Samoučinkovitost učiteljev pri obravnavi učencev s simptomi motnje pozornosti s hiperaktivnostjo

Both the quality and quantity of teachers’ experiences of self-competence in dealing with pupils with symptoms of Attention Deficit Hyperactivity Disorder have been the subject of a great deal of research. The permanent monitoring of the levels at which teachers accomplish such competencies, which have a positive effect on the improvement of teaching, is one of the tasks of educational science. The present paper determines how teachers self-assess their efficacy in teaching pupils with behavioural difficulties based on the pupils’ symptoms of attention disorder and hyperactivity. Primary school teachers from 12 counties of the Republic of Croatia participated in the research. The teachers provided data for a total of 1,383 pupils in whom they subjectively detected behavioural difficulties. The research reveals that the characteristics of the pupil best predict the teacher’s self-efficacy. More time spent in the classroom with the teacher, better academic achievement, and a lower school grade indicate higher self-efficacy in teachers. (DIPF/Orig.

Assessing glycemia in type 1 diabetic patients using a microdialysis system for continuous glucose monitoring

Background: Continuous glucose monitoring systems can monitor moment-to-moment changes in blood glucose concentration, which cannot be detected by intermittent self-monitoring. Continuing monitoring sys--tems may lead to improved glycemic control. We evaluated a microdialysis technique for improving glycemic control in type 1 diabetes patients treated by different means of basal insulin substitution. Patients and Methods: Fifty-two type 1 diabetic patients on twice daily NPH and pre-meal aspart insulin were randomized in two groups: the continuation of NPH (n=26) (group 1) or once daily glargine (n=26) (group 2). 48-hour GlucoDay registrations were started at the beginning and after 4 months. Results: At baseline, time spent in the euglycemic range (glucose between 3.9 and 8.0mmol/L) was 37.96±6.81% for the NPH group and 35.83±6.24% for the glargine group. At endpoint, time in the euglyce--mic range increased in both groups (51.02±7.22% and 57.29±10.27%, P< 0.001 vs. before treatment for both groups). Time spent in the hypoglycemic range (glucose < 3.9 mmol/L) was 9.98±2.57% for the first group and 10.24±3.55% for the second group at baseline. At endpoint, time in the hypoglycemic range decreased in both groups (8.00±2.13% and 6.59±2.04%, P< 0.001 vs. before treatment for both groups). Conclusion: The analysis of the GlucoDay data gave us information about glycemia other than HbA1c and self-monitoring of blood glucose, such us a peakless activity profile and the lower percentage of time spent in the hypoglycemic range in the glargine-treated group

Fas receptor is required for estrogen deficiency-induced bone loss in mice

Bone mass is determined by bone cell differentiation, activity, and death, which mainly occur through apoptosis. Apoptosis can be triggered by death receptor Fas (CD95), expressed on osteoblasts and osteoclasts and may be regulated by estrogen. We have previously shown that signaling through Fas inhibits osteoblast differentiation. In this study we analyzed Fas as a possible mediator of bone loss induced by estrogen withdrawal. At 4 weeks after ovariectomy (OVX), Fas gene expression was greater in osteoblasts and lower in osteoclasts in ovariectomized C57BL/6J (wild type (wt)) mice compared with sham-operated animals. OVX was unable to induce bone loss in mice with a gene knockout for Fas (Fas -/- mice). The number of osteoclasts increased in wt mice after OVX, whereas it remained unchanged in Fas -/- mice. OVX induced greater stimulation of osteoblastogenesis in Fas -/- than in wt mice, with higher expression of osteoblast-specific genes. Direct effects on bone cell differentiation and apoptosis in vivo were confirmed in vitro, in which addition of estradiol decreased Fas expression and partially abrogated the apoptotic and differentiation-inhibitory effect of Fas in osteoblast lineage cells, while having no effect on Fas-induced apoptosis in osteoclast lineage cells. In conclusion, the Fas receptor has an important role in the pathogenesis of postmenopausal osteoporosis by mediating apoptosis and inhibiting differentiation of osteoblast lineage cells. Modulation of Fas effects on bone cells may be used as a therapeutic target in the treatment of osteoresorptive disorders

Chemokine signals are crucial for enhanced homing and differentiation of circulating osteoclast progenitor cells

Abstract Background The peripheral blood (PB) monocyte pool contains osteoclast progenitors (OCPs), which contribute to osteoresorption in inflammatory arthritides and are influenced by the cytokine and chemokine milieu. We aimed to define the importance of chemokine signals for migration and activation of OCPs in rheumatoid arthritis (RA) and psoriatic arthritis (PsA). Methods PB and, when applicable, synovial fluid (SF) samples were collected from 129 patients with RA, 53 patients with PsA, and 110 control patients in parallel to clinical parameters of disease activity, autoantibody levels, and applied therapy. Receptors for osteoclastogenic factors (CD115 and receptor activator of nuclear factor-κB [RANK]) and selected chemokines (CC chemokine receptor 1 [CCR1], CCR2, CCR4, CXC chemokine receptor 3 [CXCR3], CXCR4) were determined in an OCP-rich subpopulation (CD3−CD19−CD56−CD11b+CD14+) by flow cytometry. In parallel, levels of CC chemokine ligand 2 (CCL2), CCL3, CCL4, CCL5, CXC chemokine ligand 9 (CXCL9), CXCL10, and CXCL12 were measured using cytometric bead array or enzyme-linked immunosorbent assay. Sorted OCPs were stimulated in culture by macrophage colony-stimulating factor and receptor activator of nuclear factor-κB ligand, and they were differentiated into mature osteoclasts that resorb bone. Selected chemokines (CCL2, CCL5, CXCL10, and CXCL12) were tested for their osteoclastogenic and chemotactic effects on circulatory OCPs in vitro. Results The OCP population was moderately enlarged among PB cells in RA and correlated with levels of tumor necrosis factor-α (TNF-α), rheumatoid factor, CCL2, and CCL5. Compared with PB, the RANK+ subpopulation was expanded in SF and correlated with the number of tender joints. Patients with PsA could be distinguished by increased RANK expression rather than total OCP population. OCPs from patients with arthritis had higher expression of CCR1, CCR2, CCR4, CXCR3, and CXCR4. In parallel, patients with RA had increased levels of CCL2, CCL3, CCL4, CCL5, CXCL9, and CXCL10, with significant elevation in SF vs PB for CXCL10. The subset expressing CXCR4 positively correlated with TNF-α, bone resorption marker, and rheumatoid factor, and it was reduced in patients treated with disease-modifying antirheumatic drugs. The CCR4+ subset showed a significant negative trend during anti-TNF treatment. CCL2, CCL5, and CXCL10 had similar osteoclastogenic effects, with CCL5 showing the greatest chemotactic action on OCPs. Conclusions In our study, we identified distinct effects of selected chemokines on stimulation of OCP mobilization, tissue homing, and maturation. Novel insights into migratory behaviors and functional properties of circulatory OCPs in response to chemotactic signals could open ways to new therapeutic targets in RA

Chemotactic and immunoregulatory properties of bone cells are modulated by endotoxin-stimulated lymphocytes

In our study, we explored the bidirectional communication via soluble factors between bone cells and endotoxin-stimulated splenic lymphocytes in an in vitro coculture model that mimics the inflammatory environment. Both the ability of lymphocytes to affect differentiation and immune properties of bone cells, osteoblasts (OBL) and osteoclasts (OCL), and of bone cells to modulate cytokine and activation profile of endotoxin-stimulated lymphocytes were tested. LPS-pulsed lymphocytes enhanced OCL but inhibited OBL differentiation and increased the RANKL/OPG ratio, and, at the same time, upregulated chemotactic properties of bone cells, specifically CCL2, CCL5, and CXCL10 in OCL and CCL5 and CXCL13 in OBL. In parallel, bone cells had immunosuppressive effects by downregulating the lymphocyte expression of interleukin (IL)-1, IL-6, TNF-α and co-stimulatory molecules. OCL stimulated the production of osteoclastogenic cytokine RANKL in T lymphocytes. The anti-inflammatory effect, especially of OBL, suggests a possible compensatory mechanism to limit the inflammatory reaction during infection