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"text": "\n93425\nAnger, interpersonal relationships, and health-related quality of life in bullying boys who are treated with outpatient family therapy: a randomized, prospective, controlled trial with 1 year of follow-up.\n\nNickel, MK\n\nKrawczyk, J\n\nNickel, C\n\nForthuber, P\n\nKettler, C\n\nLeiberich, P\n\nMuehlbacher, M\n\nTritt, K\n\nMitterlehner, FO\n\nLahmann, C\n\nRother, WK\n\nLoew, TH\n\nBeiträge in Fachzeitschriften\nISI:000230915600011\n16061577.0\n10.1542/peds.2004-2534\nNone\nOBJECTIVE: Ten to 30% of students engage in bullying behavior. Bullies stand out on account of increased anger, poor interpersonal relationships, and poor quality of life. Our aim was to determine the effectiveness of outpatient family psychotherapy as a monotherapy for anger reduction and improvement of behavior and interpersonal relationships and of health-related quality of life in male youths with bullying behavior. METHODS: Twenty-two boys with bullying behavior took part in a family therapy program for 6 months. The control group was also composed of 22 youths and took part in a placebo intervention program. Every 2 weeks, results were checked with the Adolescents Risky-Behavior Scale (ARBS), the State-Trait Anger Expression Inventory (STAXI), the Inventory of Interpersonal Problems (IIP-D), and the SF-36 Health Survey (SF-36). Follow-up testing took place 12 months after treatment. RESULTS: In comparison with the control group (according to the intention-to-treat principle), bullying behavior was reduced (family therapy group: from n = 22 to n = 6; control group: from n = 22 to n = 20). Significant changes on all ARBS scales and on the STAXI scales State-Anger, Trait-Anger, Anger-Out, and Anger-Control were observed after 6 months. In the IIP-D, significant differences were found on the scales for overly autocratic, overly competitive, overly introverted, overly expressive, and exploitable/compliant. In the SF-36, significant differences were observed in general health perceptions, vitality, social functioning, role-emotional, and mental health. The reduction in expression of anger correlated with a reduction in several scales of the ARBS, IIP-D, and SF-36. Follow-up after 1 year showed relatively stable, lasting treatment effects. CONCLUSION: The results of this study show that outpatient family therapy seems to be an effective method of reducing anger and improving interpersonal relationships and health-related quality of life in male youths with bullying behavior.\n\nNickel, Marius\n\n\n"
},
{
"text": "\n133548\nPredicting distant recurrence in receptor-positive breast cancer patients with limited clinicopathological risk: using the PAM50 Risk of Recurrence score in 1478 postmenopausal patients of the ABCSG-8 trial treated with adjuvant endocrine therapy alone.\n\nGnant, M\n\nFilipits, M\n\nGreil, R\n\nStoeger, H\n\nRudas, M\n\nBago-Horvath, Z\n\nMlineritsch, B\n\nKwasny, W\n\nKnauer, M\n\nSinger, C\n\nJakesz, R\n\nDubsky, P\n\nFitzal, F\n\nBartsch, R\n\nSteger, G\n\nBalic, M\n\nRessler, S\n\nCowens, JW\n\nStorhoff, J\n\nFerree, S\n\nSchaper, C\n\nLiu, S\n\nFesl, C\n\nNielsen, TO\n\nAustrian Breast and Colorectal Cancer Study Group\n\nBeiträge in Fachzeitschriften\nISI:000331269600007\n24347518.0\n10.1093/annonc/mdt494\nNone\nPAM50 is a 50-gene test that is designed to identify intrinsic breast cancer subtypes and generate a Risk of Recurrence (ROR) score. It has been developed to be carried out in qualified routine hospital pathology laboratories.\n One thousand four hundred seventy-eight postmenopausal women with estrogen receptor (ER)+ early breast cancer (EBC) treated with tamoxifen or tamoxifen followed by anastrozole from the prospective randomized ABCSG-8 trial were entered into this study. Patients did not receive adjuvant chemotherapy. RNA was extracted from paraffin blocks and analyzed using the PAM50 test. Both intrinsic subtype (luminal A/B, HER2-enriched, basal-like) and ROR score were calculated. The primary analysis was designed to test whether the continuous ROR score adds prognostic value in predicting distant recurrence (DR) over and above standard clinical variables.\n In all tested subgroups, ROR score significantly adds prognostic information to the clinical predictor (P<0.0001). PAM50 assigns an intrinsic subtype to all cases, and the luminal A cohort had a significantly lower ROR at 10 years compared with Luminal B (P<0.0001). Significant and clinically relevant discrimination between low- and high-risk groups occurred also within all tested subgroups.\n The results of the primary analysis, in combination with recently published results from the ATAC trial, constitute Level 1 evidence for clinical validity of the PAM50 test for predicting the risk of DR in postmenopausal women with ER+ EBC. A 10-year metastasis risk of <3.5% in the ROR low category makes it unlikely that additional chemotherapy would improve this outcome-this finding could help to avoid unwarranted overtreatment.\n ABCSG 8: NCT00291759.\n\nBalic, Marija\n\nStoeger, Herbert\n\n\n"
},
{
"text": "\n137010\nStrategies to manage hepatitis C virus (HCV) disease burden.\n\nWedemeyer, H\n\nDuberg, AS\n\nButi, M\n\nRosenberg, WM\n\nFrankova, S\n\nEsmat, G\n\nÖrmeci, N\n\nVan Vlierberghe, H\n\nGschwantler, M\n\nAkarca, U\n\nAleman, S\n\nBalık, I\n\nBerg, T\n\nBihl, F\n\nBilodeau, M\n\nBlasco, AJ\n\nBrandão Mello, CE\n\nBruggmann, P\n\nCalinas, F\n\nCalleja, JL\n\nCheinquer, H\n\nChristensen, PB\n\nClausen, M\n\nCoelho, HS\n\nCornberg, M\n\nCramp, ME\n\nDore, GJ\n\nDoss, W\n\nEl-Sayed, MH\n\nErgör, G\n\nEstes, C\n\nFalconer, K\n\nFélix, J\n\nFerraz, ML\n\nFerreira, PR\n\nGarcía-Samaniego, J\n\nGerstoft, J\n\nGiria, JA\n\nGonçales, FL\n\nGuimarães Pessôa, M\n\nHézode, C\n\nHindman, SJ\n\nHofer, H\n\nHusa, P\n\nIdilman, R\n\nKåberg, M\n\nKaita, KD\n\nKautz, A\n\nKaymakoglu, S\n\nKrajden, M\n\nKrarup, H\n\nLaleman, W\n\nLavanchy, D\n\nLázaro, P\n\nMarinho, RT\n\nMarotta, P\n\nMauss, S\n\nMendes Correa, MC\n\nMoreno, C\n\nMüllhaupt, B\n\nMyers, RP\n\nNemecek, V\n\nØvrehus, AL\n\nParkes, J\n\nPeltekian, KM\n\nRamji, A\n\nRazavi, H\n\nReis, N\n\nRoberts, SK\n\nRoudot-Thoraval, F\n\nRyder, SD\n\nSarmento-Castro, R\n\nSarrazin, C\n\nSemela, D\n\nSherman, M\n\nShiha, GE\n\nSperl, J\n\nStärkel, P\n\nStauber, RE\n\nThompson, AJ\n\nUrbanek, P\n\nVan Damme, P\n\nvan Thiel, I\n\nVandijck, D\n\nVogel, W\n\nWaked, I\n\nWeis, N\n\nWiegand, J\n\nYosry, A\n\nZekry, A\n\nNegro, F\n\nSievert, W\n\nGower, E\n\nBeiträge in Fachzeitschriften\nISI:000333893200004\n24713006.0\n10.1111/jvh.12249\nNone\nThe number of hepatitis C virus (HCV) infections is projected to decline while those with advanced liver disease will increase. A modeling approach was used to forecast two treatment scenarios: (i) the impact of increased treatment efficacy while keeping the number of treated patients constant and (ii) increasing efficacy and treatment rate. This analysis suggests that successful diagnosis and treatment of a small proportion of patients can contribute significantly to the reduction of disease burden in the countries studied. The largest reduction in HCV-related morbidity and mortality occurs when increased treatment is combined with higher efficacy therapies, generally in combination with increased diagnosis. With a treatment rate of approximately 10%, this analysis suggests it is possible to achieve elimination of HCV (defined as a >90% decline in total infections by 2030). However, for most countries presented, this will require a 3-5 fold increase in diagnosis and/or treatment. Thus, building the public health and clinical provider capacity for improved diagnosis and treatment will be critical. \n © 2014 John Wiley & Sons Ltd.\n\nStauber, Rudolf\n\n\n"
},
{
"text": "\n138499\nImpact of histologic subtype on cancer-specific survival in patients with renal cell carcinoma and tumor thrombus.\n\nTilki, D\n\nNguyen, HG\n\nDall'Era, MA\n\nBertini, R\n\nCarballido, JA\n\nChromecki, T\n\nCiancio, G\n\nDaneshmand, S\n\nGontero, P\n\nGonzalez, J\n\nHaferkamp, A\n\nHohenfellner, M\n\nHuang, WC\n\nKoppie, TM\n\nLorentz, CA\n\nMandel, P\n\nMartinez-Salamanca, JI\n\nMaster, VA\n\nMatloob, R\n\nMcKiernan, JM\n\nMlynarczyk, CM\n\nMontorsi, F\n\nNovara, G\n\nPahernik, S\n\nPalou, J\n\nPruthi, RS\n\nRamaswamy, K\n\nRodriguez Faba, O\n\nRusso, P\n\nShariat, SF\n\nSpahn, M\n\nTerrone, C\n\nVergho, D\n\nWallen, EM\n\nXylinas, E\n\nZigeuner, R\n\nLibertino, JA\n\nEvans, CP\n\nBeiträge in Fachzeitschriften\nISI:000340260900039\n23871402.0\n10.1016/j.eururo.2013.06.048\nNone\nAlthough different prognostic factors for patients with renal cell carcinoma (RCC) and vena cava tumor thrombus (TT) have been studied, the prognostic value of histologic subtype in these patients remains unclear.\n We analyzed the impact of histologic subtype on cancer-specific survival (CSS).\n We retrospectively analyzed the records of 1774 patients with RCC and TT who underwent radical nephrectomy and tumor thrombectomy from 1971 to 2012 at 22 US and European centers.\n Multivariable ordered logistic and Cox regression models were used to quantify the impact of tumor histology on CSS.\n Overall 5-yr CSS was 53.4% (confidence interval [CI], 50.5-56.2) in the entire group. TT level (according to the Mayo classification of macroscopic venous invasion in RCC) was I in 38.5% of patients, II in 30.6%, III in 17.3%, and IV in 13.5%. Histologic subtypes were clear cell renal cell carcinoma (cRCC) in 89.9% of patients, papillary renal cell carcinoma (pRCC) in 8.5%, and chromophobe RCC in 1.6%. In univariable analysis, pRCC was associated with a significantly worse CSS (p<0.001) compared with cRCC. In multivariable analysis, the presence of pRCC was independently associated with CSS (hazard ratio: 1.62; CI, 1.01-2.61; p<0.05). Higher TT level, positive lymph node status, distant metastasis, and fat invasion were also independently associated with CSS.\n In our multi-institutional series, we found that patients with pRCC and vena cava TT who underwent radical nephrectomy and tumor thrombectomy had significantly worse cancer-specific outcomes when compared with patients with other histologic subtypes of RCC. We confirmed that higher TT level and fat invasion were independently associated with reduced CSS.\n Copyright © 2013 European Association of Urology. Published by Elsevier B.V. All rights reserved.\n\nZigeuner, Richard\n\n\n"
},
{
"text": "\n169002\nOxidized Albumin Triggers a Cytokine Storm in Leukocytes Through P38 Mitogen-Activated Protein Kinase: Role in Systemic Inflammation in Decompensated Cirrhosis.\n\nAlcaraz-Quiles, J\n\nCasulleras, M\n\nOettl, K\n\nTitos, E\n\nFlores-Costa, R\n\nDuran-Güell, M\n\nLópez-Vicario, C\n\nPavesi, M\n\nStauber, RE\n\nArroyo, V\n\nClària, J\n\nBeiträge in Fachzeitschriften\nISI:000448844900022\n30070728.0\n10.1002/hep.30135\nNone\nDecompensated cirrhosis is characterized by exuberant systemic inflammation. Although the inducers of this feature remain unknown, the presence of circulating forms of oxidized albumin, namely human nonmercaptalbumin 1 (HNA1) and HNA2, is a common finding in cirrhosis. The aim of this study was to explore the ability of these oxidized albumin forms to induce systemic inflammation by triggering the activation of peripheral leukocytes. We observed significantly higher plasma levels of HNA1 and HNA2 in patients with cirrhosis (n = 256) compared to healthy volunteers (n = 48), which gradually increased during the course from compensated to decompensated to acute-on-chronic liver failure. Plasma HNA1 and HNA2 levels significantly correlated with inflammatory markers (i.e., interleukin-6 [IL-6], IL-1β, tumor necrosis factor-alpha [TNF-α] and IL-8) in patients with cirrhosis. To directly test the inflammatory effects of HNA1 and HNA2 on leukocytes, these oxidized albumin forms were prepared ex vivo and their posttranslational modifications monitored by liquid chromatography (LC)-quadrupole time-of-flight/mass spectrometry (MS). HNA1, but not HNA2, increased IL-1β, IL-6, and TNF-α mRNA and protein expression in leukocytes from both healthy volunteers and patients with cirrhosis. Moreover, HNA1 up-regulated the expression of eicosanoid-generating enzymes (i.e., cyclooxygenase-2 [COX-2] and microsomal prostaglandin E [PGE] synthase 1) and the production of inflammatory eicosanoids (PGE2 , PGF2α , thromboxane B2 , and leukotriene B4 ), as determined by LC-electrospray ionization-MS/MS. The inflammatory response to HNA1 was more pronounced in peripheral blood mononuclear cells (PBMCs) and marginal in polymorphonuclear neutrophils. Kinome analysis of PBMCs revealed that HNA1 induced the phosphorylation of p38 mitogen-activated protein kinase, the inhibition of which blocked HNA1-induced cytokine and COX-2 induction. Conclusion: HNA1 triggers an inflammatory response in PBMCs, providing a rationale for its removal and replacement by reduced albumin in the prevention of systemic inflammation in patients with advanced liver disease.\n © 2018 by the American Association for the Study of Liver Diseases.\n\nÖttl, Karl\n\nStauber, Rudolf\n\n\n"
},
{
"text": "\n173112\nReconstituted high density lipoprotein mediated targeted co-delivery of HZ08 and paclitaxel enhances the efficacy of paclitaxel in multidrug-resistant MCF-7 breast cancer cells.\n\nZhang, F\n\nWang, X\n\nXu, X\n\nLi, M\n\nZhou, J\n\nWang, W\n\nBeiträge in Fachzeitschriften\nISI:000381833900002\n27343697.0\n10.1016/j.ejps.2016.06.017\nNone\nIn the past decades, reconstituted high density lipoprotein (rHDL) has been successfully developed as a drug carrier since the enhanced HDL-lipids uptake is demonstrated in several human cancers. In this paper, rHDL, for the first time, was utilized to co-encapsulate two hydrophobic drugs: an anticancer drug, paclitaxel (PTX), and a new reversal agent for P-gp (P-glycoprotein)-mediated multidrug resistance (MDR) of cancer, N-cyano-1-[(3, -dimethoxyphenyl)methyl]-3, -dihydro-6, -dimethoxy-N'-octyl-2(1H)-isoquinoline-carboximidamide (HZ08). We proposed this drug co-delivery strategy to reverse PTX resistance. The study aimed to develop a biomimetic nanovector, reconstituted high density lipoprotein (rHDL), mediating targeted PTX-HZ08 delivery for cancer therapy. Using sodium cholate dialysis method, we successfully formulated dual-agent co-delivering rHDL nanoparticles (PTX-HZ08-rHDL NPs) with a typical spherical morphology, well-distributed size (~100nm), high drug encapsulation efficiency (approximately 90%), sustained drug release properties and exceptional stability even after storage for 1month or incubation in 10% fetal bovine serum (FBS) DMEM for up to 2days. Results demonstrated that PTX-HZ08-rHDL NPs significantly enhanced anticancer efficacy in vitro, including higher cytotoxicity and better ability to induce cell apoptosis against both PTX-sensitive and -resistant MCF-7 human breast cancer cell lines (MCF-7 and MCF-7/PTX cells). Mechanism studies demonstrated that these improvements could be correlated with increased cellular uptake of PTX mediated by scavenger receptor class B type I (SR-BI) as well as prolonged intracellular retention of PTX due to the HZ08 mediated drug-efflux inhibition. In addition, in vivo investigation showed that the PTX-HZ08-rHDL NPs were substantially safer, have higher tumor-targeted capacity and have stronger antitumor activity than the corresponding dosage of paclitaxel injection. These findings suggested that rHDL NPs could be an ideal tumor-targeted nanovector for simultaneous transfer of insoluble anticancer drug and drug resistance reversal agents. The PTX-HZ08-rHDL NPs co-delivery system might be a new promising strategy to overcome tumor drug resistance. \n Copyright © 2016 Elsevier B.V. All rights reserved.\n\nZhang, Fangrong\n\n\n"
},
{
"text": "\n178715\nLong-Term Prognostic Value of High-Sensitivity Troponin T Added to N-Terminal Pro Brain Natriuretic Peptide Plasma Levels Before Valve Replacement for Severe Aortic Stenosis.\n\nBarbieri, F\n\nSenoner, T\n\nAdukauskaite, A\n\nDobner, S\n\nHolfeld, J\n\nSemsroth, S\n\nLambert, T\n\nZweiker, D\n\nTheurl, T\n\nRainer, PP\n\nSchmidt, A\n\nFeuchtner, GM\n\nSteinwender, C\n\nHoppe, UC\n\nHintringer, F\n\nBauer, A\n\nMüller, S\n\nGrimm, M\n\nPfeifer, BE\n\nDichtl, W\n\nBeiträge in Fachzeitschriften\nISI:000503909900020\n31699359.0\n10.1016/j.amjcard.2019.09.014\nNone\nNatriuretic peptide plasma levels help to manage patients with severe aortic stenosis (AS). The role of troponin plasma levels in this patient cohort remains speculative. A consortium of 4 university hospital centers in Austria analyzed retrospectively 3, 95 patients admitted for valve replacement because of severe AS since 2007. The aim was to compare the additive preprocedural value of high-sensitivity troponin T (hsTnT) to N-terminal pro brain natriuretic peptide (NT-proBNP) plasma levels in predicting postoperative long-term survival in a large cohort undergoing either surgical (57.8%) or transcatheter (42.2%) aortic valve replacement. During a median follow-up of 2.93 (1.91 to 4.92) years, 919 patients (25.6%) died, in them 556 (15.5%) due to cardiovascular causes. Both normal hsTnT (<14 ng/l) and NT-proBNP (within age- and sex-corrected normal range) plasma levels were found in 481 patients (14.3%, group 1). Normal hsTnT but elevated NT-proBNP plasma levels were found in 748 patients (22.3%, group 2). Elevated hsTnT but normal NT-proBNP plasma levels were found in 258 patients (7.7%, group 3). Both elevated hsTnT and elevated NT-proBNP plasma levels were found in 1, 69 patients (55.7%, group 4). Using Log Rank tests for comparison there was a highly significant difference in both cardiovascular mortality (p <0.0001) and all-cause mortality (p <0.0001). All-cause mortality rates after 1, 3, and 5 years were 2.1%, 5.4%, 7.7% in group 1; 4.0%, 7.5%, 11.5% in group 2; 5.8%, 8.9%, 14.0% in group 3; and 12.3%, 22.6%, 28.4% in group 4. In conclusion, hsTnT adds additional impact to NT-proBNP as a routinely available biomarker for risk stratification concerning postoperative survival in patients with severe AS admitted for valve replacement. The present study supports the concept to integrate hsTnT plasma levels in the management of severe AS.\n Copyright © 2019 Elsevier Inc. All rights reserved.\n\nRainer, Peter\n\nSchmidt, Albrecht\n\nZweiker, David\n\n\n"
},
{
"text": "\n240\nAntioxidant status in patients on chronic hemodialysis therapy: impact of parenteral selenium supplementation.\n\nKoenig, JS\n\nFischer, M\n\nBulant, E\n\nTiran, B\n\nElmadfa, I\n\nDruml, W\n\nBeiträge in Fachzeitschriften\nISI:A1997WE18800004\n9037743.0\nNone\nNone\nReactive oxygen species may be involved in a broad pattern of tissue injury in patients on regular hemodialysis therapy and, in fact, increasing evidence suggests that the antioxidative system is compromized in these patients. One factor contributing to this reduction of antioxidative capacity is selenium deficiency. The present investigation was undertaken to further define the extent and type of impairment of the oxygen radical scavenger system in chronic hemodialysis patients and to evaluate the impact of selenium supplementation. Twelve non-wasted patients (6 male, 6 female, mean age of 58 years) on chronic hemodialysis for a minimum of 5 months (mean 46 months) were supplemented intravenously with 400 mg selenium (as sodium selenite) thrice weekly after each hemodialysis session over 8 weeks. Blood samples were taken before the start, at intervals of 2 weeks during, and 4 weeks after termination of supplementation. Concentrations were evaluated of selenium and alpha-tocopherol in plasma and erythrocytes, of retinol and ascorbic acid in plasma, of glutathione and the activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and, catalase (CAT) in erythrocytes. Lipid peroxidation endproducts were measured as malondialdehyde (MDA) in plasma. In patients on hemodialysis multiple alterations of the antioxidative system were present and the concentrations of selenium in plasma, of glutathione and the activity of GSH-Px in erythrocytes were profoundly decreased (p < 0.001). Selenium supplementation improved the selenium status of the patients, as indicated by an increase in selenium concentrations in plasma and erythrocytes and erythrocyte GSH-Px activity. Improvement in antioxidative capacity was further documented by an increase in alpha-tocopherol in erythrocytes. Plasma MDA showed a transient decrease after 6 weeks and increased activities of SOD and CAT were dampened. No effect was seen on plasma concentrations of ascorbic acid, a-tocopherol and retinol. We conclude that patients on chronic hemodialysis therapy manifest a profound depression in antioxidative potential and a selenium deficiency. Selenium supplementation improves the oxygen radical scavenger system and increases selenium concentrations in plasma and erythrocytes and the activity of selenium dependent glutathione peroxidase. Thus, selenium should also be considered for micronutrient supplementation in patients on chronic hemodialysis therapy.\n\nTiran, Beate\n\n\n"
},
{
"text": "\n1513\nLipoprotein(a) in health and disease.\n\nKronenberg, F\n\nSteinmetz, A\n\nKostner, GM\n\nDieplinger, H\n\nBeiträge in Fachzeitschriften\nISI:A1996WA92200003\n8989507.0\n10.3109/10408369609080056\nNone\nLipoprotein(a) [Lp(a)] represents an LDL-like particle to which the Lp(a)-specific apolipoprotein(a) is linked via a disulfide bridge. It has gained considerable interest as a genetically determined risk factor for atherosclerotic vascular disease. Several studies have described a correlation between elevated Lp(a) plasma levels and coronary heart disease, stroke, and peripheral atherosclerosis. In healthy individuals, Lp(a) plasma concentrations are almost exclusively controlled by the apo(a) gene locus on chromosome 6q2.6-q2.7. More than 30 alleles at this highly polymorphic gene locus determine a size polymorphism of apo(a). There exists an inverse correlation between the size (molecular weight) of apo(a) isoforms and Lp(a) plasma concentrations. The standardization of Lp(a) quantification is still an unresolved task due to the large particle size of Lp(a), the presence of two different apoproteins [apoB and apo(a)], and the large size polymorphism of apo(a) and its homology with plasminogen. A working group sponsored by the IFCC is currently establishing a stable reference standard for Lp(a) as well as a reference method for quantitative analysis. Aside from genetic reasons, abnormal Lp(a) plasma concentrations are observed as secondary to various diseases. Lp(a) plasma levels are elevated over controls in patients with nephrotic syndrome and patients with end-stage renal disease. Following renal transplantation, Lp(a) concentrations decrease to values observed in controls matched for apo(a) type. Controversial data on Lp(a) in diabetes mellitus result mainly from insufficient sample sizes of numerous studies. Large studies and those including apo(a) phenotype analysis came to the conclusion that Lp(a) levels are not or only moderately elevated in insulin-dependent patients. In noninsulin-dependent diabetics, Lp(a) is not elevated. Conflicting data also exist from studies in patients with familial hypercholesterolemia. Several case-control studies reported elevated Lp(a) levels in those patients, suggesting a role of the LDL-receptor pathway for degradation of Lp(a). However, recent turnover studies rejected that concept. Moreover, family studies also revealed data arguing against an influence of the LDL receptor for Lp(a) concentrations. Several rare diseases or disorders, such as LCAT- and LPL-deficiency as well as liver diseases, are associated with low plasma levels or lack of Lp(a).\n\nKostner, Gerhard\n\n\n"
},
{
"text": "\n103058\nEpendymoma of the spinal cord in children and adolescents: a retrospective series from the HIT database.\n\nBenesch, M\n\nWeber-Mzell, D\n\nGerber, NU\n\nvon Hoff, K\n\nDeinlein, F\n\nKrauss, J\n\nWarmuth-Metz, M\n\nKortmann, RD\n\nPietsch, T\n\nDriever, PH\n\nQuehenberger, F\n\nUrban, C\n\nRutkowski, S\n\nBeiträge in Fachzeitschriften\nISI:000280404400007\n20672934.0\n10.3171/2010.5.PEDS09553\nNone\nObject. Reports on spinal cord ependymoma in children are rare. The aim of this study was to evaluate the clinical spectrum, treatment, and outcome of children with primary ependymoma of the spinal cord who were registered in the database of the pediatric German brain tumor studies Hirntumor (HIT) '91 and HIT 2000. Methods. Between 1991 and 2007, 29 patients (12 male and 17 female, median age at diagnosis 13.6 years) with primary spinal cord ependymoma (myxopapillary ependymoma WHO Grade I, II, and III tumors in 6, 17, and 6 patients, respectively) were identified. Four patients had neurofibromatosis Type 2. Results. With a median follow-up of 4.2 years (range 0.48-15 years), 28 patients (96.6%) were alive. Seven patients (24.1%) developed progressive disease or relapse, 2 after gross-total resection (GTR) and 5 after incomplete resection or biopsy. One patient with anaplastic ependymoma (WHO Grade III) died 65 months after diagnosis of disease progression. Primary adjuvant treatment (radiotherapy, chemotherapy, or both) was used in 8 (50%) of 16 patients following GTR and in 9 (82%) of 11 patients who underwent less than a GTR. Three additional patients were treated adjuvantly following progression. Estimated progression-free survival and overall survival rates at 5 years were 72.3% (95% Cl 50%-86%) and 100%, respectively. Progression-free survival at 5 years is 84.4% (95% CI 50%-96%) for patients following GTR compared with 57.1% (95% CI 25%-69%) for patients who achieved a less than GTR (p = 0.088, log-rank test). A high relapse incidence (4 of 6) was observed among patients with myxopapillary ependymoma. Conclusions. Gross-total resection is the mainstay of treatment for patients with primary spinal cord ependymoma and may be achieved in about 50% of the patients using modern surgical techniques. Primary adjuvant treatment was commonly used in children with spinal cord ependymoma irrespective of the extent of resection or tumor grade. The impact of adjuvant treatment on progression-free and overall survival has to be investigated in a prospective trial. (DOI: 10.3171/2010.5.PEDS09553)\n\nBenesch, Martin\n\nQuehenberger, Franz\n\nSperl, Daniela Ingrid\n\nUrban, Ernst-Christian\n\n\n"
},
{
"text": "\n109515\nBody-image, self-concept and mental exposure in patients with pectus excavatum.\n\nHadolt, B\n\nWallisch, A\n\nEgger, JW\n\nHöllwarth, ME\n\nBeiträge in Fachzeitschriften\nISI:000290726000021\n21290134.0\n10.1007/s00383-011-2854-z\nNone\nPectus excavatum is the most common congenital anomaly of the sternum and anterior chest wall, which occurs about 3-4 times more often in boys than girls [1]. Although most patients do not report physical symptoms as cardiovascular and respiratory problems, they show a loss of self-esteem and a poor self-image. There exist very rare data about psychological state before the OP compared with data afterwards.\n This study was conducted to examine psychological changes in body-image, self-concept and mental exposure in patients with pectus excavatum, who had undergone the Nuss procedure.\n Seventeen patients (13 male, 4 female), who underwent 2003 a comprehensive psychological investigation, have been tested again in 2007 by means of the identical questionnaires to get postoperative data: OPE-FB (Wallisch; Operation-Expectation-Questionnaire), FKKS (Deusinger; Frankfurter Body Concept Scales) and SCL-90-R (Derogatis; Symptom Checklist Revised). The mean age at the second time of investigation was 19.6 years (SD = 2.5). The patients were classified into two groups based on a lower (n = 10) and a higher (n = 7) severity index of PE. Parents or a parent person were interviewed about the topics of OPE-FB by a structured interview. Data were analyzed using Mann-Whitney U test and Wilcoxon test. Interview data were evaluated with a content analysis.\n Nearly all patient's expectations in regard to the beneficial effect of the surgical procedure-investigated with the OPE-FB preoperatively-have been confirmed postoperatively. In patients with a lower severity index impairment in general interest in sports and improvements in self-assurance, health, self-acceptance of one's body and acceptance of one's body by others can be reported. Data from SCL-90-R, measuring mental exposure, had normal range. Interviews with relatives showed, that the external attribution could emphasize patient's data from the OPE-FB.\n The long-time follow-up can make us sure, that the Nuss procedure as a physical treatment has positive effects on physical as well as psychological aspects of young adults. The patient's confidence with the cosmetic result was very high, which reflects the excellent effects of the minimal invasive repair according to Nuss.\n\nEgger, Josef Wilhelm\n\nHöllwarth, Michael\n\n\n"
},
{
"text": "\n113812\nImpact of the permanent ventricular pacing site on left ventricular function in children: a retrospective multicentre survey.\n\nvan Geldorp, IE\n\nDelhaas, T\n\nGebauer, RA\n\nFrias, P\n\nTomaske, M\n\nFriedberg, MK\n\nTisma-Dupanovic, S\n\nElders, J\n\nFrüh, A\n\nGabbarini, F\n\nKubus, P\n\nIllikova, V\n\nTsao, S\n\nBlank, AC\n\nHiippala, A\n\nSluysmans, T\n\nKarpawich, P\n\nClur, SA\n\nGaname, X\n\nCollins, KK\n\nDann, G\n\nThambo, JB\n\nTrigo, C\n\nNagel, B\n\nPapagiannis, J\n\nRackowitz, A\n\nMarek, J\n\nNürnberg, JH\n\nVanagt, WY\n\nPrinzen, FW\n\nJanousek, J\n\nWorking Group for Cardiac Dysrhythmias and Electrophysiology of the Association for European Paediatric Cardiology\n\nBeiträge in Fachzeitschriften\nISI:000297687200052\n21917655.0\n10.1136/heartjnl-2011-300197\nNone\nBACKGROUND: Chronic right ventricular (RV) pacing is associated with deleterious effects on cardiac function. OBJECTIVE: In an observational multicentre study in children with isolated atrioventricular (AV) block receiving chronic ventricular pacing, the importance of the ventricular pacing site on left ventricular (LV) function was investigated. METHODS: Demographics, maternal autoantibody status and echocardiographic measurements on LV end-diastolic and end-systolic dimensions and volumes at age <18 years were retrospectively collected from patients undergoing chronic ventricular pacing (>1 year) for isolated AV block. LV fractional shortening (LVFS) and, if possible LV ejection fraction (LVEF) were calculated. Linear regression analyses were adjusted for patient characteristics. RESULTS: From 27 centres, 297 children were included, in whom pacing was applied at the RV epicardium (RVepi, n = 147), RV endocardium (RVendo, n = 113) or LV epicardium (LVepi, n = 37). LVFS was significantly affected by pacing site (p = 0.001), and not by maternal autoantibody status (p = 0.266). LVFS in LVepi (39 ± 5%) was significantly higher than in RVendo (33 ± 7%, p < 0.001) and RVepi (35 ± 8%, p = 0.001; no significant difference between RV-paced groups, p = 0.275). Subnormal LVFS (LVFS < 28%) was seen in 16/113 (14%) RVendo-paced and 21/147 (14%) RVepi-paced children, while LVFS was normal (LVFS >= 28%) in all LVepi-paced children (p = 0.049). These results are supported by the findings for LVEF (n = 122): LVEF was <50% in 17/69 (25%) RVendo- and in 10/35 (29%) RVepi-paced patients, while LVEF was >= 50% in 17/18 (94%) LVepi-paced patients. CONCLUSION: In children with isolated AV block, permanent ventricular pacing site is an important determinant of LV function, with LVFS being significantly higher with LV pacing than with RV pacing.\n\n\n"
},
{
"text": "\n151782\nAntiresorptive therapy and risk of mortality and refracture in osteoporosis-related hip fracture: a nationwide study.\n\nBrozek, W\n\nReichardt, B\n\nZwerina, J\n\nDimai, HP\n\nKlaushofer, K\n\nZwettler, E\n\nBeiträge in Fachzeitschriften\nISI:000369525500045\n26576544.0\n10.1007/s00198-015-3415-4\nNone\nWe analyzed the association of bisphosphonate therapy with mortality and hip refracture incidence among osteoporosis-related hip fracture patients in Austria. Mortality was lower in primarily female bisphosphonate users, while hip refracture incidence was generally elevated relative to controls, indicating beneficial effects of bisphosphonates other than on bone.\n The purpose of this study was to analyze mortality and hip refracture risk in osteoporotic hip fracture patients with and without antiosteoporotic medication.\n We retrospectively analyzed data on 31, 68 Austrian patients ≥50 years with a hip fracture between July 2008 and December 2010 for antiosteoporotic drug treatment with respect to outcome parameters all-cause mortality, hip refracture incidence, and hip refracture-free days. Outcomes when bisphosphonate (BP) treatment was begun before or after fracture were compared with an age- and sex-matched hip fracture control without antiosteoporotic medication.\n 27.69 % of patients (33.01 % of women, 13.13 % of men) were prescribed antiosteoporotic medication, primarily BPs. Females having initiated BP treatment before first fracture had lower odds for mortality 1 and 3 year(s) post-fracture, whereas hip refracture incidence under pre-fracture BP initiation was generally higher. Treatment that was started after fracture, however, entailed significantly lower mortality hazards for both genders (HR 0.43, 95 %CI 0.36-0.52, p < 0.0001 after 1 year) but significantly higher hip refracture incidence except for patients aged 50-69 years and more hip refracture free days for females. Hip refractures overall amounted to 29.22/1000 patient years differing significantly between women and men (31.03 vs. 23.89, respectively, p < 0.0001), and longer hip refracture free survival was observed for women than for men (499 vs. 466 median days, respectively, p < 0.0001).\n Although BP use is associated with reduced mortality after hip fracture, notably among women, hip refracture incidences are likewise elevated, which is most likely accounted for by a high probability of BP prescription to more comorbid patients suffering from more severe osteoporosis. Concomitantly, through possible effects other than on bone, BPs might be able to curtail mortality. Male hip fracture patients' low treatment frequency in particular reflects underdiagnosis and undertreatment of osteoporosis in Austria.\n\nDimai, Hans\n\n\n"
},
{
"text": "\n177417\n<i>In Silico</i> Pelvis and Sacroiliac Joint Motion: Refining a Model of the Human Osteoligamentous Pelvis for Assessing Physiological Load Deformation Using an Inverted Validation Approach.\n\nRamezani, M\n\nKlima, S\n\nde la Herverie, PLC\n\nCampo, J\n\nLe Joncour, JB\n\nRouquette, C\n\nScholze, M\n\nHammer, N\n\nBeiträge in Fachzeitschriften\nISI:000456553700001\n30729122.0\n10.1155/2019/3973170\nPMC6343175\nIntroduction. Computational modeling of the human pelvis using the finite elements (FE) method has become increasingly important to understand the mechanisms of load distribution under both healthy and pathologically altered conditions and to develop and assess novel treatment strategies. The number of accurate and validated FE models is however small, and given models fail resembling the physiologic joint motion in particular of the sacroiliac joint. This study is aimed at using an inverted validation approach, using in vitro load deformation data to refine an existing FE model under the same mode of load application and to parametrically assess the influence of altered morphology and mechanical data on the kinematics of the model. Materials and Methods. An osteoligamentous FE model of the pelvis including the fifth lumbar vertebra was used, with highly accurate representations of ligament orientations. Material properties were altered parametrically for bone, cartilage, and ligaments, followed by changes in bone geometry (solid versus 3 and 2 mm shell) and material models (linear elastic, viscoelastic, and hyperelastic isotropic), and the effects of varying ligament fiber orientations were assessed. Results. Elastic modulus changes were more decisive in both linear elastic and viscoelastic bone, cartilage, and ligaments models, especially if shell geometries were used for the pelvic bones. Viscoelastic material properties gave more realistic results. Surprisingly little change was observed as a consequence of altering SIJ ligament orientations. Validation with in vitro experiments using cadavers showed close correlations for movements especially for 3 mm shell viscoelastic model. Discussion. This study has used an inverted validation approach to refine an existing FE model, to give realistic and accurate load deformation data of the osteoligamentous pelvis and showed which variation in the outcomes of the models are attributed to altered material properties and models. The given approach furthermore shows the value of accurate validation and of using the validation data to fine tune FE models.\n\nHammer, Niels\n\n\n"
},
{
"text": "\n181875\nDevelopment of treatment and clinical results in childhood AML in Austria (1993-2013).\n\nBoztug, H\n\nMühlegger, N\n\nGlogova, E\n\nMann, G\n\nUrban, C\n\nMeister, B\n\nSchmitt, K\n\nJones, N\n\nAttarbaschi, A\n\nHaas, O\n\nStrehl, S\n\nLion, T\n\nPötschger, U\n\nFink, FM\n\nGadner, H\n\nDworzak, M\n\nBeiträge in Fachzeitschriften\nNone\n32288851.0\n10.1007/s12254-014-0135-y\nPMC7102234\nSince the early 1990s, three consecutive pediatric acute myeloid leukemia (AML) trials have been performed in Austria (AML-Berlin-Frankfurt-Münster (BFM) 93, AML-BFM 98, and AML-BFM 2004) in close cooperation with the international BFM study center. Herein, we review the pertinent patient characteristics, therapy, and outcome data.\n From January 1993 to April 2013, 249 children and adolescents (193 protocol patients) diagnosed with AML were enrolled in the three BFM studies. Patients were mainly treated in one of five pediatric hematology/oncology centers distributed over Austria.\n Many characteristics and outcome parameters were not statistically different between the three trials. Almost similar proportions of patients were stratified into two risk groups: standard risk (SR) (approximately 37 % overall) and high-risk (HR) (61 %). MLL rearrangements were found in 23 % of patients overall as the most frequent genetic aberration subtype. Complete remission (CR) was achieved by 84-95 % of patients. The most important type of event was leukemic relapse (5-year cumulative incidence 40 ± 8 %, 21 ± 5 %, and 39 ± 6 %; p = 0.058), with a trend to a higher rate specifically in SR patients of study AML-BFM 2004 compared with AML-BFM 98. Importantly, the frequency of death from causes other than relapse sequelae declined over the years (AML-BFM 93: 5/42 12 %, AML-BFM 98: 5/57 9 %, and AML-BFM 2004: 5/94 5 %). Altogether, event-free survival at 5 years varied insignificantly (48 ± 8 %, 61 ± 7 %, and 50 ± 6 %; p = 0.406). Nevertheless, survival (pSU) apparently improved from BFM 93 to subsequent studies, both overall (57 ± 8 %, 75 ± 6 %, and 62 ± 6 %; p = 0.046) and regarding the HR group (5-year-probability of survival (pSU) 40 ± 10 %, 66 ± 8 %, and 52 ± 8 %; p = 0.039).\n Treatment of pediatric AML in Austria renders survival rates in the range of international best practice. However, unambiguous statistical comparison of treatment periods is eventually hampered by small numbers and inequalities of recruitment. Hence, only internationally collaborative trials will allow developing treatment further to achieve higher cure rates with fewer events.\n © Springer-Verlag Wien 2014.\n\nUrban, Ernst-Christian\n\n\n"
},
{
"text": "\n187837\nMicroRNA expression profiling with a Droplet Digital PCR assay enables molecular diagnosis and prognosis of cancers of unknown primary (CUPs).\n\nLaprovitera, N\n\nRiefolo, M\n\nPorcellini, E\n\nDurante, G\n\nGarajova, I\n\nVasuri, F\n\nAigelsreiter, A\n\nDandachi, N\n\nBenvenuto, G\n\nAgostinis, F\n\nSabbioni, S\n\nBerindan Neagoe, I\n\nRomualdi, C\n\nArdizzoni, A\n\nTrerè, D\n\nPichler, M\n\nD'Errico, A\n\nFerracin, M\n\nBeiträge in Fachzeitschriften\nNone\n34075699.0\n10.1002/1878-0261.13026\nNone\nMetastasis is responsible for the majority of cancer-related deaths. Particularly challenging is the management of metastatic cancer of unknown primary site (CUP), whose tissue of origin (TOO) remains undetermined even after extensive investigations and whose therapy is rather unspecific and poorly effective. Molecular approaches to identify the most probable TOO of CUPs can overcome some of these issues. In this study, we applied a pre-determined set of 89 microRNAs (miRNAs) to infer the TOO of 53 metastatic cancers of unknown or uncertain origin. The miRNA expression was assessed with Droplet Digital PCR in 159 samples, including primary tumors from 17 tumor classes (reference set), and metastases of known and unknown origin (test set). We combined two different statistical models for class prediction to obtain the most probable TOOs: the nearest shrunken centroids approach of Prediction Analysis of Microarrays (PAMR) and the Least Absolute Shrinkage and Selection Operator (LASSO) models. The molecular test was successful for all formalin-fixed paraffin-embedded samples and provided a TOO identification within 1 week from the biopsy procedure. The most frequently predicted origins were gastrointestinal, pancreas, breast, lung and bile duct. The assay was applied also to multiple metastases from the same CUP, collected from different metastatic sites: the predictions showed a strong agreement, intrinsically validating our assay. The final CUPs' TOO prediction was compared with the clinico-pathological hypothesis of primary site. Moreover, a panel of 13 miRNAs proved to have prognostic value and be associated with overall survival in CUP patients. Our study demonstrated that miRNA expression profiling in CUP samples could be employed as diagnostic and prognostic test. Our molecular analysis can be performed on request, concomitantly with standard diagnostic workup and in association with genetic profiling, to offer valuable indications about the possible primary site, thereby supporting treatment decisions.\n This article is protected by copyright. All rights reserved.\n\nAigelsreiter, Ariane\n\nDandachi, Nadia\n\nPichler, Martin\n\n\n"
},
{
"text": "\n75\nA new high-resolution esophageal electrocardiography recording technique: an experimental approach for the detection of myocardial ischemia.\n\nMächler, HE\n\nLueger, A\n\nRehak, P\n\nBerger, J\n\nVeith, W\n\nKühbacher, C\n\nKoidl, C\n\nStark, G\n\nMetzler, H\n\nBeiträge in Fachzeitschriften\nISI:000071155100007\n9428847.0\nNone\nNone\nCriteria for ischemic changes in the esophageal electrocardiograph (E-ECG) have not been standardized and validated. The main goal of this study was to evaluate the experimental esophageal recording of myocardial ischemia and to assess the association between ST segment alternans in the E-ECG and ischemia. Experiments were performed on 18 anesthetized sheep with occlusion of a branch of the left anterior descending artery. The bipolar signals were recorded via an esophageal lead containing three chloridized silver electrodes. Electrical signals were amplified in a self-designed, battery-supported preamplifier (gain 1000, frequency range 0.01-2000 Hz, common mode rejection 140 dB, signal noise 5-7 microV p-p), then sent to a digital oscilloscope for display and to a pulse code-modulated recorder. Surface electrocardiography (S-ECG) data were also recorded. Ischemia E-ECG revealed homogenous ST segments without any beat-to-beat alternans. Two minutes after occlusion, 14 of 15 sheep (93%) showed repetitive beat-to-beat fluctuations within the ST segment on the E-ECG. Of the 15 sheep, 7 (47%) showed ischemia in the S-ECG (P < 0.01). For calculation of the dynamic changes in the ST segment in the E-ECG, the difference in the amplitudes of the ST segment of five successive beats to the next beat, performed for 200 consecutive beats, was calculated. The central tendency of the sum of these values before versus during ischemia was 2000 mV/ms versus 5000 mV/ms (Hodges-Lehmann point estimator) (95% confidence intervals 1700/2500 versus 3350/9250 [lower limit/upper limit]). The authors have established a close temporal relationship between the magnitude of ST segment alternans recorded via E-ECG and myocardial ischemia. Implications: The study presents the use of an esophageal electrocardiograph for detection of progressive changes of myocardial ischemia and infarction. During acute myocardial ischemia and infarction in sheep, the esophageal electrocardiograph has visually apparent ST alternans of amplitude in the millivolt range, in part due to a special amplifier (0.01-2000 Hz). This is therefore one very promising technique for better evaluation of electrocardiographic changes of ischemia.\n\nKoidl, Christoph\n\nLueger, Andreas\n\nMächler, Heinrich\n\nMetzler, Helfried\n\n\n"
},
{
"text": "\n3295\nIntracellular distribution and mobilization of unesterified cholesterol in adipocytes: triglyceride droplets are surrounded by cholesterol-rich ER-like surface layer structures.\n\nPrattes, S\n\nHörl, G\n\nHammer, A\n\nBlaschitz, A\n\nGraier, WF\n\nSattler, W\n\nZechner, R\n\nSteyrer, E\n\nBeiträge in Fachzeitschriften\nISI:000089441900006\n10934037.0\nNone\nNone\nIn addition to their central role in triglyceride storage, fat cells are a primary depot of unesterified cholesterol (FC) in the body. In comparison, peripheral cells contain very little FC. This difference in adipocytes versus peripheral tissues is inconsistent with the current theory of cholesterol homeostasis. Attempting to resolve this discrepancy, we examined intracellular storage sites of FC in murine 3T3-F442A adipocytes. Using the cholesterol-binding antibiotic, filipin, in combination with high resolution fluorescence microscopy, intense fluorescent staining characteristically decorated the periphery of triglyceride droplets (TGD) as well as the plasma membrane (PM) of fat cells. Filipin-staining was not visible inside the lipid droplets. Purification of TGD by subcellular fractionation demonstrated that the rise in total FC content of adipocytes upon differentiation was attributable to an increase in TGD-FC, which contributed up to one third of the total cellular FC. The protein component of purified TGD from cultured adipocytes as well as from murine adipocytes obtained from fresh tissues contained the lumenal endoplasmic reticulum (ER) immunoglobulin binding protein (BiP) and the integral ER membrane protein calnexin. Efflux experiments using the extracellular FC acceptors (&bgr;)-cyclodextrin or apolipoprotein A-I demonstrated that TGD-associated FC was releasable from TGD. Whereas FC efflux from adipocytes was unaffected in the presence of brefeldin A or monensin, the secretion of a control protein, lipoprotein lipase, was effectively reduced. In summary, our findings identify the TGD surface layer as primary intracellular storage site for FC within adipocytes. We suggest that the structural role of ER-resident proteins in this adipocyte TGD envelope has been previously neglected. Our findings support the suggestion that an ER-like structure, albeit of modified lipid composition, constitutes the lipid droplets' surface layer. Finally, the efflux process of FC from adipocytes upon extracellular stimulation with (beta)-cyclodextrin provides evidence for an energy-dependent intracellular trafficking route between the TGD-FC pool and the PM-FC sites which is distinct from the secretory pathway of proteins.\n\nGraier, Wolfgang\n\nHammer, Astrid\n\nHörl, Gerd\n\nSattler, Wolfgang\n\nSteyrer, Ernst\n\n\n"
},
{
"text": "\n4845\nHeterogeneity of microvascular endothelial cells isolated from human term placenta and macrovascular umbilical vein endothelial cells.\n\nLang, I\n\nPabst, MA\n\nHiden, U\n\nBlaschitz, A\n\nDohr, G\n\nHahn, T\n\nDesoye, G\n\nBeiträge in Fachzeitschriften\nISI:000182847700002\n12751902.0\n10.1078/0171-9335-00306\nNone\nThe present study compares some phenotypic and physiologic characteristics of microvascular and macrovascular endothelial cells from within one human organ. To this end microvascular endothelial cells from human full-term placenta (PLEC) were isolated using a new method and compared with macrovascular human umbilical vein endothelial cells (HUVEC) and an SV40-transformed placental venous endothelial cell line (HPEC-A2). PLEC were isolated by enzymatic perfusion of small placental vessels, purified on a density gradient and cultured subsequently. Histological sections of the enzyme-treated vessels showed a selective removal of the endothelial lining in the perfused placental cotyledons. The endothelial identity of the cells was confirmed by staining with the endothelial markers anti-von Willebrand factor, Ulex europaeus lectin and anti-QBEND10. The cells internalized acetylated low-density lipoprotein and did not show immunoreactivity with markers for macrophages, smooth muscle cells and fibroblasts. The spindle-shaped PLEC grew in swirling patterns similar to that described for venous placental endothelial cells. However, scanning electron microscopic examination clearly showed that PLEC remained elongated at the confluent state, in contrast to the more polygonal phenotype of HPEC-A2 and HUVEC that were studied in parallel. The amount of vasoactive substances (endothelin-1, , thromboxane, angiotensin II, prostacyclin) released into the culture medium and the proliferative response to cytokines was more similar to human dermal microvessels (MIEC) derived from non-fetal tissue than to HUVEC. Potent mitogens such as vascular endothelial growth factors (VEGF121, VEGF165) and basic fibroblast growth factor (FGF-2) induced proliferation of all endothelial cell types. Placental growth factors PIGF-1 and PIGF-2 effectively stimulated cell proliferation on PLEC (142 +/- 7% and 173 +/- 10%) and MIEC (160 +/- 20% and 143 +/- 28%) in contrast to HUVEC (9 +/- 8% and 15 +/- 20%) and HPEC-A2 (15 +/- 7% and 24 +/- 6%) after 48 h incubation time under serum-free conditions. These data support evidence for (1) the microvascular identity of the isolated PLEC described in this study, and (2) the phenotypic and physiologic heterogeneity of micro- and macrovascular endothelial cells within one human organ.\n\nDesoye, Gernot\n\nDohr, Gottfried\n\nHiden, Ursula\n\nLang-Olip, Ingrid\n\nPabst, Maria-Anna\n\n\n"
},
{
"text": "\n5581\nAlterations in gap junction protein expression in human benign prostatic hyperplasia and prostate cancer.\n\nHabermann, H\n\nRay, V\n\nHabermann, W\n\nPrins, GS\n\nBeiträge in Fachzeitschriften\nISI:000173212600061\n11792947.0\n10.1097%2F00005392-200112000-00054\nNone\nPURPOSE: Gap junctions composed of connexin proteins have an essential role in intercellular communication and differentiation. Dysregulation of connexin expression is believed to have a role in carcinogenesis. The human prostate has been reported to express connexin 32 and 43. However, the expression pattern in prostate cancer is controversial, while to our knowledge connexin expression has not been reported in benign prostatic hyperplasia (BPH). To understand the potential involvement in prostate disease connexin 32 and 43 expression was evaluated in a series of normal prostate, BPH and prostate cancer specimens that were surgically removed due to bladder outlet obstruction. MATERIALS AND METHODS: Frozen sections of 23 normal, 43 BPH and 40 cancer involved prostates were evaluated for the presence, staining intensity and pattern of connexin 32 and 43 by immunocytochemical testing. RESULTS: In all specimens examined connexin 43 stain was punctate along the borders of the basal epithelial cells, whereas connexin 32 immunolocalized to luminal epithelial cells. In normal prostate connexin 43 and 32 were present in 87% and 65% of specimens, respectively, at low to moderate stain intensity. Importantly none of the normal samples were negative foreach connexin. In BPH specimens there was a marked increase in the incidence and intensity of connexin 43 and 32 immunostaining within epithelial cells. In addition, 23% of BPH samples showed strong connexin 43 expression in stromal cells. In contrast, connexin was decreased in prostate cancer specimens, of which 65% and 38% were negative for connexin 43 and 32, respectively, and 28% were negative for each type. In poorly differentiated tumors connexin 43 and 32 were present in only 10% and 40% of tumors, respectively, at low immunostaining intensity. CONCLUSIONS: In normal human prostate basal cells communicate via connexin 43 gap junctions, whereas luminal cells communicate via connexin 32 gap junctions. In BPH gap junctional intercellular communication is increased in epithelial and stromal cells, which may have a role in BPH pathogenesis. In prostate cancer gap junctional intercellular communication is decreased, is as indicated by decreased expression of connexin 43 and 32 with severe loss in poorly differentiated prostate cancer. These alterations in connexin expression may have a role in dedifferentiation and tumor progression.\n\n\n"
}
]
}