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=124660",
"previous": "https://api-test.medunigraz.at/v1/research/search/publication/?format=api&limit=20&offset=124620",
"results": [
{
"text": "\n131035\nGenome-wide and gene-centric analyses of circulating myeloperoxidase levels in the charge and care consortia.\n\nReiner, AP\n\nHartiala, J\n\nZeller, T\n\nBis, JC\n\nDupuis, J\n\nFornage, M\n\nBaumert, J\n\nKleber, ME\n\nWild, PS\n\nBaldus, S\n\nBielinski, SJ\n\nFontes, JD\n\nIllig, T\n\nKeating, BJ\n\nLange, LA\n\nOjeda, F\n\nMüller-Nurasyid, M\n\nMunzel, TF\n\nPsaty, BM\n\nRice, K\n\nRotter, JI\n\nSchnabel, RB\n\nTang, WH\n\nThorand, B\n\nErdmann, J\n\nCARDIoGRAM Consortium\n\nJacobs, DR\n\nWilson, JG\n\nKoenig, W\n\nTracy, RP\n\nBlankenberg, S\n\nMärz, W\n\nGross, MD\n\nBenjamin, EJ\n\nHazen, SL\n\nAllayee, H\n\nBeiträge in Fachzeitschriften\nISI:000322341300018\n23620142.0\n10.1093/hmg/ddt189\nPMC3723315\nIncreased systemic levels of myeloperoxidase (MPO) are associated with the risk of coronary artery disease (CAD). To identify the genetic factors that are associated with circulating MPO levels, we carried out a genome-wide association study (GWAS) and a gene-centric analysis in subjects of European ancestry and African Americans (AAs). A locus on chromosome 1q31.1 containing the complement factor H (CFH) gene was strongly associated with serum MPO levels in 9305 subjects of European ancestry (lead SNP rs800292; P = 4.89 × 10(-41)) and in 1690 AA subjects (rs505102; P = 1.05 × 10(-8)). Gene-centric analyses in 8335 subjects of European ancestry additionally identified two rare MPO coding sequence variants that were associated with serum MPO levels (rs28730837, P = 5.21 × 10(-12); rs35897051, P = 3.32 × 10(-8)). A GWAS for plasma MPO levels in 9260 European ancestry subjects identified a chromosome 17q22 region near MPO that was significantly associated (lead SNP rs6503905; P = 2.94 × 10(-12)), but the CFH locus did not exhibit evidence of association with plasma MPO levels. Functional analyses revealed that rs800292 was associated with levels of complement proteins in serum. Variants at chromosome 17q22 also had pleiotropic cis effects on gene expression. In a case-control analysis of ∼80 000 subjects from CARDIoGRAM, none of the identified single-nucleotide polymorphisms (SNPs) were associated with CAD. These results suggest that distinct genetic factors regulate serum and plasma MPO levels, which may have relevance for various acute and chronic inflammatory disorders. The clinical implications for CAD and a better understanding of the functional basis for the association of CFH and MPO variants with circulating MPO levels require further study.\n\nMärz, Winfried\n\n\n"
},
{
"text": "\n138764\nMast cell reactivity at the margin of human skin wounds: an early cell marker of wound survival?\n\nOehmichen, M\n\nGronki, T\n\nMeissner, C\n\nAnlauf, M\n\nSchwark, T\n\nBeiträge in Fachzeitschriften\nISI:000270526700001\n19560296.0\n10.1016/j.forsciint.2009.05.020\nNone\nDetecting the vitality of mechanical skin wounds (antemortem versus postmortem injury) in human cadavers remains a specifically forensic problem. To determine whether skin mast cells (MCs) are activated during the very early phase of human wound healing we performed a histomorphometric evaluation of the extent of MC enzyme loss as an indication of MC degranulation at the wound margins of skin wounds in 64 human cadavers. We compared the number of tryptase-reactive MCs, which are said not to loose all of their enzyme activity during degranulation process, with the number of naphthol AS-D chloroacetate esterase (NAS-DClAE)-positive MCs, which loose their complete enzyme activity in the form of enzyme-positive granula after activation. The enzyme activity was evaluated on sequential histological sections after autopsy as an indirect quantification of the number of degranulated MCs. Most of the victims had died within 10-60 min after injury (n=50), 12 survived between 60 min and 24h, and only 2 victims survived more than 24h (12 days each). The number of enzyme-positive MCs were counted in six successive visual fields (0.785 mm(2)) on the one hand located parallel to and--on the other hand--at increasing distances outward from the wound margins. In victims surviving the injury less than 60 min the average number of NAS-DClAE-reactive MCs next to the wound margin was significantly lower than the number of tryptase-reactive MCs. The extent of the reduction in NAS-DClAE-reactive MC counts correlated inversely with the distance from the wound edges. Our findings show that MCs undergo very early loss of NAS-DClAE activity at wound margins, and thus appear to be an early cell marker of wound survival. However, definitive evidence that the enzyme loss (degranulation) represents a vital process can only be obtained by comparing MC enzyme loss induced by injury during intact circulation with the MC reaction to injury inflicted very shortly after cardiac arrest, a question that can only be answered by animal experiments.\n\nSchwark, Thorsten\n\n\n"
},
{
"text": "\n142819\nLysyl oxidase expression is decreased in the developing diaphragm and lungs of nitrofen-induced congenital diaphragmatic hernia.\n\nTakahashi, T\n\nFriedmacher, F\n\nTakahashi, H\n\nDaniel Hofmann, A\n\nPuri, P\n\nBeiträge in Fachzeitschriften\nISI:000348524500006\n25111273.0\n10.1055/s-0034-1386644\nNone\nMalformation of the nonmuscular tissue components in congenital diaphragmatic hernia (CDH) is thought to underlie the diaphragmatic defect, causing intrathoracic herniation of abdominal viscera and thus disturbing normal lung development. It has been shown that diaphragmatic and pulmonary morphogeneses require the structural integrity of connective tissue, and developmental mutations that inhibit the formation of extracellular matrix (ECM) result in CDH with hypoplastic lungs. Lysyl oxidase (lox), an extracellular enzyme that catalyzes the cross-linking of ECM proteins, plays an essential role during diaphragmatic and pulmonary development by controlling the formation of connective tissue. Furthermore, lox (-/-) knockouts exhibit abnormal connective tissue with diaphragmatic defects and impaired airway morphogenesis. We designed this study to investigate the hypothesis that diaphragmatic and pulmonary lox expression is decreased in the nitrofen-induced CDH model.\n Timed-pregnant Sprague-Dawley rats were exposed to either nitrofen or vehicle on gestational day 9 (D9), and fetuses were harvested on selected time points D15 and D18. The micro-dissected fetal diaphragms (n=48) and lungs (n=48) were divided into two groups: control and nitrofen-exposed samples (n=12 per specimen and time point, respectively). Diaphragmatic and pulmonary gene expression levels of lox were analyzed by quantitative real-time polymerase chain reaction. Immunohistochemical staining was performed to evaluate lox protein expression in diaphragms and lungs.\n Relative mRNA expression of lox was significantly reduced in diaphragms and lungs of nitrofen-exposed fetuses on D15 (0.29 ± 0.08 vs. 0.12 ± 0.05; p<0.05 and 0.52 ± 0.44 vs. 0.20 ± 0.04; p<0.05) and D18 (0.90 ± 0.25 vs. 0.57 ± 0.23; p<0.05 and 0.59 ± 0.26 vs. 0.35 ± 0.09; p<0.05) compared with controls. Diaphragmatic and pulmonary immunoreactivity of lox was markedly decreased in nitrofen-exposed fetuses on D15 and D18 compared with controls.\n Decreased lox expression during diaphragmatic development and lung branching morphogenesis may interfere with normal cross-linking of ECM proteins, disrupting the integrity of connective tissue, and contributing to the diaphragmatic defect and impaired airway formation in the nitrofen-induced CDH model.\n Georg Thieme Verlag KG Stuttgart · New York.\n\n\n"
},
{
"text": "\n144381\nGalectin-3 in patients with heart failure with preserved ejection fraction: results from the Aldo-DHF trial.\n\nEdelmann, F\n\nHolzendorf, V\n\nWachter, R\n\nNolte, K\n\nSchmidt, AG\n\nKraigher-Krainer, E\n\nDuvinage, A\n\nUnkelbach, I\n\nDüngen, HD\n\nTschöpe, C\n\nHerrmann-Lingen, C\n\nHalle, M\n\nHasenfuss, G\n\nGelbrich, G\n\nStough, WG\n\nPieske, BM\n\nBeiträge in Fachzeitschriften\nISI:000349675200016\n25418979.0\n10.1002/ejhf.203\nNone\nGalectin-3 is a marker of myocardial fibrosis and mediates aldosterone-induced cardiovascular inflammation and fibrosis. Characteristics of galectin-3 and its response to spironolactone have not been evaluated in heart failure with preserved ejection fraction (HFpEF). The aim of this study was to determine the association between galectin-3 levels and patient characteristics in HFpEF; to evaluate the interaction between spironolactone and galectin-3 levels; and to assess the association between galectin-3 and clinical outcomes.\n Aldo-DHF investigated spironolactone 25 mg once daily vs. placebo for 12 months in patients with NYHA class II-III, LVEF ≥50%, grade ≥ I diastolic dysfunction, and peakVO2 ≤ 25 mL/kg/min. Galectin-3 levels were obtained at baseline, and at 6 and 12 months. The association between baseline galectin-3, change in galectin-3, and all-cause death or hospitalization was evaluated, and the interaction between galectin-3 and treatment was assessed. Median baseline galectin-3 was 12.1 ng/mL. After multivariable adjustment, baseline galectin-3 inversely correlated with peak VO2 (P = 0.021), 6 min walk distance (P = 0.002), and Short Form 36 (SF-36) physical functioning (P = 0.001), and directly correlated with NYHA class (P = 0.007). Baseline NT-proBNP correlated with E/e' velocity ratio (P ≤ 0.001), left atrial volume index (P < 0.001), and LV mass index (P = 0.009). Increasing galectin-3 at 6 or 12 months was associated with all-cause death or hospitalization independent of treatment arm [hazard ratio (HR) 3.319, 95% confidence interval (CI) 1.214-9.07, P = 0.019] and NT-proBNP (HR 3.127, 95% CI 1.144-8.549, P = 0.026). Spironolactone did not influence galectin-3 levels.\n Galectin-3 levels are modestly elevated in patients with stable HFpEF and relate to functional performance and quality of life. Increasing galectin-3 was associated with worse outcome, independent of treatment or NT-proBNP.\n © 2014 The Authors. European Journal of Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.\n\nSchmidt, Albrecht\n\n\n"
},
{
"text": "\n145036\nIncreases in pre-hospitalization serum 25(OH)D concentrations are associated with improved 30-day mortality after hospital admission: A cohort study.\n\nAmrein, K\n\nLitonjua, AA\n\nMoromizato, T\n\nQuraishi, SA\n\nGibbons, FK\n\nPieber, TR\n\nCamargo, CA\n\nGiovannucci, E\n\nChristopher, KB\n\nBeiträge in Fachzeitschriften\nISI:000373865200030\n25935851.0\n10.1016/j.clnu.2015.03.020\nNone\nPre-hospital vitamin D status may be a modifiable risk factor for all-cause mortality among hospitalized patients.\n To examine the association between increases in serum 25-hydroxyvitamin D [25(OH)D] levels during the year before hospitalization and risk of 30-day all-cause mortality after hospital admission.\n Retrospective cohort study.\n Two Boston teaching hospitals.\n We studied 4344 adults hospitalized between 1993 and 2011 who had serum 25(OH)D concentrations measured at least twice within 7-365 days before the index hospitalization.\n None.\n The exposure of interest was change in pre-hospital serum 25(OH)D concentrations. The main outcome was 30-day all-cause mortality. We used mixed-effects logistic regression to describe how 30-day mortality differed with changes in pre-hospital 25(OH)D concentrations. Additionally, the odds of 30-day mortality in patients with pre-hospital 25(OH)D increases of ≥10 ng/mL was compared to that of patients with increases of <10 ng/mL.\n In a mixed-effect logistic regression model adjusted for age, gender, race, type (medical/surgical), Deyo-Charlson Index, creatinine and hematocrit, 30-day all-cause mortality rate was 8% (95%CI: 1-15) lower for each 10 ng/mL increase in pre-hospital 25(OH)D (P = 0.025) compared with the 30-day all-cause mortality rate in the entire cohort. In an adjusted logistic regression model, absolute changes of ≥10 ng/mL in patients with initial 25(OH)D concentrations < 20 ng/mL (n = 1944) decreased the odds of 30-day all-cause mortality by 48% (adjusted OR 0.52; 95%CI 0.30-0.93; P = 0.026) compared to patients with changes of <10 ng/mL.\n In patients with initial 25(OH)D < 20 ng/mL, subsequent improvements in vitamin D status before hospitalization are associated with decreased odds of 30-day all-cause mortality after hospital admission. A causal relation may not be inferred from this observational study.\n Copyright © 2015 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.\n\nAmrein, Karin\n\nPieber, Thomas\n\n\n"
},
{
"text": "\n146444\nStable gastric pentadecapeptide BPC 157 in trials for inflammatory bowel disease (PL-10, PLD-116, PL14736, Pliva, Croatia) heals ileoileal anastomosis in the rat.\n\nVuksic, T\n\nZoricic, I\n\nBrcic, L\n\nSever, M\n\nKlicek, R\n\nRadic, B\n\nCesarec, V\n\nBerkopic, L\n\nKeller, N\n\nBlagaic, AB\n\nKokic, N\n\nJelic, I\n\nGeber, J\n\nAnic, T\n\nSeiwerth, S\n\nSikiric, P\n\nBeiträge in Fachzeitschriften\nISI:000248983600008\n17713731.0\n10.1007/s00595-006-3498-9\nNone\nGastric pentadecapeptide BPC 157 (BPC 157), which has been shown to be safe in clinical trials for inflammatory bowel disease (PL-10, PLD-116, PL14736, Pliva, Croatia), may be able to cure intestinal anastomosis dehiscence. This antiulcer peptide shows no toxicity, is limit test negative, and a lethal dose is not achieved. It is stable in human gastric juice. In comparison with other standard treatments it is more effective for ulcers and various wounds, and can be used without a carrier needed for other peptides, both locally and systemically (i.e., perorally, parenterally). We studied the effectiveness of BPC 157 for ileoileal anastomosis healing in rats.\n We assessed ileoileal anastomosis dehiscence macroscopically, histologically, and biomechanically (volume [ml] infused through a syringe-perfusion pump system (1 ml/10 s), and pressure [mmHg] to leak induction [catheter connected to a chamber and a monitor, at 10 cm proximal to anastomosis]), at 1, 2, 3, 4, 5, 6, 7, and 14 days. BPC 157 (10 microg, 10 ng, 10 pg/kg i.p. (or saline [5 ml/kg]) was first administered after surgery, while it was last given 24 h before either assessment or sacrifice.\n Throughout the experiment, both higher doses of BPC 157 were shown to improve all parameters of anastomotic wound healing. The formation of adhesions remained slight, the blood vessels were filled with blood, and a mild intestinal passage obstruction was only temporarily observed. Anastomosis without leakage induces markedly higher volume and pressure values, with a continuous increase toward healthy values. From day 1, edema was markedly attenuated and the number of granulocytes decreased, while from days 4 or 5 necrosis decreased and granulation tissue, reticulin, and collagen formation substantially increased, thus resulting in increased epithelization.\n This study showed BPC 157 to have a beneficial effect on ileoileal anastomosis healing in the rat.\n\nBrcic, Luka\n\n\n"
},
{
"text": "\n148201\nInhibition of intestinal bile acid absorption improves cholestatic liver and bile duct injury in a mouse model of sclerosing cholangitis.\n\nBaghdasaryan, A\n\nFuchs, CD\n\nÖsterreicher, CH\n\nLemberger, UJ\n\nHalilbasic, E\n\nPåhlman, I\n\nGraffner, H\n\nKrones, E\n\nFickert, P\n\nWahlström, A\n\nStåhlman, M\n\nPaumgartner, G\n\nMarschall, HU\n\nTrauner, M\n\nBeiträge in Fachzeitschriften\nISI:000370292300019\n26529078.0\n10.1016/j.jhep.2015.10.024\nNone\nApproximately 95% of bile acids (BAs) excreted into bile are reabsorbed in the gut and circulate back to the liver for further biliary secretion. Therefore, pharmacological inhibition of the ileal apical sodium-dependent BA transporter (ASBT/SLC10A2) may protect against BA-mediated cholestatic liver and bile duct injury.\n Eight week old Mdr2(-/-) (Abcb4(-/-)) mice (model of cholestatic liver injury and sclerosing cholangitis) received either a diet supplemented with A4250 (0.01% w/w) - a highly potent and selective ASBT inhibitor - or a chow diet. Liver injury was assessed biochemically and histologically after 4weeks of A4250 treatment. Expression profiles of genes involved in BA homeostasis, inflammation and fibrosis were assessed via RT-PCR from liver and ileum homogenates. Intestinal inflammation was assessed by RNA expression profiling and immunohistochemistry. Bile flow and composition, as well as biliary and fecal BA profiles were analyzed after 1week of ASBT inhibitor feeding.\n A4250 improved sclerosing cholangitis in Mdr2(-/-) mice and significantly reduced serum alanine aminotransferase, alkaline phosphatase and BAs levels, hepatic expression of pro-inflammatory (Tnf-α, Vcam1, Mcp-1) and pro-fibrogenic (Col1a1, Col1a2) genes and bile duct proliferation (mRNA and immunohistochemistry for cytokeratin 19 (CK19)). Furthermore, A4250 significantly reduced bile flow and biliary BA output, which correlated with reduced Bsep transcription, while Ntcp and Cyp7a1 were induced. Importantly A4250 significantly reduced biliary BA secretion but preserved HCO3(-) and biliary phospholipid secretion resulting in an increased HCO3(-)/BA and PL/BA ratio. In addition, A4250 profoundly increased fecal BA excretion without causing diarrhea and altered BA pool composition, resulting in diminished concentrations of primary BAs tauro-β-muricholic acid and taurocholic acid.\n Pharmacological ASBT inhibition attenuates cholestatic liver and bile duct injury by reducing biliary BA concentrations in mice.\n Copyright © 2015 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.\n\nBaghdasaryan, Anna\n\nFickert, Peter\n\nTatscher, Elisabeth\n\n\n"
},
{
"text": "\n159406\nTreatment of Dupuytren's disease with collagenase - a 1-year follow-up of 37 patients].\n\nBinter, A\n\nNeuwirth, M\n\nRab, M\n\nBeiträge in Fachzeitschriften\nISI:000347712000007\n25564949.0\n10.1055/s-0034-1395604\nNone\nThe efficiency of collagenase of Clostridium histolyticum (CCH; Xiapex) in the treatment of Dupuytren's contracture has been proved in phase III studies. This retrospective study aims to evaluate our clinical results after the use of CCH.\n The study included 40 Dupuytren's contractures in 37 patients. There were 32 male and 5 female patients; their average age was 66 years. The most affected finger was the ring finger (55%; 22/40), followed by the little finger (30%; 12/40) and the middle finger (15; 6/40). 14 fingers (35%) presented isolated contractures of the metacarpophalangeal joint whereas an isolated contracture of the proximal interphalangeal joint was evident in 8 (20%) fingers. 18 (45%) fingers presented combined MCP and PIP flexion contractures. None of the patients underwent any treatment prior to this study. A retrospective chart review was performed of all patients. Follow-up examinations were performed seven days, fourteen days, three months, six months and one year after the intervention. The follow-up examination included goniometry of each affected finger to assess the range of motion (ROM) before and after cord breaking. Further patient-reported outcome was accessed concerning postinterventional complaints, impairment of sensibility and satisfaction with the treatment.\n The range of motion improved in all fingers. Full extension of the affected finger without any contracture could be observed in 93% of the MCP contractures, 38% of the PIP contractures and in 28% of the combined MCP and PIP contractures. Incomplete cord breaking could be observed in 9 (22.5%) fingers. In 8 fingers (20%) skin tears occurred after joint manipulation but healed up without any further surgical intervention. The recurrence rate at the latest follow-up was 2.5% (1/40). Patient satisfaction was high and none of the patients reported any complaints at the latest follow-up.\n The best results could be achieved in patients with isolated contractures of the MCP joint. Regarding the good functional results, the low complication rates and the high patient satisfaction, CCH represents a simple and effective treatment for Dupuytren's contracture in selected cases.\n © Georg Thieme Verlag KG Stuttgart · New York.\n\nNeuwirth, Maximilian\n\n\n"
},
{
"text": "\n168276\nRisk factors for hyperglycemia in pregnancy in the DALI study differ by period of pregnancy and OGTT time point.\n\nMendoza, LC\n\nHarreiter, J\n\nSimmons, D\n\nDesoye, G\n\nAdelantado, JM\n\nJuarez, F\n\nChico, A\n\nDevlieger, R\n\nvan Assche, A\n\nGaljaard, S\n\nDamm, P\n\nMathiesen, ER\n\nJensen, DM\n\nAndersen, LLT\n\nTanvig, M\n\nLapolla, A\n\nDalfra, MG\n\nBertolotto, A\n\nMantaj, U\n\nWender-Ozegowska, E\n\nZawiejska, A\n\nHill, D\n\nJelsma, JG\n\nSnoek, FJ\n\nvan Poppel, MNM\n\nWorda, C\n\nBancher-Todesca, D\n\nKautzky-Willer, A\n\nDunne, FP\n\nCorcoy, R\n\nDALI Core Investigator Group\n\nBeiträge in Fachzeitschriften\nISI:000439468700009\n29739812.0\n10.1530/EJE-18-0003\nNone\nRisk factors are widely used to identify women at risk for gestational diabetes mellitus (GDM) without clear distinction by pregnancy period or oral glucose tolerance test (OGTT) time points. We aimed to assess the clinical risk factors for Hyperglycemia in pregnancy (HiP) differentiating by these two aspects.\n Nine hundred seventy-one overweight/obese pregnant women, enrolled in the DALI study for preventing GDM. OGTTs were performed at ≤19 + 6, 24-28 and 35-37 weeks (IADPSG/WHO2013 criteria). Women with GDM or overt diabetes at one time point did not proceed to further OGTTs. Potential independent variables included baseline maternal and current pregnancy characteristics.\n Multivariate logistic regression.\n Clinical characteristics independently associated with GDM/overt diabetes were at ≤19 + 6 weeks, previous abnormal glucose tolerance (odds ratio (OR): 3.11; 95% CI: 1.41-6.85), previous GDM (OR: 2.22; 95% CI: 1.20-4.11), neck circumference (NC) (OR: 1.58; 95% CI: 1.06-2.36 for the upper tertile), resting heart rate (RHR, OR: 1.99; 95% CI: 1.31-3.00 for the upper tertile) and recruitment site; at 24-28 weeks, previous stillbirth (OR: 2.92; 95% CI: 1.18-7.22), RHR (OR: 3.32; 95% CI: 1.70-6.49 for the upper tertile) and recruitment site; at 35-37 weeks, maternal height (OR: 0.41; 95% CI: 0.20-0.87 for upper tertile). Clinical characteristics independently associated with GDM/overt diabetes differed by OGTT time point (e.g. at ≤19 + 6 weeks, NC was associated with abnormal fasting but not postchallenge glucose).\n In this population, most clinical characteristics associated with GDM/overt diabetes were non-modifiable and differed by pregnancy period and OGTT time point. The identified risk factors can help define the target population for future intervention trials.\n © 2018 European Society of Endocrinology.\n\nDesoye, Gernot\n\n\n"
},
{
"text": "\n168442\nAntibody Concentrations Decrease 14-Fold in Children With Celiac Disease on a Gluten-Free Diet but Remain High at 3 Months.\n\nPetroff, D\n\nWolf, J\n\nRichter, T\n\nAuth, MKH\n\nUhlig, HH\n\nLaass, MW\n\nLauenstein, P\n\nKrahl, A\n\nHändel, N\n\nde Laffolie, J\n\nHauer, AC\n\nHeiduk, M\n\nFlemming, G\n\nSchmidt, A\n\nHasenclever, D\n\nMothes, T\n\nBeiträge in Fachzeitschriften\nISI:000441570500021\n29654912.0\n10.1016/j.cgh.2018.04.008\nNone\nCeliac disease can be identified by a serologic test for IgA against tissue transglutaminase (IgA-TTG) in a large proportion of children. However, the increased concentrations of antibody rarely normalize within the months after children are placed on a gluten-free diet (GFD). Early serologic predictors of sufficient adherence to GFD are required for optimal treatment.\n In a prospective study, we observed the response to a GFD in 345 pediatric patients (67% girls; mean age, 8.4 y) who underwent duodenal biopsy to confirm or refute celiac disease from October 2012 through December 2015. Baseline serum samples were tested centrally for IgA-TTG and IgG against deamidated gliadin. Follow-up serologic analyses of children on a GFD were performed about 3 months later.\n The geometric mean concentration of IgA-TTG decreased from 72.4-fold to 5.2-fold the upper limit of normal (ULN), or by a factor of 14.0 (95% CI, 12.0-16.4). A substantial response (defined as a larger change than the typical variation in patients not on a GFD) was observed in 80.6% of the children. Only 28.1% of patients had a substantial response in the concentration of IgG against deamidated gliadin. Concentration of IgA-TTG remained above 1-fold the ULN in 83.8% of patients, and above 10-fold the ULN in 26.6% of patients with a substantial response.\n Serum concentration of IgA-TTG decreases substantially in most children with celiac disease within 3 months after they are placed on a GFD, but does not normalize in most. This information on changes in antibody concentrations can be used to assess patient response to the diet at short-term follow-up evaluations. Patients with a substantial response to a GFD often still have high antibody levels after 3 months. German Clinical Trials Registry no. DRKS00003854.\n Copyright © 2018 AGA Institute. Published by Elsevier Inc. All rights reserved.\n\nHauer, Almuthe\n\n\n"
},
{
"text": "\n171840\nPrevalence and Clinical Features of Mazabraud Syndrome: A Multicenter European Study.\n\nMajoor, BCJ\n\nvan de Sande, MAJ\n\nAppelman-Dijkstra, NM\n\nLeithner, A\n\nJutte, PC\n\nVélez, R\n\nPerlaky, T\n\nStaals, EL\n\nBovée, JVMG\n\nHamdy, NAT\n\nDijkstra, SPD\n\nBeiträge in Fachzeitschriften\nISI:000458570700013\n30653046.0\n10.2106/JBJS.18.00062\nNone\nMazabraud syndrome is a rare disorder, characterized by the presence of fibrous dysplasia (FD) with associated intramuscular myxomas. Data are scarce on the prevalence, clinical features, and natural history of this disorder and outcomes. In this multicenter study, we evaluated a series of patients from 6 European centers.\n All centers affiliated with the European Musculo-Skeletal Oncology Society (EMSOS) were invited to include data on all patients with Mazabraud syndrome who were seen between 1980 and 2015. The study investigated the prevalence of Mazabraud syndrome, the type, severity, and localization of FD lesions in relation to myxomas, the histopathology of myxomas, and results of GNAS-mutation analysis, when available.\n Thirty-two patients (22 female) from 6 centers were included. The prevalence of Mazabraud syndrome was 2.2% in the combined cohort of 1, 46 patients with FD, and the syndrome was diagnosed at a mean of 10.1 years after diagnosis of FD. The myxomas were predominantly localized in the upper leg. Excision was performed in 20 patients, recurrence occurred in 6 of these patients (30%) at a median of 8.5 years (range, 1.9 to 16.0 years), and revision surgery was necessary in 5 (25%). High cellularity of myxomas was associated with recurrence (p < 0.05). A GNAS mutation was identified in the myxoma tissue of 5 (83%) of 6 patients with GNAS-mutation analysis.\n This study is the first, to our knowledge, to provide data on the prevalence of Mazabraud syndrome in a relatively large cohort. Although the outcomes of surgical resection were good, a quarter of the patients required revision surgery despite clear resection margins. High cellularity of myxomas was associated with recurrence. GNAS mutations were identified in 83% (5 of 6), emphasizing the shared origin of FD and myxomas. Our data show that patients with FD who have disproportionate complaints, irrespective of FD type, extent, or severity, should be investigated for the possible presence of myxomas.\n Prognostic Level IV. See Instructions for Authors for a complete description of levels of evidence.\n\nLeithner, Andreas\n\n\n"
},
{
"text": "\n176839\nThe Role of Attachment in Poly-Drug Use Disorder: An Overview of the Literature, Recent Findings and Clinical Implications.\n\nHiebler-Ragger, M\n\nUnterrainer, HF\n\nBeiträge in Fachzeitschriften\nISI:000482807900001\n31507461.0\n10.3389/fpsyt.2019.00579\nPMC6720034\nBackground: Substance use disorders (SUDs) represent a worldwide epidemic with extensive costs to the individual and to society. Occasionally described as an attachment disorder, they have been linked to various impairments in self-regulation and social functioning. However, while there have been significant advances in the development and validation of treatment strategies for SUD in recent years, the components of these treatment approaches have yet to be fully explored. The characteristics of polydrug use disorder (PUD) especially need to be addressed in more detail, as this diagnosis is highly common in individuals seeking treatment, while simultaneously being associated with poor treatment success. Aim and Scope: This review aims at further exploring the relevance of attachment in PUD and its treatment. To this end, this review provides a concise summary of relevant theories on the development and treatment of SUD in general, including related parameters of attachment, emotion regulation, and neuroscience. Furthermore, several studies focused specifically on PUD are described in more detail. These studies explored the connections between attachment, personality structure, primary and higher emotions (including spirituality), as well as structural and functional neural parameters in inpatients with PUD as well as in healthy controls. Most notably, the described studies highlight that insecure attachment and impairments in personality structure are present in inpatients with PUD. In addition, these characteristics are paralleled by extensive impairments in white matter integrity, especially in tracts connected to facets of emotion regulation. Conclusions: Based on our findings, we emphasize conceptualization of PUD as an Attachment Disorder, on a behavioral as well as on a neural level. Furthermore, we point out the importance of an integrated bio-psycho-social approach in this research area. Consequently, future studies might more closely focus on the influence of attachment-based interventions on emotion regulation abilities as well as a potentially related neuroplasticity. Neuroplastic changes, which are still rather unexplored, might represent important parameters for the assessment of treatment outcomes especially in long-term SUD treatment.\n\nUnterrainer, Human-Friedrich\n\n\n"
},
{
"text": "\n181824\nNon-Coding microRNAs as Novel Potential Tumor Markers in Testicular Cancer.\n\nRegouc, M\n\nBelge, G\n\nLorch, A\n\nDieckmann, KP\n\nPichler, M\n\nBeiträge in Fachzeitschriften\nISI:000530232300225\n32235691.0\n10.3390/cancers12030749\nPMC7140096\nTesticular cancer is an important disease with increasing incidence and a high burden of morbidity and mortality in young men worldwide. Histological examination of the testicular tissue after orchiectomy plays an important role alongside patient history, imaging, clinical presentation and laboratory parameters. Surgical procedures and chemotherapeutic treatment provide a high chance of cure in early stages, though some patients in advanced stages belonging to a poor risk group experience cancer-related death. Though conventional serum-based tumor markers, including α-fetoprotein (AFP), the β-subunit of human chorionic gonadotropin (β-hCG), and lactate dehydrogenase (LDH), are useful as prognostic and diagnostic biomarkers, unfortunately, these tumor markers only have a sensitivity of about 60%, and in pure seminoma even lower with about 20%. Therefore, the development of new tumor markers is an important and intensively ongoing issue. The analysis of epigenetic modification and non-coding RNA microRNAs (miRNAs) are carrying most promising potential as tumor markers in future. miRNAs are small RNAs secreted by testicular tumor cells and circulate and be measurable in body fluids. In recent years, miRNAs of the miR-371-373 cluster in particular have been identified as potentially superior tumor markers in testicular cancer patients. Studies showed that miR-371a-3p and miR-302/367 expression significantly differ between testicular tumors and healthy testicular tissue. Several studies including high prospective multi-center trials clearly demonstrated that these miRNAs significantly exceed the sensitivity and specificity of conventional tumor markers and may help to facilitate the diagnosis, follow-up, and early detection of recurrences in testicular cancer patients. In addition, other miRNAs such as miR-223-3p, miR-449, miR-383, miR-514a-3p, miR-199a-3p, and miR-214 will be discussed in this review. However, further studies are needed to identify the value of these novel markers in additional clinical scenarios, including the monitoring in active surveillance or after adjuvant chemotherapy, but also to show the limitations of these tumor markers. The aim of this review is to give an overview on the current knowledge regarding the relevance of non-coding miRNAs as biomarkers in testicular cancer.\n\nPichler, Martin\n\n\n"
},
{
"text": "\n186836\nCombined testing of copeptin and high-sensitivity cardiac troponin T at presentation in comparison to other algorithms for rapid rule-out of acute myocardial infarction.\n\nMueller-Hennessen, M\n\nLindahl, B\n\nGiannitsis, E\n\nVafaie, M\n\nBiener, M\n\nHaushofer, AC\n\nSeier, J\n\nChrist, M\n\nAlquézar-Arbé, A\n\ndeFilippi, CR\n\nMcCord, J\n\nBody, R\n\nPanteghini, M\n\nJernberg, T\n\nPlebani, M\n\nVerschuren, F\n\nFrench, JK\n\nChristenson, RH\n\nDinkel, C\n\nKatus, HA\n\nMueller, C\n\nBeiträge in Fachzeitschriften\nNone\n30404726.0\n10.1016/j.ijcard.2018.10.084\nNone\nWe aimed to directly compare the diagnostic and prognostic performance of a dual maker strategy (DMS) with combined testing of copeptin and high-sensitivity (hs) cardiac troponin T (cTnT) at time of presentation with other algorithms for rapid rule-out of acute myocardial infarction (AMI).\n 922 patients presenting to the emergency department with suspected AMI and available baseline copeptin measurements qualified for the present TRAPID-AMI substudy. Diagnostic measures using the DMS (copeptin <10, <14 or < 20 pmol/L and hs-cTnT≤14 ng/L), the 1 h-algorithm (hs-cTnT<12 ng/L and change <3 ng/L at 1 h), as well as the hs-cTnT limit-of-blank (LoB, <3 ng/L) and -detection (LoD, <5 ng/L) were compared. Outcomes were assessed as combined end-points of death and myocardial re-infarction.\n True-negative rule-out using the DMS could be achieved in 50.9%-62.3% of all patients compared to 35.0%, 45.3% and 64.5% using LoB, LoD or the 1 h-algorithm, respectively. The DMS showed NPVs of 98.1%-98.3% compared to 99.2% for the 1 h-algorithm, 99.4% for the LoB and 99.3% for the LoD. Sensitivities were 93.5%-94.8%, as well as 96.8%, 98.7% and 98.1%, respectively. Addition of clinical low-risk criteria such as a HEART-score ≤ 3 to the DMS resulted in NPVs and sensitivities of 100% with a true-negative rule-out to 33.8%-41.6%. Rates of the combined end-point of death/MI within 30 days ranged between 0.2% and 0.3% for all fast-rule-out protocols.\n Depending on the applied copeptin cut-off and addition of clinical low-risk criteria, the DMS might be an alternative to the hs-cTn-only-based algorithms for rapid AMI rule-out with comparable diagnostic measures and outcomes.\n Copyright © 2018. Published by Elsevier B.V.\n\n\n"
},
{
"text": "\n52969\nMutations in the apolipoprotein (apo) B-100 receptor-binding region: detection of apo B-100 (Arg3500-->Trp) associated with two new haplotypes and evidence that apo B-100 (Glu3405-->Gln) diminishes receptor-mediated uptake of LDL.\n\nFisher, E\n\nScharnagl, H\n\nHoffmann, MM\n\nKusterer, K\n\nWittmann, D\n\nWieland, H\n\nGross, W\n\nMärz, W\n\nBeiträge in Fachzeitschriften\nISI:000081286100015\n10388479.0\nNone\nNone\nBACKGROUND: Ligand-defective apolipoprotein (apo) B-100 is a major cause of hypercholesterolemia. For many years, apo B-100 (Arg3500-->Gln) has been the only mutation known to cause ligand-defective apo B-100. METHODS: Using temperature gradient gel electrophoresis, we screened 297 unrelated individuals with LDL-cholesterol >1.55 g/L and triglycerides <2.0 g/L for sequence variants of the putative LDL receptor-binding domain of apo B-100. RESULTS: We found apo B-100 (Arg3500-->Gln) in 21 individuals (7.1%). When extrapolated to the general population, this corresponds to the highest prevalence of apo B-100 (Arg3500-->Gln) reported to date. Furthermore, we identified three unrelated carriers (1%) of a silent substitution (CTG-->CTA) affecting the codon for leucine3350, four carriers (1.3%) of apo B-100 (Glu3405-->Gln), and two subjects (0.7%) with apo B-100 (Arg3500-->Trp). apo B-100 (Arg3500-->Trp) was assigned to two different, previously unknown haplotypes. The binding, uptake, and degradation of apo B-100 (Arg3500-->Trp) was lower than that of normal LDL, but higher than with apo B-100 (Arg3500-->Gln), implying that the substitution of Trp3500 for Arg may cause less severe reduction of binding than the substitution of Gln. LDL from individuals heterozygous for apo B-100 (Glu3405-->Gln) bound to LDL receptors at the same rate as normal LDL, but was taken up and degraded at significantly reduced rates, suggesting that domains of apo B-100 involved in binding and uptake do not completely overlap. CONCLUSIONS: In Germany, apo B-100 (Arg3500-->Gln) may be more frequent than previously assumed. Both apo B-100 (Arg3500-->Trp) and apo B-100 (Glu3405-->Gln) may contribute to the phenotype of ligand-defective LDL. These variants will be missed if screening is confined to apo B-100 (Arg3500-->Gln) only.\n\nMärz, Winfried\n\nScharnagl, Hubert\n\n\n"
},
{
"text": "\n62562\nOxidation of methionine residues to methionine sulfoxides does not decrease potential antiatherogenic properties of apolipoprotein A-I.\n\nPanzenböck, U\n\nKritharides, L\n\nRaftery, M\n\nRye, KA\n\nStocker, R\n\nBeiträge in Fachzeitschriften\nISI:000087941300016\n10751387.0\n10.1074/jbc.M000458200\nNone\nThe initial stage of oxidation of high density lipoproteins (HDL) is accompanied by the lipid hydroperoxide-dependent, selective oxidation of two of the three Met residues of apolipoprotein A-I (apoA-I) to Met sulfoxides (Met(O)). Formation of such selectively oxidized apoA-I (i.e. apoA-I(+32)) may affect the antiatherogenic properties of HDL, because it has been suggested that Met(86) and Met(112) are important for cholesterol efflux and Met(148) is involved in the activation of lecithin:cholesterol acyl transferase (LCAT). We therefore determined which Met residues were oxidized in apoA-I(+32) and how such oxidation of apoA-I affects its secondary structure, the affinity for lipids, and its ability to remove lipids from human macrophages. We also assessed the capacity of discoidal reconstituted HDL containing apoA-I(+32) to act as substrate for LCAT, and the dissociation of apoA-I and apoA-I(+32) from reconstituted HDL. Met(86) and Met(112) were present as Met(O), as determined by amino acid sequencing and mass spectrometry of isolated peptides derived from apoA-I(+32). Selective oxidation did not alter the alpha-helicity of lipid-free and lipid-associated apoA-I as assessed by circular dichroism, and the affinity for LCAT was comparable for reconstituted HDL containing apoA-I or apoA-I(+32). Cholesteryl ester transfer protein mediated the dissociation of apoA-I more readily from reconstituted HDL containing apoA-I(+32) than unoxidized apoA-I. Also, compared with native apoA-I, apoA-I(+32) had a 2- to 3-fold greater affinity for lipid (as determined by the rate of clearance of multilamellar phospholipid vesicles) and its ability to cause efflux of [(3)H]cholesterol, [(3)H]phospholipid, and [(14)C]alpha-tocopherol from lipid-laden human monocyte-derived macrophages was significantly enhanced. By contrast, no difference was observed for cholesterol and alpha-tocopherol efflux to lipid-associated apolipoproteins. Together, these results suggest that selective oxidation of Met residues enhances rather than diminishes known antiatherogenic activities of apoA-I, consistent with the overall hypothesis that detoxification of lipid hydroperoxides by HDL is potentially antiatherogenic.\n\n\n"
},
{
"text": "\n101872\nAddition of inhaled treprostinil to oral therapy for pulmonary arterial hypertension: a randomized controlled clinical trial.\n\nMcLaughlin, VV\n\nBenza, RL\n\nRubin, LJ\n\nChannick, RN\n\nVoswinckel, R\n\nTapson, VF\n\nRobbins, IM\n\nOlschewski, H\n\nRubenfire, M\n\nSeeger, W\n\nBeiträge in Fachzeitschriften\nISI:000277084900003\n20430262.0\n10.1016/j.jacc.2010.01.027\nNone\nOBJECTIVES: This study assessed the efficacy and safety of inhaled treprostinil in pulmonary arterial hypertension (PAH) patients receiving therapy with either bosentan or sildenafil. BACKGROUND: There is no cure for PAH, despite effective treatments, and outcomes remain suboptimal. The addition of inhaled treprostinil, a long-acting prostacyclin analog, might be a safe and effective treatment addition to other PAH-specific oral therapies. METHODS: Two hundred thirty-five PAH patients with New York Heart Association (NYHA) functional class III (98%) or IV symptoms and a 6-min walk distance (6MWD) of 200 to 450 m while treated with bosentan (70%) or sildenafil were randomized to inhaled treprostinil (up to 54 mug) or inhaled placebo 4 times daily. The primary end point was peak 6MWD at 12 weeks. Secondary end points included time to clinical worsening, Borg Dyspnea Score, NYHA functional class, 12-week trough 6MWD, 6-week peak 6MWD, quality of life, and PAH signs and symptoms. The biomarker N-terminal pro-brain natriuretic peptide (NT-proBNP) was assessed. RESULTS: Twenty-three patients withdrew from the study prematurely (13 treprostinil, 10 placebo). The Hodges-Lehmann between-treatment median difference in change from baseline in peak 6MWD was 19 m at week 6 (p = 0.0001) and 20 m at week 12 (p = 0.0004). Hodges-Lehmann between-treatment median difference in change from baseline in trough 6MWD at week 12 was 14 m (p = 0.0066). Quality of life measures and NT-proBNP improved on active therapy. There were no improvements in other secondary end points, including time to clinical worsening, Borg Dyspnea Score, NYHA functional class, and PAH signs and symptoms. Inhaled treprostinil was safe and well-tolerated. CONCLUSIONS: This trial demonstrates that, among PAH patients who remain symptomatic on bosentan or sildenafil, inhaled treprostinil improves exercise capacity and quality of life and is safe and well-tolerated. (TRIUMPH I: Double Blind Placebo Controlled Clinical Investigation Into the Efficacy and Tolerability of Inhaled Treprostinil Sodium in Patients With Severe Pulmonary Arterial Hypertension; NCT00147199).\n\nOlschewski, Horst\n\n\n"
},
{
"text": "\n103219\nGadobenate dimeglumine and gadofosveset trisodium for MR angiography of the renal arteries: Multicenter intraindividual crossover comparison.\n\nSchneider, G\n\nPasowicz, M\n\nVymazal, J\n\nSeidl, Z\n\nAschauer, M\n\nKonopka, M\n\nBilecen, D\n\nIezzi, R\n\nBallarati, C\n\nBeiträge in Fachzeitschriften\nISI:000280197800029\n20651208.0\n10.2214/AJR.09.3868\nNone\nThis prospective multicenter intraindividual crossover study was designed to compare gadobenate dimeglumine and gadofosveset trisodium at approved doses with respect to the image quality and diagnostic performance of contrast-enhanced MR angiography (CE-MRA) in the detection of clinically relevant renal artery stenosis.\n Thirty-nine subjects (17 men, 22 women; age range, 30-86 years; mean 62 +/- 13.3 [SD] years) with known or suspected renovascular disease underwent a first CE-MRA examination with 0.1 mmol/kg gadobenate dimeglumine and a second examination 3-12 days later with 0.03 mmol/kg gadofosveset. Identical T1-weighted spoiled gradient-refocused echo coronal first-pass images were acquired for 38 of the 39 patients. For 15 of the 38 patients, additional sagittal or axial images or both were acquired with gadofosveset during the steady-state phase. Thirty-four patients underwent digital subtraction angiography, which was the reference standard. Three independent blinded readers assessed source images and maximum-intensity-projection reconstructions to detect clinically relevant (> 50%) renal artery stenosis. Diagnostic performance (sensitivity, specificity, accuracy, positive and negative predictive values) was evaluated with the McNemar and Wald tests. Matched-pair determinations of diagnostic preference were evaluated with Wilcoxon's signed rank test. Reader agreement was determined with kappa analysis, and safety was assessed.\n Comparison of first-pass images revealed superior sensitivity (75.7-86.5% vs 68.4-76.3%), specificity (92.1-98.6% vs 90.5-93.9%), accuracy (88.9-96.2% vs 85.9-90.3%), positive predictive value (70.0-94.1% vs 65.0-76.3%), and negative predictive value (94.0-96.6% vs 91.7-93.9%) with gadobenate dimeglumine. Significant superiority was noted for specificity (p < or = 0.02), accuracy (p < or = 0.005), and positive predictive value (p < or = 0.018). Steady-state images showed no benefit of gadofosveset. Reader agreement was good to excellent (gadobenate dimeglumine, kappa = 0.855; gadofosveset, kappa = 0.776). Reader preference was for gadobenate dimeglumine in 11, 17, and 13 patients and for gadofosveset in five, four, and five patients. No safety concerns were noted.\n Better diagnostic performance and reader preference were found for gadobenate dimeglumine than gadofosveset in first-pass renal CE-MRA.\n\nAschauer, Manuela\n\n\n"
},
{
"text": "\n108401\nA role for Mac-1 (CDIIb/CD18) in immune complex-stimulated neutrophil function in vivo: Mac-1 deficiency abrogates sustained Fcgamma receptor-dependent neutrophil adhesion and complement-dependent proteinuria in acute glomerulonephritis.\n\nTang, T\n\nRosenkranz, A\n\nAssmann, KJM\n\nGoodman, MJ\n\nGutierrezRamos, JC\n\nCarroll, MC\n\nCotran, RS\n\nMayadas, TN\n\nBeiträge in Fachzeitschriften\nISI:A1997YK68100007\n9382884.0\n10.1084/jem.186.11.1853\nPMC2211718\nMac-1 (alphambeta2), a leukocyte adhesion receptor, has been shown in vitro to functionally interact with Fcgamma receptors to facilitate immune complex (IC)-stimulated polymorphonuclear neutrophil (PMN) functions. To investigate the relevance of Mac-1-FcgammaR interactions in IC-mediated injury in vivo, we induced a model of Fc-dependent anti-glomerular basement membrane (GBM) nephritis in wild-type and Mac-1-deficient mice by the intravenous injection of anti-GBM antibody. The initial glomerular PMN accumulation was equivalent in Mac-1 null and wild-type mice, but thereafter increased in wild-type and decreased in mutant mice. The absence of Mac-1 interactions with obvious ligands, intercellular adhesion molecule 1 (ICAM-1), and C3 complement, is not responsible for the decrease in neutrophil accumulation in Mac-1- deficient mice since glomerular PMN accumulation in mice deficient in these ligands was comparable to those in wild-type mice. In vitro studies showed that spreading of Mac-1-null PMNs to IC-coated dishes was equivalent to that of wild-type PMNs at 5-12 min but was markedly reduced thereafter, and was associated with an inability of mutant neutrophils to redistribute filamentous actin. This suggests that in vivo, Mac-1 is not required for the initiation of Fc-mediated PMN recruitment but that Mac-1-FcgammaR interactions are required for filamentous actin reorganization leading to sustained PMN adhesion, and this represents the first demonstration of the relevance of Mac-1-FcgammaR interactions in vivo. PMN-dependent proteinuria, maximal in wild-type mice at 8 h, was absent in Mac-1 mutant mice at all time points. Complement C3-deficient mice also had significantly decreased proteinuria compared to wild-type mice. Since Mac-1 on PMNs is the principal ligand for ic3b, an absence of Mac-1 interaction with C3 probably contributed to the abrogation of proteinuria in Mac-1-null mice.\n\nRosenkranz, Alexander\n\n\n"
},
{
"text": "\n112372\nModulation of motor cortex excitability by different levels of whole-hand afferent electrical stimulation.\n\nGolaszewski, SM\n\nBergmann, J\n\nChristova, M\n\nKunz, AB\n\nKronbichler, M\n\nRafolt, D\n\nGallasch, E\n\nStaffen, W\n\nTrinka, E\n\nNardone, R\n\nBeiträge in Fachzeitschriften\nISI:000298324800025\n21764634.0\n10.1016/j.clinph.2011.06.010\nNone\nOBJECTIVE: In a previous transcranial magnetic stimulation (TMS) study we demonstrated that suprathreshold mesh-glove (MG) whole-hand stimulation elicits lasting changes in motor cortical excitability. Currently, there is no consensus with regard to the optimal parameters for the induction of sensorimotor cortical plasticity using peripheral electrical stimulation. Thus, in the present study we explore the modulatory effects of MG stimulation at different stimulus intensities and different frequencies in order to identify an optimal stimulation protocol. METHODS: MG stimulation was performed on 12 healthy subjects in separate sessions at different stimulation levels: sub-sensory at 50 Hz, sensory at 50 Hz and motor at 2 Hz. To verify if stimulation at lower frequencies is less effective, an additional experiment at sensory level with 2 Hz was performed. TMS was used to assess motor threshold (MT), motor evoked potentials (MEPs) recruitment curve (RC), short latency intracortical inhibition (SICI) and intracortical facilitation (ICF) to paired-pulse TMS at baseline (T0), immediately after (T1) and 1h (T2) after 30 min of MG stimulation. F-wave studies were performed to assess spinal motoneuron excitability. RESULTS: MG stimulation at sub-sensory/50 Hz and sensory/2 Hz level determines no significant cortical excitability changes; at sensory/50 Hz level and at motor/2 Hz level we found decreased MT, increased MEP RC as well as reduced SICI and increased ICF at T1 and T2. CONCLUSIONS: MG stimulation at sensory/50 Hz and motor/2 Hz level induces similar long-lasting modulatory effects on motor cortical excitability. Both the strength of the corticospinal projections and the intracortical networks are influenced to the same extend. SIGNIFICANCE: The study provides further evidence that stimulation intensity and frequency can independently modulate motor cortical plasticity. The selection of optimal stimulation parameters has potentially important implications for the neurorehabilitation of patients after brain damage (e.g. stroke, traumatic brain injury) with hand motor deficits. Copyright © 2011 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.\n\nChristova, Monica\n\nGallasch, Eugen\n\n\n"
}
]
}