[Change Mechanisms in Group Therapy: A Questionnaire to Measure Therapeutic Perspectives]. / Wirkfaktoren in der Gruppentherapie: Fragebogen zur Messung der therapeutischen Perspektive.

Group therapy was shown to be an effective and economic intervention. To date few instruments exist to empirically assess mechanisms of therapeutic change in group therapy. The Group Therapy Process Questionnaire for Therapists (FEPiG-T) measuring change mechanisms in group therapy as viewed from the perspectives of therapists was developed and validated in this study based on the conceptualizations of Grawe,Yalom and Bordin and in reference to the previously developed measure for patients. The FEPiG-T subscales show good internal consistencies and small to large correlations with convergent measures. Subscales at beginning of therapy correlated with improvement of interpersonal problems over time. Further associations with symptom scales remained more vague. However, intersections with the established version for patients allow routinely implemented evaluation of the 2 perspectives in clinical practice, but inevitably need careful interpretation where the instruments differ in their factor structure.

Validation of the URICA-S in Group Therapy: Associations of Stages of Change with Therapeutic Factors and Treatment Outcome.

Stages of change could be driving forces to activate the realization of therapeutic factors and symptom change. Consequently, the aims of the present study were to investigate whether the stages of change concept is valid in group therapy settings shown by factor analysis, internal consistencies, and criterion validity. A total of 377 patients completed measures of stages of change, symptom change, and therapeutic factors. A confirmatory factor analysis replicated the stages of change factors for group therapy. Related to the criterion validity, stages of change demonstrated only low, non-significant associations with symptom change, but some stages of change were significant predictors of certain therapeutic factors. Further research is needed to explore whether a stronger focus on motivational stages of change could help to intensify the realization of therapeutic factors in group therapy.

[Change Factors in Group Therapy: Development and Validation of a Questionnaire]. / Wirkfaktoren in der Gruppentherapie: Entwicklung und Validierung eines Fragebogens.

While the efficacy of group therapy is sufficiently confirmed, there is a research gap concerning relevant therapeutic processes. Particularly, there is a dearth of integrative instruments that assess a broad spectrum of group therapeutic change factors. Hence, the aim of the current investigation was the validation of the newly developed "Scale for the assessment of therapeutic processes in group therapy (FEPiG)" based on Grawe's general psychotherapy and Yalom's conception of change factors in group therapy. 303 Patients (110 outpatients, 193 inpatients) participated in the study and completed the FEPiG as well as established measures concerning group processes. The outpatients additionally received established questionnaires concerning clinical symptomatology and filled out all instruments at the beginning and end of treatment. Factor analysis demonstrated an excellent factor structure of the FEPiG, which corresponded to the theoretically predicted subscales. Internal consistencies of the FEPiG were good to excellent and correlated with established process measures, which indicated convergent validity. While the FEPiG change factors subscales at the beginning of therapy were not correlated with outcome, associations between increases in change factors across the course of therapy and symptom reduction could be demonstrated.

Safety and efficacy of intensified versus standard dosing regimens of enteric-coated mycophenolate sodium in de novo renal transplant patients.

BACKGROUND: Efficacy and safety of an intensified dosing (ID) regimen of enteric-coated mycophenolate sodium (EC-MPS), which achieves higher mycophenolic acid exposure early posttransplantation, were evaluated in comparison with a standard dosing (SD) regimen. METHODS: In total, 128 de novo kidney transplant recipients treated with basiliximab induction, cyclosporine A, and steroids were randomized (1:1) to receive EC-MPS as SD (1440 mg/day; n=65) or ID (days 0-14: 2880 mg/day; days 15-42: 2160 mg/day; followed by 1440 mg/day; n=63). Efficacy parameters, safety, and tolerability were assessed over a 6-month study period. The primary endpoint was mean time to first occurrence of treatment failure. RESULTS: Mean time to treatment failure was 130 days (95% confidence interval [CI]: 81-n/a) in the ID group versus 114 days (95% CI: 15-155) in the SD group (P=0.36). Similar percentages (ID 30.2%; SD 36.9%) experienced treatment failure. Biopsy-proven acute rejection occurred in 2 (3.2%) ID versus 11 (16.9%) SD patients (P<0.001). Three (2.3%) deaths (2 SD, 1 ID) and five (3.9%) graft losses (3 SD, 2 ID) occurred. Renal function, incidence of infection, and hematologic disorders were comparable in both study cohorts. Gastrointestinal disorders occurred in 51 (81.0%) ID and 49 (75.4%) SD patients with overall similar tolerability as assessed by the Gastrointestinal Symptom Rating Scale. CONCLUSION: In this exploratory study, the EC-MPS ID regimen reduced the incidence of rejection and showed a comparable safety and tolerability profile to SD. Further examination of this approach in a larger patient cohort is now warranted to confirm these findings.

Pharmacokinetics and pharmacodynamics of intensified versus standard dosing of mycophenolate sodium in renal transplant patients.

BACKGROUND AND OBJECTIVES: Adequate early mycophenolic acid (MPA) exposure is an important determinant for effective rejection prophylaxis. This pharmacokinetic study investigated whether an intensified dosing regimen of enteric-coated mycophenolate sodium (EC-MPS) could achieve higher mycophenolic acid (MPA) exposure early after transplantation versus a standard dosing regimen. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: De novo kidney transplant recipients (n = 75) who were treated with basiliximab induction and cyclosporine were randomly assigned to receive EC-MPS as either standard dosing (1440 mg/d; n = 37) or intensified dosing (days 0 through 14: 2880 mg/d; days 15 through 42: 2160 mg/d; followed by 1440 mg/d; n = 38). Full 12-hour pharmacokinetic and pharmacodynamic profiles were taken at six time points during the first 3 months. Exploratory analysis of inosine monophosphate dehydrogenase (IMPDH) activity was also performed for better understanding of the pharmacokinetic-pharmacodynamic relationship between MPA exposure and IMPDH activity in the early posttransplantation period. Preliminary efficacy parameters, safety, and tolerability were assessed. RESULTS: Exposure to MPA was significantly higher on days 3 and 10 after transplantation in the intensified versus standard EC-MPS group, with 52.9 versus 22.2% (P < 0.05) of patients reaching MPA exposure >40 mg/h per L in the first week. The intensified regimen resulted in significantly lower IMPDH activity on day 3 after transplantation, and the overall safety was comparable for both groups. CONCLUSIONS: These pharmacokinetic and safety data support further research on the hypothesis that early adequate MPA exposure could improve clinical outcome.

Glyceroltrinitrate facilitates stimulated CGRP release but not gene expression of CGRP or its receptor components in rat trigeminal ganglia.

Nitric oxide (NO) donors induce delayed headaches in migraineurs. In a corresponding rat model NO donors cause delayed ongoing activity in central trigeminal neurons which process intracranial afferent input. Cellular models indicate that NO may increase the release or production of calcitonin gene-related peptide (CGRP), a key mediator in primary headaches. CGRP release from intact isolated trigeminal ganglia of adult male Wistar rats was investigated in vitro. Exposure to high NO donor concentrations did not affect basal or stimulated CGRP release. After a two hour infusion of the NO donor glyceroltrinitrate (250microg/kg/h), however, inflammatory mediators-induced CGRP release was 80% higher compared to control animals. Administration of the soluble guanylate cyclase inhibitor ODQ or the application of 8Br-cGMP revealed a cGMP-independent mechanism. In four groups of separate experiments total mRNA was extracted from rat trigeminal ganglia up to 6h after glyceroltrinitrate or saline infusion. Gene expression of CGRP and the CGRP-receptor components, receptor activity-modifying protein 1, receptor component protein and calcitonin receptor-like receptor was measured by quantitative RT-PCR. Glyceroltrinitrate infusion did not change mRNA levels of these genes compared to infusion of saline. The present data suggest that prolonged increase in NO levels facilitates stimulated CGRP release from trigeminal ganglion neurons. The underlying mechanism appears to be independent of the cGMP pathway and not to interact with CGRP in the trigeminal ganglion. Delayed headaches induced by NO may change CGRP or CGRP-receptor expression.

Autonomic renal denervation ameliorates experimental glomerulonephritis.

Increasing evidence indicates that inflammation of visceral organs is significantly affected by the autonomic nervous system. Such neuroimmune interactions have not been studied in the kidney. Here, we show that the rat kidney is innervated by both tyrosine hydroxylase-positive sympathetic efferent nerve fibers and calcitonin gene-related peptide-positive primary afferent nerve fibers, both of which are found in proximity to macrophages and dendritic cells. Complete surgical bilateral renal denervation was performed 2 d before glomerulonephritis was induced by injecting the monoclonal anti-Thy-1.1 antibody OX-7. Denervation significantly reduced albuminuria, mesangiolysis, formation of microaneurysms, deposition of glomerular collagen IV, and expression of TGF-beta compared with sham-operated controls. Accordingly, inflammation, identified by accumulation of interstitial macrophages and renal expression of TNF-alpha, and mesangial cell proliferation were significantly reduced. These findings indicate that autonomic renal denervation ameliorates and, by inference, innervation exacerbates acute inflammation in the kidney; therefore, neurotransmitters or neuropeptides and their receptors might represent novel targets for the treatment of acute glomerulonephritis.