[Pictograms for assessing pain quality in foreign language-speaking patients: a quality improvement study]. / Piktogramme zur Erfassung der Schmerzqualität bei fremdsprachigen Patient_innen.

Pictograms for assessing pain quality in foreign language-speaking patients: a quality improvement study Abstract. Background: Numerical assessment instruments allow foreign language patients to quantify their pain. However, for a complete assessment of the pain situation, the description of pain quality is also important. Problem: To assess pain quality completely, the treatment team lacked a tool. Objective: Foreign language-speaking patients can communicate their pain to the treatment team and are actively involved in the treatment process. The treatment team develops tools for recording the quality of pain and reflects on their experiences. Method: In a practice development project, pictograms of the Iconic Pain Assessment Tool 2 (IPAT2) where chosen to assess pain quality. The pictograms were prepared for everyday use, tested, and evaluated. Results: With the help of pictograms, quality of pain of 72 patients was documented almost 50% more frequently than before the study. The nursing team experienced IPAT2 as helpful in obtaining information and deepening the quality of the relationship. A feeling of being seen and understood emerged. Discussion: Pictograms are a valid method for nonverbal pain assessment. However, there is a risk of misunderstanding. The study only allowed an external assessment of patient's perceptions. An empirical investigation of the patient's view would be desirable. Conclusions: Further use and development of pictograms for communicating with foreign language-speaking patients are recommended.

Optimized quantification of lymphocyte subsets by use of CD7 and CD33.

Identification and quantification of lymphocyte subsets is based on the expression of specific cell surface antigens. As only a minority of these structures is lineage-restricted gating strategies were established, which should permit to include a maximum of lymphocytes, to reach a high purity within the gate and to avoid specific loss of subsets. Two problems remain: First, the incomplete removal of nonlymphoid cells when CD14 is used to exclude them from the lymphocyte gate. Second, the lack of a restricted marker to identify NK cells that are usually defined as CD3(-) /CD16/56(+) lymphocytes, though contaminating monocyte subsets share the expression of CD16, respectively, CD56. This study demonstrates the advantage of CD33 over CD14 at the creation of a pure lymphocyte gate, because CD33 enables the exclusion of all monocyte subpopulations as well as basophils and granulocytes. Independent of the applied NK cell marker mean purity was significantly higher, when CD33 was used (P < 0.001). For the identification of NK cells, CD7 was compared with CD16/56 and with single stained CD56. CD7 and CD16/56 exhibited as equivalent in various CD33 settings (P ≥ 0.173), whereas the mean proportion of CD56(+) NK cells was significantly lower (P ≤ 0.008). Use of CD14 entailed a significantly higher amount of CD3(-) /CD16/56(+) cells than of CD3(-) /CD7(+) cells (P = 0.008) because of the remaining CD14(-) /CD16(+) monocytes. As CD7 is restricted to T cells and NK cells in peripheral blood, misclassification of contaminating monocytes is avoided and CD7(+) NK cells can be identified by lack of CD3. Applying this new selection of mAbs, we reached a mean purity of ≥99.50% within the revised lymphocyte gate. As gates can be set very broadly, high inclusivity and high purity are not mutually exclusive. We propose the adoption of CD7 and CD33 for the quantification of lymphocyte subsets.

Molecular correlates of age-dependent seizures in an inherited neonatal-infantile epilepsy.

Many idiopathic epilepsy syndromes have a characteristic age dependence, the underlying molecular mechanisms of which are largely unknown. Here we propose a mechanism that can explain that epileptic spells in benign familial neonatal-infantile seizures occur almost exclusively during the first days to months of life. Benign familial neonatal-infantile seizures are caused by mutations in the gene SCN2A encoding the voltage-gated Na(+) channel Na(V)1.2. We identified two novel SCN2A mutations causing benign familial neonatal-infantile seizures and analysed the functional consequences of these mutations in a neonatal and an adult splice variant of the human Na(+) channel Na(V)1.2 expressed heterologously in tsA201 cells together with beta1 and beta2 subunits. We found significant gating changes leading to a gain-of-function, such as an increased persistent Na(+) current, accelerated recovery from fast inactivation or altered voltage-dependence of steady-state activation. Those were restricted to the neonatal splice variant for one mutation, but more pronounced for the adult form for the other, suggesting that a differential developmental splicing does not provide a general explanation for seizure remission. We therefore analysed the developmental expression of Na(V)1.2 and of another voltage-gated Na(+) channel, Na(V)1.6, using immunohistochemistry and real-time reverse transcription-polymerase chain reaction in mouse brain slices. We found that Na(V)1.2 channels are expressed early in development at axon initial segments of principal neurons in the hippocampus and cortex, but their expression is diminished and they are gradually replaced as the dominant channel type by Na(V)1.6 during maturation. This finding provides a plausible explanation for the transient expression of seizures that occur due to a gain-of-function of mutant Na(V)1.2 channels.