[The Medical Examination - Between Desire and Reality - Analysis of Consensus Between the Second Part of the Medical Licensing Exam (IMPP) and the National Catalogue of Expertise-based Learning Goals in Surgery (NKLC)]. / Medizinische Prüfung zwischen Wunsch und Wirklichkeit ­ Analyse der Übereinstimmung zwischen dem 2. Abschnitt der ärztlichen Prüfung und dem Nationalen Kompetenzbasierten Lernzielkatalog Chirurgie.

Background The working party of the German Society for Surgery (DGCH) on undergraduate surgical education has developed a national expertise-based catalogue of learning goals in surgery (NKLC). This study analyses the extent to which the questions of the German second medical licensing examination compiled by the IMPP are congruent with the NKLC and which thematic focus is emphasised. Materials and Methods Firstly, a guideline and evaluation sheet were developed in order to achieve documentation of the individual examination questions of the second licensing examination with respect to the learning goals of the NKLC. In a retrospective analysis from autumn 2009 to autumn 2014, eleven licensing examinations in human medicine were screened independently by three different reviewers. In accordance with the guideline, the surgical questions were identified and subsequently matched to the learning goals of the NKLC. The analysis included the number of surgical learning goals as well as the number of surgical questions for each examination, learning goal, and different levels of expertise (LE). Results Thirteen reviewers from six surgical disciplines participated in the analysis. On average, reviewers agreed on the differentiation between surgical and non-surgical questions in 79.1% of all 3480 questions from 11 licensing examinations. For each examination (n = 320 questions), 98.8 ± 22.6 questions (min.: 69, max.: 150) were rated as surgical. For each surgical learning goal addressed, 2.2 ± 0.3 questions (min.: 1, max.: 16) were asked. For each examination, 23.5 ± 6.3 questions (min.: 11; max.: 31) referred to learning goals of LE 3, 52.5 ± 16.7 questions (min.: 34; max.: 94) addressed learning goals of LE 2 and 22.8 ± 7.7 questions (min.: 9; max.: 34) were related to learning goals of LE 1. 64 learning goals (27.8% of all learning goals of the NKLC) were not reflected in the examinations. With a total of 70 questions, the most frequently examined surgical topic was "disorders of the rheumatic spectrum". Conclusion The number of surgical examination questions in the German second medical licensing examination seems to be sufficient. However, the questions seem to be unevenly distributed between different surgical areas of undergraduate education. In order to achieve a more homogenous representation of relevant surgical topics, improved alignment is needed between the state examination with existing catalogues of learning goals by the IMPP.

Differential Relevance of NF-κB and JNK in the Pathophysiology of Hemorrhage/Resususcitation-Induced Liver Injury after Chronic Ethanol Feeding.

BACKGROUND: Chronic ethanol (EtOH) abuse worsens pathophysiological derangements after hemorrhagic shock and resuscitation (H/R) that induce hepatic injury and strong inflammatory changes via JNK and NF-κB activation. Inhibiting JNK with a cell-penetrating, protease-resistant peptide D-JNKI-1 after H/R in mice with healthy livers ameliorated these effects. Here, we studied if JNK inhibition by D-JNKI-1 in chronically EtOH-fed mice after hemorrhagic shock prior to the onset of resuscitation also confers protection. METHODS: Male mice were fed a Lieber-DeCarli diet containing EtOH or an isocaloric control (ctrl) diet for 4 weeks. Animals were hemorrhaged for 90 min (32 ± 2 mm Hg) and randomly received either D-JNKI-1 (11 mg/kg, intraperitoneally, i. p.) or sterile saline as vehicle (veh) immediately before the onset of resuscitation. Sham animals underwent surgical procedures without H/R and were either D-JNKI-1 or veh treated. Two hours after resuscitation, blood samples and liver tissue were harvested. RESULTS: H/R induced hepatic injury with increased systemic interleukin (IL)-6 levels, and enhanced local gene expression of NF-κB-controlled genes such as intercellular adhesion molecule (ICAM)-1 and matrix metallopeptidase (MMP)9. c-Jun and NF-κB phosphorylation were increased after H/R. These effects were further increased in EtOH-fed mice after H/R. D-JNKI-1 application inhibited the proinflammatory changes and reduced significantly hepatic injury after H/R in ctrl-fed mice. Moreover, D-JNKI-1 reduces in ctrl-fed mice the H/R-induced c-Jun and NF-κB phosphorylation. However, in chronically EtOH-fed mice, JNK inhibition did not prevent the H/R-induced hepatic damage and proinflammatory changes nor c-Jun and NF-κB phosphorylation after H/R. CONCLUSIONS: These results indicate, that JNK inhibition is protective only in not pre-harmed liver after H/R. In contrast, the pronounced H/R-induced liver damage in mice being chronically fed with ethanol cannot be prevented by JNK inhibition after H/R and seems to be under the control of NF-κB.

Chronic ethanol feeding modulates inflammatory mediators, activation of nuclear factor-κB, and responsiveness to endotoxin in murine Kupffer cells and circulating leukocytes.

Chronic ethanol abuse is known to increase susceptibility to infections after injury, in part, by modification of macrophage function. Several intracellular signalling mechanisms are involved in the initiation of inflammatory responses, including the nuclear factor-κB (NF-κB) pathway. In this study, we investigated the systemic and hepatic effect of chronic ethanol feeding on in vivo activation of NF-κB in NF-κB(EGFP) reporter gene mice. Specifically, the study focused on Kupffer cell proinflammatory cytokines IL-6 and TNF-α and activation of NF-κB after chronic ethanol feeding followed by in vitro stimulation with lipopolysaccharide (LPS). We found that chronic ethanol upregulated NF-κB activation and increased hepatic and systemic proinflammatory cytokine levels. Similarly, LPS-stimulated IL-1 ß release from whole blood was significantly enhanced in ethanol-fed mice. However, LPS significantly increased IL-6 and TNF-α levels. These results demonstrate that chronic ethanol feeding can improve the responsiveness of macrophage LPS-stimulated IL-6 and TNF-α production and indicate that this effect may result from ethanol-induced alterations in intracellular signalling through NF-κB. Furthermore, LPS and TNF-α stimulated the gene expression of different inflammatory mediators, in part, in a NF-κB-dependent manner.

Long-term prospective teaching effectivity of practical skills training and a first OSCE in cranio maxillofacial surgery for dental students.

Basic skills in oral/CMF surgery should be taught effectively to dental students as surgical skills training is traditionally under-represented in the dental curriculum compared to its later need in daily clinical practice. Rigid curricular time frames and prospectively condensed professional education foster new effective teaching and examination formats. Transmitting and assessing clinical competence objectively (independent of subjective bias), reliably (repeatable, inter-rater consistency) and valid (representative, structured task selection) was intended and evaluated in oral/CMF surgery skills acquisition starting in summer 2009. A small-group practical skills training (PST) day initiated a one-week practical training course, covering previously formulated learning objectives. An objective structured clinical evaluation (OSCE) was held at the end of each semester. Theoretical background knowledge and clinical skills should have to be memorized within a representative number of practical tasks (test stations). A first semester (26 students) used classical practical training alone as controls, the following semesters (171 students) had PST, considered as a study group. All 197 students were assessed with OSCE's over a 3-year period. An instructor held PST based on presentations, videos and practical training, including mannequins, with pairs of students. This included history taking, communication and interpretation of laboratory/image diagnostics, structured clinical facial examination, fracture diagnosis, venipuncture, suturing, biopsy and wire loops on pig jaws for manual and clinical skills, which were later incorporated in OSCE stations. OSCE average results increased from 63.3 ± 9.7% before and to 75.5 ± 10% after the inclusion of PST (p < 0.05). Knowledge diffusion between sittings on the same test date and between consecutive semesters was insignificant. Students and faculty rated their learning/teaching experience "very good" to "good". PST was effective in optimizing clinical skills as evaluated by OSCE.

Delayed wound repair in sepsis is associated with reduced local pro-inflammatory cytokine expression.

Sepsis is one of the main causes for morbidity and mortality in hospitalized patients. Moreover, sepsis associated complications involving impaired wound healing are common. Septic patients often require surgical interventions that in-turn may lead to further complications caused by impaired wound healing. We established a mouse model to the study delayed wound healing during sepsis distant to the septic focus point. For this reason cecal ligation and puncture (CLP) was combined with the creation of a superficial wound on the mouse ear. Control animals received the same procedure without CPL. Epithelialization was measured every second day by direct microscopic visualization up to complete closure of the wound. As interplay of TNF-α, TGF-ß, matrix metalloproteinases (MMP), and tissue inhibitors of metalloproteinases (TIMP) is important in wound healing in general, TNF-α, TGF-ß, MMP7, and TIMP1 were assessed immunohistochemical in samples of wounded ears harvested on days 2, 6, 10 and 16 after wounding. After induction of sepsis, animals showed a significant delay in wound epithelialization from day 2 to 12 compared to control animals. Complete wound healing was attained after mean 12.2± standard deviation (SD) 3.0 days in septic animals compared to 8.7± SD 1.7 days in the control group. Septic animals showed a significant reduction in local pro-inflammatory cytokine level of TNF-α on day 2 and day 6 as well as a reduced expression of TGF-ß on day 2 in wounds. A significant lower expression of MMP7 as well as TIMP1 was also observed on day 2 after wounding. The induction of sepsis impairs wound healing distant to the septic focus point. We could demonstrate that expression of important cytokines for wound repair is deregulated after induction of sepsis. Thus restoring normal cytokine response locally in wounds could be a good strategy to enhance wound repair in sepsis.