A third protein shown to interact with laforin, selleck called PTG, is a regulatory subunit of protein phosphatese-1 (PP1) that enhances glycogen accumulation (21). It was shown that the G240S missense mutation identified in some LD patients disrupts the interaction between laforin and PTG (while glycogen binding and phosphatase activity remain preserved). This observation suggests that PTG is critical for laforin function and that laforin is part of a complex of proteins associated with glycogen and may have a role in regulating its metabolism. Studies using a mammalian two-hybrid system demonstrated that laforin interacts with glycogen synthase kinase-3 (GSK3). Furthermore, laforin

reduces GSK3 Ser 9 phosphorylation (25, 26). Inhibitors,research,lifescience,medical GSK3 is a potent glycogen synthase (GS) inhibitor. The relationship between GSK3, GS, laforin and LBs is discussed below. EPM2B gene was identified through genome-wide linkage scan followed by haplotype analysis and homozygosity Inhibitors,research,lifescience,medical mapping performed in a cluster of French-Canadian families from Quebec (11, 27). To date, 40 mutations have been found in the EMP2B gene, including insertion, missense Inhibitors,research,lifescience,medical and nonsense changes, frameshifts and deletions in both compound heterozygous as well as homozygous states. The EMP2B gene product encodes a 395 amino acid protein

named malin which contains a zinc finger of the RING type at the N-terminus and six NHL-repeat motifs at the C-terminus. NHL motifs are likely involved in protein-protein interactions, while the RING-finger motif of malin is typical of E3 ubiquitin ligases. Sub-celllular localization studies showed that MYC-tagged malin, similarly to laforin, also localizes to the cytoplasm at Inhibitors,research,lifescience,medical the ER and the nucleus (16, 17, 28). The E3 ubiquitin ligase activity of malin was confirmed in vitro (25, 29). At least two mutations associated with LD (Cys26Ser and Phe33Ser) result in inactivation of malin’s

ubiquitinase function (13, 25). Ubiquitination can serve several purposes Inhibitors,research,lifescience,medical including targeting the ubiquitinated protein for destruction or actively regulating its function (30, 31). Recent studies demonstrated that laforin and malin interact and that this interaction occurs at the central regions of both proteins (25, 29). There is data suggesting that malin ubiquitinates laforin, targeting laforin for destruction, but this is presently difficult to understand, as destruction Rolziracetam of laforin by malin would be expected to result in Lafora disease (29). Finally, it was demonstrated through co-immunoprecipitation studies that malin and glycogen synthase (GS) interact, although the result of such interaction is not known. Animal models of Lafora Disease Animal models of Lafora Disease known to date include a naturally occurring dog, one transgenic mouse and one knockout mouse. The canine model was observed in approximately 5% of Miniature Wirehaired Dachshunds (MWHDs) in England. The identified mutation was a dodecamer expansion in the EPM2B gene (32).

27 Resulting loss of dopaminergic modulation of the early stages of visual processing28 is associated with impaired color perception and reduced spatial and temporal contrast sensitivity,29,30 as well as electroretinographic abnormalities and altered patternevoked potentials.31,32 These visual disturbances are correlated with disease severity33 and can be partially reversed with levodopa therapy.34,35 Table I. Clinical correlates of neuron loss in Parkinson’s disease. DA, dopamine; NA, noradrenaline;

5-HT, 5-hydroxytryptamine (serotonin); VP, vasopressin; Glu, glutamate; ACh, acetylcholine; CRF, corticotrophin-releasing factor; Inhibitors,research,lifescience,medical CCK, cholecystokinin; RBD, rapid … Olfactory DA neurons Olfactory dysfunction occurs early and often in PD, in association with early neuron loss and LB formation in the anterior olfactory nucleus and extensive Inhibitors,research,lifescience,medical LB pathology in the olfactory bulb.36,37 Hyposmia is demonstrable in up to 90% of PD patients in whom olfaction is formally tested,38 but this deficit is unrelated to disease duration or severity and is typically asymptomatic.39 In contrast to the characteristic depletion

Inhibitors,research,lifescience,medical of DA neurons in SNc, the population of DA neurons in the olfactory bulb actually increases in PD (in fact it more than doubles), mainly within the glomerular layer.40 While this increase may appear paradoxical, its association with hyposmia is consistent with – and may be explained

by40 – separate evidence that olfactory transmission Inhibitors,research,lifescience,medical within the glomerular level is inhibited by DA“41 due to a local predominance of d2 receptor types.42 A similar increase in the population of intrinsic DA neurons of the striatum Inhibitors,research,lifescience,medical occurs in the MPTP model of PD.43 The normally small population of these tyrosine hydroxylase (TH)-positive interneurons44 increased more than threefold in the putamen of monkeys rendered parkinsonian by destruction of the nigrostriatal DA neurons.43 Pontine GSK1120212 chemical structure noradrenergic neurons By the time of SNc involvement in PD, extranigral pathology has generally extended to other vulnerable cell groups within the brain stem.45 Notable among these are the noradrenergic neurons of the locus ceruleus (LC)46,47 and the serotonergic nuclei of the median raphe (nMR).37,48 The Carnitine palmitoyltransferase II wide-ranging and profuse axonal projections of LC neurons provide noradrenergic innervation to virtually the entire central nervous system (CNS) – except for the basal ganglia.49 Apart from a restricted portion of the ventral striatum (the shell region of the nucleus accumbens), neither the striatum nor the globus pallidus receives significant input from LC49 ; noradrenergic innervation of the subthalamic nucleus appears to be minimal in primates.50 Loss of LC neurons in PD results in marked reductions in NA levels in cerebellum51 and frontal cortex.

All of these models commonly propose that, in early PD patients, the withdrawal of dopaminergic medication has a detrimental effect on cognitive functions associated with the dorsolateral loop, and a beneficial effect on the cognitive functions associated with the orbital loop; this pattern has been recently

confirmed and better specified by a study that matched Inhibitors,research,lifescience,medical behavioral performances of PD patients ‘on’ and ‘off’ dopaminergic drugs and fMRI findings in healthy subjects in a simple selection task [MacDonald et al. 2011]. Findings confirmed that ventral striatum and the related orbital frontostriatal circuit is involved in learning new stimulus–stimulus

associations and its functioning Inhibitors,research,lifescience,medical is impaired in early PD stages by dopaminergic drugs; on the other hand, dorsal striatum and the related dorsolateral frontostriatal circuit is involved in the assimilation of new and relevant information for the production of more accurate selections, for example shifting attention to more salient stimuli, and its functioning is enhanced in early PD stages by dopaminergic drugs. This double dissociation involving cognitive effects of dopaminergic drugs Inhibitors,research,lifescience,medical is therefore evident when directly comparing patients ‘on’ and ‘off’ dopaminergic medication and was first suggested by the ‘dopamine overdose hypothesis’ [Gotham et al. 1986, 1988], stating that the administration of dopaminergic medication to early PD patients may replete dopamine-depleted circuits (including the dorsal striatum), thus improving Inhibitors,research,lifescience,medical performances in

tasks related to the dorsolateral loop while ‘overdosing’ relatively intact circuits (including the orbital loop). As levodopa mainly elevates dopamine levels Inhibitors,research,lifescience,medical in the striatum [Hornykiewicz, 1974; Maruyama et al. 1996], these differential effects are likely due to opposing effects of levodopa in the dorsal and the ventral striatum, which are connected to different cortical areas via segregated frontostriatal loops [Alexander et al. 1986]. MRIP The neurocomputational model of frontostriatal circuitry functioning in PD [Frank et al. 2004] proposed that basal ganglia modulate the selection of actions under consideration in the PFC. Two main projection pathways from the striatum travel up to the cortex through the thalamus via different basal ganglia output structures. The subthalamic nucleus provides a self-adaptive, dynamic control signal that temporarily prevents the execution of any response, depending on decision conflict [Frank, 2006]. The direct frontostriatal ‘orbital’ pathway is excitatory and the indirect frontostriatal ‘orbital’ pathway is Epigenetics inhibitor inhibitory.

Over 90% of patients who undergo modified radical mastectomy for their locally advanced disease requiring adjuvant chest wall radiotherapy develop radiation dermatitis. Breast cancer patients receiving chest wall radiotherapy develop acute skin toxicity (radiation dermatitis) during the course of radiotherapy or a short period after

the completion of radiotherapy.1,2 Chest Inhibitors,research,lifescience,medical wall radiation dermatitis can decrease tolerance for continuing radiotherapy, negatively influence quality of life, postpone treatment, and cause treatment failure.1 For the all the research hitherto conducted on the management of radiation-induced dermatitis, a consensus has yet to emerge as to what constitutes the http://www.selleckchem.com/products/SB-202190.html optimal care.2 Topical corticosteroids Inhibitors,research,lifescience,medical comprise one group of the suggested agents for the treatment of radiation-induced dermatitis. Corticosteroids have anti-inflammatory effects, which may play a crucial role in alleviating patients’ complaints. Recent evidence Inhibitors,research,lifescience,medical shows the efficacy of topical corticosteroids in this category.2,3 In addition, other local treatments such as Dexpanthenol, Calendula, and honey ointment have been recommended for treating dermatitis.4,5 Another drug which has newly been introduced for the management of burning and infectious wounds is natural Henna (Lawsonia inermis linn),6 with some investigators providing evidence

for its antimicrobial and antioxidant properties in wound healing as well.7-10 The data regarding the efficacy of Henna compounds in the management of burn and infected wounds are, however,

insufficient, and there are no optimal recommendations for skin care in breast cancer patients suffering Inhibitors,research,lifescience,medical radiation dermatitis. This Inhibitors,research,lifescience,medical study aimed to compare topical Alpha ointment and topical hydrocortisone cream (1%) in terms of their efficacy in the healing of radiation-induced dermatitis in breast cancer patients undergoing post-mastectomy chest wall radiotherapy. Patients and Methods This study is an open, randomized, controlled, phase II clinical trial. Eligible patients had newly pathologically proven, locally advanced breast cancer (treated with modified below radical mastectomy, followed by sequential adjuvant chemotherapy and chest wall radiotherapy [45-50.4 Gy]) and grade 2 and/or 3 radiation-induced dermatitis. Exclusion criteria consisted of any history of collagen vascular diseases, diabetes mellitus, taking any drugs interfering with the wound healing process like systemic steroids, previous history of chest wall radiotherapy, and concurrent use of chemotherapy. All the patients had to sign the consent form before participating in the study. This clinical trial was approved by the local Research Ethics Committee of Shiraz University of Medical Sciences.

EDH and SDH showed the largest odds ratio (22.6 and 13.7 respectively) Adjusted analysis After adjusting for all potential confounding variables, there was an increased

risk of haematoma INCB28060 evacuation for both SDH and EDH. The magnitude of the association was larger for large haematomas, intermediate for those coded as NFS and smallest for the small ones. The odds ratio for large EDH and SDH were, respectively, 25.58 (95% CI: 18.80-34.81) and 15.47 (95% CI: 11.88-20.13). After multivariate analysis none of the categories of IPH remained Inhibitors,research,lifescience,medical positively associated with evacuation. Similar results were obtained when excluding GCS and brain swelling from the multivariable adjustment. Comparison between large and small haemorrhages In table ​table44 it can be seen that large IB, wherever the location,

were associated with an increased risk of mortality, in comparison with small IB lesions. Inhibitors,research,lifescience,medical After adjusting for potential confounders (model 1) the odds ratio for mortality was 2.86 (95% CI: 1.86-4.38) for large EDH, 3.41 (95% CI: 2.68-4.33) for large SDH and 3.47 (95% CI: 2.26-5.33) for large IPH. Patients with EDH coded as NFS had an odds ratio for Inhibitors,research,lifescience,medical mortality of 1.89 (95% CI: 1.20-2.99) in comparison with those with small EDH. There was no strong evidence of increased risk of mortality for those Inhibitors,research,lifescience,medical patients with SDH or IPH coded as NFS when compared with patients with the corresponding lesions coded as small. Table 4 Odds ratios (95% confidence intervals) for mortality with small haemorrhages as baseline Discussion This analysis of over 13,000 patients with TBI showed

that patients with a large EDH, SDH or IPH have a substantially higher mortality than patients with either no bleeding or a small bleed. Even after adjusting for other CT findings, such as contusions and brain swelling, and other potential confounding variables, such as age and GCS, large bleeds substantially increased the probability of death. Patients with Inhibitors,research,lifescience,medical large IPH or large SDH had more than a threefold increased in mortality odds in comparison with patients with small IB in the same location, while large EDH showed more nearly than a doubling in the mortality odds in comparison with patients with small EDH. Small IB were not associated with an increased in mortality after adjustment for other potentially confounding variables. Patients with IB coded as NFS had generally a risk which was intermediate between that reported for patients with large and the one reported for patients with small IB. The frequency of IB after a TBI varies according to the inclusion criteria of the different studies. The incidence of IB in our analysis was higher than other series because of the TARN inclusion criteria.

Key Words: Fructose, insulin resistance, Urtica dioica Introduction Diabetes mellitus

occurs when the body can’t use glucose normally, and is associated with increased serum triglycerides, decreased serum HDL and sometimes increased serum LDL.1 According to ancient medical texts, Urtica dioica may be used for the treatment of high blood sugar.2 Hypoglycemic activity of Urtica dioica was detected in a large pharmacological screen of European species with known potential anti-diabetic effects.3 It has also been reported that the extract of the leaves or other parts of Inhibitors,research,lifescience,medical the plan were of GSK1120212 datasheet benefits in conditions such as prostatic hyperplasia, Inflammation, arthritis rheumatoid, hypertension and allergic Inhibitors,research,lifescience,medical rhinitis.4 Urtica dioica has been reported to have histamine, formic acid, acetylcholine, acetic acid, butyric acid, leukotrienes, 5-hydroxytryptamine, and other irritants.5,6 This study aimed to evaluate the effect of Urtica dioica leaf extract on blood glucose, lipid profile, insulin and leptin in rat model of fructose-induced insulin resistance. Inhibitors,research,lifescience,medical Materials and Methods Animal

Maintenance Forty male Wistar rats, weighting 200-250 g were obtained from the Animal Breeding Center, Jundishapur University of Medical Sciences, and were kept under standard conditions (12/12 light-dark cycle, 20-24oC, 55% humidity) with free access to water and food. All procedures were performed in accordance with the University guidelines Inhibitors,research,lifescience,medical for care and use of laboratory animals. Plant Extraction Urtica dioica was collected around the city of Ahwaz and identified by a faculty of the Department of Pharmacognosy, Jundishapur University of Medical Sciences. The leaves were dried under the shade and ground to powder by an electrical grinder. The extraction was prepared using maceration method. The powder was macerated for 72 hours at

room temperature using 70% ethanol and 30% water. The mixture was filtered with Whatman filter paper (No 1), and the filtrate was centrifuged Inhibitors,research,lifescience,medical at 3000 rpm for 20 min. The supernatant was evaporated at ambient temperature and the extract powder (15.1% of leaf powder) was kept at 4˚C until used.7 Experimental Studies One below group of rats was assigned as sham group (n=8) and given tap water. Thirty two rats, given daily fresh fructose 10% in drinking water,8 for eight weeks. Starting from the 6th week, they were randomly divided into four groups (n=8 each) including a control receiving intraperitoneal (IP) vehicle for Urtica dioica, and three other groups receiving single administrations of IP hydro-alcoholic extract of Urtica dioica at 50, 100 or 200 mg/kg.9 Twenty four hours after the last IP injection, the animals were lightly anesthetized and blood samples were obtained by cardiac puncture.

According to the service configurations, XML-based descriptions are generated that contain the information needed by client applications to call the services correctly. At runtime, the jETI SPS receives calls and data from the client, which it forwards to the corresponding registered tool, collects the result, and sends it back to the client. For providing pieces of FiatFlux functionality that are directly accessible by the SPS and that are adequate for workflow modeling, we applied a set of purpose-built

scripts to handle (aggregated) function calls and the required data transfers. More precisely, Inhibitors,research,lifescience,medical each FiatFlux function of interest (available as a single MATLAB function or as specific sequence Inhibitors,research,lifescience,medical of MATLAB functions)

is encapsulated by a MATLAB script, which can be executed by MATLAB in headless mode. This invocation of MATLAB is again wrapped as a service into a shell script that can then be called by the jETI SPS. It turned out that a coarse-grained service library, which provides predefined variants of the major analysis steps, rather than exposing computational details of the analysis steps to the workflow level, is advantageous. Inhibitors,research,lifescience,medical Thus, we finally provide the following services: – MSdataExtraction: Mass spectrometry (MS) data extraction from .cdf format. – METAFoR: Predefined, complete metabolic flux ratio analysis. Performs the user emulation steps Cyclosporin A described above. – netFlux: Predefined, complete net flux distribution analysis. Performs the user emulation steps described above. – netFlux_CustomModel: Predefined, Inhibitors,research,lifescience,medical complete 13C flux analysis based on a user-defined network model. Performs the user emulation

steps described above. – netFlux_JointRatios: Predefined, complete 13C flux analysis that uses several results from complimentary datasets as Inhibitors,research,lifescience,medical input. Performs the user emulation steps described above. Combining data from experiments with different isotopomer mixtures is valuable as it increases the resolution of network fluxes. The jETI SPS is able to generate clients for the registered services, particularly in the form of jABC workflow building blocks, which take care of exchanging the necessary data with the surrounding workflow and manage the communication with the jETI SPS. The different FiatFlux services can thus be combined with various other services, allowing the user to work with Montelukast Sodium FiatFlux in a highly flexible and automated manner. In the following we give a short introduction to workflow modeling with jABC, before we describe three of the many possible Flux-P workflows that we realized using jABC as a jETI client. 2.7. Workflows for 13C-data Analysis The jABC framework (Figure 2), which provides the graphical user interface for Bio-jETI, supports the orchestration of processes from heterogeneous services.

A frequent and difficult problem in DM2 is the peculiar muscle pain described earlier (35, 29). The exact mechanism underlying the pain is unknown, and there is no well-established, effective treatment. Carbamazepine or mexiletine along with nonsteroidal anti-inflammatory medications or tylenol ameliorate this pain in some patients. Concluding remarks The myotonic dystrophies are dominantly inherited multisystemic disorders that include two genetically distinct Inhibitors,research,lifescience,medical types. DM1 is the commonest cause of adult onset muscular dystrophy with an estimated prevalence of 1/8000. Due to the lack of awareness of the disease among clinicians, DM2 this website remains largely underdiagnosed and the prevalence of DM2 is not well established.

These diseases have been called ‘spliceopathies’ and are mediated by a primary disorder of RNA rather than proteins,

however, spliceopathy may not fully explain the multisystemic disease spectrum. Although the two forms Inhibitors,research,lifescience,medical of myotonic dystrophy share many features, there are definite differences with respect to clinical, Inhibitors,research,lifescience,medical muscle biopsy, and genetic findings. In DM2 the core symptoms include proximal muscle weakness, myotonia, cataracts, cardiac conduction defects, insulin resistance and male hypogonadism. In DM1, the muscle weakness and wasting are more severe, preferentially distal and facial with ptosis, and with later evolving dysphagia, generalized weakness, and respiratory failure. A severe congenital form associated with DM1 has not been observed in DM2, and anticipation is the exception in DM2. In contrast to DM1, type 2 fiber are preferentially involved in DM2 with the presence Inhibitors,research,lifescience,medical of very atrophic type 2 fibers early in

muscle pathogenesis. The basis for the differences between DM1 and DM2 has not been clarified at the molecular level. There is currently no cure but effective management is likely to significantly Inhibitors,research,lifescience,medical reduce the morbidity and mortality of patients. The enormous advances in the understanding of the molecular pathogenesis of DM1 and DM2 has revealed pathways of molecular pathogenesis more complex than previously appreciated that could be the right track towards the development of effective therapies. Acknowledgements This work was supported by AFM – Association Française contre les Myopathies, CMN – Centro per lo Studio delle Malattie Neuromuscolari and FMM – Fondazione Malattie PD184352 (CI-1040) Miotoniche
Because I am a neuromyologist that has dealt for many years with muscle hypertonia, I decided to write my memories in order to motivate younger researchers to try to duplicate the same observations and experiences. We defined a whole range of conditions and symptoms, partly or in full. That is the first crucial step on the way to suppressing or relieving suffering. In some cases there was nothing we could do. In the other cases, we managed to diminish the uncomfortable symptoms. In still other cases, we cured the diseases, at least for a while.

Conflict of interest statement: DKT has received honoraria from Lilly UK and Roche for educational talks. Contributor Information Kayleigh M. Brown, Institute of Psychiatry, King’s College London, PO Box 63, De Crespigny Park, Denmark Hill, London SE5 8AF, UK. Derek K. Tracy, The Institute of Psychiatry, King’s College, London, UK and Oxleas NHS Foundation Trust,

UK.
Quetiapine is a dibenzothiazepine derivative that is licensed for the treatment of schizophrenia Inhibitors,research,lifescience,medical in an immediate-release (IR) formulation. An extended-release (ER) formulation has also been licensed in the UK (March 2010) for use in depression and in bipolar disorder. Quetiapine is provided in 25, 100, 150, 200 and 300 mg quetiapine fumarate IR and ER tablets; a 400 mg ER tablet is also available. The maximum licensed daily dose of quetiapine for the treatment of schizophrenia is 750 mg/day,

and for Inhibitors,research,lifescience,medical the treatment of depression and of mania in bipolar disorder 600 and 800 mg/day, respectively [BNF, 2012]. Quetiapine has a plasma half-life of some 7 hours and maximum plasma concentrations are obtained 1–2 hours postdose [Hiemke et al. 2011; Sparshatt et al. 2011]. It is metabolized to sulfoxide, Inhibitors,research,lifescience,medical 7-hydroxy, N-desalkyl, O-desalkyl, and 7-hydroxy-N-desalkyl metabolites by cytochromes P450 (CYP) 3A4 and CYP3A5, with a possible minor contribution from CYP2D6 [Sparshatt et al. 2011; Spina and de Leon, 2007; Bakken et al. 2011]. The 7-hydroxy- and 7-hydroxy-N-desalkyl- metabolites are pharmacologically active and accumulate in plasma to concentrations of less than 10% of Inhibitors,research,lifescience,medical those of quetiapine itself [DeVane and Nemeroff, 2001]. N-Desalkylquetiapine may be a major contributor to the antidepressant effect of quetiapine [Jensenet al. 2008]. Quetiapine

plasma concentrations and its Inhibitors,research,lifescience,medical effectiveness in therapy may be associated with the P-glycoprotein status of the patient [Nikischet al. 2010]. Optimal efficacy of quetiapine IR in treating the positive symptoms of schizophrenia is seen at doses of 150–750 mg/day; for treating the negative symptoms of schizophrenia a dose of 300 mg/day is recommended [Arvanitis and Miller, 1997]. For quetiapine ER doses of 600 Rutecarpine and 800 mg/day are most effective at treating both the positive and negative symptoms of schizophrenia [Sparshatt et al. 2008]. There is currently no widely accepted target range for predose plasma quetiapine concentrations associated with either optimal clinical response, or minimal adverse effects when used to treat schizophrenia. However, target ranges of 50–100 µg/l (upper limit uncertain), 100–500 µg/l and 70–170 µg/l have been suggested [Taylor et al. 2012; Hiemke et al. 2011; PFT�� manufacturer Baumann et al. 2004]. There are also no accepted target ranges for plasma quetiapine concentrations when used to treat depression, although quetiapine doses of 150 mg/day (quetiapine ER) have been suggested [El-Khalili et al. 2010].

Committee for “Emergency Medical Care and Simulation” In 1998, Burdick et al. stated correctly that society has a right to expect that every physician is able to manage acute problems of patients and that a basic knowledge of emergency medical care has to exist [2]. Following this postulation, and based on the developments initiated through

legal changes, the “Committee for Emergency Medical Care and simulation” was Inhibitors,research,lifescience,medical founded within the “German Association for Medical Education” (GMA) by medical professionals engaged in medical education and simulation [2,3]; their professional backgrounds – internal medicine, traumatology and anaesthesiology – emphasize the interdisciplinary approach of the committee. The objective of this committee is to establish an interdisciplinary, nationwide forum for discussion, exchange Inhibitors,research,lifescience,medical of ideas and concepts of continuous improvement in education of emergency medical care as Inhibitors,research,lifescience,medical well as the

implementation of simulation find more technology in this field. The committee is explicitly interdisciplinary and accessible for all interested professionals involved in education with respect to emergency medical care, which includes paramedic and nursing staff as well. The overall goal of the committee is to define the education at the level of competence in emergency medical care as a fundamental part of undergraduate medical

education. Purpose of survey Inhibitors,research,lifescience,medical The committee decided to collect data about the current status of undergraduate medical education in emergency medical care at German Inhibitors,research,lifescience,medical medical schools. This survey should build the foundation for further committee work, especially in finding a useful minimal standard for a nationwide curriculum in emergency medical care and in identifying research and development topics in this particular Parvulin field of education. Additionally, this survey was intended to discover weaknesses in form and content as well as applied assessment and teaching methods, and to give the participating schools feedback about their program as compared to the others. Methods Methodology and item selection The survey was conducted in the context of the postgraduate-degree programme “Master of Medical Education-Germany” and arranged by the authors. In order to keep the questionnaire as simple as possible and yet as informative as necessary, the number of items had to be restricted to a reasonable and answerable amount.