HTTP 200 OK
Allow: GET, HEAD, OPTIONS
Content-Type: application/json
Vary: Accept
{
"count": 127182,
"next": "https://api-test.medunigraz.at/v1/research/search/publication/?format=api&limit=20&offset=125140",
"previous": "https://api-test.medunigraz.at/v1/research/search/publication/?format=api&limit=20&offset=125100",
"results": [
{
"text": "\n96133\nDevelopment of an anatomically detailed MRI-derived rabbit ventricular model and assessment of its impact on simulations of electrophysiological function.\n\nBishop, MJ\n\nPlank, G\n\nBurton, RA\n\nSchneider, JE\n\nGavaghan, DJ\n\nGrau, V\n\nKohl, P\n\nBeiträge in Fachzeitschriften\nISI:000273780400049\n19933417.0\n10.1152/ajpheart.00606.2009\nPMC2822578\nRecent advances in magnetic resonance (MR) imaging technology have unveiled a wealth of information regarding cardiac histoanatomical complexity. However, methods to faithfully translate this level of fine-scale structural detail into computational whole ventricular models are still in their infancy, and, thus, the relevance of this additional complexity for simulations of cardiac function has yet to be elucidated. Here, we describe the development of a highly detailed finite-element computational model (resolution: approximately 125 microm) of rabbit ventricles constructed from high-resolution MR data (raw data resolution: 43 x 43 x 36 microm), including the processes of segmentation (using a combination of level-set approaches), identification of relevant anatomical features, mesh generation, and myocyte orientation representation (using a rule-based approach). Full access is provided to the completed model and MR data. Simulation results were compared with those from a simplified model built from the same images but excluding finer anatomical features (vessels/endocardial structures). Initial simulations showed that the presence of trabeculations can provide shortcut paths for excitation, causing regional differences in activation after pacing between models. Endocardial structures gave rise to small-scale virtual electrodes upon the application of external field stimulation, which appeared to protect parts of the endocardium in the complex model from strong polarizations, whereas intramural virtual electrodes caused by blood vessels and extracellular cleft spaces appeared to reduce polarization of the epicardium. Postshock, these differences resulted in the genesis of new excitation wavefronts that were not observed in more simplified models. Furthermore, global differences in the stimulus recovery rates of apex/base regions were observed, causing differences in the ensuing arrhythmogenic episodes. In conclusion, structurally simplified models are well suited for a large range of cardiac modeling applications. However, important differences are seen when behavior at microscales is relevant, particularly when examining the effects of external electrical stimulation on tissue electrophysiology and arrhythmia induction. This highlights the utility of histoanatomically detailed models for investigations of cardiac function, in particular for future patient-specific modeling.\n\nPlank, Gernot\n\n\n"
},
{
"text": "\n98170\nNeuroendocrine circuitry and endometriosis: progesterone derivative dampens corticotropin-releasing hormone-induced inflammation by peritoneal cells in vitro.\n\nTariverdian, N\n\nRücke, M\n\nSzekeres-Bartho, J\n\nBlois, SM\n\nKarpf, EF\n\nSedlmayr, P\n\nKlapp, BF\n\nKentenich, H\n\nSiedentopf, F\n\nArck, PC\n\nBeiträge in Fachzeitschriften\nISI:000275461700007\n19898767.0\n10.1007/s00109-009-0559-8\nNone\nClinical symptoms of endometriosis, such as pain and infertility, can be described as persistent stressors. Such continuous exposure to stress may severely affect the equilibrium and bidirectional communication of the endocrine and immune system, hereby further aggravating the progression of endometriosis. In the present study, we aimed to tease apart mediators that are involved in the stress response as well as in the progression of endometriosis. Women undergoing diagnostic laparoscopy due to infertility were recruited (n = 69). Within this cohort, early stage of endometriosis were diagnosed in n = 30 and advanced stage of endometriosis in n = 8. Levels of progesterone in serum were determined. Frequency of progesterone receptor (PR) expression on CD56(+) and CD8(+) peritoneal lymphocytes was analysed by flow cytometry. The production of tumour necrosis factor (TNF) and interleukin (IL)-10 by peritoneal leukocytes upon stimulation with the potent stress mediator corticotropin-releasing hormone (CRH) and the progesterone derivative dydrogesterone, or both, were evaluated. Furthermore, the production of progesterone-induced blocking factor (PIBF) by peritoneal leukocytes and the expression of PR in endometriotic tissue were investigated. Levels of progesterone in serum were decreased in women with endometriosis and inversely correlated to pain scores. Furthermore, an increased frequency of CD56(+)PR(+) and CD8(+)PR(+) peritoneal lymphocytes was present in advanced endometriosis. The TNF/IL-10 ratio, reflecting cytokine secretion by peritoneal cells, was higher in cells derived from endometriosis patients and could be further heightened by CRH stimulation, whereas stimulation with dydrogesterone abrogated the CRH-mediated inflammation. Finally, the expression of PIBF by peritoneal leukocytes was increased in endometriosis. Low levels of progesterone in the follicular phase could be responsible for the progression of endometriosis and related pain. Peripheral CRH, increasing upon high psychological stress, might contribute to the peritoneal inflammation present in endometriosis. The therapeutic application of progesterone derivatives, CRH blocking agents as well as improvement of stress coping may disrupt the vicious circle between the chronic peritoneal inflammation and high perception of psychological stress in endometriosis.\n\nKampelmühler, Eva\n\nSedlmayr, Peter\n\n\n"
},
{
"text": "\n119562\nThe analgesic NSAID lornoxicam inhibits cyclooxygenase (COX)-1/-2, inducible nitric oxide synthase (iNOS), and the formation of interleukin (IL)-6 in vitro.\n\nBerg, J\n\nFellier, H\n\nChristoph, T\n\nGrarup, J\n\nStimmeder, D\n\nBeiträge in Fachzeitschriften\nISI:000081691400003\n10450786.0\n10.1007/s000110050474\nNone\nOBJECTIVE: To investigate anti-inflammatory effects of lornoxicam in vitro on COX-1/COX-2, on NO formation from iNOS and on the formation of the pro-inflammatory cytokines TNF-alpha, IL-1beta, IL-6, and IL-8. MATERIALS AND METHODS: COX-1 inhibition in intact cells was assessed employing two systems: measurement of aggregation in human washed platelets and assessment of TXB2 formation in HEL cells. COX-2 inhibition was assessed by measuring 6-keto-PGF1alpha in supernatants of intact cells of LPS-stimulated J774.2 cells (murine) and of Mono Mac 6 cells (human). In whole blood inhibition of COX-1 was performed by measuring TXB2 formation after clotting, and COX-2 inhibition was examined in LPS-stimulated whole blood cultures. The reduction of NO levels as a measure of the inhibition of cellular NO formation was assayed in supernatants of LPS-stimulated RAW 264.7 cells using the Griess reaction. Compound influence on the formation ofTNF-alpha, IL-1beta, IL-6, and IL-8 was examined using LPS-stimulated monocytic cells (THP-1) and measurement of cytokine concentrations by specific ELISAs. RESULTS: In intact human cells, lornoxicam showed a balanced inhibition of COX-1/-2 exhibiting the lowest IC50 (0.005 microM/0.008 microM) of the large panel of NSAIDs tested. Similar results were obtained in the whole blood for COX-1/-2. NO formation was dose-dependently inhibited by lornoxicam (IC50 of 65 microM) whereas piroxicam, diclofenac, ibuprofen, ketorolac and naproxen inhibited the NO formation markedly less. Indomethacin was approximately equipotent with lornoxicam. In stimulated monocytic cells (THP-1), lornoxicam showed a marked inhibition of IL-6 formation (IC50 54 microM) while the formation ofTNF-alpha, IL-1beta and IL-8 was only moderately affected. CONCLUSIONS: Of the panel of NSAIDs tested, lornoxicam was found to be the most potent balanced inhibitor of human COX-1/-2. The equipotent COX-isoenzyme inhibition by lornoxicam is complemented by a marked inhibition of IL-6 production and of iNOS-derived NO formation. The in vitro activities described support the marked anti-inflammatory and analgesic activities of lornoxicam found in animal models as well as in clinical studies.\n\n\n"
},
{
"text": "\n127708\nHigh risk vs. "metabolically healthy" phenotype in juvenile obesity - neck subcutaneous adipose tissue and serum uric acid are clinically relevant.\n\nWeghuber, D\n\nZelzer, S\n\nStelzer, I\n\nPaulmichl, K\n\nKammerhofer, D\n\nSchnedl, W\n\nMolnar, D\n\nMangge, H\n\nBeiträge in Fachzeitschriften\nISI:000321692500002\n23519645.0\n10.1055/s-0033-1341440\nNone\nSince obesity and its associated co-morbidities do not only have effect on the individual patient, but also on society and the health system, it is of great importance to investigate this lifestyle-disease. The rationale of this study was to distinguish metabolically healthy from unhealthy overweight/obese patients as compared to healthy normal weight children and adolescents by means of a comprehensive anthropometric, laboratory and sonomorphological vascular assessment.\n 299 study participants were derived from the prospective, observational study STYJOBS/EDECTA (STYrian Juvenile Obesity Study/Early DEteCTion of Arteriosclerosis). Standard anthropometric data were obtained for each subject. This study comprised different diagnostic steps: extended anthropometry (Lipometer®), carotid artery ultrasound, various laboratory measurements, blood pressure measurement, oral glucose tolerance test. Ow/ob juveniles were classified as "metabolically healthy" (no laboratory criteria of metabolic syndrome fulfilled) vs. "metabolically unhealthy" (≥ 3 criteria of metabolic syndrome). Results underwent statistical evaluation, including t-test or Mann-Whitney U-test, regression analysis and a p-value < 0.05 was considered statistically significant.\n In the study's central European cohort only about 16% (n=48/299) of the overweight/obese juveniles can be regarded as metabolically healthy. About 36% (n=108/299) of the overweight/obese patients fulfilled the criteria for metabolic syndrome. High visceral fat stores (p<0.001) and their clinical surrogate waist circumference (p<0.001) determine an adverse metabolic phenotype. Several parameters, including uric acid (p<0.001), adiponectin (p<0.05), insulin resistance (HOMA-Index, p<0.001), nuchal SAT thickness (p<0.001), arteriosclerosis of the carotids (p<0.001), and others are responsible for the distinction between -metabolically healthy and unhealthy juveniles. Nevertheless, "healthy obesity" only defines a sub-phenotype of a disease effecting rising numbers of young patients.\n Since obesity in children and adolescents is not a consistent entity, it remains crucial to differ between metabolically healthy and unhealthy obese children in order to achieve appropriate intervention and prevention for our patients.\n © J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York.\n\nMangge, Harald\n\nStelzer, Ingeborg\n\nZelzer, Sieglinde\n\n\n"
},
{
"text": "\n139563\nDefinition of a standard lymphadenectomy in surgery for pancreatic ductal adenocarcinoma: a consensus statement by the International Study Group on Pancreatic Surgery (ISGPS).\n\nTol, JA\n\nGouma, DJ\n\nBassi, C\n\nDervenis, C\n\nMontorsi, M\n\nAdham, M\n\nAndrén-Sandberg, A\n\nAsbun, HJ\n\nBockhorn, M\n\nBüchler, MW\n\nConlon, KC\n\nFernández-Cruz, L\n\nFingerhut, A\n\nFriess, H\n\nHartwig, W\n\nIzbicki, JR\n\nLillemoe, KD\n\nMilicevic, MN\n\nNeoptolemos, JP\n\nShrikhande, SV\n\nVollmer, CM\n\nYeo, CJ\n\nCharnley, RM\n\nInternational Study Group on Pancreatic Surgery\n\nBeiträge in Fachzeitschriften\nISI:000341228200014\n25061003.0\n10.1016/j.surg.2014.06.016\nNone\nThe lymph node (Ln) status of patients with resectable pancreatic ductal adenocarcinoma is an important predictor of survival. The survival benefit of extended lymphadenectomy during pancreatectomy is, however, disputed, and there is no true definition of the optimal extent of the lymphadenectomy. The aim of this study was to formulate a definition for standard lymphadenectomy during pancreatectomy.\n During a consensus meeting of the International Study Group on Pancreatic Surgery, pancreatic surgeons formulated a consensus statement based on available literature and their experience.\n The nomenclature of the Japanese Pancreas Society was accepted by all participants. Extended lymphadenectomy during pancreatoduodenectomy with resection of Ln's along the left side of the superior mesenteric artery (SMA) and around the celiac trunk, splenic artery, or left gastric artery showed no survival benefit compared with a standard lymphadenectomy. No level I evidence was available on prognostic impact of positive para-aortic Ln's. Consensus was reached on selectively removing suspected Ln's outside the resection area for frozen section. No consensus was reached on continuing or terminating resection in cases where these nodes were positive.\n Extended lymphadenectomy cannot be recommended. Standard lymphadenectomy for pancreatoduodenectomy should strive to resect Ln stations no. 5, 6, 8a, 12b1, 12b2, 12c, 13a, 13b, 14a, 14b, 17a, and 17b. For cancers of the body and tail of the pancreas, removal of stations 10, 11, and 18 is standard. Furthermore, lymphadenectomy is important for adequate nodal staging. Both pancreatic resection in relatively fit patients or nonresectional palliative treatment were accepted as acceptable treatment in cases of positive Ln's outside the resection plane. This consensus statement could serve as a guide for surgeons and researchers in future directives and new clinical studies.\n Copyright © 2014 Mosby, Inc. All rights reserved.\n\n\n"
},
{
"text": "\n148135\nPersistence, adherence, and medication-taking behavior in women with postmenopausal osteoporosis receiving denosumab in routine practice in Germany, Austria, Greece, and Belgium: 12-month results from a European non-interventional study.\n\nHadji, P\n\nPapaioannou, N\n\nGielen, E\n\nFeudjo Tepie, M\n\nZhang, E\n\nFrieling, I\n\nGeusens, P\n\nMakras, P\n\nResch, H\n\nMöller, G\n\nKalouche-Khalil, L\n\nFahrleitner-Pammer, A\n\nBeiträge in Fachzeitschriften\nISI:000361639700010\n26018090.0\n10.1007/s00198-015-3164-4\nPMC4575374\nPersistence with and adherence to osteoporosis therapy are critical for fracture reduction. This non-interventional study is evaluating medication-taking behavior of women with postmenopausal osteoporosis (PMO) receiving denosumab in Germany, Austria, Greece, and Belgium. Patients were representative of the PMO population and highly persistent with and adherent to denosumab at 12 months.\n Persistence with and adherence to osteoporosis therapy are important for optimal treatment efficacy, namely fracture reduction. This ongoing, non-interventional study will evaluate medication-taking behavior of women with postmenopausal osteoporosis (PMO) receiving denosumab in routine practice in four European countries.\n The study enrolled women who had been prescribed subcutaneous denosumab (60 mg every 6 months) in accordance with prescribing information and local guidelines. Persistence was defined as receiving the subsequent injection within 6 months + 8 weeks of the previous injection. Adherence was defined as receiving two consecutive injections within 6 months ± 4 weeks of each other. Medication coverage ratio (MCR) was calculated using the time a patient was covered with denosumab, as assessed from prescription records. Treatment was assigned prior to and independently of enrollment; outcomes are recorded during routine practice.\n These planned 12-month interim analyses included data from 1500 patients from 141 sites. Mean age was 66.4-72.4 years, mean baseline total hip T-scores ranged from -2.0 to -2.1 and femoral neck T-scores from -2.2 to -2.6, and 30.7-62.1% of patients had prior osteoporotic fracture. Persistence was 87.0-95.3%, adherence 82.7-89.3%, and MCR 91.3-95.4%. In a univariate analysis, increased age, decreased mobility, and increased distance to the clinic were associated with significantly decreased persistence; parental history of hip fracture was associated with significantly increased persistence.\n These data extend the real-world evidence regarding persistence with and adherence to denosumab, both of which are critical for favorable clinical outcomes, including fracture risk reduction.\n\nFahrleitner-Pammer, Astrid\n\n\n"
},
{
"text": "\n154158\nOverexpression of KCNJ3 gene splice variants affects vital parameters of the malignant breast cancer cell line MCF-7 in an opposing manner.\n\nRezania, S\n\nKammerer, S\n\nLi, C\n\nSteinecker-Frohnwieser, B\n\nGorischek, A\n\nDeVaney, TT\n\nVerheyen, S\n\nPassegger, CA\n\nTabrizi-Wizsy, NG\n\nHackl, H\n\nPlatzer, D\n\nZarnani, AH\n\nMalle, E\n\nJahn, SW\n\nBauernhofer, T\n\nSchreibmayer, W\n\nBeiträge in Fachzeitschriften\nISI:000384181000001\n27519272.0\n10.1186/s12885-016-2664-8\nPMC4983040\nOverexpression the KCNJ3, a gene that encodes subunit 1 of G-protein activated inwardly rectifying K(+) channel (GIRK1) in the primary tumor has been found to be associated with reduced survival times and increased lymph node metastasis in breast cancer patients.\n In order to survey possible tumorigenic properties of GIRK1 overexpression, a range of malignant mammary epithelial cells, based on the MCF-7 cell line that permanently overexpress different splice variants of the KCNJ3 gene (GIRK1a, GIRK1c, GIRK1d and as a control, eYFP) were produced. Subsequently, selected cardinal neoplasia associated cellular parameters were assessed and compared.\n Adhesion to fibronectin coated surface as well as cell proliferation remained unaffected. Other vital parameters intimately linked to malignancy, i.e. wound healing, chemoinvasion, cellular velocities / motilities and angiogenesis were massively affected by GIRK1 overexpression. Overexpression of different GIRK1 splice variants exerted differential actions. While GIRK1a and GIRK1c overexpression reinforced the affected parameters towards malignancy, overexpression of GIRK1d resulted in the opposite. Single channel recording using the patch clamp technique revealed functional GIRK channels in the plasma membrane of MCF-7 cells albeit at very low frequency.\n We conclude that GIRK1d acts as a dominant negative constituent of functional GIRK complexes present in the plasma membrane of MCF-7 cells, while overexpression of GIRK1a and GIRK1c augmented their activity. The core component responsible for the cancerogenic action of GIRK1 is apparently presented by a segment comprising aminoacids 235-402, that is present exclusively in GIRK1a and GIRK1c, but not GIRK1d (positions according to GIRK1a primary structure).\n The current study provides insight into the cellular and molecular consequences of KCNJ3 overexpression in breast cancer cells and the mechanism upon clinical outcome in patients suffering from breast cancer.\n\nBauernhofer, Thomas\n\nGhaffari Tabrizi-Wizsy, Nassim\n\nGorischek, Astrid\n\nJahn, Stephan\n\nMalle, Ernst\n\nPassegger, Christina Angelika\n\nPlatzer, Dieter\n\nRezania, Simin\n\nSchreibmayer, Wolfgang\n\nSteinecker-Frohnwieser, Bibiane\n\nVerheyen, Sarah\n\n\n"
},
{
"text": "\n174431\nAdhesion Prevention Efficacy of Composite Meshes Parietex<sup>®</sup>, Proceed<sup>®</sup> and 4DryField<sup>®</sup> PH Covered Polypropylene Meshes in an IPOM Rat Model.\n\nWinny, M\n\nMaegel, L\n\nGrethe, L\n\nLippmann, T\n\nJonigk, D\n\nSchrem, H\n\nKaltenborn, A\n\nKlempnauer, J\n\nPoehnert, D\n\nBeiträge in Fachzeitschriften\nISI:000391041900006\n27994499.0\n10.7150/ijms.16215\nPMC5165687\nBackground: Adhesions to intraperitoneally implanted meshes (IPOM) are a common problem following hernia surgery and may cause severe complications. Recently, we showed that missing peritoneal coverage of the intestine is a decisive factor for adhesion formation and 4DryField® PH (4DF) gel significantly prevents intestine-to-mesh adhesions even with use of uncoated Ultrapro® polypropylene mesh (UPM). The present study investigates adhesion prevention capability of coated Parietex® mesh (PTM) and Proceed® mesh (PCM) in comparison to 4DF treated UPM. Methods: 20 rats were randomized into two groups. A 1.5 x 2 cm patch of PTM or PCM was attached to the abdominal wall and the cecum was depleted from peritoneum by abrasion. After seven days incidence of intestine-to-mesh adhesions was evaluated using Lauder and Hoffmann adhesion scores. Histological specimens were evaluated; statistics were performed using student's t-test. The data were compared with recently published data of 4DF treated uncoated UPM. Results: Use of PTM or PCM did not significantly diminish development of intestine-to-mesh adhesions (adhesion reduction rate PTM: 29%, p = 0.069 and PCM: 25%, p = 0.078). Histological results confirmed macroscopic finding of agglutination of intestine and abdominal wall with the mesh in between. Compared to these data, the use of UPM combined with 4DF gel reveals significantly better adhesion prevention capability (p < 0.0001) as shown in earlier studies. However, in clinical situation interindividual differences in adhesion induction mechanisms cannot be excluded by this experimental approach as healing responses towards the different materials might vary. Conclusion: This study shows that in case of impaired intestinal peritoneum coated PTM and PCM do not provide significant adhesion prevention. In contrast, use of UPM combined with 4DF gel achieved a significant reduction of adhesions. Hence, in case of injury of the visceral peritoneum, application of a polysaccharide barrier device such as 4DF gel might be considered more effective in reducing intestine-to-mesh adhesions than coated mesh devices.\n\nSchrem, Harald Heinrich\n\n\n"
},
{
"text": "\n178985\nDevelopment and external validation of a dynamic prognostic nomogram for primary extremity soft tissue sarcoma survivors.\n\nCallegaro, D\n\nMiceli, R\n\nBonvalot, S\n\nFerguson, PC\n\nStrauss, DC\n\nvan Praag, VVM\n\nLevy, A\n\nGriffin, AM\n\nHayes, AJ\n\nStacchiotti, S\n\nPèchoux, CL\n\nSmith, MJ\n\nFiore, M\n\nTos, APD\n\nSmith, HG\n\nCatton, C\n\nSzkandera, J\n\nLeithner, A\n\nvan de Sande, MAJ\n\nCasali, PG\n\nWunder, JS\n\nGronchi, A\n\nBeiträge in Fachzeitschriften\nNone\n31891146.0\n10.1016/j.eclinm.2019.11.008\nPMC6933187\nPrognostic nomograms for patients with extremity soft tissue sarcoma (eSTS) typically predict survival or the occurrence of local recurrence or distant metastasis at time of surgery. Our aim was to develop and externally validate a dynamic prognostic nomogram for overall survival in eSTS survivors for use during follow-up.\n All primary eSTS patients operated with curative intent between 1994 and 2013 at three European and one Canadian sarcoma centers formed the development cohort. Patients with Fédération Française des Centres de Lutte Contre le Cancer (FNCLCC) grade II and grade III eSTS operated between 2000 and 2016 at seven other European reference centers formed the external validation cohort. We used a landmark analysis approach and a multivariable Cox model to create a dynamic nomogram; the prediction window was fixed at five years. A backward procedure based on the Akaike Information Criterion was adopted for variable selection. We tested the nomogram performance in terms of calibration and discrimination.\n The development and validation cohorts included 3740 and 893 patients, respectively. The variables selected applying the backward procedure were patient's age, tumor size and its interaction with landmark time, tumor FNCLCC grade and its interaction with landmark time, histology, and both local recurrence and distant metastasis (as first event) indicator variables. The nomogram showed good calibration and discrimination. Harrell C indexes at different landmark times were between 0.776 (0.761-0.790) and 0.845 (0.823-0.862) in the development series and between 0.675 (0.643-0.704) and 0.810 (0.775-0.844) in the validation series.\n A new dynamic nomogram is available to predict 5-year overall survival at different times during the first three years of follow-up in patients operated for primary eSTS. This nomogram allows physicians to update the individual survival prediction during follow-up on the basis of baseline variables, time elapsed from surgery and first-event history.\n © 2019 Published by Elsevier Ltd.\n\nLeithner, Andreas\n\nSzkandera, Joanna\n\n\n"
},
{
"text": "\n183889\nEuropean dermatology forum - updated guidelines on the use of extracorporeal photopheresis 2020 - part 1.\n\nKnobler, R\n\nArenberger, P\n\nArun, A\n\nAssaf, C\n\nBagot, M\n\nBerlin, G\n\nBohbot, A\n\nCalzavara-Pinton, P\n\nChild, F\n\nCho, A\n\nFrench, LE\n\nGennery, AR\n\nGniadecki, R\n\nGollnick, HPM\n\nGuenova, E\n\nJaksch, P\n\nJantschitsch, C\n\nKlemke, C\n\nLudvigsson, J\n\nPapadavid, E\n\nScarisbrick, J\n\nSchwarz, T\n\nStadler, R\n\nWolf, P\n\nZic, J\n\nZouboulis, C\n\nZuckermann, A\n\nGreinix, H\n\nBeiträge in Fachzeitschriften\nISI:000608483800056\n33025659.0\n10.1111/jdv.16890\nPMC7820969\nFollowing the first investigational study on the use of extracorporeal photopheresis for the treatment of cutaneous T-cell lymphoma published in 1983, this technology has received continued use and further recognition for additional earlier as well as refractory forms. After the publication of the first guidelines for this technology in the JEADV in 2014, this technology has maintained additional promise in the treatment of other severe and refractory conditions in a multi-disciplinary setting. It has confirmed recognition in well-known documented conditions such as graft-versus-host disease after allogeneic bone marrow transplantation, systemic sclerosis, solid organ transplant rejection including lung, heart and liver and to a lesser extent inflammatory bowel disease.\n In order to further provide recognized expert practical guidelines for the use of this technology for all indications, the European Dermatology Forum (EDF) again proceeded to address these questions in the hands of the recognized experts within and outside the field of dermatology. This was done using the recognized and approved guidelines of EDF for this task. All authors had the opportunity to review each contribution as it was added.\n These updated 2020 guidelines provide at present the most comprehensive available expert recommendations for the use of extracorporeal photopheresis based on the available published literature and expert consensus opinion. The guidelines are divided in two parts: PART I covers cutaneous T-cell lymphoma, chronic graft-versus-host disease and acute graft-versus-host disease while PART II will cover scleroderma, solid organ transplantation, Crohn's disease, use of ECP in paediatrics practice, atopic dermatitis, type 1 diabetes, pemphigus, epidermolysis bullosa acquisita and erosive oral lichen planus.\n © 2020 The Authors. Journal of the European Academy of Dermatology and Venereology published by John Wiley & Sons Ltd on behalf of European Academy of Dermatology and Venereology.\n\nGreinix, Hildegard\n\nWolf, Peter\n\n\n"
},
{
"text": "\n185232\nThe gut bacterium <i>Extibacter muris</i> produces secondary bile acids and influences liver physiology in gnotobiotic mice.\n\nStreidl, T\n\nKarkossa, I\n\nSegura Muñoz, RR\n\nEberl, C\n\nZaufel, A\n\nPlagge, J\n\nSchmaltz, R\n\nSchubert, K\n\nBasic, M\n\nSchneider, KM\n\nAfify, M\n\nTrautwein, C\n\nTolba, R\n\nStecher, B\n\nDoden, HL\n\nRidlon, JM\n\nEcker, J\n\nMoustafa, T\n\nvon Bergen, M\n\nRamer-Tait, AE\n\nClavel, T\n\nBeiträge in Fachzeitschriften\nISI:000604003200001\n33382950.0\n10.1080/19490976.2020.1854008\nPMC7781625\nExtibacter muris is a newly described mouse gut bacterium which metabolizes cholic acid (CA) to deoxycholic acid (DCA) via 7α-dehydroxylation. Although bile acids influence metabolic and inflammatory responses, few in vivo models exist for studying their metabolism and impact on the host. Mice were colonized from birth with the simplified community Oligo-MM12 with or without E. muris. As the metabolism of bile acids is known to affect lipid homeostasis, mice were fed either a low- or high-fat diet for eight weeks before sampling and analyses targeting the gut and liver. Multiple Oligo-MM12 strains were capable of deconjugating primary bile acids in vitro. E. muris produced DCA from CA either as pure compound or in mouse bile. This production was inducible by CA in vitro. Ursodeoxycholic, chenodeoxycholic, and β-muricholic acid were not metabolized under the conditions tested. All gnotobiotic mice were stably colonized with E. muris, which showed higher relative abundances after HF diet feeding. The presence of E. muris had minor, diet-dependent effects on Oligo-MM12 communities. The secondary bile acids DCA and surprisingly LCA and their taurine conjugates were detected exclusively in E. muris-colonized mice. E. muris colonization did not influence body weight, white adipose tissue mass, liver histopathology, hepatic aspartate aminotransferase, or blood levels of cholesterol, insulin, and paralytic peptide (PP). However, proteomics revealed shifts in hepatic pathways involved in amino acid, glucose, lipid, energy, and drug metabolism in E. muris-colonized mice. Liver fatty acid composition was substantially altered by dietary fat but not by E. muris.In summary, E. muris stably colonized the gut of mice harboring a simplified community and produced secondary bile acids, which affected proteomes in the liver. This new gnotobiotic mouse model can now be used to study the pathophysiological role of secondary bile acids in vivo.\n\nMoustafa, Tarek\n\nZaufel, Alex\n\n\n"
},
{
"text": "\n77899\nImpact of age, body mass index, insulin resistance and proteinuria on the kidney function in obese patients with Type 2 diabetes and renal insufficiency.\n\nKoch, M\n\nBeien, A\n\nFusshller, A\n\nZitta, S\n\nHaastert, B\n\nTrapp, R\n\nBeiträge in Fachzeitschriften\nISI:000252665000003\n18218312.0\nNone\nNone\nAIMS: To date, several different equations to predict the glomerular filtration rate (GFR) in patients with renal insufficiency have been developed for different patients groups. Our aim was to determine the prognostic factors of GFR in our homogenous patient group of obese, water-loaded patients with Type 2 diabetes and renal insufficiency, since we assumed that the endogenous creatinine clearance (ECC) alone may not be an accurate method to predict GFR. METHOD: We recruited 46 obese patients (37 men) with Type 2 diabetes and renal insufficiency in our nephrology center in Mettmann (Germany). However, two male patients were excluded from the analysis due to an outlying insulin level or low inulin clearance. The inulin clearance as a measure of renal function performed by the single shot method was compared with the GFR estimated by ECC, Cystatin C, and MDRD formula. Several multiple regression models were built to test the impact of the prognostic factors age, sex, body mass index (BMI), insulin resistance according to the homeostasis model assessment (HOMA), body water (TBW), brain natriuretic peptide (BNP), and proteinuria on the inulin clearance. In the main regression model to predict the inulin clearance by ECC, only the statistically significant prognostic factors of these models were selected, as well as the interaction between GFR predicted by ECC (GFR_ECC) and BMI. RESULTS: The prognostic factors GFR_ECC, age, BMI, HOMA and proteinuria had a statistically significant impact on the inulin clearance (the gold standard of the GFR) in our patient population (p < 0.05). However, the interaction of GFR_ECC and BMI was not significant (p = 0.06) in our model. The model was validated and considered well-fitted with a coefficient of determination (R2) of 0.69. CONCLUSIONS: The independent prognostic factors to determine GFR in obese, water-loaded diabetic patients are GFR_ECC, age, BMI, HOMA and proteinuria. However, our model should be revalidated and tested in a larger sample size to probably detect an interaction between GFR_ECC and BMI as an additional prognostic factor.\n\nZitta, Sabine\n\n\n"
},
{
"text": "\n106822\nDesign of the Coronary ARtery DIsease Genome-Wide Replication And Meta-Analysis (CARDIoGRAM) Study: A Genome-wide association meta-analysis involving more than 22 000 cases and 60 000 controls.\n\nPreuss, M\n\nKonig, IR\n\nThompson, JR\n\nErdmann, J\n\nAbsher, D\n\nAssimes, TL\n\nBlankenberg, S\n\nBoerwinkle, E\n\nChen, L\n\nCupples, LA\n\nHall, AS\n\nHalperin, E\n\nHengstenberg, C\n\nHolm, H\n\nLaaksonen, R\n\nLi, MY\n\nMarz, W\n\nMcPherson, R\n\nMusunuru, K\n\nNelson, CP\n\nBurnett, MS\n\nEpstein, SE\n\nO'Donnell, CJ\n\nQuertermous, T\n\nRader, DJ\n\nRoberts, R\n\nSchillert, A\n\nStefansson, K\n\nStewart, AFR\n\nThorleifsson, G\n\nVoight, BF\n\nWells, GA\n\nZiegler, A\n\nKathiresan, S\n\nReilly, MP\n\nSamani, NJ\n\nSchunkert, H\n\nBeiträge in Fachzeitschriften\nISI:000283163100012\n20923989.0\n10.1161/CIRCGENETICS.109.899443\nPMC3070269\nBackground-Recent genome-wide association studies (GWAS) of myocardial infarction (MI) and other forms of coronary artery disease (CAD) have led to the discovery of at least 13 genetic loci. In addition to the effect size, power to detect associations is largely driven by sample size. Therefore, to maximize the chance of finding novel susceptibility loci for CAD and MI, the Coronary ARtery DIsease Genome-wide Replication And Meta-analysis (CARDIoGRAM) consortium was formed. Methods and Results-CARDIoGRAM combines data from all published and several unpublished GWAS in individuals with European ancestry; includes >22 000 cases with CAD, MI, or both and >60 000 controls; and unifies samples from the Atherosclerotic Disease VAscular functioN and genetiC Epidemiology study, CADomics, Cohorts for Heart and Aging Research in Genomic Epidemiology, deCODE, the German Myocardial Infarction Family Studies I, II, and III, Ludwigshafen Risk and Cardiovascular Heath Study/AtheroRemo, MedStar, Myocardial Infarction Genetics Consortium, Ottawa Heart Genomics Study, PennCath, and the Wellcome Trust Case Control Consortium. Genotyping was carried out on Affymetrix or Illumina platforms followed by imputation of genotypes in most studies. On average, 2.2 million single nucleotide polymorphisms were generated per study. The results from each study are combined using meta-analysis. As proof of principle, we meta-analyzed risk variants at 9p21 and found that rs1333049 confers a 29% increase in risk for MI per copy (P=2x10(-20)). Conclusion-CARDIoGRAM is poised to contribute to our understanding of the role of common genetic variation on risk for CAD and MI. (Circ Cardiovasc Genet. 2010;3:475-483.)\n\nMärz, Winfried\n\n\n"
},
{
"text": "\n107637\nDisturbance of parathyroid hormone-related protein signaling in the nitrofen-induced hypoplastic lung.\n\nDoi, T\n\nLukosiute, A\n\nRuttenstock, E\n\nDingemann, J\n\nPuri, P\n\nBeiträge in Fachzeitschriften\nISI:000273094400007\n19855984.0\n10.1007/s00383-009-2506-8\nNone\nDespite remarkable progress in resuscitation and intensive care, the morbidity and mortality rates in congenital diaphragmatic hernia (CDH) remain high due to severe pulmonary hypoplasia. The pathogenesis of pulmonary hypoplasia associated with CDH is still not clearly understood. Pulmonary parathyroid hormone-related protein (PTHrP) is expressed in the type II epithelial cells and stimulates surfactant production by a paracrine feedback loop regulated by PTHrP receptor (PTHrP-R), which is expressed in the mesenchyme, during terminal airway differentiation. It has been reported that PTHrP knockout and PTHrP-R null mice both exhibit pulmonary hypoplasia, disrupting alveolar maturation before birth. We designed this study to test the hypothesis that gene expression of PTHrP and PTHrP-R is downregulated in the late stages of lung morphogenesis in the nitrofen-induced hypoplastic lung. Pregnant rats were exposed to either olive oil or nitrofen on day 9 of gestation (D9). Fetal lungs were harvested on D15, 18, and 21 and divided into three groups: control, nitrofen without CDH [CDH(-)], and nitrofen with CDH [CDH(+)] (n = 8 at each time point for each group, respectively). Total mRNA was extracted from fetal lungs and mRNA expression of PTHrP and PTHrP-R was analyzed by real-time RT-PCR and the significant differences between the groups were accepted at P < 0.05 by statistical analysis. Immunohistochemical studies were also performed to evaluate PTHrP and PTHrP-R protein expression at each time point. Pulmonary mRNA expression of PTHrP-R was significantly decreased in both nitrofen groups [CDH(-) and CDH(+)] compared to controls at D18 and 21. The mRNA level of PTHrP was significantly decreased at D21 in both nitrofen groups compared to controls. Immunoreactivity of PTHrP and PTHrP-R at D18 and 21 was diminished in the distal epithelium and in the mesenchyme, respectively, in the nitrofen-induced hypoplastic lung compared to control lungs. There were no significant differences in both gene/protein expression of PTHrP and PTHrP-R on D15. Downregulation of PTHrP and PTHrP-R gene expression during late lung morphogenesis may cause pulmonary hypoplasia in the nitrofen CDH model, disrupting alveolar maturation and surfactant production by interfering with mesenchymal-epithelial interactions.\n\n\n"
},
{
"text": "\n135831\nVitamin D status and its association with season, hospital and sepsis mortality in critical illness.\n\nAmrein, K\n\nZajic, P\n\nSchnedl, C\n\nWaltensdorfer, A\n\nFruhwald, S\n\nHoll, A\n\nPurkart, T\n\nWünsch, G\n\nValentin, T\n\nGrisold, A\n\nStojakovic, T\n\nAmrein, S\n\nPieber, TR\n\nDobnig, H\n\nBeiträge in Fachzeitschriften\nISI:000339627400065\n24661739.0\n10.1186/cc13790\nPMC4057427\nVitamin D plays a key role in immune function. Deficiency may aggravate the incidence and outcome of infectious complications in critically ill patients. We aimed to evaluate the prevalence of vitamin D deficiency and the correlation between serum 25-hydroxyvitamin D (25(OH) D) and hospital mortality, sepsis mortality and blood culture positivity.\n In a single-center retrospective observational study at a tertiary care center in Graz, Austria, 655 surgical and nonsurgical critically ill patients with available 25(OH) D levels hospitalized between September 2008 and May 2010 were included. Cox regression analysis adjusted for age, gender, severity of illness, renal function and inflammatory status was performed. Vitamin D levels were categorized by month-specific tertiles (high, intermediate, low) to reflect seasonal variation of serum 25(OH) D levels.\n Overall, the majority of patients were vitamin D deficient (<20 ng/ml; 60.2%) or insufficient (≥20 and <30 ng/dl; 26.3%), with normal 25(OH) D levels (>30 ng/ml) present in only 13.6%. The prevalence of vitamin D deficiency and mean 25(OH) D levels was significantly different in winter compared to summer months (P <0.001). Hospital mortality was 20.6% (135 of 655 patients). Adjusted hospital mortality was significantly higher in patients in the low (hazard ratio (HR) 2.05, 95% confidence interval (CI) 1.31 to 3.22) and intermediate (HR 1.92, 95% CI 1.21 to 3.06) compared to the high tertile. Sepsis was identified as cause of death in 20 of 135 deceased patients (14.8%). There was no significant association between 25(OH) D and C-reactive protein (CRP), leukocyte count or procalcitonin levels. In a subgroup analysis (n = 244), blood culture positivity rates did not differ between tertiles (23.1% versus 28.2% versus 17.1%, P = 0.361).\n Low 25(OH) D status is significantly associated with mortality in the critically ill. Intervention studies are needed to investigate the effect of vitamin D substitution on mortality and sepsis rates in this population.\n\nAmrein, Karin\n\nFruhwald, Sonja\n\nGrisold, Andrea\n\nPieber, Thomas\n\nUrbanic Purkart, Tadeja\n\nValentin, Thomas\n\nWaltensdorfer, Andreas\n\nWünsch, Gerit\n\nZajic, Paul\n\n\n"
},
{
"text": "\n142817\nDisruption of copper-dependent signaling pathway in the nitrofen-induced congenital diaphragmatic hernia.\n\nTakahashi, T\n\nFriedmacher, F\n\nTakahashi, H\n\nHofmann, AD\n\nPuri, P\n\nBeiträge in Fachzeitschriften\nISI:000347291400004\n25319798.0\n10.1007/s00383-014-3620-9\nNone\nNormal development of the fetal diaphragm requires muscularization of the diaphragm as well as the structural integrity of its underlying connective tissue components. Developmental mutations that inhibit the formation of extracellular matrix (ECM) have been shown to result in congenital diaphragmatic hernia (CDH). Copper (Cu) is an important element during diaphragm morphogenesis by participating in cross-linking of collagen and elastin fibers. Cu transport is strictly regulated by two membrane proteins: Cu-uptake transporter 1 (CTR1) and the Cu-efflux pump ATP7A. Animals lacking Cu-dependent enzymes exhibit abnormal connective tissue with diaphragmatic defects. However, the molecular basis of disruptions in Cu-mediated ECM formation in CDH remains unclear. We designed this study to investigate the hypothesis that diaphragmatic expression of CTR1 and ATP7A is decreased in the nitrofen-induced CDH model.\n Timed-pregnant rats were exposed to either nitrofen or vehicle on gestational day 9 (D9), and fetuses were harvested on selected time-points D15 and D18. Microdissected fetal diaphragms (n = 48) were divided into control and nitrofen-induced CDH samples (n = 12 per experimental group and time-point). Diaphragmatic gene expression levels of CTR1 and ATP7A were analyzed by quantitative real-time polymerase chain reaction. Immunohistochemistry was performed to evaluate CTR1 and ATP7A protein expression in fetal diaphragms, which was combined with specific rhodanine staining to determine diaphragmatic Cu content.\n Relative mRNA levels of CTR1 and ATP7A were significantly reduced in diaphragms of nitrofen-exposed fetuses on D15 (0.06 ± 0.02 vs. 0.18 ± 0.08; p < 0.05 and 0.04 ± 0.02 vs. 0.08 ± 0.02; p < 0.05) and D18 (0.10 ± 0.03 vs. 0.17 ± 0.02; p < 0.05 and 0.09 ± 0.03 vs. 0.16 ± 0.04; p < 0.05) compared to controls. Immunoreactivity of CTR1 and ATP7A was markedly decreased in the malformed diaphragmatic ECM of nitrofen-exposed fetuses on D15 and D18, which was associated with a significantly decreased diaphragmatic Cu content on D15 (7.22 ± 2.91 vs. 17.50 ± 3.09; p < 0.05) and D18 (17.60 ± 3.54 vs. 28.20 ± 4.63; p < 0.05) compared to controls.\n Reduced diaphragmatic expression of CTR1 and ATP7A during morphogenesis may impair the activity of Cu-dependent enzymes and thus contribute to defective ECM during diaphragmatic development.\n\n\n"
},
{
"text": "\n146438\nStable gastric pentadecapeptide BPC 157 in trials for inflammatory bowel disease (PL-10, PLD-116, PL 14736, Pliva, Croatia). Full and distended stomach, and vascular response.\n\nSikiric, P\n\nSeiwerth, S\n\nBrcic, L\n\nBlagaic, AB\n\nZoricic, I\n\nSever, M\n\nKlicek, R\n\nRadic, B\n\nKeller, N\n\nSipos, K\n\nJakir, A\n\nUdovicic, M\n\nTonkic, A\n\nKokic, N\n\nTurkovic, B\n\nMise, S\n\nAnic, T\n\nBeiträge in Fachzeitschriften\nNone\n17186181.0\n10.1007/s10787-006-1531-7\nNone\nGastric pentadecapeptide BPC 157 (GEPPPGKPADDAGLV, M.W. 1419, safe in clinical trials for inflammatory bowel disease (PL 10, PLD 116, PLD 14736, Pliva, Croatia)) has a particular cytoprotective/adaptive cytoprotective activity. The cytoprotective/adaptive cytoprotection researches largely neglect that stomach distension could per se jeopardize the mucosal integrity, with constantly stretched mucosa and blood vessels, and sphincters more prone for reflux induction. After absolute alcohol instillation in fully distended rat stomach, gastric, esophageal and duodenal lesions occur. Throughout next 3 min, left gastric artery blood vessels clearly disappear at the serosal site, indicative for loss of vessels both integrity and function. Contrary, constant vessels presentation could predict the beneficial effect of applied agent. After pentadecapeptide BPC 157 instillation into the stomach the vessels presentation remains constant, and lesions of stomach, esophagus, and duodenum are inhibited. Standards (atropine, ranitidine, omeprazole) could only slightly improve the vessels presentation compared to control values, and they have only a partial effect on the lesions. In this review we emphasize BPC 157 unusual stability, and some of its important effects: effectiveness against various lesions in gastrointestinal tract, on nitric oxide (NO)-system, and NO-agents effects, on somatosensory neurons, salivary glands function, recovery of AMP-ADP-ATP system, endothelium protection, effect on endothelin, and on angiogenesis promotion. It also antagonizes other alcohol effects, including acute and chronic intoxication. Given peripherally, it counteracts the consequence of central dopamine system disturbances (receptor blockade), and induces serotonin release in substantia nigra. Therapeutic potential of BPC 157 as a cytoprotective agent is also seen in its capability to heal various wounds. Given directly into the stomach, BPC 157 instantly recovers disturbed lower esophageal and pyloric sphincter pressure in rats after 12-20 months of untreated esophagitis. All these could be suggestive for its role as a natural protectant in gastric juice with particular function throughout stomach distension.\n\nBrcic, Luka\n\n\n"
},
{
"text": "\n146930\nEffects of High-Intensity Interval Exercise versus Moderate Continuous Exercise on Glucose Homeostasis and Hormone Response in Patients with Type 1 Diabetes Mellitus Using Novel Ultra-Long-Acting Insulin.\n\nMoser, O\n\nTschakert, G\n\nMueller, A\n\nGroeschl, W\n\nPieber, TR\n\nObermayer-Pietsch, B\n\nKoehler, G\n\nHofmann, P\n\nBeiträge in Fachzeitschriften\nISI:000360299100089\n26317981.0\n10.1371/journal.pone.0136489\nPMC4552855\nWe investigated blood glucose (BG) and hormone response to aerobic high-intensity interval exercise (HIIE) and moderate continuous exercise (CON) matched for mean load and duration in type 1 diabetes mellitus (T1DM).\n Seven trained male subjects with T1DM performed a maximal incremental exercise test and HIIE and CON at 3 different mean intensities below (A) and above (B) the first lactate turn point and below the second lactate turn point (C) on a cycle ergometer. Subjects were adjusted to ultra-long-acting insulin Degludec (Tresiba/ Novo Nordisk, Denmark). Before exercise, standardized meals were administered, and short-acting insulin dose was reduced by 25% (A), 50% (B), and 75% (C) dependent on mean exercise intensity. During exercise, BG, adrenaline, noradrenaline, dopamine, cortisol, glucagon, and insulin-like growth factor-1, blood lactate, heart rate, and gas exchange variables were measured. For 24 h after exercise, interstitial glucose was measured by continuous glucose monitoring system.\n BG decrease during HIIE was significantly smaller for B (p = 0.024) and tended to be smaller for A and C compared to CON. No differences were found for post-exercise interstitial glucose, acute hormone response, and carbohydrate utilization between HIIE and CON for A, B, and C. In HIIE, blood lactate for A (p = 0.006) and B (p = 0.004) and respiratory exchange ratio for A (p = 0.003) and B (p = 0.003) were significantly higher compared to CON but not for C.\n Hypoglycemia did not occur during or after HIIE and CON when using ultra-long-acting insulin and applying our methodological approach for exercise prescription. HIIE led to a smaller BG decrease compared to CON, although both exercises modes were matched for mean load and duration, even despite markedly higher peak workloads applied in HIIE. Therefore, HIIE and CON could be safely performed in T1DM.\n ClinicalTrials.gov NCT02075567 http://www.clinicaltrials.gov/ct2/show/NCT02075567.\n\nKöhler, Gerd\n\nMoser, Othmar\n\nObermayer-Pietsch, Barbara\n\nPieber, Thomas\n\n\n"
},
{
"text": "\n149838\nSexual Activity, Psychosexual Distress, and Fear of Progression in Women With Human Papillomavirus-Related Premalignant Genital Lesions.\n\nNagele, E\n\nReich, O\n\nGreimel, E\n\nDorfer, M\n\nHaas, J\n\nTrutnovsky, G\n\nBeiträge in Fachzeitschriften\nISI:000384726100016\n26782607.0\n10.1016/j.jsxm.2015.12.012\nNone\nGenital human papillomavirus (HPV) infections are very common in women 18 to 30 years old and substantially affect women's sexual health.\n To examine sexual activity, psychosexual distress, and fear of progression in women diagnosed with HPV-related precancerous genital lesions.\n In this observational study, women diagnosed with premalignant lesions of the cervix, vagina, or vulva were recruited from a university hospital-based colposcopy clinic.\n Quantitative data from three validated patient-administered questionnaires (Sexual Activity Questionnaire, German version of the Cervical Dysplasia Distress Questionnaire, and Fear of Progression Questionnaire) were compared within the study population, according to the location of the genital lesion, and with relevant reference populations. Qualitative data from two written open-ended questions about women's thoughts regarding diagnosis and information were analyzed.\n Two-hundred nine women completed the questionnaires. Seventy-eight percent of women (n = 162) were referred for evaluation of suspect lesions of the cervix, 8% (n = 17) of the vagina, and 14% (n = 30) of the vulva. There were no significant differences in questionnaire results among the three patient groups, except for sexual consequences (Cervical Dysplasia Distress Questionnaire) and recent sexual activity (Sexual Activity Questionnaire). Women with vulvar lesions were most likely to worry about sexual consequences (ie, being unable to have children, being sexually less attractive, or infecting a sexual partner; P = .04). The Sexual Activity Questionnaire subscales sexual pleasure (P = .15) and sexual habits (P = 1.00) were similar to those in a healthy control population, whereas sexual discomfort (P = .51) was comparable to that in a reference population of women who survived cervical cancer. The subscale partner-specific concerns (Fear of Progression Questionnaire) was similar to that in a reference population of patients with cancer (P = .28).\n HPV-related precancerous genital lesions, especially of the vulva, are likely to cause concerns about sexual health. Effective information and communication are important to lessen negative sexual consequences and anxiety.\n Copyright © 2016 International Society for Sexual Medicine. Published by Elsevier Inc. All rights reserved.\n\nGreimel, Elfriede Renate\n\nHaas, Josef\n\nNagele, Eva Helene\n\nReich, Olaf\n\nTrutnovsky, Gerda\n\n\n"
},
{
"text": "\n155004\n20 Years of Pediatric Benchmarking in Germany and Austria: Age-Dependent Analysis of Longitudinal Follow-Up in 63,967 Children and Adolescents with Type 1 Diabetes.\n\nBohn, B\n\nKarges, B\n\nVogel, C\n\nOtto, KP\n\nMarg, W\n\nHofer, SE\n\nFröhlich-Reiterer, E\n\nHolder, M\n\nPlamper, M\n\nWabitsch, M\n\nKerner, W\n\nHoll, RW\n\nDPV Initiative\n\nBeiträge in Fachzeitschriften\nISI:000381487600051\n27532627.0\n10.1371/journal.pone.0160971\nPMC4988648\nTo investigate changes in diabetes treatment over the last two decades in three age-groups of children and adolescents with type 1 diabetes (T1D) from Germany and Austria.\n 63, 67 subjects (<18yr) with T1D documented between 1995 and 2014 from the DPV-database were included and stratified according to age (0.5-<6, 6-<12, 12-<18yr). Regression models were applied for insulin regimens (<3 and ≥4 injection time points/day, or continuous subcutaneous insulin infusion (CSII)), use of rapid- and long acting insulin analogues, NPH insulin, and frequency of self-monitoring of blood glucose (SMBG)/day. Models were adjusted for sex, diabetes duration, and migration background. P-value for trend was given.\n The number of subjects with <3 injection time points/day decreased from 1995 to 2014 to <5% in all age-groups (p<0.0001). Proportion of patients with ≥4 injections/day increased until the early 2000s, and then declined until 2014. This trend was not found in 6-<12yr olds (p = 0.3403). CSII increased in all age-groups (p<0.0001) with the highest increase in children <6 years (from 0.4% to 79.2%), and the lowest increase in 12-<18 year olds (from 1.0% to 38.9%). NPH insulin decreased in all age-groups (p<0.0001). Insulin analogues, especially rapid-acting, became more frequent in all age-groups (p<0.0001), accounting for 78.4% in 2014 for all subjects. The highest use was found in the youngest children (in 2014: 85.6%), the lowest use in 6-<12 year olds (in 2014: 72.9%). The number of SMBG/day increased from 2.2 to 6.4 with a similar rise in all age-groups (p<0.0001). Frequency was highest in subjects <6yr.\n In all age-groups, T1D treatment was intensified over the last 20 years. Age-specific differences in trends were particularly observed in the number of patients on CSII, in the number of patients with 4 or more injections/day, and in the frequency of SMBG/day.\n\nFröhlich-Reiterer, Elke\n\n\n"
}
]
}