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Background: It has been reported that 50% of patients with atrophic body gastritis have positive Helicobacter pylori antibody titres only. In atrophic body gastritis, a decrease in H. pylori antibodies after eradication treatment has been reported, suggesting that serology may indicate an active H. pylori infection. Aim: To investigate the time course of H. pylori antibodies and gastric inflammation after eradication treatment in patients with atrophic body gastritis, and to determine whether serology alone can be considered as a valid tool to assess the efficacy of eradication treatment in patients with atrophic body gastritis. Methods: Twenty-seven patients with atrophic body gastritis (12 serologically H. pylori -positive only, ABG-S+; 15 H. pylori -positive at histology and serology, ABG-H+) were included in the treatment group, and 17 patients (all ABG-S+) in the no treatment group. All patients had gastroscopy plus biopsies evaluated according to the updated Sydney system and H. pylori immunoglobulin G determination: in the treatment group, at baseline and 6 and 24 months after eradication (bismuth-based triple regimens); in the no treatment group, at baseline and after 3 years. Results: In the treatment group, in ABG-S+ patients, H. pylori antibodies decreased significantly 6 months after treatment [37.5 U/mL (16–100 U/mL) vs. 15 U/mL (0–100 U/mL), P < 0.01], but 2 years after treatment no further decrease occurred. In addition, in ABG-H+ patients, a significant decrease in H. pylori antibodies occurred 6 months after treatment [45 U/mL (12.5–100 U/mL) vs. 31 U/mL (0–65 U/mL), P < 0.01], but a further decrease was also observed 2 years after treatment [20 U/mL (0–56 U/mL), P < 0.01]. In ABG-S+ patients, no correlation was observed between the H. pylori antibodies and gastric inflammation score, whereas, in the ABG-H+ group, this correlation was extremely significant (r =0.5991, P < 0.0001). In the no treatment group, at... [ABSTRACT FROM AUTHOR]

We have examinied the frequencies of Tγδ cells in blood, synovial fluids, and synovial membrances of patients with rheumatoid arthritis (RA) and in blood from age-matched controls. Immunocyto-chemical and immunohistochemical techniques were used with monoclonal antibodies BB3 and A13 to define a major and minor blood subset of Tγδ cells respectively. Together, these antibodies identify the majority (if not all) of the peripheral blood Tγδ cells [ABSTRACT FROM AUTHOR]

A minor population of T cells expresses a heterodimeric antigen receptor composed of γ and &delta chain (TcR-1). In blood from adults, two subsets pf Tγ&delta cells can be identified by the monoclonal antibodies (MoAb) BB3 and A13. Little is known about the distribution and markers of these subsets early in life. We have therefore examined both the frequencies of these cells in cord blood and their expression of the cytotoxicity-associated marker serine esterase (SE), using immunocytochemical techniques. Our data show lower percentages of TcR-1+ cells in the blood of newborns compared with that in adults. However, the ratio of the A13+/BB3+ cells was significantly higher in cord than in adult blood. Whereas virtually all the adult TcR-1+ cells in blood were SE-positive, only a small proportion of the cord blood cells carried this enzyme. This was restricted to the BB3+ Tγδ-cells subset in the cord. Our data suggest different characteristic of the TcR-1+ cells in blood from newborns compared with adult blood, and study of the functions of the different subsets, e.g. cytotoxicity, will be important in understanding their particular role in immunity. [ABSTRACT FROM AUTHOR]

Human peripheral blood large granular lymphocytes (LGL)--that is, cells with intracytoplasmic azurophilic (electron-dense) granules, with a positivity for the cytochemical localization of certain acid hydrolases, and with avid surface receptors for the Fc portion of IgG--have been purified on Percoll density gradients. Approximately 30% of these cells expressed receptors for the third complement component (C3R). They were separated into C3R-positive and C3R-negative cells. C3R+ cells had a significantly greater natural killer (NK) activity against K562 target cells than C3R+ cells. This difference was unrelated to the presence in the C3R+ cells of a contaminant cell type incapable of NK activity, since cytochemical and ultrastructural analysis revealed that C3R+ and C3R- fractions contained comparable LGL numbers. Agarose cytotoxicity assays at the single-cell level demonstrated that C3R+ LGL contained a large number of cells that bound to but did not lyse the target. The remaining fully cytotoxic C3R+ LGL had, however, the same killing and recycling properties as the cells from the C3R- fraction. Electron microscopy and cytochemical studies showed that C3R+ cells had fewer electron-dense granules than C3R- cells and stained more faintly for the localization of alpha-naphtyl acetate esterase. In contrast to C3R- cells, C3R+ LGL displayed morphological features suggesting that an active process of granule formation was taking place. Taken together, the data indicate that C3R+ cells represent a discrete subset or a maturational stage of LGL. [ABSTRACT FROM AUTHOR]

The comparison of hemodilution at the end of surgery is of limited use as it represents only a snapshot of a dynamic phenomenon. This study was undertaken to compare the perioperative hemoglobin curves of isolated coronary artery bypass grafting performed with minimized extracorporeal circulation, traditional cardiopulmonary bypass, and off-pump technique. The propensity score method was used to select three groups of patients, homogenous regarding preoperative and operative data, who underwent isolated coronary artery bypass grafting. A generalized linear mixed model was used for estimating differences in perioperative hemoglobin trends among groups. The three groups were each composed of 50 patients with no differences in demographic data, preoperative risk profile, preoperative hemoglobin, or type of surgery. There was no significant difference in major postoperative complications. The pattern of the hemodilution curves was similar in patients operated with mini-circuit and off-pump technique (P > 005). Mini-circuit led to a 3.1 ± 11.9% hemoglobin reduction, which was similar to the off-pump group (1.6 ± 8.9%, P = 0.99 at ANOVA) and significantly different from the standard extracorporeal circuit group (16.0 ± 10.3%, P < 0.001 at ANOVA). The generalized linear mixed model determined that the standard circuit was the only independent predictor for increased hemodilution. Its effect on hemodilution was time-dependent and the slope of the hemoglobin curve was more pronounced between systemic heparinization and the end of surgery. Perioperative hemoglobin trends of patients who underwent myocardial revascularization with mini-circuit were similar to those of off-pump surgery and significantly less pronounced than those of standard extracorporeal circulation., (© 2012, Copyright the Authors. Artificial Organs © 2012, International Center for Artificial Organs and Transplantation and Wiley Periodicals, Inc.)

Peptides and proteins can convert from their soluble forms into highly ordered fibrillar aggregates, giving rise to pathological conditions ranging from neurodegenerative disorders to systemic amyloidoses. It is increasingly recognized that protein oligomers forming early in the process of fibril aggregation represent the pathogenic species in protein deposition diseases. The N-terminal domain of the HypF protein from Escherichia coli (HypF-N) has previously been shown to form, under distinct conditions, two types of HypF-N oligomers with indistinguishable morphologies but distinct structural features at the molecular level. Only the oligomer type exposing hydrophobic surfaces and possessing sufficient structural plasticity is toxic (type A), whereas the other type is benign to cultured cells (type B). Here we show that only type A oligomers are able to induce a Ca(2+) influx from the cell medium to the cytosol, to penetrate the plasma membrane, to increase intracellular reactive oxygen species production, lipid peroxidation and release of intracellular calcein, resulting in the activation of the apoptotic pathway. Remarkably, these oligomers can also induce a loss of cholinergic neurons when injected into rat brains. By contrast, markers of cellular stress and viability were unaffected in cultured and rat neuronal cells exposed to type B oligomers. The analysis of the time scales of such effects indicates that the difference of toxicity between the two oligomer types involve the early events of the toxicity cascade, shedding new light on the mechanism of action of protein oligomers and on the molecular targets for the therapeutic intervention against protein deposition diseases., (© 2011 The Authors Journal of Cellular and Molecular Medicine © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.)

Background and Aim of the Study: The aim of this study was to evaluate the early and mid-term off-pump coronary artery bypass surgery (OPCAB) results in a single surgical unit, assessing the impact of completeness of revascularization., Methods: Three hundred and twelve patients underwent OPCAB between August 2000 and January 2005. In-hospital data were collected prospectively for all patients undergoing OPCAB. Complete revascularization (CR) was derived by comparing significantly stenotic vessels at cardiac catheterization with surgically grafted coronary vessels. Grafting of all the significantly stenotic coronary vessels was considered CR. In-hospital outcomes were compared between patients with CR and incomplete revascularization (IR). A multivariate analysis based on the Cox proportional hazards regression model was performed., Results: Patients receiving IR (105 patients, 43.7%) presented a worse preoperative risk profile then those having CR (mean Euroscore 6.8 +/- 2.9 vs. 4.3 +/- 2.8, p < 0.0001). IR was not associated with a higher incidence of early adverse events. Five-year freedom from death and major adverse cardiac events (MACE) were 0.88 (0.02 SE) and 0.86 (0.03 SE), respectively. Complete revascularization was protective for mid-term unstable angina recurrence [heart rate (HR) = 0.24, 95% confidence interval (CI) 0.10 to 0.58], acute myocardial infarction (HR = 0.25, 95% CI 0.09 to 0.73), all-cause repeat revascularization (HR = 0.35, 95% CI 0.13 to 0.90), and MACE (HR = 0.2, 95% CI 0.1 to 0.5)., Conclusion: Our study suggests that, although incomplete revascularization may not result in increased short-term morbidity and mortality, it increases the incidence of mid-term MACE.

Background: Helicobacter pylori is involved in the induction of atrophic body gastritis (ABG). During the progression of atrophic gastritis the disappearance of H. pylori has been documented and in time serology is the only sign that indicates a previous infection. It has been shown that a positive serology, in ABG patients without histological evidence of infection, indicates an active H. pylori infection., Aim: To investigate in a population of patients with ABG the prevalence of H. pylori infection on the basis of histology and serology., Patients: A total of 150 consecutive outpatients with atrophic body gastritis were diagnosed on the basis of a screening system., Methods: All patients had a detailed assessment including measurement of specific anti-H. pylori antibodies, parietal cell antibodies, and fasting gastrin, gastroscopy with biopsies from gastric antrum and body., Results: 24.6% of patients were histologically and serologically negative (Group A). 52.7% H. pylori was not detected on histology but IgG to H. pylori were in all these patients elevated (Group B). 22.6% of patients were found to be positive at histology in the corpus mucosa; all but one of these patients had elevated circulating IgG to H. pylori (Group C). Mean corporal atrophy score in Group B patients was statistically lower than in Group A patients (2.43 +/- 0.08 vs. 2.75 +/- 0.09; p <.05), but was statistically higher than in Group C patients (1.79 +/- 0.11; p <.001). Thus, in corporal mucosa a gradient of atrophy was shown: Group C < Group B < Group A. A similar gradient was observed for the presence of pernicious anemia being lowest in Group C 11.8% increasing to 45.6% in Group B and being highest in Group C 75.6%. A statistical correlation was obtained (r =.04791, p <.05) between the histological score of corporal atrophy and the titer of antibodies to parietal cells and an inverse correlation was obtained (r = -.2322, p <.0001) between the histological score of corporal atrophy and IgG to H. pylori., Conclusion: This study shows that two-thirds of ABG patients have evidence of H. pylori infection. This suggests that atrophic gastritis of the corpus is a spectrum of damage where H. pylori is a key agent able to induce gastric atrophic damage and also gastric autoimmunity.

Phenotypic and functional abnormalities within the residual non-B-cell compartment of B-cell chronic lymphocytic leukaemia (CLL) suggest an interaction between tumour cells and host immune effectors. To explore the possibility of a polarized Th1/Th2 response we have studied CD30 antigen expression and the pattern of cytokine production by purified CLL T cells. Activated T cells from CLL patients showed a significant increase in the expression of CD30 compared to normal controls. Accordingly, high levels of soluble CD30 were detected in supernatants from activated T-cell cultures, as well as in CLL serum samples. Messenger RNA for IL4 was found in both resting and, to a greater extent, in activated CLL T lymphocytes. The latter cells were also capable of releasing IL4. Three-colour immunofluorescence analyses revealed a strong CD30 expression in the CD3+/CD8+/CD28- large granular lymphocyte subset, which is considerably expanded in CLL. Production of IL4, as well as expression and release of CD30 by these T cells, was conclusively demonstrated at the clonal level. These findings document an expansion of a peculiar subset of 'Th2-like' cells in CLL, with an increased IL4 production and CD30 expression and release, that are likely to contribute to both the B-cell accumulation and immune-defects characteristic of this disease.