 levels and the percentages of CD4+CD27+ cells in SF correlated positively with the levels of rheumatoid factors in serum and SF. The findings presented in this study suggest a continuous influx of preactivated CD4+CD45RO+CD27+ cells from the PB into the rheumatoid ST and further activation and differentiation to CD4+CD45RO+CD27- cells in situ, followed by migration to the SF. These activated T-cells are likely to play a role in synovial inflammation.     

Human hepatitis B virus and hepatocellular carcinoma. I. Experimental infection of tree shrews with hepatitis B virus

A cross-sectional study involving 771 children under the age of one year, was carried out in a traditional area of urban Ilorin, Nigeria, to determine how socio-economic conditions and feeding practices relate to diarrhoeal disease among infants. After adjustment has been made (through logistic regression) for covariates, five factors had significant association with diarrhoeal disease. These are the age of the child, parity, mother's education, availability of household kitchen and the feeding of semi-solid food to the infants. The lowest diarrhoeal rate occurred in infants aged 0-3 months while the highest rate occurred among infants seven to nine months old (Odds Ratio = 4.2). Children who were of the fifth or higher birth order had significantly higher risk of diarrhoea when compared with those who were of the first or second birth order (OR = 1.62; P < 0.05). Children of mothers with secondary education had significantly higher risk of diarrhoea compared with children of illiterates (OR = 1.9; P < 0.05). Households that had no kitchen had significantly higher risk of infantile diarrhoea than households with kitchen facilities (P < 0.01). Finally, infants receiving semi-solid food had higher risk of diarrhoea compared to those children not receiving semi-solid food (P < 0.05). Diarrhoeal disease awareness campaign to educate mothers on the dangers of childhood diarrhoea and how to prevent it, through proper hygiene, especially, food hygiene, is advocated.     

Functional defects in peripheral blood T cells of multiple sclerosis patients. Diminished in vitro responsiveness in accessory cell dependent activation systems

Function and phenotype of peripheral blood (PB) T cells in multiple sclerosis (MS) patients were analyzed. In whole blood cultures, T cell proliferation of multiple sclerosis (MS) patients, using soluble CD3 mAb and CD2 mAb as stimulants, was reduced in comparison to healthy controls. A similar difference was seen when isolated PBMC were tested after stimulation with soluble CD3 mAb. However, in accessory cell-independent activation systems, i.e. after stimulation of PBMC with immobilized CD3 mAb or after co-stimulation with CD28 mAb, both patients and controls responded equally well. Phenotypical analysis of the circulating T cell population showed that there were no differences in the percentage of CD26+, 'memory' (CD45R0+) or 'effector' (CD4+CD45R0+CD27-) cells between MS patients and healthy controls. Finally, although MS patients did show an enhanced proportion of 'naive' (CD4+CD45RA+) T cells, this did not correlate with the observed functional defects.     

Regulation of CD27 expression on subsets of mature T-lymphocytes

CD27, a lymphocyte-specific member of the TNF/NGF-R family, is expressed on the majority of peripheral blood T cells. Activation of T cells via TCR/CD3 induces high CD27 surface expression and the release of a soluble extracellular part of the molecule. After prolonged activation in vitro, CD27 becomes gradually switched off. There is evidence that also in vivo, CD4+ cells that have persistently been stimulated by Ag, accumulate within the CD45RA-CD27- subset. In addition, an increase of CD27- T cells has been observed under certain immunopathologic conditions and during aging. This study was undertaken to analyze the regulation of CD27 on different T-cell subsets and to determine whether the loss of CD27 expression is an irreversible event and may thereby mark T-cell differentiation. In agreement with earlier findings, all CD4+CD45RA+CD45RO- T cells were found to express CD27, whereas a small fraction of the CD4+CD45RA-CD45RO+ subset lacks the molecule. In contrast, within the CD8+ compartment CD27- subsets were found both in the CD45RA+ and CD45RA- subpopulations. After stimulation with CD3 mAb, both CD27 membrane expression and release was equally up-regulated in CD4+ and CD8+ subpopulations. This stimulus, however, provoked a strikingly predominant up-regulation of membrane CD27 on CD45RO- cells as compared with CD45RA- cells. On CD4+CD45RA-CD27- T cells and long-term grown CD45RA-CD27- TLC, CD27 expression could not be reinduced after stimulation of the TCR/CD3 complex, neither at the protein nor at the mRNA level. Comparison of CD27 expression with its structural homologue FAS/APO-1 showed that down-regulation after prolonged activation is not a general feature of TNF/NGF-R family members. The CD27 ligand was recently identified and was shown to give a co-stimulatory signal to PHA-activated T cells. The restricted up-regulation of CD27 on CD45RA+ cells after T-cell stimulation may point at a discrete role of CD27-CD27 ligand interaction during transition of CD45RO- to CD45RA- T cells. In addition, the CD27 negative phenotype seems a stable reflection of differentiation rather than of activation.     

Idiopathic avascular necrosis of a vertebral body. Case report and literature review

STUDY DESIGN: Case report and literature review. OBJECTIVES: To review the English literature pertaining to idiopathic avascular necrosis of a vertebral body. As an illustrative example, the case of a 60-year-old woman with idiopathic avascular necrosis of L4 is presented. SUMMARY OF BACKGROUND DATA: Avascular necrosis of a vertebral body is an uncommon entity. Avascular necrosis has been described in the context of other underlying lesions, such as with malignancy, infection, radiation therapy, and systemic steroid treatment. The intravertebral vacuum cleft phenomenon seen on plain films has been strongly associated with vertebral body avascular necrosis. METHODS: Literature and chart review was carried out. Vertebral body avascular necrosis was initially identified with imaging studies and confirmed with biopsy. A comprehensive preoperative evaluation did not identify a specific cause of avascular necrosis. The patient underwent vertebral body resection with fibula allograft struts. CONCLUSIONS: Although vertebral body collapse in an osteoporotic individual is relatively common, a case is reported of vertebral body collapse and subsequent necrosis without evidence of underlying disease at 48-month follow-up. The current findings support the diagnosis of idiopathic avascular necrosis of L4.     

Reference Raman spectra of eleven miscellaneous pesticides

The Raman spectra of ICP (propham), CIPC (chlorpropham), carbaryl, EPTC (ethyl N,N-dipropyl (3-chlorophenyl) carbamate), pebulate, CDEC (2-chloroallyl diethyldithiocarbamate), thiram, maneb, zineb, ferbam, and nicotine have been recorded. These spectra are presented, along with tables giving values for the frequencies.     

Hemidesmosome formation is initiated by the beta4 integrin subunit, requires complex formation of beta4 and HD1/plectin, and involves a direct interaction between beta4 and the bullous pemphigoid antigen 180

Hemidesmosomes (HDs) are stable anchoring structures that mediate the link between the intermediate filament cytoskeleton and the cell substratum. We investigated the contribution of various segments of the beta4 integrin cytoplasmic domain in the formation of HDs in transient transfection studies using immortalized keratinocytes derived from an epidermolysis bullosa patient deficient in beta4 expression. We found that the expression of wild-type beta4 restored the ability of the beta4-deficient cells to form HDs and that distinct domains in the NH2- and COOH-terminal regions of the beta4 cytoplasmic domain are required for the localization of HD1/plectin and the bullous pemphigoid antigens 180 (BP180) and 230 (BP230) in these HDs. The tyrosine activation motif located in the connecting segment (CS) of the beta4 cytoplasmic domain was dispensable for HD formation, although it may be involved in the efficient localization of BP180. Using the yeast two-hybrid system, we could demonstrate a direct interaction between beta4 and BP180 which involves sequences within the COOH-terminal part of the CS and the third fibronectin type III (FNIII) repeat. Immunoprecipitation studies using COS-7 cells transfected with cDNAs for alpha6 and beta4 and a mutant BP180 which lacks the collagenous extracellular domain confirmed the interaction of beta4 with BP180. Nevertheless, beta4 mutants which contained the BP180-binding region, but lacked sequences required for the localization of HD1/plectin, failed to localize BP180 in HDs. Additional yeast two- hybrid assays indicated that the 85 COOH-terminal residues of beta4 can interact with the first NH2-terminal pair of FNIII repeats and the CS, suggesting that the cytoplasmic domain of beta4 is folded back upon itself. Unfolding of the cytoplasmic domain may be part of a mechanism by which the interaction of beta4 with other hemidesmosomal components, e.g., BP180, is regulated.