Klaus Höcherl

Background: The subject catalogue (SC) for the First State Examination in Pharmacy (P1) is a nationwide, concise list of subjects covered in the first two years of German pharmacy programmes. In its current form, however, it does not provide any information about the competencies to which knowledge of these subjects contributes. Methods: The subjects in this catalogue were mapped to competencies that are considered to be achievable within the first two years of the curriculum. On the basis of this draft competency-based catalogue, we conducted an online survey of pharmacy faculty at German universities on the added value of a competency-based SC. Results: On average, about 75% of the participants (N = 158) agreed or partly agreed with the assumptions made in this survey about the benefits of a competency-based SC. Non-professors and younger teachers are generally more open to the concept than full professors and more experienced teachers. Professors, in particular, expressed their fears of regimentation and infringement of their freedom of teaching. Conclusion: The attitude of the participating German pharmacy teachers towards a competency-based SC is predominantly positive. Many points of criticism could be addressed in a participatory process of SC development.

Background: Competency-based education models (CBEM) are gaining growing importance in the qualification of healthcare professionals. However, the need for a pharmaceutical CBEM in Germany, particularly a competency-based Subject Catalogue (SC), remains controversial and has not been previously explored. Hence, a survey was conducted to evaluate the expectations of German pharmacy students regarding this topic. Methods: An anonymous online survey was administered between December 2022 and January 2023 to all pharmacy students in Germany. The questionnaire primarily used a 4-point Likert scale ranging from “disagree” to “agree”. Results: The majority of participants (N = 605) expected benefits from a competency-based SC. More than 90% supported a detailed and precise formulation of learning objectives, along with additional elements, such as competency levels and application examples. Conclusion: The study provides recommendations to improve the SC, facilitating pharmacy students’ preparation for the first state examination. Furthermore, findings highlight the need for better integrating theoretical knowledge into application-related content.

It has been reported that the serine protease kallikrein stimulates and that aprotinin, a protease inhibitor, inhibits renal renin secretion. Since direct stimulation of the protease-activated receptor (PAR) 2 increases renin secretion in isolated perfused mouse kidneys, we hypothesized that activation of PAR2 receptors by serine proteases could be involved in the synthesis and secretion of renin in vivo. We therefore determined the response of plasma renin concentration (PRC) to acute intraperitoneal administration of the PAR2 agonist SLIGRL, isoproterenol, hydralazine, furosemide, losartan, or lipopolysaccharide in conscious wild-type (WT) and Par2-deficient mice. Basal PRC was not different in Par2-deficient mice compared with WT mice. All six acute treatments caused significant increases of PRC in both WT and Par2-deficient mice. The response was significantly lower only in endotoxin-treated Par2-deficient mice. Chronic treatment with losartan, low salt intake, the combination of both, or furosemide caused an increase of PRC and renin mRNA in WT mice, whereas a high salt intake caused a decrease. Alterations in PRC and renal renin mRNA expression were not different between WT and Par2 -/- mice in response to chronic treatments. Par2-deficiency did not alter furosemide-induced diuresis and natriuresis. Systolic blood pressure responses to chronic treatments were not different between WT and Par2 -/- mice. In conclusion, deficiency of Par2 receptors does not alter renin secretion and renin gene expression modulated by a variety of typical maneuvers. However, activation of Par2 receptors by serine proteases seems to be of importance for renin secretion in the context of inflammation.

Magnesium (Mg²⁺) abnormalities during sepsis have been reported, but the underlying mechanisms during acute inflammation are poorly understood. We hypothesized that a decrease in GFR and/or changes in transporters or channels for Mg²⁺ could be responsible for the observed Mg²⁺ abnormalities. Therefore, we studied the metabolism of Mg²⁺ in a murine model of endotoxemia. LPS-induced hypermagnesemia was paralleled by a decrease in creatinine clearance and an increase in the fractional excretion of Mg²⁺. In agreement with an altered renal Mg²⁺ handling, endotoxemia decreased the renal expression of claudin (Cldn) 10b, Cldn16, Cldn19, parvalbumin, and of the solute carrier family (Slc) 41a3. Further, LPS increased the renal expression of Cldn14 and Slc41a1. The renal expression of the transient receptor potential melastin (Trpm) 6, Trpm7, and of cyclin M (Cnnm) 2 was unaltered in response to LPS. In vitro studies support a direct effect on the expression of Cldn10b, Cldn14, Cldn16, and Cldn19. Further, endotoxemia increased the fractional excretion of sodium, which was paralleled by a decrease of important renal sodium transporters. In the large intestine, the expression of Trpm7 was increased in response to LPS, whereas the expression of Trpm6 was decreased. Cnnm4 mRNA levels were unchanged in the large intestine. Further, Cldn12 and Na⁺-H⁺ exchanger 3 (Slc9a3) expressions were decreased in the small intestine in response to LPS. Our findings indicate that endotoxemia is associated with hypermagnesemia and a disturbed Mg²⁺ handling. It seems likely that LPS-induced hypermagnesemia is due to the decrease in renal function in response to LPS.