The Erasmus programme for postgraduate education in orthodontics in Europe: an update of the guidelines

In 1989, the ERASMUS Bureau of the European Cultural Foundation of the Commission of the European Communities funded the development of a new 3-year curriculum for postgraduate education in orthodontics. The new curriculum was created by directors for orthodontic education representing 15 European countries. The curriculum entitled ‘Three years Postgraduate Programme in Orthodontics: the Final Report of the Erasmus Project' was published 1992. In 2012, the ‘Network of Erasmus Based European Orthodontic Programmes' developed and approved an updated version of the guidelines. The core programme consists of eight sections: general biological and medical subjects; basic orthodontic subjects; general orthodontic subjects; orthodontic techniques; interdisciplinary subjects; management of health and safety; practice management, administration, and ethics; extramural educational activities. The programme goals and objectives are described and the competencies to be reached are outlined. These guidelines may serve as a baseline for programme development and quality assessment for postgraduate programme directors, national associations, and governmental bodies and could assist future residents when selecting a postgraduate programm

Vanishing influence of the band gap on the charge exchange of slow highly charged ions in freestanding single-layer MoS2

Charge exchange and kinetic energy loss of slow highly charged xenon ions transmitted through freestanding monolayer MoS2 are studied. Two distinct exit charge state distributions, characterized by high and low charge states, are observed. They are accompanied by smaller and larger kinetic energy losses, as well as scattering angles, respectively. High charge exchange is attributed to two-center neutralization processes, which take place in close impact collisions with the target atoms. Experimental findings are compared to graphene as a target material and simulations based on a time-dependent scattering potential model. Independent of the target material, experimentally observed charge exchange can be modeled by the same electron capture and de-excitation rates for MoS2 and graphene. A common dependence of the kinetic energy loss on the charge exchange for MoS2 as well as graphene is also observed. Considering the similarities of the zero band-gap material graphene and the 1.9 eV band-gap material MoS2, we suggest that electron transport on the femtosecond timescale is dominated by the strong influence of the ion’s Coulomb potential in contrast to the dispersion defined by the material’s band structure

Contributions of the international plant science community to the fight against infectious diseases in humans-part 2: Affordable drugs in edible plants for endemic and re-emerging diseases.

The fight against infectious diseases often focuses on epidemics and pandemics, which demand urgent resources and command attention from the health authorities and media. However, the vast majority of deaths caused by infectious diseases occur in endemic zones, particularly in developing countries, placing a disproportionate burden on underfunded health systems and often requiring international interventions. The provision of vaccines and other biologics is hampered not only by the high cost and limited scalability of traditional manufacturing platforms based on microbial and animal cells, but also by challenges caused by distribution and storage, particularly in regions without a complete cold chain. In this review article, we consider the potential of molecular farming to address the challenges of endemic and re-emerging diseases, focusing on edible plants for the development of oral drugs. Key recent developments in this field include successful clinical trials based on orally delivered dried leaves of Artemisia annua against malarial parasite strains resistant to artemisinin combination therapy, the ability to produce clinical-grade protein drugs in leaves to treat infectious diseases and the long-term storage of protein drugs in dried leaves at ambient temperatures. Recent FDA approval of the first orally delivered protein drug encapsulated in plant cells to treat peanut allergy has opened the door for the development of affordable oral drugs that can be manufactured and distributed in remote areas without cold storage infrastructure and that eliminate the need for expensive purification steps and sterile delivery by injection

Contributions of the international plant science community to the fight against human infectious diseases - part 1: epidemic and pandemic diseases.

Infectious diseases, also known as transmissible or communicable diseases, are caused by pathogens or parasites that spread in communities by direct contact with infected individuals or contaminated materials, through droplets and aerosols, or via vectors such as insects. Such diseases cause ~17% of all human deaths and their management and control places an immense burden on healthcare systems worldwide. Traditional approaches for the prevention and control of infectious diseases include vaccination programmes, hygiene measures and drugs that suppress the pathogen, treat the disease symptoms or attenuate aggressive reactions of the host immune system. The provision of vaccines and biologic drugs such as antibodies is hampered by the high cost and limited scalability of traditional manufacturing platforms based on microbial and animal cells, particularly in developing countries where infectious diseases are prevalent and poorly controlled. Molecular farming, which uses plants for protein expression, is a promising strategy to address the drawbacks of current manufacturing platforms. In this review article, we consider the potential of molecular farming to address healthcare demands for the most prevalent and important epidemic and pandemic diseases, focussing on recent outbreaks of high-mortality coronavirus infections and diseases that disproportionately affect the developing world

eLearning at the Hannover Medical School

In the recent years various multimedia learning modules were developed at the Hannover Medical School. So, for example the web-based content management system Schoolbook is used to collect medical cases for education. It enables authors to present their specialised knowledge in the World Wide Web without the need to be familiar with internet technologies. The System provides access to several sources of medical knowledge and is used as an elearning platform for different medical departments. Furthermore it was established in combination with the learning management system ILIAS which contains web-based learning units as well as self-tests (multiple choice) with direct feedback.In den vergangenen Jahren wurden an der Medizinischen Hochschule Hannover (MHH) zahlreiche multimediale Lernmodule erstellt. So werden mit dem web-basierten Autorentool Schoolbook Lernszenarien realisiert, die die spezifischen Anforderungen der fallbasierten Lehre in der ärztlichen und zahnärztlichen Aus-, Weiter- und Fortbildung berücksichtigen. Das Schoolbook ermöglicht den Ärzten medizinisch interessante Fälle innerhalb des Klinikbetriebes in digitaler Form zu sammeln und didaktisch aufbereitet für die Lehre zur Verfügung zu stellen. Weiterhin werden in enger Zusammenarbeit mit Lehrkräften unterschiedlicher Fachgebiete in der MHH eLearning-Module (Lerneinheiten) sowie Online-Tests (MC-Fragen) entwickelt und im web-basierten Lern-Management-System ILIAS zum Internet-basierten Lehren und Lernen bereitgestellt

Inhibition of c-jun n-terminal kinase after hemorrhage but before resuscitation mitigates hepatic damage and inflammatory response in male rats

Inhibition of c-Jun N-terminal kinase (JNK) by a cell-penetrating, protease-resistant JNK peptide (D-JNKI-1) before hemorrhage and resuscitation (H/R) ameliorated the H/R-induced hepatic injury and blunted the proinflammatory changes. Here we tested the hypothesis if JNK inhibition at a later time point-after hemorrhagic shock but before the onset of resuscitation-in a rat model of H/R also confers protection. Twenty-four male Sprague-Dawley rats (250 - 350 g) were randomly divided into 4 groups: 2 groups of shock animals were hemorrhaged to a MAP of 32 to 37 mmHg for 60 min and randomly received either D-JNKI-1 (11 mg/kg i.p.) or sterile saline as vehicle immediately before the onset of resuscitation. Two groups of sham-operated animals underwent surgical procedures without H/R and were either D-JNKI-1 or vehicle treated. Rats were killed 2 h later. Serum activity of alanine aminotransferase and serum lactate dehydrogenase after H/R increased 3.5-fold in vehicle-treated rats as compared with D-JNKI-1-treated rats. Histopathological analysis revealed that hepatic necrosis and apoptosis (hematoxylin-eosin, TUNEL, and M30, respectively) were significantly inhibited in D-JNKI-1-treated rats after H/R. Hepatic oxidative (4-hydroxynonenal) and nitrosative (3-nitrotyrosine) stress as well as markers of inflammation (hepatic and serum IL-6 levels and hepatic infiltration with polymorphonuclear leukocytes) were also reduced in D-JNKI-1-treated rats. LPS-stimulated TNF-alpha release from whole blood from hemorrhaged and resuscitated animals was higher in vehicle-treated rats as compared with D-JNKI-1-treated rats. c-Jun N-terminal kinase inhibition after hemorrhage before resuscitation resulted in a reduced activation of c-Jun. Taken together, these results indicate that D-JNKI-1 application after hemorrhagic shock before resuscitation blunts hepatic damage and proinflammatory changes during resuscitation. Hence, JNK inhibition is even protective when initiated after blood loss before resuscitation. These experimental results indicate that the JNK pathway may be a possible treatment option for the harmful consequences of H/R

A peptide inhibitor of C-jun N-terminal kinase modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation

Hemorrhage and resuscitation (H/R) leads to phosphorylation of mitogen-activated stress kinases, an event that is associated with organ damage. Recently, a specific, cell-penetrating, protease-resistant inhibitory peptide of the mitogen-activated protein kinase c-JUN N-terminal kinase (JNK) was developed (D-JNKI-1). Here, using this peptide, we tested if inhibition of JNK protects against organ damage after H/R. Male Sprague-Dawley rats were treated with D-JNKI-1 (11 mg/kg, i.p.) or vehicle. Thirty minutes later, rats were hemorrhaged for 1 h to a MAP of 30 to 35 mmHg and then resuscitated with 60% of the shed blood and twice the shed blood volume as Ringer lactate. Tissues were harvested 2 h later. ANOVA with Tukey post hoc analysis or Kruskal-Wallis ANOVA on ranks, P < 0.05, was considered significant. c-JUN N-terminal kinase inhibition decreased serum alanine aminotransferase activity as a marker of liver injury by 70%, serum creatine kinase activity by 67%, and serum lactate dehydrogenase activity by 60% as compared with vehicle treatment. The histological tissue damage observed was blunted after D-JNKI-1 pretreatment both for necrotic and apoptotic cell death. Hepatic leukocyte infiltration and serum IL-6 levels were largely diminished after D-JNKI-1 pretreatment. The extent of oxidative stress as evaluated by immunohistochemical detection of 4-hydroxynonenal was largely abrogated after JNK inhibition. After JNK inhibition, activation of cJUN after H/R was also reduced. Hemorrhage and resuscitation induces a systemic inflammatory response and leads to end-organ damage. These changes are mediated, at least in part, by JNK. Therefore, JNK inhibition deserves further evaluation as a potential treatment option in patients after resuscitated blood loss