[Educational intervention to improve diagnostic accuracy regarding psychological morbidity in general practice]. / Verbessert eine Schulungsintervention die Diagnostik von psychischen Erkrankungen in der hausärztlichen Praxis?

INTRODUCTION: The aim of this pilot study was to evaluate the effectiveness of a complex educational intervention to improve the diagnostic competencies of general practitioners (GPs) regarding the detection of depression, anxiety and somatization. METHODS: Cluster-randomized controlled pilot study with six practices each in the intervention group and in the control group. Psychological morbidity was determined by patient self-report using the Patient Health Questionnaire (PHQ-D). GPs rated the extent of psychological morbidity on a numerical rating scale from 0 (no co-morbidity) to 10 (maximum) of the individual patient after the consultation, independent of the reason for encounter. RESULTS: 364 patients participated. There were moderate correlations between GP rating and the PHQ scales (Spearman correlation between 0.27 and 0.42). There was no significant difference between intervention and control group. Diagnostic accuracy of the GPs, as determined with areas under the curves (AUCs), ranged between 0.52 (95%KI 0.30-0.73) and 0.84 (95%KI 0.67-1.00). The AUCs showed significant heterogeneity (Cochran Q=25.0; p<0.01). The regression analysis with 'presence of psychological disorder' (in PHQ) as the dependent variable showed that longer duration of doctor-patient-relationship was negatively associated with psychological morbidity (OR 0.96; 95%KI 0.92-0.99; p=0.01). There was a significant interaction between the factors 'time of doctor-patient relationship' and 'GP rating' (ß=0.02; OR 1.02, 95%KI 1.01-1.03; p<0.001), pointing towards increasing diagnostic accuracy when patients are known for a longer time. DISCUSSION: We found no significant effect regarding the educational intervention. The GPs' estimation regarding psychological morbidity correlated significantly with the self-rating of the patients on PHQ scales. However, there was a considerable inter-individual variation between the GPs' diagnostic accuracy. The diagnostic estimation improved with increasing duration of doctor-physician relationship. CONCLUSION: A one-time educational intervention seems not to be sufficient to improve diagnostic competencies in the detection of psychological morbidity. The considerable variation of the diagnostic accuracy might explain why 'one-size-fits-all' educational interventions will not help improve diagnostic competencies.

Evaluation of a Computer-Based Training Program for Enhancing Arithmetic Skills and Spatial Number Representation in Primary School Children.

Calcularis is a computer-based training program which focuses on basic numerical skills, spatial representation of numbers and arithmetic operations. The program includes a user model allowing flexible adaptation to the child's individual knowledge and learning profile. The study design to evaluate the training comprises three conditions (Calcularis group, waiting control group, spelling training group). One hundred and thirty-eight children from second to fifth grade participated in the study. Training duration comprised a minimum of 24 training sessions of 20 min within a time period of 6-8 weeks. Compared to the group without training (waiting control group) and the group with an alternative training (spelling training group), the children of the Calcularis group demonstrated a higher benefit in subtraction and number line estimation with medium to large effect sizes. Therefore, Calcularis can be used effectively to support children in arithmetic performance and spatial number representation.

Energetics and reaction mechanisms for the competitive losses of H2, CH4 and C2H4 from protonated methylbenzenes--implications to the methanol- to-hydrocarbons (MTH) process.

We report the unimolecular decomposition following collisional activation of protonated mono-, di- and trimethylbenzenes as a function of collision energy. The resulting energy-resolved mass spectra are then used for the quality control of high-level quantum chemical models of the respective potential energy surfaces. Distinction is made between direct dissociation products (CH(4) or H(2)) and indirect products (alkenes), since formation of the latter requires extensive rearrangement of the molecular skeleton. Very good consistency was found between model and experiment. The models thereby provide a solid foundation for discussing the reaction mechanisms of the industrial methanol-to-hydrocarbon process. The losses of CH(4), C(2)H(4) and C(3)H(6) from mesitylenium ions have been studied by (13)C and (2)H labelling and the alkene losses were found to occur via irreversible isomerisation pathways.

Expression of the chemokine receptor CCR1 in human renal allografts.

BACKGROUND: Chemokines are involved in the recruitment of leukocytes to vascularized allografts. CCR1 is a receptor for various proinflammatory chemokines and CCR1 blockade reduces renal allograft injury in rabbits. The purpose of the study was to characterize CCR1-positive cells in human renal allografts. METHODS: Formalin-fixed, paraffin-embedded allograft nephrectomies (n = 9) and non-involved parts of tumour nephrectomies (n = 10) were studied. Immunohistochemistry for CCR1, CD3 and CD68 was performed on consecutive sections. Double immunofluorescence for CCR1 and CD3, CD20, CD68, DC-SIGN and S100 was used on selected cases. Expression of CCR1 mRNA and the ligands CCL3 and CCL5 was studied in renal allograft biopsies with acute rejection (n = 10), with chronic allograft nephropathy (n = 8) and controls (n = 8). RESULTS: CCR1 protein was expressed by circulating cells in glomerular and peritubular capillaries, colocalizing with CD68. In renal allografts CCR1-positive cells were present within glomerular tufts, but only scattered CCR1-positive cells were found in tubulointerstitial infiltrates. CCR1 did not colocalize with the majority of CD68-positive cells in the interstitium. The small number of CCR1-positive interstitial cells were identified as CD20- or DC-SIGN-positive by double immunofluorescence. CCR1 mRNA was significantly increased in renal biopsies with acute allograft rejection (P < 0.001), and with chronic allograft nephropathy (P < 0.05), it correlated with the expression of CCL3 and CCL5, and with serum-creatinine. CONCLUSIONS: CCR1 mRNA expression was associated with renal function in allografts. CCR1 protein expression was restricted to monocytes, CD20-positive B cells and DC-SIGN-positive dendritic cells. Thus most interstitial macrophages were CCR1 negative, which may relate to down-regulation after migration into the interstitium in human renal allografts.

Analysis of NF-kappaB nuclear translocation in PMN-neutrophils of major trauma patients in the early post-traumatic period: a pilot study.

BACKGROUND: Post-traumatic inflammation is connected to polymorphonuclear neutrophil (PMN)-dysfunction characterized by reduced nuclear translocation of NF-kappaB during the post-traumatic period. However, the dynamic of NF-kappaB translocation in PMN of major trauma patients remains unclear. Hence, the aim of this pilot study was to analyze NF-kappaB in PMN from multiply injured patients immediately after trauma. PATIENTS AND METHODS: Blood samples of major trauma patients (ISS > 16) were drawn on admission within 90 minutes after trauma and at 6, 12, 24, 48, and 72 hours after trauma. Neutrophilic NF-kappaB-translocation was analyzed by EMSA and quantified by densitometry as (arbitrary units). In addition, PMN of healthy volunteers were analyzed either in their native state (-control) or after LPS stimulation (+control). RESULTS: Twelve patients (NISS: 34 +/- 10 [mean +/- SEM]) were enrolled. NF-kappaB translocation was significantly increased in trauma patients on admission and after 6 hours. Interestingly, a second activity peak was present after 24 hours. In patients who later died, NF-kappaB activity was significantly elevated initially, to be rapidly diminished after 6 hours, while it increased in the survivors group. After 24 hours NF-kappaB activity increased significantly in the survivors group, to become reduced in both groups at a later time. CONCLUSIONS: Within this pilot study, the dynamic of NF-kappaB translocation in PMN of multiply injured patients immediately after trauma was analyzed for the first time. Enabled by closely matched sequential blood sampling strictly standardized to the traumatic event, an essential biphasic increase of neutrophilic signal transduction could be investigated in the very early post-traumatic period, which preceded the downregulation of the innate immune system.

Initial posttraumatic translocation of NF-kappaB and TNF-alpha mRNA expression in peripheral blood monocytes of trauma patients with multiple injuries: a pilot study.

Post-traumatic inflammation is connected to monocyte dysfunction characterized by reduced NF-kappaB translocation during the first post-traumatic days. Because the exact dynamic of monocytic NF-kappaB translocation in patients directly after trauma remains unclear, the aim of this pilot study was to measure the intranuclear presence of NF-kappaB in monocytes from patients with multiple injuries initially after the trauma and during the early post-traumatic period and to compare these results with downstream-placed mRNA expression alteration of TNF-alpha, as well as with clinical data. Eleven patients were enrolled with an Injury Severity Score of 16 to 66 points, and blood samples were drawn on admission within 90 min and at 6, 12, 24, 48, and 72 h after trauma. NF-kappaB translocation of monocytic nuclear protein was analyzed by electrophoretic mobility shift assay and was quantified by densitometry as arbitrary units. In addition, monocytes of healthy volunteers were analyzed either native (-, control) or after LPS stimulation (+, control). For determination of downstream mRNA encoding for TNF-alpha, quantitative reverse transcriptase-PCR was performed. For both parameters, the negative control values were set as baseline (=1) and results from positive controls and patients were given as a relative alteration ratio without unit. Initial post-traumatic NF-kappaB translocation was significantly increased in trauma patients on admission (88 +/- 37) and 6 h after trauma (59 +/- 28) compared with the baseline level. In contrast, TNF-alpha mRNA was not increased on admission (1.7 +/- 0.9) and decreased even below baseline after 12 h. The substantial information of our study arises from the analysis of the dynamic of NF-kappaB translocation of monocytes. Enabled by closely matched sequential blood sampling strictly standardized to the traumatic event, an essential increase of monocytic signal transduction and transcription could be elucidated in the very early post-traumatic period, which precedes the down-regulation of the innate immune system.