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"text": "\n181933\nPleuropulmonary blastoma type I might arise in congenital pulmonary airway malformation type 4 by acquiring a Dicer 1 mutation.\n\nBrcic, L\n\nFakler, F\n\nEidenhammer, S\n\nThueringer, A\n\nKashofer, K\n\nKulka, J\n\nPopper, H\n\nBeiträge in Fachzeitschriften\nISI:000521039900001\n32193603.0\n10.1007/s00428-020-02789-6\nPMC7443180\nCongenital pulmonary airway malformation (CPAM) occurs most commonly in infants. It is divided into 5 types. The most common types 1 and 2 are cystic, type 0 presents as bronchial buds without alveolar tissue, most likely corresponding to alveolar dysgenesis, while type 3 is composed of branching bronchioles and appears as a solid lesion. A defect in the epithelial-mesenchymal crosstalk might be the underlying mechanism for all. Type 4 is a peripheral cystic lesion with a thin cyst wall covered by pneumocytes. CPAM 4 has been mixed up with pleuropulmonary blastoma (PPB) type I and some authors question its existence. We investigated five cases of CPAM type 4 for the presence or absence of rhabdomyoblasts, and for markers associated with CPAM development. In addition, all cases were evaluated for mutations within the Dicer gene and for mutations of the RAS family of oncogenes. All five cases showed smooth muscle actin and desmin-positive cells; however, only one case showed a few cells positive for MyoD. The same case showed a mutation of Dicer 1. All cases were negative for mutations of the RAS family of genes. Fibroblast growth factor 10 was similarly expressed in all cases, and thus cannot be used to differentiate CPAM4 from PPB-I. Low expression of the proliferation marker Ki67 was seen in our CPAM 4 cases and the probable PPB-I case. YingYang-1 protein seems to play an active role in the development of PPB-I. CPAM 4 can be separated from PPB-I based on the presence of rhabdomyoblasts and mutations in Dicer 1 gene. These cells might not be numerous; therefore, all available tissue has to be evaluated. As CPAM 4 morphologically looks very similar to PPB-I, it might be speculated, that there exists a potential for progression from CPAM 4 to PPB-I, by acquiring somatic mutations in Dicer 1.\n\nBrcic, Luka\n\nEidenhammer, Sylvia\n\nKashofer, Karl\n\nPopper, Helmuth\n\n\n"
},
{
"text": "\n4987\nSirolimus and mycophenolate mofetil after liver transplantation.\n\nKniepeiss, D\n\nIberer, F\n\nGrasser, B\n\nSchaffellner, S\n\nTscheliessnigg, KH\n\nBeiträge in Fachzeitschriften\nISI:000184854200008\n12687325.0\n10.1007/s00147-003-0579-1\nNone\nSince the approval of sirolimus (SRL) as an immunosuppressive agent in renal transplantation, several liver transplant centres have introduced this agent to the immunosuppression regimen. We present here a retrospective follow-up study of late conversion to sirolimus and mycophenolate mofetil (MMF) as immunosuppressive agents after liver transplantation (LTX). From July 2001 to March 2002, seven liver transplant recipients (three female, 59 (41-66) years old) were enrolled in this study. Indications for liver transplantation were hepatitis B and/or hepatitis C (three), alcohol-induced cirrhosis (three) and Wilson's syndrome (hepatolenticular degeneration) (one). LTX was performed by standard (four) or piggy-back (three) technique. The switch to SRL was performed 62 (37-118) months after LTX; the reasons for the switch from cyclosporine or tacrolimus to SRL were renal (six) or neurological (one) impairment. As immunosuppressive therapy, SRL at trough levels of 4-10 ng/ml and MMF at trough levels of approximately 1 micro g/ml were administered. Mean follow-up time under SRL per patient was 137 (26-258 days). Patient and graft survival was 100% during SRL therapy, and there were neither rejection episodes nor infections. Renal function improved in five of the six patients (83.3%) whom we had switched to SRL due to renal impairment. In the patient whom we switched to SRL due to neurological impairment, the neurological symptoms abated, and renal function improved. Side effects (hypertriglyceridaemia, hypercholesterolaemia, exanthema) became manifest in three patients (42.8%). Cessation of therapy due to side effects was necessary in two patients (exanthema: one, hypertriglyceridaemia: one). One patient refused to continue the therapy with SRL because he wanted tablets, and we only had SRL in fluid form. The data of our study suggest that SRL is a potent immunosuppressive agent of potential benefit in clinical LTX. SRL in combination with MMF provided sufficient immunosuppression of liver allografts in the late course after LTX. Side effects were reversible with dose reduction or cessation of therapy. We can thus conclude that SRL might offer an immunosuppressive therapy for patients with renal or neurological impairment after LTX.\n\nKniepeiss, Daniela\n\nSchaffellner, Silvia\n\n\n"
},
{
"text": "\n88209\nInsulin-like growth factor binding protein-3 levels during early and late follow-up after surgery in acromegalic patients.\n\nCharalampaki, P\n\nHildebrandt, G\n\nSchaeffer, HJ\n\nSchönau, E\n\nKlug, N\n\nBeiträge in Fachzeitschriften\nISI:000073500200007\n9628244.0\n10.1055/s-0029-1211964\nNone\nDisease activity in acromegaly is accurately reflected by growth hormone (GH) concentration during oral glucose tolerance test (OGTT) and insulin-like growth factor-I (IGF-I) levels, representing an integrated index of GH activity. This prospective study was performed to evaluate whether plasma IGF binding protein 3 (IGFBP-3) might also reflect the hormonal disease activity in pituitary acromegaly after operative treatment during early and late follow-up. Twenty-two acromegalic patients were studied. Data were obtained pre-, intra- and post-operatively in 13 cases. In 9 patients the acromegalic activity was studied only after treatment. The hormonal assessment included repeated blood samples for estimation of IGF-I, IGFBP-3 and repeated OGTTs. In each case 100 sigma g octreotide (Sandostatin lambda, Sandoz, Basel) was injected to test the acute response of GH, IGF-I and IGFBP-3. Intraoperatively, GH levels were estimated to examine acutely the influence of tumour reduction on GH levels. Patients were considered cured when GH levels (GH60min) were less than 2 ng/ml during OGTT 4 weeks after surgery. The data outlined that in patients with normalized GH60min levels, normalized IGFBP-3 levels were noticed 4 weeks and 12 months post-operatively. In non-cured patients normalized IGFBP-3 concentrations were found in 11 out of 15 cases in the late post-treatment phase. In contrast only 1 of 7 cured patients had persistently elevated IGF-I levels within the first month post-operatively, whereas no case of the non-cured patients had IGF-I values in the normal range. Despite these observations a strong correlation of IGF-I and IGFBP-3 did not exist before one year post-operatively -- either in the cured or in the non-cured patients. Serum IGFBP-3 in patients with pituitary acromegaly does not provide a predictive value of appreciable magnitude concerning cure or non-cure from the disease- whether examined early or late in the post-operative period. Absolute levels of IGFBP-3 may thus cause misinterpretation concerning cure of acromegalics after surgery.\n\n\n"
},
{
"text": "\n88567\nLong-term cardiac-targeted RNA interference for the treatment of heart failure restores cardiac function and reduces pathological hypertrophy.\n\nSuckau, L\n\nFechner, H\n\nChemaly, E\n\nKrohn, S\n\nHadri, L\n\nKockskämper, J\n\nWestermann, D\n\nBisping, E\n\nLy, H\n\nWang, X\n\nKawase, Y\n\nChen, J\n\nLiang, L\n\nSipo, I\n\nVetter, R\n\nWeger, S\n\nKurreck, J\n\nErdmann, V\n\nTschope, C\n\nPieske, B\n\nLebeche, D\n\nSchultheiss, HP\n\nHajjar, RJ\n\nPoller, WC\n\nBeiträge in Fachzeitschriften\nISI:000264004800010\n19237664.0\n10.1161/CIRCULATIONAHA.108.783852\nNone\nBackground-RNA interference (RNAi) has the potential to be a novel therapeutic strategy in diverse areas of medicine. Here, we report on targeted RNAi for the treatment of heart failure, an important disorder in humans that results from multiple causes. Successful treatment of heart failure is demonstrated in a rat model of transaortic banding by RNAi targeting of phospholamban, a key regulator of cardiac Ca2+ homeostasis. Whereas gene therapy rests on recombinant protein expression as its basic principle, RNAi therapy uses regulatory RNAs to achieve its effect. Methods and Results-We describe structural requirements to obtain high RNAi activity from adenoviral and adeno-associated virus (AAV9) vectors and show that an adenoviral short hairpin RNA vector (AdV-shRNA) silenced phospholamban in cardiomyocytes (primary neonatal rat cardiomyocytes) and improved hemodynamics in heart-failure rats 1 month after aortic root injection. For simplified long-term therapy, we developed a dimeric cardiotropic adeno-associated virus vector (rAAV9-shPLB) to deliver RNAi activity to the heart via intravenous injection. Cardiac phospholamban protein was reduced to 25%, and suppression of sacroplasmic reticulum Ca2+ ATPase in the HF groups was rescued. In contrast to traditional vectors, rAAV9 showed high affinity for myocardium but low affinity for liver and other organs. rAAV9-shPLB therapy restored diastolic (left ventricular end-diastolic pressure, dp/dt(min), and tau) and systolic (fractional shortening) functional parameters to normal ranges. The massive cardiac dilation was normalized, and cardiac hypertrophy, cardiomyocyte diameter, and cardiac fibrosis were reduced significantly. Importantly, no evidence was found of microRNA deregulation or hepatotoxicity during these RNAi therapies. Conclusions-Our data show for the first time the high efficacy of an RNAi therapeutic strategy in a cardiac disease. (Circulation. 2009; 119: 1241-1252.)\n\nBisping, Egbert Hubertus\n\n\n"
},
{
"text": "\n115618\nExpression of Trp3 determines sensitivity of capacitative Ca2+ entry to nitric oxide and mitochondrial Ca2+ handling: evidence for a role of Trp3 as a subunit of capacitative Ca2+ entry channels.\n\nThyagarajan, B\n\nPoteser, M\n\nRomanin, C\n\nKahr, H\n\nZhu, MX\n\nGroschner, K\n\nBeiträge in Fachzeitschriften\nISI:000172927000056\n11600493.0\n10.1074/jbc.M103977200\nNone\nThe role of Trp3 in cellular regulation of Ca(2+) entry by NO was studied in human embryonic kidney (HEK) 293 cells. In vector-transfected HEK293 cells (controls), thapsigargin (TG)-induced (capacitative Ca(2+) entry (CCE)-mediated) intracellular Ca(2+) signals and Mn(2+) entry were markedly suppressed by the NO donor 2-(N, -diethylamino)diazenolate-2-oxide sodium salt (3 microm) or by authentic NO (100 microm). In cells overexpressing Trp3 (T3-9), TG-induced intracellular Ca(2+) signals exhibited an amplitude similar to that of controls but lacked sensitivity to inhibition by NO. Consistently, NO inhibited TG-induced Mn(2+) entry in controls but not in T3-9 cells. Moreover, CCE-mediated Mn(2+) entry into T3-9 cells exhibited a striking sensitivity to inhibition by extracellular Ca(2+), which was not detectable in controls. Suppression of mitochondrial Ca(2+) handling with the uncouplers carbonyl cyanide m-chlorophenyl hydrazone (300 nm) or antimycin A(1) (-AA(1)) mimicked the inhibitory effect of NO on CCE in controls but barely affected CCE in T3-9 cells. T3-9 cells exhibited enhanced carbachol-stimulated Ca(2+) entry and clearly detectable cation currents through Trp3 cation channels. NO as well as carbonyl cyanide m-chlorophenyl hydrazone slightly promoted carbachol-induced Ca(2+) entry into T3-9 cells. Simultaneous measurement of cytoplasmic Ca(2+) and membrane currents revealed that Trp3 cation currents are inhibited during Ca(2+) entry-induced elevation of cytoplasmic Ca(2+), and that this negative feedback regulation is blunted by NO. Our results demonstrate that overexpression of Trp3 generates phospholipase C-regulated cation channels, which exhibit regulatory properties different from those of endogenous CCE channels. Moreover, we show for the first time that Trp3 expression determines biophysical properties as well as regulation of CCE channels by NO and mitochondrial Ca(2+) handling. Thus, we propose Trp3 as a subunit of CCE channels.\n\nGroschner, Klaus\n\n\n"
},
{
"text": "\n136251\nAnalysis of clinical, dermoscopic and histopathological features of primary melanomas of patients with metastatic disease--a retrospective study at the Department of Dermatology, Medical University of Graz, 2000-2010.\n\nRichtig, G\n\nRichtig, E\n\nMassone, C\n\nHofmann-Wellenhof, R\n\nBeiträge in Fachzeitschriften\nISI:000345348800025\n24576192.0\n10.1111/jdv.12413\nNone\nIncidence rates of malignant melanoma have been increasing worldwide and metastatic melanoma is still a significant problem despite widespread prevention programmes.\n We made a systemic review of all metastasized melanoma patients treated at the Department of Dermatology, Medical University of Graz in the years 2000-2010 and looked at the kind of melanoma type, e.g. if it has been slowly growing superficial spreading melanoma (SSM) or fast growing nodular melanoma (NM).\n Histological slides and clinical images of patients treated at our department between 2000 and 2010, who received chemotherapy because of proven metastatic disease were analysed with regard to growth type of their primary tumours.\n A total of 88 patients met the inclusion criteria. Mean age of all patients was 57 years (median 59 years, SD ± 15 years). Of these 88 patients 51 patients (58%) (28 male patients and 23 female patients) had SSM; mean age 58 years (median 58 years, SD ± 14 years) and 37 patients (42%) (18 male patients and 19 female patients) had NM; mean age 56 years (median 61 years, SD ± 17 years). Mean Breslow thickness in the SSM group was 2.26 mm (median: 1.6 mm, SD ± 2.11 mm). In the NM group, mean Breslow thickness was 4.59 mm (median: 3.50 mm, SD ± 4.07 mm). When separated by gender, 46 melanomas were seen in the male group (28 SSM and 18 NM) and 42 melanomas in the female group (23 SSM and 19 NM).\n Our results showed that more than half of the patients with metastatic disease had SSMs and not, as suspected, NMs. As SSMs are growing over a longer period to become invasive and potentially metastatic, there might be a chance to focus primary and secondary prevention programmes not only on fast growing tumours but also on slowly changes of tumours.\n © 2014 European Academy of Dermatology and Venereology.\n\nHofmann-Wellenhof, Rainer\n\nRichtig, Erika\n\nRichtig, Georg\n\n\n"
},
{
"text": "\n147063\n2015 Recommendations for the management of polymyalgia rheumatica: a European League Against Rheumatism/American College of Rheumatology collaborative initiative.\n\nDejaco, C\n\nSingh, YP\n\nPerel, P\n\nHutchings, A\n\nCamellino, D\n\nMackie, S\n\nAbril, A\n\nBachta, A\n\nBalint, P\n\nBarraclough, K\n\nBianconi, L\n\nButtgereit, F\n\nCarsons, S\n\nChing, D\n\nCid, M\n\nCimmino, M\n\nDiamantopoulos, A\n\nDocken, W\n\nDuftner, C\n\nFashanu, B\n\nGilbert, K\n\nHildreth, P\n\nHollywood, J\n\nJayne, D\n\nLima, M\n\nMaharaj, A\n\nMallen, C\n\nMartinez-Taboada, V\n\nMaz, M\n\nMerry, S\n\nMiller, J\n\nMori, S\n\nNeill, L\n\nNordborg, E\n\nNott, J\n\nPadbury, H\n\nPease, C\n\nSalvarani, C\n\nSchirmer, M\n\nSchmidt, W\n\nSpiera, R\n\nTronnier, D\n\nWagner, A\n\nWhitlock, M\n\nMatteson, EL\n\nDasgupta, B\n\nEuropean League Against Rheumatism\n\nAmerican College of Rheumatology\n\nBeiträge in Fachzeitschriften\nISI:000361043200006\n26359488.0\n10.1136/annrheumdis-2015-207492\nNone\nTherapy for polymyalgia rheumatica (PMR) varies widely in clinical practice as international recommendations for PMR treatment are not currently available. In this paper, we report the 2015 European League Against Rheumatism (EULAR)/American College of Rheumatology (ACR) recommendations for the management of PMR. We used the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) methodology as a framework for the project. Accordingly, the direction and strength of the recommendations are based on the quality of evidence, the balance between desirable and undesirable effects, patients' and clinicians' values and preferences, and resource use. Eight overarching principles and nine specific recommendations were developed covering several aspects of PMR, including basic and follow-up investigations of patients under treatment, risk factor assessment, medical access for patients and specialist referral, treatment strategies such as initial glucocorticoid (GC) doses and subsequent tapering regimens, use of intramuscular GCs and disease modifying anti-rheumatic drugs (DMARDs), as well as the roles of non-steroidal anti-rheumatic drugs and non-pharmacological interventions. These recommendations will inform primary, secondary and tertiary care physicians about an international consensus on the management of PMR. These recommendations should serve to inform clinicians about best practices in the care of patients with PMR.\n Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.\n\nDejaco, Christian\n\n\n"
},
{
"text": "\n147515\nClinical onset and course, response to treatment and outcome in 24 patients with the cblE or cblG remethylation defect complemented by genetic and in vitro enzyme study data.\n\nHuemer, M\n\nBürer, C\n\nJešina, P\n\nKožich, V\n\nLandolt, MA\n\nSuormala, T\n\nFowler, B\n\nAugoustides-Savvopoulou, P\n\nBlair, E\n\nBrennerova, K\n\nBroomfield, A\n\nDe Meirleir, L\n\nGökcay, G\n\nHennermann, J\n\nJardine, P\n\nKoch, J\n\nLorenzl, S\n\nLotz-Havla, AS\n\nNoss, J\n\nParini, R\n\nPeters, H\n\nPlecko, B\n\nRamos, FJ\n\nSchlune, A\n\nTsiakas, K\n\nZerjav Tansek, M\n\nBaumgartner, MR\n\nBeiträge in Fachzeitschriften\nISI:000360436700021\n25526710.0\n10.1007/s10545-014-9803-7\nNone\nThe cobalamin E (cblE) (MTRR, methionine synthase reductase) and cobalamin G (cblG) (MTR, methionine synthase) defects are rare inborn errors of cobalamin metabolism leading to impairment of the remethylation of homocysteine to methionine.\n Information on clinical and laboratory data at initial full assessment and during the course of the disease, treatment, outcome and quality of life was obtained in a survey-based, retrospective study from physicians caring for patients with the CblE or CblG defect. In addition, data on enzyme studies in cultured skin fibroblasts and mutations in the MTRR and MTR gene were analysed.\n In 11 cblE and 13 cblG patients, failure to thrive, feeding problems, delayed milestones, muscular hypotonia, cognitive impairment and macrocytic anaemia were the most frequent symptoms. Delay in diagnosis depended on age at first symptom and clinical pattern at presentation and correlated significantly with impaired communication abilities at follow-up. Eighteen/22 patients presented with brain atrophy or white matter disease. Biochemical response to treatment with variable combinations of betaine, cobalamin, folate was significant. The overall course was considered improving (n = 8) or stable (n = 15) in 96% of patients, however the average number of CNS symptoms per patient increased significantly over time and 16 of 23 patients were classified as developmentally delayed or severely handicapped. In vitro enzyme analysis data showed no correlation with outcome. Predominantly private mutations were detected and no genotype- phenotype correlations evident.\n The majority of patients with the cblE and cblG defect show limited clinical response to treatment and have neurocognitive impairment.\n\nPlecko, Barbara\n\n\n"
},
{
"text": "\n154620\nAntibodies to MOG and AQP4 in children with neuromyelitis optica and limited forms of the disease.\n\nLechner, C\n\nBaumann, M\n\nHennes, EM\n\nSchanda, K\n\nMarquard, K\n\nKarenfort, M\n\nLeiz, S\n\nPohl, D\n\nVenkateswaran, S\n\nPritsch, M\n\nKoch, J\n\nSchimmel, M\n\nHäusler, M\n\nKlein, A\n\nBlaschek, A\n\nThiels, C\n\nLücke, T\n\nGruber-Sedlmayr, U\n\nKornek, B\n\nHahn, A\n\nLeypoldt, F\n\nSandrieser, T\n\nGallwitz, H\n\nStoffels, J\n\nKorenke, C\n\nReindl, M\n\nRostásy, K\n\nBeiträge in Fachzeitschriften\nISI:000380392200016\n26645082.0\n10.1136/jnnp-2015-311743\nNone\nTo determine the frequency and clinical-radiological associations of antibodies to myelin oligodendrocyte glycoprotein (MOG) and aquaporin-4 (AQP4) in children presenting with neuromyelitis optica (NMO) and limited forms.\n Children with a first event of NMO, recurrent (RON), bilateral ON (BON), longitudinally extensive transverse myelitis (LETM) or brainstem syndrome (BS) with a clinical follow-up of more than 12 months were enrolled. Serum samples were tested for MOG- and AQP4-antibodies using live cell-based assays.\n 45 children with NMO (n=12), LETM (n=14), BON (n=6), RON (n=12) and BS (n=1) were included. 25/45 (56%) children had MOG-antibodies at initial presentation (7 NMO, 4 BON, 8 ON, 6 LETM). 5/45 (11%) children showed AQP4-antibodies (3 NMO, 1 LETM, 1 BS) and 15/45 (33%) were seronegative for both antibodies (2 NMO, 2 BON, 4 RON, 7 LETM). No differences were found in the age at presentation, sex ratio, frequency of oligoclonal bands or median EDSS at last follow-up between the three groups. Children with MOG-antibodies more frequently (1) had a monophasic course (p=0.018) after one year, (2) presented with simultaneous ON and LETM (p=0.004) and (3) were less likely to receive immunosuppressive therapies (p=0.0002). MRI in MOG-antibody positive patients (4) less frequently demonstrated periependymal lesions (p=0.001), (5) more often were unspecific (p=0.004) and (6) resolved more frequently (p=0.016).\n 67% of all children presenting with NMO or limited forms tested positive for MOG- or AQP4-antibodies. MOG-antibody positivity was associated with distinct features. We therefore recommend to measure both antibodies in children with demyelinating syndromes.\n Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/\n\n\n"
},
{
"text": "\n154766\nPostoperative Nomogram for Relapse-Free Survival in Patients with High Grade Upper Tract Urothelial Carcinoma.\n\nKrabbe, LM\n\nEminaga, O\n\nShariat, SF\n\nHutchinson, RC\n\nLotan, Y\n\nSagalowsky, AI\n\nRaman, JD\n\nWood, CG\n\nWeizer, AZ\n\nRoscigno, M\n\nMontorsi, F\n\nBolenz, C\n\nNovara, G\n\nKikuchi, E\n\nFajkovic, H\n\nRapoport, LM\n\nGlybochko, PV\n\nZigeuner, R\n\nRemzi, M\n\nBensalah, K\n\nKassouf, W\n\nMargulis, V\n\nBeiträge in Fachzeitschriften\nISI:000395869600015\n27670916.0\n10.1016/j.juro.2016.09.078\nNone\nWe developed a prognostic nomogram for patients with high grade urothelial carcinoma of the upper urinary tract after extirpative surgery.\n Clinical data were available for 2, 26 patients diagnosed with high grade urothelial carcinoma of the upper urinary tract who underwent extirpative surgery. Cox proportional hazard regression models identified independent prognosticators of relapse in the development cohort (838). A backward step-down selection process was applied to achieve the most informative nomogram with the least number of variables. The L2-regularized logistic regression was applied to generate the novel nomogram. Harrell's concordance indices were calculated to estimate the discriminative accuracy of the model. Internal validation processes were performed using bootstrapping, random sampling, tenfold cross-validation, LOOCV, Brier score, information score and F1 score. External validation was performed on an external cohort (2, 88). Decision tree analysis was used to develop a risk classification model. Kaplan-Meier curves were applied to estimate the relapse rate for each category.\n Overall 35.3% and 30.7% of patients experienced relapse in the development and external validation cohort. The final nomogram included age, pT stage, pN stage and architecture. It achieved a discriminative accuracy of 0.71 and 0.76, and the AUC was 0.78 and 0.77 in the development and external validation cohort, respectively. Rigorous testing showed constant results. The 5-year relapse-free survival rates were 88.6%, 68.1%, 40.2% and 12.5% for the patients with low risk, intermediate risk, high risk and very high risk disease, respectively.\n The current nomogram, consisting of only 4 variables, shows high prognostic accuracy and risk stratification for patients with high grade urothelial carcinoma of the upper urinary tract following extirpative surgery, thereby adding meaningful information for clinical decision making.\n Copyright © 2017 American Urological Association Education and Research, Inc. Published by Elsevier Inc. All rights reserved.\n\nZigeuner, Richard\n\n\n"
},
{
"text": "\n156460\nVagal denervation inhibits the increase in pulmonary blood flow during partial lung aeration at birth.\n\nLang, JA\n\nPearson, JT\n\nBinder-Heschl, C\n\nWallace, MJ\n\nSiew, ML\n\nKitchen, MJ\n\nTe Pas, AB\n\nLewis, RA\n\nPolglase, GR\n\nShirai, M\n\nHooper, SB\n\nBeiträge in Fachzeitschriften\nISI:000398112300023\n27902842.0\n10.1113/JP273682\nPMC5330930\nLung aeration at birth significantly increases pulmonary blood flow, which is unrelated to increased oxygenation or other spatial relationships that match ventilation to perfusion. Using simultaneous X-ray imaging and angiography in near-term rabbits, we investigated the relative contributions of the vagus nerve and oxygenation to the increase in pulmonary blood flow at birth. Vagal denervation inhibited the global increase in pulmonary blood flow induced by partial lung aeration, although high inspired oxygen concentrations can partially mitigate this effect. The results of the present study indicate that a vagal reflex may mediate a rapid global increase in pulmonary blood flow in response to partial lung aeration.\n Air entry into the lungs at birth triggers major cardiovascular changes, including a large increase in pulmonary blood flow (PBF) that is not spatially related to regional lung aeration. To investigate the possible underlying role of a vagally-mediated stimulus, we used simultaneous phase-contrast X-ray imaging and angiography in near-term (30 days of gestation) vagotomized (n = 15) or sham-operated (n = 15) rabbit kittens. Rabbits were imaged before ventilation, when one lung was ventilated (unilateral) with 100% nitrogen (N2 ), air or 100% oxygen (O2 ), and after all kittens were switched to unilateral ventilation in air and then ventilation of both lungs using air. Compared to control kittens, vagotomized kittens had little or no increase in PBF in both lungs following unilateral ventilation when ventilation occurred with 100% N2 or with air. However, relative PBF did increase in vagotomized animals ventilated with 100% O2 , indicating the independent stimulatory effects of local oxygen concentration and autonomic innervation on the changes in PBF at birth. These findings demonstrate that vagal denervation inhibits the previously observed increase in PBF with partial lung aeration, although high inspired oxygen concentrations can partially mitigate this effect.\n © 2016 The Authors. The Journal of Physiology © 2016 The Physiological Society.\n\nBinder-Heschl, Corinna\n\n\n"
},
{
"text": "\n165460\nAn Easy-to-Use Prognostic Model for Survival Estimation for Patients with Symptomatic Long Bone Metastases.\n\nWilleumier, JJ\n\nvan der Linden, YM\n\nvan der Wal, CWPG\n\nJutte, PC\n\nvan der Velden, JM\n\nSmolle, MA\n\nvan der Zwaal, P\n\nKoper, P\n\nBakri, L\n\nde Pree, I\n\nLeithner, A\n\nFiocco, M\n\nDijkstra, PDS\n\nBeiträge in Fachzeitschriften\nISI:000427284900011\n29406340.0\n10.2106/JBJS.16.01514\nNone\nA survival estimation for patients with symptomatic long bone metastases (LBM) is crucial to prevent overtreatment and undertreatment. This study analyzed prognostic factors for overall survival and developed a simple, easy-to-use prognostic model.\n A multicenter retrospective study of 1, 20 patients treated for symptomatic LBM between 2000 and 2013 at the radiation therapy and/or orthopaedic departments was performed. Primary tumors were categorized into 3 clinical profiles (favorable, moderate, or unfavorable) according to an existing classification system. Associations between prognostic variables and overall survival were investigated using the Kaplan-Meier method and multivariate Cox regression models. The discriminatory ability of the developed model was assessed with the Harrell C-statistic. The observed and expected survival for each survival category were compared on the basis of an external cohort.\n Median overall survival was 7.4 months (95% confidence interval [CI], 6.7 to 8.1 months). On the basis of the independent prognostic factors, namely the clinical profile, Karnofsky Performance Score, and presence of visceral and/or brain metastases, 12 prognostic categories were created. The Harrell C-statistic was 0.70. A flowchart was developed to easily stratify patients. Using cutoff points for clinical decision-making, the 12 categories were narrowed down to 4 categories with clinical consequences. Median survival was 21.9 months (95% CI, 18.7 to 25.1 months), 10.5 months (95% CI, 7.9 to 13.1 months), 4.6 months (95% CI, 3.9 to 5.3 months), and 2.2 months (95% CI, 1.8 to 2.6 months) for the 4 categories.\n This study presents a model to easily stratify patients with symptomatic LBM according to their expected survival. The simplicity and clarity of the model facilitate and encourage its use in the routine care of patients with LBM, to provide the most appropriate treatment for each individual patient.\n Prognostic Level IV. See Instructions for Authors for a complete description of levels of evidence.\n\nLeithner, Andreas\n\nSmolle, Maria Anna\n\n\n"
},
{
"text": "\n170107\nLipid-modifying therapy and low-density lipoprotein cholesterol goal attainment in patients with familial hypercholesterolemia in Germany: The CaReHigh Registry.\n\nSchmidt, N\n\nDressel, A\n\nGrammer, TB\n\nGouni-Berthold, I\n\nJulius, U\n\nKassner, U\n\nKlose, G\n\nKönig, C\n\nKoenig, W\n\nOtte, B\n\nParhofer, KG\n\nReinhard, W\n\nSchatz, U\n\nSchunkert, H\n\nSteinhagen-Thiessen, E\n\nVogt, A\n\nLaufs, U\n\nMärz, W\n\nBeiträge in Fachzeitschriften\nISI:000445908000048\n30270065.0\n10.1016/j.atherosclerosis.2018.08.050\nNone\nFamilial hypercholesterolemia (FH) is amongst the most common genetic disorders encountered in primary care. Yet, only a minority of affected patients is diagnosed and treated. This interim analysis of the CaRe High Registry aims at examining the state of treatment and attainment of lipid goals in German FH patients.\n The CaRe High registry includes FH patients from lipid clinics and private practices. Data have been collected using questionnaires filled in by the recruiting physicians and by interviewing the participating patients.\n We examined 512 F H patients diagnosed according to clinical criteria. Median age at the time of the first FH diagnosis was 39 (25th and 75th percentile: 27-50) years, median treatment naïve LDL cholesterol (LDL-C) was 239.4 mg/dl (6.19 mmol/l), 25th to 75th percentile 191.8-342.5 mg/dl (4.96-8.86 mmol/l). 27% of the participants did not receive lipid-lowering drugs. Among the patients treated with lipid-lowering drugs, 19% received a PCSK9 inhibitor (PCSK9i) in combination with a statin, 9% were treated with a PCSK9i alone and 3% were treated with a combination of PCSK9i and a non-statin drug. Patients with pre-existing CVD were more likely to be treated with lipid-lowering drugs and more likely to receive a PCSK9i, but LDL-C targets were only achieved by a minority of patients (<20%). Gap to target LDL-C was lowest and the median achieved LDL-C reduction was 1.4 times higher with PCSK9i treatment than with (oral) lipid-lowering therapy without PCSK9i.\n The Care High registry has included patients with the typical clinical features of familial hypercholesterolemia. PCSK9i treatment in addition to standard therapy allows attainment of target values in many patients with initially very high LDL-C.\n Copyright © 2018 The Authors. Published by Elsevier B.V. All rights reserved.\n\nMärz, Winfried\n\n\n"
},
{
"text": "\n182596\nSensitive and broadly applicable residual disease detection in acute myeloid leukemia using flow cytometry-based leukemic cell enrichment followed by mutational profiling.\n\nDaga, S\n\nRosenberger, A\n\nKashofer, K\n\nHeitzer, E\n\nQuehenberger, F\n\nHalbwedl, I\n\nGraf, R\n\nKrisper, N\n\nPrietl, B\n\nHöfler, G\n\nReinisch, A\n\nZebisch, A\n\nSill, H\n\nWölfler, A\n\nBeiträge in Fachzeitschriften\nISI:000557466600001\n32602117.0\n10.1002/ajh.25918\nPMC7540028\nPersistent measurable residual disease (MRD) is an increasingly important prognostic marker in acute myeloid leukemia (AML). Currently, MRD is determined by multi-parameter flow cytometry (MFC) or PCR-based methods detecting leukemia-specific fusion transcripts and mutations. However, while MFC is highly operator-dependent and difficult to standardize, PCR-based methods are only available for a minority of AML patients. Here we describe a novel, highly sensitive and broadly applicable method for MRD detection by combining MFC-based leukemic cell enrichment using an optimized combinatorial antibody panel targeting CLL-1, TIM-3, CD123 and CD117 followed by mutational analysis of recurrently mutated genes in AML. In dilution experiments this method showed a sensitivity of 10-4 to 10-5 for residual disease detection. In prospectively collected remission samples this marker combination allowed for a median 67-fold cell enrichment with sufficient DNA quality for mutational analysis using next generation sequencing (NGS) or digital PCR in 39 out of 41 patients. Twenty-one samples (53.8%) tested MRD positive, whereas 18 (46.2%) were negative. With a median follow-up of 559 days 71.4% of MRD positive (15/21) and 27.8% (5/18) of MRD negative patients relapsed (p=0.0065). The cumulative incidence of relapse (CIR) was higher for MRD positive patients (5-year CIR: 90.5% vs 28%, p<0.001). In multivariate analysis, MRD positivity was a prominent factor for CIR. Thus, MFC-based leukemic cell enrichment using antibodies against CLL-1, TIM-3, CD123 and CD117 followed by mutational analysis allows high sensitive MRD detection and is informative on relapse risk in the majority of AML patients. This article is protected by copyright. All rights reserved.\n This article is protected by copyright. All rights reserved.\n\nGraf, Ricarda\n\nHalbwedl, Iris\n\nHeitzer, Ellen\n\nHöfler, Gerald\n\nKashofer, Karl\n\nPrietl, Barbara\n\nQuehenberger, Franz\n\nReinisch, Andreas\n\nSchlacher, Angelika\n\nSill, Heinz\n\nWoelfler, Albert\n\nZebisch, Armin\n\n\n"
},
{
"text": "\n182813\nMechanical properties of human oral mucosa tissues are site dependent: A combined biomechanical, histological and ultrastructural approach.\n\nChoi, JJE\n\nZwirner, J\n\nRamani, RS\n\nMa, S\n\nHussaini, HM\n\nWaddell, JN\n\nHammer, N\n\nBeiträge in Fachzeitschriften\nISI:000544926000001\n32618130.0\n10.1002/cre2.305\nPMC7745080\nTo investigate load-deformation properties of Thiel-embalmed human oral mucosa tissues and to compare three different anatomical regions in terms of mechanical, histological and ultrastructural characteristic with focus on the extracellular matrix.\n Thirty specimens from three different regions of the oral cavity: attached gingiva, buccal mucosa and the hard palate were harvested from two Thiel-embalmed cadavers. Mechanical properties were obtained, combining strain evaluation and digital image correlation in a standardised approach. Elastic modulus, tensile strength, strain at maximum load and strain to failure were computed and analysed statistically. Subsamples were also analysed using scanning electron microscopy (SEM) and histological analysis.\n The highest elastic modulus of 37.36 ± 17.4 MPa was found in the attached gingiva group, followed by the hard palate and buccal mucosa. The elastic moduli of attached gingiva differed significantly to the buccal mucosa (p = .01) and hard palate (p = .021). However, there was no difference in the elastic moduli between the buccal mucosa and hard palate (p > .22). The tensile strength of the tissue samples ranged from 1.54 ± 0.5MPa to 3.81 ± 0.9 MPa, with a significant difference between gingiva group and buccal mucosa or hard palate (p = .001). No difference was found in the mean tensile strength between the buccal mucosa and hard palate (p = .92). Ultrastructural imaging yielded a morphological basis for the various mechanical properties found intraorally; the attached gingiva showed unidirectional collagen fibre network whereas the buccal mucosa and hard palate showed multi-directional network, which was more prone to tension failure and less elasticity.\n This is the first study assessing the various morphological-mechanical relationships of intraoral soft tissues, utilising Thiel-embalmed tissues. The findings of this study suggest that the tissues from different intraoral regions showed various morphological-mechanical behaviour which was also confirmed under the SEM and in the histological analysis.\n © 2020 The Authors. Clinical and Experimental Dental Research published by John Wiley & Sons Ltd.\n\nHammer, Niels\n\n\n"
},
{
"text": "\n187652\nPrognostic impact of PD-1 and PD-L1 expression in malignant pleural mesothelioma: an international multicenter study.\n\nBrcic, L\n\nKlikovits, T\n\nMegyesfalvi, Z\n\nMosleh, B\n\nSinn, K\n\nHritcu, R\n\nLaszlo, V\n\nCufer, T\n\nRozman, A\n\nKern, I\n\nMohorcic, K\n\nJakopovic, M\n\nSamarzija, M\n\nSeiwerth, S\n\nKolek, V\n\nFischer, O\n\nJakubec, P\n\nŠkarda, J\n\nGieszer, B\n\nHegedus, B\n\nFillinger, J\n\nRenyi-Vamos, F\n\nBuder, A\n\nBilecz, A\n\nBerger, W\n\nGrusch, M\n\nHoetzenecker, K\n\nKlepetko, W\n\nHoda, MA\n\nFilipits, M\n\nDome, B\n\nBeiträge in Fachzeitschriften\nNone\n34012777.0\n10.21037/tlcr-20-1114\nPMC8107750\nProgrammed cell death 1/programmed death ligand 1 (PD-1/PD-L1) immune-checkpoint blockade is a promising new therapeutic strategy in cancer. However, expression patterns and prognostic significance of PD-L1 and PD-1 are still controversial in human malignant pleural mesothelioma (MPM).\n Formalin-fixed paraffin-embedded (FFPE) tumor samples from 203 MPM patients receiving standard treatment without immunotherapy were collected from 5 European centers. PD-L1 and PD-1 expression of tumor cells (TCs) and tumor-infiltrating lymphocytes (TILs) were measured by immunohistochemistry and correlated with clinical parameters and long-term outcome.\n High (>10%) PD-L1 TC and PD-1 TILs expressions were found in 18 (8%) and 39 (24%) patients, respectively. PD-L1 was rarely expressed by TILs [≥1%, n=13 (8%); >10%, n=1]. No significant associations were found between the PD-L1 or PD-1 expression of TCs or TILs and clinicopathological parameters such as stage or histological subtype. Notably, patients with high (>10%) TC-specific PD-L1 expression exhibited significantly worse median overall survival (OS) (6.3 vs. 15.1 months of those with low TC PD-L1 expression; HR: 2.51, P<0.001). In multivariate cox regression analysis adjusted for clinical parameters, high TC PD-L1 expression (>10%) proved to be an independent negative prognostic factor for OS (HR: 2.486, P=0.005). There was no significant correlation between PD-L1 or PD-1 expression of TILs and OS.\n In this multicenter cohort study, we demonstrate that high (>10%) PD-L1 expression of TCs independently predicts worse OS in MPM. Further studies are warranted to investigate the value of PD-L1/PD-1 expression as a marker for treatment response in MPM patients receiving immunotherapy.\n 2021 Translational Lung Cancer Research. All rights reserved.\n\nBrcic, Luka\n\n\n"
},
{
"text": "\n4040\nKetoprofen-induced cyclooxygenase inhibition in renal medulla and platelets of rats treated with caffeine.\n\nSommerauer, M\n\nAtes, M\n\nGühring, H\n\nBrune, K\n\nAmann, R\n\nPeskar, BA\n\nBeiträge in Fachzeitschriften\nISI:000172790300006\n11729362.0\n10.1159/000056139\nNone\nIt has been suggested that caffeine can augment analgesic activity and aggravate side effects of nonsteroidal anti-inflammatory drugs (NSAIDs). The aim of the present study was to investigate a possible interaction between ketoprofen and caffeine on prostaglandin (PG) biosynthesis and cyclooxygenase (COX) mRNA expression in the rat renal medulla ex vivo. Treatment of rats with ketoprofen (60 min before) resulted in a dose-dependent (estimated ID(50) 0.3 mg/kg p.o.) reduction of PGE(2) biosynthesis in renal medulla ex vivo. Ketoprofen (0.3 mg/kg)-induced inhibition of PGE(2) biosynthesis was stable between 30 and 180 min and still detectable 300 min after drug administration. Caffeine (10 mg/kg) did not cause a detectable effect on its own, nor did it significantly affect ketoprofen-induced inhibition of renal medullary PGE(2) biosynthesis. Similar results were obtained with repeated daily drug administration for 1 week: there was no significant effect of caffeine on ketoprofen-induced inhibition of renal medullary PGE(2) biosynthesis. The absence of significant caffeine effects on ketoprofen-induced inhibition of renal medullary PGE(2) biosynthesis was paralleled by experiments showing no significant effect of caffeine on ketoprofen-induced inhibition of platelet thromboxane (TX)B(2) biosynthesis. Additional experiments showed increased COX-2 mRNA expression in the renal medulla 60 min after ketoprofen administration, that was not significantly influenced by concomitant caffeine treatment. Treatment of rats with ketoprofen for 1 week had no significant effects on COX-2 mRNA expression. The present results show that ketoprofen caused inhibition of PGE(2) biosynthesis in the rat renal medulla ex vivo with a potency similar to that reported for in vivo models suggesting that the ex vivo approach is a valid model to test a possible interference of caffeine with ketoprofen-induced COX inhibition. The absence of detectable effects of caffeine on time course or magnitude of ketoprofen-induced suppression of PGE(2) biosynthesis in this model indicates, therefore, that possible adverse actions of co-administered caffeine on renal function are not related to interference with renal COX inhibition.\n\nPeskar, Bernhard\n\n\n"
},
{
"text": "\n70911\nAlterations in intracellular calcium handling associated with the inverse force-frequency relation in human dilated cardiomyopathy.\n\nPieske, B\n\nKretschmann, B\n\nMeyer, M\n\nHolubarsch, C\n\nWeirich, J\n\nPosival, H\n\nMinami, K\n\nJust, H\n\nHasenfuss, G\n\nBeiträge in Fachzeitschriften\nISI:A1995RR27600018\n7648662.0\n10.1161/01.CIR.92.5.1169\nNone\nBACKGROUND: The present study was performed to test the hypothesis that the altered force-frequency relation in human failing dilated cardiomyopathy may be attributed to alterations in intracellular calcium handling. METHODS AND RESULTS: The force-frequency relation was investigated in isometrically contracting ventricular muscle strip preparations from 5 nonfailing human hearts and 7 hearts with end-stage failing dilated cardiomyopathy. Intracellular calcium cycling was measured simultaneously by use of the bioluminescent photoprotein aequorin. Stimulation frequency was increased stepwise from 15 to 180 beats per minute (37 degrees C). In nonfailing myocardium, twitch tension and aequorin light emission rose with increasing rates of stimulation. Maximum average twitch tension was reached at 150 min-1 and was increased to 212 +/- 34% (P < .05) of the value at 15 min-1. Aequorin light emission was lowest at 15 min-1 and was maximally increased at 180 min-1 to 218 +/- 39% (P < .01). In the failing myocardium, average isometric tension was maximum at 60 min-1 (106 +/- 7% of the basal value at 15 min-1, P = NS) and then decreased continuously to 62 +/- 9% of the basal value at 180 min-1 (P < .002). In the failing myocardium, aequorin light emission was highest at 15 min-1. At 180 min-1, it was decreased to 71 +/- 7% of the basal value (P < .01). Including both failing and nonfailing myocardium, there was a close correlation between the frequencies at which aequorin light emission and isometric tension were maximum (r = .92; n = 19; P < .001). Action potential duration decreased similarly with increasing stimulation frequencies in nonfailing and end-stage failing myocardium. Sarcoplasmic reticulum 45Ca2+ uptake, measured in homogenates from the same hearts, was significantly reduced in failing myocardium (3.60 +/- 0.51 versus 1.94 +/- 0.18 (nmol/L).min-1.mg protein-1, P < .005). CONCLUSIONS: These data indicate that the altered force-frequency relation of the failing human myocardium results from disturbed excitation-contraction coupling with decreased calcium cycling at higher rates of stimulation.\n\n\n"
},
{
"text": "\n88058\nAspirin and extended-release dipyridamole versus clopidogrel for recurrent stroke.\n\nSacco, RL\n\nDiener, HC\n\nYusuf, S\n\nCotton, D\n\nOunpuu, S\n\nLawton, WA\n\nPalesch, Y\n\nMartin, RH\n\nAlbers, GW\n\nBath, P\n\nBornstein, N\n\nChan, BP\n\nChen, ST\n\nCunha, L\n\nDahlöf, B\n\nDe Keyser, J\n\nDonnan, GA\n\nEstol, C\n\nGorelick, P\n\nGu, V\n\nHermansson, K\n\nHilbrich, L\n\nKaste, M\n\nLu, C\n\nMachnig, T\n\nPais, P\n\nRoberts, R\n\nSkvortsova, V\n\nTeal, P\n\nToni, D\n\nVandermaelen, C\n\nVoigt, T\n\nWeber, M\n\nYoon, BW\n\nPRoFESS Study Group\n\nBeiträge in Fachzeitschriften\nISI:000259259900007\n18753638.0\n10.1056/NEJMoa0805002\nPMC2714259\nBACKGROUND: Recurrent stroke is a frequent, disabling event after ischemic stroke. This study compared the efficacy and safety of two antiplatelet regimens--aspirin plus extended-release dipyridamole (ASA-ERDP) versus clopidogrel. METHODS: In this double-blind, 2-by-2 factorial trial, we randomly assigned patients to receive 25 mg of aspirin plus 200 mg of extended-release dipyridamole twice daily or to receive 75 mg of clopidogrel daily. The primary outcome was first recurrence of stroke. The secondary outcome was a composite of stroke, myocardial infarction, or death from vascular causes. Sequential statistical testing of noninferiority (margin of 1.075), followed by superiority testing, was planned. RESULTS: A total of 20, 32 patients were followed for a mean of 2.5 years. Recurrent stroke occurred in 916 patients (9.0%) receiving ASA-ERDP and in 898 patients (8.8%) receiving clopidogrel (hazard ratio, 1.01; 95% confidence interval [CI], 0.92 to 1.11). The secondary outcome occurred in 1333 patients (13.1%) in each group (hazard ratio for ASA-ERDP, 0.99; 95% CI, 0.92 to 1.07). There were more major hemorrhagic events among ASA-ERDP recipients (419 [4.1%]) than among clopidogrel recipients (365 [3.6%]) (hazard ratio, 1.15; 95% CI, 1.00 to 1.32), including intracranial hemorrhage (hazard ratio, 1.42; 95% CI, 1.11 to 1.83). The net risk of recurrent stroke or major hemorrhagic event was similar in the two groups (1194 ASA-ERDP recipients [11.7%], vs. 1156 clopidogrel recipients [11.4%]; hazard ratio, 1.03; 95% CI, 0.95 to 1.11). CONCLUSIONS: The trial did not meet the predefined criteria for noninferiority but showed similar rates of recurrent stroke with ASA-ERDP and with clopidogrel. There is no evidence that either of the two treatments was superior to the other in the prevention of recurrent stroke. (ClinicalTrials.gov number, NCT00153062.)\n\nHorner, Susanna\n\n\n"
},
{
"text": "\n95316\nCan routine gynecologic examination contribute to the diagnosis of cervical involvement by primary endometrial cancer?\n\nPristauz, G\n\nWinter, R\n\nFischerauer, E\n\nHaas, J\n\nBjelic-Radisic, V\n\nBader, AA\n\nPetru, E\n\nBeiträge in Fachzeitschriften\nISI:000270030600005\n19899399.0\nNone\nNone\nObjective: There are few data in the literature as to whether findings at routine preoperative gynecologic examination of patients with primary endometrial cancer including cervical cytology, colposcopy and rectovaginal bimanual pelvic exam Could predict cervical extension of the disease. Methods and Materials: The present retrospective study was undertaken to preoperatively identify potential clinical parameters associated with the histological diagnosis of cervical involvement by primary endometrial cancer in the hysterectomy specimen. We reviewed the records of 104 patients with Stage 11 endometrial cancer treated at our institution between 1985 and 2005 by simple or radical abdominal hysterectomy with special emphasis on cervical Pap smear, colposcopy, cervical palpation as well as rectal parametrial assessment. Patients with Stage I disease operated on before and after each study patient were selected as controls (n = 208). Patients with more advanced disease were excluded. Results: Overall, 312 records of patients with primary endometrial cancer were reviewed. Patients with Stage 11 disease had a significantly lower prevalence (p < 0.0001) of endometrioid carcinomas and a significantly higher (p < 0.01) prevalence of G3 tumors compared to the control patients. Pap smears and colposcopic findings were abnormal in 39% of patients with Stage 11 and in 9% and 10% of patients with Stage I disease (l) < 0.0001). Of patients with Stage 11 disease, 42% had a suspicious cervical palpation compared to only 4% of patients with Stage I disease (p < 0.0005). Parametrial assessment was suspicious in 16% of patients with Stage H disease and in no patient with Stage I disease (p < 0.001). Conclusion: The four routine clinical parameters Pap smear, colposcopy, cervical palpation and rectal parametrial examination are significantly more often pathologic in patients with Stage 11 than in Stage I disease. The majority of patients with Stage 11 disease had at least one of these tests positive. Thus they may be useful to preoperatively detect cervical involvement by primary endometrial cancer.\n\nAmerstorfer, Eva\n\nBader, Arnim\n\nBjelic-Radisic, Vesna\n\nHaas, Josef\n\nPetru, Edgar\n\nPristauz-Telsnigg, Gunda\n\n\n"
}
]
}