GET /v1/research/search/publication/?format=api&offset=124780
HTTP 200 OK
  Allow: GET, HEAD, OPTIONS
  Content-Type: application/json
  Vary: Accept
  
  {
    "count": 127182,
    "next": "https://api-test.medunigraz.at/v1/research/search/publication/?format=api&limit=20&offset=124800",
    "previous": "https://api-test.medunigraz.at/v1/research/search/publication/?format=api&limit=20&offset=124760",
    "results": [
        {
            "text": "\n1051\nFamotidine versus omeprazole in combination with clarithromycin and metronidazole for eradication of Helicobacter pylori--a randomized, controlled trial.\n\nGschwantler, M\n\nDragosics, B\n\nSchütze, K\n\nWurzer, H\n\nHirschl, AM\n\nPasching, E\n\nWimmer, M\n\nKlimpfinger, M\n\nOberhuber, G\n\nBrandstätter, G\n\nHentschel, E\n\nWeiss, W\n\nBeiträge in Fachzeitschriften\nISI:000082101900011\n10468682.0\n10.1046/j.1365-2036.1999.00563.x\nNone\nBACKGROUND: One-week low-dose triple therapy is currently considered the gold standard regimen for treatment of Helicobacter pylori infection. However, the mechanisms involved in the synergy between antibiotics and proton pump inhibitors are controversial. AIMS: To test the hypothesis that acid suppression represents the crucial mechanism by which the antibacterial activity of antibiotics can be enhanced, and to assess the impact of primary resistance on treatment outcome. METHODS: One hundred and twenty patients with H. pylori infection and duodenal ulcer, gastric ulcer or non-ulcer dyspepsia were randomly assigned to a 1 week course of either famotidine 80 mg b.d., clarithromycin 250 mg b.d. and metronidazole 500 mg b.d. (FCM group; n = 60) or omeprazole 20 mg o.d., clarithromycin 250 mg b.d. and metronidazole 500 mg b.d. (OCM group; n = 60). Gastroscopy was performed at baseline and 5 weeks after completion of treatment. H. pylori status was assessed by biopsy urease test, histology and culture. RESULTS: In the intention-to-treat analysis, eradication of H. pylori was achieved in 47 of 60 patients (78%; 95% CI: 66-88%) in the FCM group, compared to 44 of 60 patients (73%; 95% CI: 60-84%) in the OCM group (N.S.). Using per protocol analysis, eradication therapy was successful in 47 of 52 patients (90%; 95% CI: 79-97%) treated with FCM and 44 of 57 patients (77%; 95% CI: 64-87%) treated with OCM (N.S.). Primary metronidazole resistance was present in 27% and primary clarithromycin resistance in 8% of strains. Overall per protocol eradication rates in strains susceptible to both antibiotics and strains with isolated metronidazole resistance were 93% and 84%, respectively. No patient with clarithromycin resistance responded to treatment. CONCLUSIONS: High-dose famotidine and omeprazole, combined with clarithromycin and metronidazole, are equally effective for eradication of H. pylori. In 1-week low-dose triple therapy, metronidazole resistance has no major impact on eradication rates whereas clarithromycin resistance is associated with a poor treatment outcome.\n\n\n"
        },
        {
            "text": "\n1881\nOxidation of high-density lipoprotein HDL3 leads to exposure of apo-AI and apo-AII epitopes and to formation of aldehyde protein adducts, and influences binding of oxidized low-density lipoprotein to type I and type III collagen in vitro1.\n\nGreilberger, J\n\nJürgens, G\n\nBeiträge in Fachzeitschriften\nISI:000072972500024\n9512478.0\n10.1042/bj3310185\nPMC1219337\nThe changes in the immunological properties of apolipoprotein AI (apo-AI) and AII (apo-AII) during the oxidation of the high-density lipoprotein HDL3 and its influence on the binding of heavily oxidized low-density lipoprotein (LDL) to type I and III collagen were investigated. Oxidation of HDL3 or Eu3+-labelled HDL3 was performed with CuSO4, varying the time of oxidation. Oxidation of HDL3 resulted in an increase in lipid hydroperoxides and enhanced the negative charge of this lipoprotein. Immunological studies with a solid-phase sandwich immunoassay revealed a strong increase in binding of Eu3+-labelled HDL3 to polyclonal antibodies against apo-AI and apo-AII within the first 4 h of oxidation. Neo-epitopes were also formed by interaction of the apolipoproteins with degradation products from the lipid peroxidation of polyunsaturated fatty acids, as evidenced by an immunoreaction of oxidized Eu3+-labelled HDL3 with antibodies to 4-hydroxynonenal (4-HNE)- and malondialdehyde (MDA)-protein adducts. Western blot analysis of oxidized HDL3 samples showed, as well as apo-AI and apo-AII bands, larger aggregated apolipoproteins, occurring after 0.5-2.5 h of oxidation. These aggregates were recognized by antibodies to apo-AI and apo-AII as well as by antibodies to 4-HNE- and MDA-protein adducts. Furthermore the original apo-AI monomers and apo-AII dimers decreased during the oxidation. The ability of native and oxidized HDL3 to prevent the binding of Eu3+-labelled 24 h-oxidized LDL to collagen on microtitration plates was estimated. Interestingly, 2 h-oxidized HDL3 competed most with the binding of 24 h-oxidized LDL on collagen type I and type III, followed by native HDL3. However, 24 h-oxidized HDL3 was a weaker competitor. Thus oxidative modification of HDL3 strongly alters the immunological properties of this lipoprotein and its binding affinity for collagen.\n\nGreilberger, Joachim\n\nJürgens, Günther\n\n\n"
        },
        {
            "text": "\n2609\nThe relevance of adjuvant therapy in primary carcinoma of the fallopian tube, stages I and II: irradiation vs. chemotherapy.\n\nKlein, M\n\nRosen, A\n\nLahousen, M\n\nGraf, AH\n\nRainer, A\n\nBeiträge in Fachzeitschriften\nISI:000165604600021\n11121643.0\n10.1016%2FS0360-3016%2800%2901381-X\nNone\nINTRODUCTION: Primary carcinoma of the Fallopian tube (FTC) is a rare but extremely aggressive neoplasm. It must be expected to cause up to 40% of tumor-related deaths even in Stage I, and up to 57% in Stage II. Due to its rarity, there exist only a few and divergent reports on the value of adjuvant therapy. Therefore the present study aims at evaluating the influence of postoperative adjuvant therapy on FTC by studying the effects of irradiation and chemotherapy on the overall survival of patients in Stages I and II. PATIENTS AND METHODS: We investigated 95 cases of FTC in Stages I (n = 66) and II (n = 29) in a retrospective multicenter study. Group I (n = 32) are patients who underwent a complete irradiation with cobalt or photon energies of 23 MV (administering a daily dose of 2 Gy resulted in a total of 45-52 Gy in the pelvic areas). Group II (n = 31) consists of those cases who received postoperative chemotherapy with platinum. Thirty-two women were excluded from this study because they had other chemotherapies, incomplete irradiation, or no adjuvant therapy at all. RESULTS: Median survival time was 57 months in Group I patients (95% confidence interval 33-81 months), compared to 73 months (95% confidence interval, 68-78 months) in the chemotherapeutically treated Group II. This difference did not prove to be statistically significant (p = 0.476).If primary surgical therapy is included in the evaluation, and patients with total abdominal hysterectomy (TAH) and bilateral salpingo-oophorectomy (BSO) are compared to those with additional radical lymphadenectomy (TAH+BSO+lymph nodes), the latter group's overall survival essentially improves but fails to reach statistical significance. Their 5-year survival rate is 83% against 58% in the TAH+BSO group (p = 0.12). CONCLUSION: Chemotherapy and irradiation are two adjuvant therapies that are similarly effective in FTC of Stages I and II, with chemotherapy being preferred at the present time. Primary surgical treatment, however, is of crucial impact on the prognosis of FTC.\n\n\n"
        },
        {
            "text": "\n3230\nRisk factors and determinants of neurodevelopmental outcome in cystic periventricular leucomalacia.\n\nResch, B\n\nVollaard, E\n\nMaurer, U\n\nHaas, J\n\nRosegger, H\n\nMüller, W\n\nBeiträge in Fachzeitschriften\nISI:000088937600006\n11014465.0\n10.1007/PL00008403\nNone\nThe aim of the study was to determine risk factors for the development of cystic periventricular leucomalacia (PVL) and to correlate ultrasound findings with neurodevelopmental outcome. By means of a retrospective case-control study (matched for gestational age, birth weight, sex, and year of birth) and a cohort analysis of all preterm infants with cystic PVL documented by ultrasound scans hospitalised at a local tertiary care centre between 1988 and 1998, 98 preterm infants with a gestational age ranging from 26 to 35 weeks were diagnosed as having cystic PVL. The mean day of diagnosis of periventricular echodensities was 3 +/- 2 days (range 1-11 days), and of cystic PVL 21 +/- 8 days (range 2-47 days). Of 79 infants (1988-1997) eligible for neurodevelopmental follow-up (91%), hemi-, di-, or tetraplegia was diagnosed in 61 (77%), normal mental outcome in 22 (28%), associated visual disorders in 41 (52%) and seizure disorders in 12 (15%) infants. Significant risk factors associated with the development of cystic PVL were premature rupture of membranes, chorioamnionitis, and hyperbilirubinaemia (odds ratios 4.665, 6.026, and 2.460 respectively). Subgroup analysis according to gestational age (26-28, 29-32, 33-35 weeks) revealed similar results despite spontaneous labour (26-28 weeks; odds ratio 4.808) and pre-eclampsia (33-35 weeks; odds ratio 3.517). Multiple pregnancy was associated with a twofold increased risk (odds ratio 2.075). The white matter damage probably accounted for the significantly higher prevalence of apnoeas (P < 0.001) and neonatal seizures (P < 0.001). Cysts located bilateral or parieto-occipital were associated with a higher risk of cerebral palsy (odds ratios 6.933 and 4.327 respectively). Solely anterior located cysts were associated with normal neurological outcome. Increasing size of the cysts was associated with increasing risk of cerebral palsy with a cut-off value of 10 mm (odds ratio 3.300 and above) and all infants with cysts of more than 20 mm diameter had cerebral palsy. CONCLUSION: The high prevalence of premature rupture of the membranes and chorioamnionitis further supports the role of intra-uterine infection in the pathogenesis of periventricular leucomalacia. The overall prognosis of cystic periventricular leucomalacia is poor.\n\nHaas, Josef\n\nMüller, Wilhelm\n\nResch, Bernhard\n\n\n"
        },
        {
            "text": "\n123959\nPalmitate Induced IL-6 and MCP-1 Expression in Human Bladder Smooth Muscle Cells Provides a Link between Diabetes and Urinary Tract Infections.\n\nOberbach, A\n\nSchlichting, N\n\nBluher, M\n\nKovacs, P\n\nTill, H\n\nStolzenburg, JU\n\nNeuhaus, J\n\n\n\nBeiträge in Fachzeitschriften\nISI:000278222100011\n20526368.0\n10.1371/journal.pone.0010882\nPMC2878332\nBACKGROUND: Urinary tract infections (UTI) are more frequent in type-2 diabetes mellitus patients than in subjects with normal glucose metabolism. The mechanisms underlying this higher prevalence of UTI are unknown. However, cytokine levels are altered in diabetic patients and may thus contribute to the development of UTI. Increased levels of free fatty acids (FFA), as observed in obese patients, can induce IL-6 production in various cell types. Therefore we studied the effects of the free fatty acid palmitate and bacterial lipopolysaccharide (LPS) on interleukin-6 (IL-6) and monocyte chemotactic protein-1 (MCP-1) expression and secretion in cultured human bladder smooth muscle cells (hBSMC).\r\n\r\nMETHODOLOGY/PRINCIPAL FINDINGS: Biopsies were taken from patients undergoing cystectomy due to bladder cancer. Palmitate or LPS stimulated hBSMC were analysed for the production and secretion of the IL-6, gp80, gp80soluble, gp130, MCP-1, pSTAT3, SOCS3, NF-kappaB and SHP2 by quantitative PCR, ELISA, Western blotting, and confocal immunofluorescence. In signal transduction inhibition experiments we evaluated the involvement of NF-kappaB and MEK1 in IL-6 and MCP-1 regulation. Palmitate upregulates IL-6 mRNA expression and secretion via NF-kappaB dependent pathways in a concentration- and time-dependent manner. MCP-1 was moderately upregulated by palmitate but was strongly upregulated by LPS involving NF-kappaB and MEK1 dependent pathways. Soluble IL-6 receptor (gp80soluble) was downregulated by palmitate and LPS, while membrane-bound gp80 was moderately upregulated. LPS increased SOCS3 and SHP2, whereas palmitate only induced SOCS3. Secondary finding: most of the IL-6 is secreted.\r\n\r\nCONCLUSIONS/SIGNIFICANCE: Bacterial infection (LPS) or metabolic alterations (palmitate) have distinct effects on IL-6 expression in hBSMC, (i) short term LPS induced autocrine JAK/STAT signaling and (ii) long-term endocrine regulation of IL-6 by palmitate. Induction of IL-6 in human bladder smooth muscle cells by fatty acids may represent a pathogenetic factor underlying the higher frequency and persistence of urinary tract infections in patients with metabolic diseases.\n\nTill, Holger\n\n\n"
        },
        {
            "text": "\n134844\nStrategies for assignment of HIV-HCV genotype-1-coinfected patients to either dual-therapy or direct-acting antiviral agent-based triple-therapy.\n\nMandorfer, M\n\nNeukam, K\n\nRivero, A\n\nPuoti, M\n\nBoesecke, C\n\nBaumgarten, A\n\nGrzeszczuk, A\n\nZangerle, R\n\nErnst, D\n\nRockstroh, JK\n\nTrauner, M\n\nPineda, JA\n\nPeck-Radosavljevic, M\n\nReiberger, T\n\nBeiträge in Fachzeitschriften\nISI:000348601800010\n24342953.0\n10.3851/IMP2717\nNone\nThe aim of this study was to evaluate strategies for assignment of HIV-HCV genotype-1-coinfected patients (HIV-HCV-GT1) to either dual-therapy or direct-acting antiviral agent (DAA)-based triple-therapy.\n                A total of 148 treatment-naive HIV-HCV-GT1 who received antiviral therapy with pegylated interferon/ribavirin were included in this multinational, retrospective analysis. Patients with rapid virological response (RVR) were treated for 48 weeks, while patients without RVR received either 48 or 72 weeks of treatment. IL28B rs12979860 (IL28B) non-C/C, advanced liver fibrosis and high HCV RNA were considered as established risk factors for treatment failure.\n                A trend toward higher sustained virological response (SVR) rates in patients with IL28B C/C (65% [37/57] versus 51% [40/79]; P=0.097) was observed. Higher SVR rates were observed in patients without advanced liver fibrosis (61% [47/77] versus 42% [22/52]); P=0.036) and without high HCV RNA (73% [35/48] versus 49% [49/100]; P=0.006), as well as in patients with RVR (90% [35/39] versus 45% [49/109]; P<0.001). SVR rates varied statistically significantly between the risk factors for treatment failure subgroups (86% [6/7] versus 69% [34/49] versus 48% [21/44] versus 20% [4/20] for zero, one, two and three risk factors, respectively; P<0.001). In patients without RVR, higher rates of SVR were observed in those treated for 72 weeks (62% [23/37]), when compared to patients treated for 48 weeks (36% [26/72]; P=0.01).\n                RVR had an excellent positive predictive value for the response to dual-therapy in HIV-HCV-GT1, emphasizing the utility of a lead-in phase for assigning these patients to dual-therapy or DAA-based triple-therapy. The use of an IL28B-guided approach was suboptimal, while a combination of established baseline predictors may provide guidance for individual treatment decisions prior to the initiation of antiviral therapy. However, the extension of treatment duration to 72 weeks in HIV-HCV-GT1 without RVR should be strongly considered if triple-therapy is not available.\n\n\n"
        },
        {
            "text": "\n144240\nPlatelet-Rich Plasma Reduces Retear Rates After Arthroscopic Repair of Small- and Medium-Sized Rotator Cuff Tears but Is Not Cost-Effective.\n\nVavken, P\n\nSadoghi, P\n\nPalmer, M\n\nRosso, C\n\nMueller, AM\n\nSzoelloesy, G\n\nValderrabano, V\n\nBeiträge in Fachzeitschriften\nISI:000365761000027\n25767267.0\n10.1177/0363546515572777\nNone\nIt has been suggested that platelet-rich plasma (PRP) improves healing after arthroscopic rotator cuff repair. The current literature provides ample but inconsistent data on this topic.\n                To systematically review the current in vivo evidence for the use of platelet concentrates (PRP) in the arthroscopic treatment of rotator cuff tears to assess effectiveness, safety, and cost-effectiveness.\n                Meta-analysis and cost-effectiveness analysis.\n                Published evidence from controlled, human trials of rotator cuff repair augmented with platelet concentrates was systematically gathered, and data on retear rates were extracted. Mathematical and clinical heterogeneity was evaluated, and fixed-effect meta-analysis was performed to calculate the risk ratio (RR) of retears and the number needed to treat (NNT). Subgroup analyses were made for small/medium tears (n = 404) and large/massive tears (n = 374). Cost-effectiveness was assessed using data from this meta-analysis and using cost data from the literature, including extensive sensitivity analyses, to calculate the incremental cost-effectiveness ratio (ICER).\n                Thirteen studies published between 2010 and 2014 were identified for analysis. The RR for retear for all patients was 0.87 (95% CI, 0.67-1.12; P = .286). For small- and medium-sized tears (<3 cm), the RR for retear was 0.60 (95% CI, 0.37-0.97), consistent with a significant difference in favor of PRP use (P = .038). This translated into an NNT of 14 (95% CI, 7-125). However, at an ICER of US$127, 93 per quality-adjusted life year gained, assuming a 5% revision rate, the use of PRP was not cost-effective for small- and medium-sized tears.\n                In large tears, even with double-row repair, the beneficial effects of PRP alone are insufficient to compensate the progressed tissue damage. The study data suggest that PRP may promote healing of small- and medium-sized tears to reduce retear rates. However, despite the substantial biological effect, at current cost, the use of PRP is not cost-effective in arthroscopic repair of small- and medium-sized tears.\n                © 2015 The Author(s).\n\nSadoghi, Patrick\n\n\n"
        },
        {
            "text": "\n161456\nEAACI guidelines on allergen immunotherapy: Hymenoptera venom allergy.\n\nSturm, GJ\n\nVarga, EM\n\nRoberts, G\n\nMosbech, H\n\nBilò, MB\n\nAkdis, CA\n\nAntolín-Amérigo, D\n\nCichocka-Jarosz, E\n\nGawlik, R\n\nJakob, T\n\nKosnik, M\n\nLange, J\n\nMingomataj, E\n\nMitsias, DI\n\nOllert, M\n\nOude Elberink, JNG\n\nPfaar, O\n\nPitsios, C\n\nPravettoni, V\n\nRuëff, F\n\nSin, BA\n\nAgache, I\n\nAngier, E\n\nArasi, S\n\nCalderón, MA\n\nFernandez-Rivas, M\n\nHalken, S\n\nJutel, M\n\nLau, S\n\nPajno, GB\n\nvan Ree, R\n\nRyan, D\n\nSpranger, O\n\nvan Wijk, RG\n\nDhami, S\n\nZaman, H\n\nSheikh, A\n\nMuraro, A\n\nBeiträge in Fachzeitschriften\nISI:000430164500003\n28748641.0\n10.1111/all.13262\nNone\nHymenoptera venom allergy is a potentially life-threatening allergic reaction following a honeybee, vespid, or ant sting. Systemic-allergic sting reactions have been reported in up to 7.5% of adults and up to 3.4% of children. They can be mild and restricted to the skin or moderate to severe with a risk of life-threatening anaphylaxis. Patients should carry an emergency kit containing an adrenaline autoinjector, H1 -antihistamines, and corticosteroids depending on the severity of their previous sting reaction(s). The only treatment to prevent further systemic sting reactions is venom immunotherapy. This guideline has been prepared by the European Academy of Allergy and Clinical Immunology's (EAACI) Taskforce on Venom Immunotherapy as part of the EAACI Guidelines on Allergen Immunotherapy initiative. The guideline aims to provide evidence-based recommendations for the use of venom immunotherapy, has been informed by a formal systematic review and meta-analysis and produced using the Appraisal of Guidelines for Research and Evaluation (AGREE II) approach. The process included representation from a range of stakeholders. Venom immunotherapy is indicated in venom-allergic children and adults to prevent further moderate-to-severe systemic sting reactions. Venom immunotherapy is also recommended in adults with only generalized skin reactions as it results in significant improvements in quality of life compared to carrying an adrenaline autoinjector. This guideline aims to give practical advice on performing venom immunotherapy. Key sections cover general considerations before initiating venom immunotherapy, evidence-based clinical recommendations, risk factors for adverse events and for relapse of systemic sting reaction, and a summary of gaps in the evidence.\n                © 2017 EAACI and John Wiley and Sons A/S. Published by John Wiley and Sons Ltd.\n\nSturm, Gunter\n\nVarga, Eva-Maria\n\n\n"
        },
        {
            "text": "\n162503\nRegularity of beating of small clusters of embryonic chick ventricular heart-cells: experiment vs. stochastic single-channel population model.\n\nKrogh-Madsen, T\n\nKold Taylor, L\n\nSkriver, AD\n\nSchaffer, P\n\nGuevara, MR\n\nBeiträge in Fachzeitschriften\nISI:000412093600044\n28964156.0\n10.1063/1.5001200\nNone\nThe transmembrane potential is recorded from small isopotential clusters of 2-4 embryonic chick ventricular cells spontaneously generating action potentials. We analyze the cycle-to-cycle fluctuations in the time between successive action potentials (the interbeat interval or IBI). We also convert an existing model of electrical activity in the cluster, which is formulated as a Hodgkin-Huxley-like deterministic system of nonlinear ordinary differential equations describing five individual ionic currents, into a stochastic model consisting of a population of ∼20 000 independently and randomly gating ionic channels, with the randomness being set by a real physical stochastic process (radio static). This stochastic model, implemented using the Clay-DeFelice algorithm, reproduces the fluctuations seen experimentally: e.g., the coefficient of variation (standard deviation/mean) of IBI is 4.3% in the model vs. the 3.9% average value of the 17 clusters studied. The model also replicates all but one of several other quantitative measures of the experimental results, including the power spectrum and correlation integral of the voltage, as well as the histogram, Poincaré plot, serial correlation coefficients, power spectrum, detrended fluctuation analysis, approximate entropy, and sample entropy of IBI. The channel noise from one particular ionic current (IKs), which has channel kinetics that are relatively slow compared to that of the other currents, makes the major contribution to the fluctuations in IBI. Reproduction of the experimental coefficient of variation of IBI by adding a Gaussian white noise-current into the deterministic model necessitates using an unrealistically high noise-current amplitude. Indeed, a major implication of the modelling results is that, given the wide range of time-scales over which the various species of channels open and close, only a cell-specific stochastic model that is formulated taking into consideration the widely different ranges in the frequency content of the channel-noise produced by the opening and closing of several different types of channels will be able to reproduce precisely the various effects due to membrane noise seen in a particular electrophysiological preparation.\n\nSchaffer, Peter\n\n\n"
        },
        {
            "text": "\n169168\nThe influence of glucocorticoid receptor single nucleotide polymorphisms on outcome after haematopoietic stem cell transplantation.\n\nNorden, J\n\nPearce, KF\n\nIrving, JAE\n\nCollin, MP\n\nWang, XN\n\nWolff, D\n\nKolb, HJ\n\nSocie, G\n\nKuzmina, Z\n\nGreinix, H\n\nHoller, E\n\nRocha, V\n\nGluckman, E\n\nHromadnikova, I\n\nDickinson, AM\n\nBeiträge in Fachzeitschriften\nISI:000441962400002\n30043490.0\n10.1111/iji.12380\nNone\nHaematopoietic stem cell transplantation (HSCT) remains the only cure for most haematological malignancies, however, the mortality rate remains high. Complications after HSCT include relapse, graft versus host disease (GvHD), graft rejection and infection. Over the last few years several groups, have demonstrated that non-HLA gene polymorphisms can be predictive of outcome after HSCT. Since the glucocorticoid cortisol is pivotal in the regulation of the immune system, we decided to examine single nucleotide polymorphisms (SNPs; rs6198, rs33388 and rs33389) within the glucocorticoid receptor (GR) and correlate with HSCT outcome. The training set consisted of patients (n = 458) who underwent HSCT for acute leukaemia between 1983 and 2005. In the recipients, the absence of the ACT haplotype and absence of the T allele of rs33388 were associated with decreased OS and the absence of the ACT haplotype, the absence of the T allele of rs33388 and the presence of the ATA haplotype were associated with increased risk of relapse. In addition, the presence of the ACT haplotype in the recipient showed a trend to be associated with increased risk of chronic graft versus host disease (cGvHD). The patients in this cohort received mainly myeloablative conditioning (n = 327). The SNPs in the glucocorticoid receptor were then investigated in a validation set (n = 251) of HSCT patients transplanted for acute leukaemia from 2006. This cohort contained significantly more patients that had received reduced intensity conditioning (RIC). Some of the results could be validated in these patients. However, contrary to the training set, the absence of the haplotype ACT in the donor in this cohort was associated with increased risk of cGvHD. Differences in the conditioning were shown to influence the results. These results are the first to associate GR SNPs with HSCT outcome and demonstrate the inherent problems of replicating SNP association studies in HSCT, due to different pre-transplant regimens.\n                © 2018 John Wiley & Sons Ltd.\n\nGreinix, Hildegard\n\n\n"
        },
        {
            "text": "\n170096\nAcute and long-term mental and physical sequelae in the aftermath of traumatic exposure - some remarks on &quot;the body keeps the score&quot;.\n\nKapfhammer, HP\n\nBeiträge in Fachzeitschriften\nISI:000445798700002\n30267517.0\n10.24869/psyd.2018.254\nNone\nTraumata, by definition, refer to exterior events that expose a person to experiences of overwhelming threat and catastrophe and elicit feelings of death anxiety, panic, horror, helplessness, loss of personal control, and intractability. Most affected persons respond with at least some distressing symptoms of trauma-related memory intrusions, autonomic hyperarousal, dissociation, and depression in the acute aftermath. Fortunately, the majority of traumatized individuals succeed in coping with this major stress quite well during the following weeks and months unless the process of recovery is hampered by additional adverse psychosocial circumstances, psychological disposition or biological vulnerability. In a subgroup of persons a transition to acute and posttraumatic stress disorder or other major psychiatric disorders, e.g. depressive, anxiety, substance-related disorders may be observed. Posttraumatic stress disorders very often run a chronic course of illness enduring for many years or even life-long. The typical course of illness in PTSD is characterized not only by major psychiatric comorbidities contributing to a dramatically reduced health-related quality of life, to many deficits of psychosocial adaptation and a heightened suicide risk. It is also associated with a lot of major somatic health problems both in acute and long-term stages. The main focus here is on this special dimension of physical comorbidities in posttraumatic disorders. Empirical evidence underscores that trauma exposure, and in particular PTSD is significantly associated with major physical health problems in addition to well-known PTSD-related psychological, behavioural, and psychosocial impairments. Both self-report-based and objective assessments emphasized significantly increased rates of somatoform/functional syndromes and physical comorbidities, premature all-cause and specific mortality rates, heightened medical utilization behaviours, major socioeconomic costs, and reduced health-related quality of life in the aftermath of trauma exposure and posttraumatic stress disorders, thus defining a major challenge to any medical care system. Complex psycho-behavioural-somatic and somato-psycho-behavioural models are needed to better understand both acute and long-term effects of a perpetuating stress system on physical health.\n\nKapfhammer, Hans-Peter\n\n\n"
        },
        {
            "text": "\n174421\nIndependent Pre-Transplant Recipient Cancer Risk Factors after Kidney Transplantation and the Utility of G-Chart Analysis for Clinical Process Control.\n\nSchrem, H\n\nSchneider, V\n\nKurok, M\n\nGoldis, A\n\nDreier, M\n\nKaltenborn, A\n\nGwinner, W\n\nBarthold, M\n\nLiebeneiner, J\n\nWinny, M\n\nKlempnauer, J\n\nKleine, M\n\nBeiträge in Fachzeitschriften\nISI:000379508100007\n27398803.0\n10.1371/journal.pone.0158732\nPMC4939933\nThe aim of this study is to identify independent pre-transplant cancer risk factors after kidney transplantation and to assess the utility of G-chart analysis for clinical process control. This may contribute to the improvement of cancer surveillance processes in individual transplant centers.\n                1655 patients after kidney transplantation at our institution with a total of 9, 25 person-years of follow-up were compared retrospectively to the general German population using site-specific standardized-incidence-ratios (SIRs) of observed malignancies. Risk-adjusted multivariable Cox regression was used to identify independent pre-transplant cancer risk factors. G-chart analysis was applied to determine relevant differences in the frequency of cancer occurrences.\n                Cancer incidence rates were almost three times higher as compared to the matched general population (SIR = 2.75; 95%-CI: 2.33-3.21). Significantly increased SIRs were observed for renal cell carcinoma (SIR = 22.46), post-transplant lymphoproliferative disorder (SIR = 8.36), prostate cancer (SIR = 2.22), bladder cancer (SIR = 3.24), thyroid cancer (SIR = 10.13) and melanoma (SIR = 3.08). Independent pre-transplant risk factors for cancer-free survival were age <52.3 years (p = 0.007, Hazard ratio (HR): 0.82), age >62.6 years (p = 0.001, HR: 1.29), polycystic kidney disease other than autosomal dominant polycystic kidney disease (ADPKD) (p = 0.001, HR: 0.68), high body mass index in kg/m2 (p<0.001, HR: 1.04), ADPKD (p = 0.008, HR: 1.26) and diabetic nephropathy (p = 0.004, HR = 1.51). G-chart analysis identified relevant changes in the detection rates of cancer during aftercare with no significant relation to identified risk factors for cancer-free survival (p<0.05).\n                Risk-adapted cancer surveillance combined with prospective G-chart analysis likely improves cancer surveillance schemes by adapting processes to identified risk factors and by using G-chart alarm signals to trigger Kaizen events and audits for root-cause analysis of relevant detection rate changes. Further, comparative G-chart analysis would enable benchmarking of cancer surveillance processes between centers.\n\nSchrem, Harald Heinrich\n\n\n"
        },
        {
            "text": "\n182842\nMutations in SREBF1, Encoding Sterol Regulatory Element Binding Transcription Factor 1, Cause Autosomal-Dominant IFAP Syndrome.\n\nWang, H\n\nHumbatova, A\n\nLiu, Y\n\nQin, W\n\nLee, M\n\nCesarato, N\n\nKortüm, F\n\nKumar, S\n\nRomano, MT\n\nDai, S\n\nMo, R\n\nSivalingam, S\n\nMotameny, S\n\nWu, Y\n\nWang, X\n\nNiu, X\n\nGeng, S\n\nBornholdt, D\n\nKroisel, PM\n\nTadini, G\n\nWalter, SD\n\nHauck, F\n\nGirisha, KM\n\nCalza, AM\n\nBottani, A\n\nAltmüller, J\n\nBuness, A\n\nYang, S\n\nSun, X\n\nMa, L\n\nKutsche, K\n\nGrzeschik, KH\n\nBetz, RC\n\nLin, Z\n\nBeiträge in Fachzeitschriften\nISI:000546685300004\n32497488.0\n10.1016/j.ajhg.2020.05.006\nPMC7332643\nIFAP syndrome is a rare genetic disorder characterized by ichthyosis follicularis, atrichia, and photophobia. Previous research found that mutations in MBTPS2, encoding site-2-protease (S2P), underlie X-linked IFAP syndrome. The present report describes the identification via whole-exome sequencing of three heterozygous mutations in SREBF1 in 11 unrelated, ethnically diverse individuals with autosomal-dominant IFAP syndrome. SREBF1 encodes sterol regulatory element-binding protein 1 (SREBP1), which promotes the transcription of lipogenes involved in the biosynthesis of fatty acids and cholesterols. This process requires cleavage of SREBP1 by site-1-protease (S1P) and S2P and subsequent translocation into the nucleus where it binds to sterol regulatory elements (SRE). The three detected SREBF1 mutations caused substitution or deletion of residues 527, 528, and 530, which are crucial for S1P cleavage. In vitro investigation of SREBP1 variants demonstrated impaired S1P cleavage, which prohibited nuclear translocation of the transcriptionally active form of SREBP1. As a result, SREBP1 variants exhibited significantly lower transcriptional activity compared to the wild-type, as demonstrated via luciferase reporter assay. RNA sequencing of the scalp skin from IFAP-affected individuals revealed a dramatic reduction in transcript levels of low-density lipoprotein receptor (LDLR) and of keratin genes known to be expressed in the outer root sheath of hair follicles. An increased rate of in situ keratinocyte apoptosis, which might contribute to skin hyperkeratosis and hypotrichosis, was also detected in scalp samples from affected individuals. Together with previous research, the present findings suggest that SREBP signaling plays an essential role in epidermal differentiation, skin barrier formation, hair growth, and eye function.\n                Copyright © 2020 American Society of Human Genetics. Published by Elsevier Inc. All rights reserved.\n\nKroisel, Peter\n\n\n"
        },
        {
            "text": "\n183443\n<i>Pseudomonas</i> Species Diversity Along the Danube River Assessed by <i>rpoD</i> Gene Sequence and MALDI-TOF MS Analyses of Cultivated Strains.\n\nMulet, M\n\nMontaner, M\n\nRomán, D\n\nGomila, M\n\nKittinger, C\n\nZarfel, G\n\nLalucat, J\n\nGarcía-Valdés, E\n\nBeiträge in Fachzeitschriften\nISI:000572242000001\n32983072.0\n10.3389/fmicb.2020.02114\nPMC7492575\nA collection of 611 Pseudomonas isolated from 14 sampling sites along the Danube River were identified previously by MALDI-TOF MS with the VITEK MS system and were grouped in 53 clusters by their main protein profiles. The strains were identified in the present study at the phylospecies level by rpoD gene sequencing. Partial sequences of the rpoD gene of 190 isolates representatives of all clusters were analyzed. Strains in the same MALDI-TOF cluster were grouped in the same phylospecies when they shared a minimum 95% similarity in their rpoD sequences. The sequenced strains were assigned to 34 known species (108 strains) and to 32 possible new species (82 strains). The 611 strains were identified at the phylospecies level combining both methods. Most strains were assigned to phylospecies in the Pseudomonas putida phylogenetic group of species. Special attention was given to 14 multidrug resistant strains that could not be assigned to any known Pseudomonas species and were considered environmental reservoir of antibiotic resistance genes. Coverage indices and rarefaction curves demonstrated that at least 50% of the Pseudomonas species in the Danube River able to grow in the isolation conditions have been identified at the species level. Main objectives were the confirmation of the correlation between the protein profile clusters detected by MALDI-TOF MS and the phylogeny of Pseudomonas strains based on the rpoD gene sequence, the assessment of the higher species discriminative power of the rpoD gene sequence, as well as the estimation of the high diversity of Pseudomonas ssp. along the Danube river. This study highlights the Pseudomonas species diversity in freshwater ecosystems and the usefulness of the combination of MALDI-TOF mass spectrometry for the dereplication of large sets of strains and the rpoD gene sequences for rapid and accurate identifications at the species level.\n                Copyright © 2020 Mulet, Montaner, Román, Gomila, Kittinger, Zarfel, Lalucat and García-Valdés.\n\nKittinger, Clemens\n\nZarfel, Gernot\n\n\n"
        },
        {
            "text": "\n183718\nGlucose management for exercise using continuous glucose monitoring (CGM) and intermittently scanned CGM (isCGM) systems in type 1 diabetes: position statement of the European Association for the Study of Diabetes (EASD) and of the International Society for Pediatric and Adolescent Diabetes (ISPAD) endorsed by JDRF and supported by the American Diabetes Association (ADA).\n\nMoser, O\n\nRiddell, MC\n\nEckstein, ML\n\nAdolfsson, P\n\nRabasa-Lhoret, R\n\nvan den Boom, L\n\nGillard, P\n\nNørgaard, K\n\nOliver, NS\n\nZaharieva, DP\n\nBattelino, T\n\nde Beaufort, C\n\nBergenstal, RM\n\nBuckingham, B\n\nCengiz, E\n\nDeeb, A\n\nHeise, T\n\nHeller, S\n\nKowalski, AJ\n\nLeelarathna, L\n\nMathieu, C\n\nStettler, C\n\nTauschmann, M\n\nThabit, H\n\nWilmot, EG\n\nSourij, H\n\nSmart, CE\n\nJacobs, PG\n\nBracken, RM\n\nMader, JK\n\nBeiträge in Fachzeitschriften\nISI:000577086900002\n33047169.0\n10.1007/s00125-020-05263-9\nNone\nPhysical exercise is an important component in the management of type 1 diabetes across the lifespan. Yet, acute exercise increases the risk of dysglycaemia, and the direction of glycaemic excursions depends, to some extent, on the intensity and duration of the type of exercise. Understandably, fear of hypoglycaemia is one of the strongest barriers to incorporating exercise into daily life. Risk of hypoglycaemia during and after exercise can be lowered when insulin-dose adjustments are made and/or additional carbohydrates are consumed. Glycaemic management during exercise has been made easier with continuous glucose monitoring (CGM) and intermittently scanned continuous glucose monitoring (isCGM) systems; however, because of the complexity of CGM and isCGM systems, both individuals with type 1 diabetes and their healthcare professionals may struggle with the interpretation of given information to maximise the technological potential for effective use around exercise (i.e. before, during and after). This position statement highlights the recent advancements in CGM and isCGM technology, with a focus on the evidence base for their efficacy to sense glucose around exercise and adaptations in the use of these emerging tools, and updates the guidance for exercise in adults, children and adolescents with type 1 diabetes. Graphical abstract.\n\nMader, Julia\n\nMoser, Othmar\n\nSourij, Harald\n\n\n"
        },
        {
            "text": "\n2671\nTime course of plasma soluble intercellular adhesion molecule-1 (sICAM-1) is related to severity of acute pancreatitis.\n\nKaufmann, P\n\nDemel, U\n\nTilz, GP\n\nKrejs, GJ\n\nBeiträge in Fachzeitschriften\nISI:000082596700091\n10522042.0\nNone\nNone\nBACKGROUND/AIMS: In severe acute pancreatitis the release of cytokines indicates a key step from local to systemic inflammation. Increased plasma concentrations of circulating soluble intercellular adhesion molecule-1 (sICAM-1), a marker of leukocyte activation, were detected in necrotizing pancreatitis at the time of diagnosis, however, the exact role of sICAM-1 in the development of complications such as shock or organ dysfunction is unclear. Therefore, we investigated in what manner the time course of plasma sICAM-1 is associated with the development of severe pancreatitis and whether these results are of any predictive value for the further course of the disease. METHODOLOGY: In a medical intensive care unit we studied 29 consecutive patients admitted for acute pancreatitis. Plasma levels of sICAM-1 were measured serially over a period of 6 days and the time courses were assigned either to a group of patients with uncomplicated, mild disease or to patients who developed complications including multiple organ failure. RESULTS: In mild pancreatitis, decreasing and peak sICAM-1 concentrations were found in 88% of the patients with a mean maximal level of 574 +/- 59ng/ml (SE) (upper limit of normal: 400ng/ml) on day 1. Partial pancreatic necrosis was present in 24% and no deaths were observed. In severe pancreatitis an increase of sICAM-1 levels or an initial fall followed by an increase (relapsing response) was the predominant pattern (92%). Maximal values of 1453 +/- 136ng/ml occurred on day 6, significantly different when compared to mild disease (p<0.0001). Necrotizing pancreatitis was diagnosed in 75% and the mortality rate was 58%. The sensitivity in predicting severe pancreatitis using sICAM-1 plasma levels with an increasing or relapsing pattern was much higher (92%) when compared with serial C-reactive protein measurements (42%). CONCLUSIONS: In acute pancreatitis, increasing or relapsing plasma levels of sICAM-1 over 6 days after admission to hospital are associated with a high rate of pancreatic necrosis and a high mortality. Daily measurements of sICAM-1 would allow early recognition of patients prone to develop complications and follow a severe course.\n\nDemel, Ulrike\n\nKrejs, Günter Josef\n\nTilz, Gernot\n\n\n"
        },
        {
            "text": "\n4672\nEosinophilic fungal rhinosinusitis: a common disorder in Europe?\n\nBraun, H\n\nBuzina, W\n\nFreudenschuss, K\n\nBeham, A\n\nStammberger, H\n\nBeiträge in Fachzeitschriften\nISI:000180929200013\n12567080.0\n10.1097%2F00005537-200302000-00013\nNone\nOBJECTIVES/HYPOTHESIS: The traditional criteria for the diagnosis of allergic fungal sinusitis include chronic rhinosinusitis, "allergic mucin" (mucus containing clusters of eosinophils), and detection of fungi by means of histological examination or culture. In 1999, a group of Mayo Clinic researchers, with a novel method of mucus collection and fungal culturing technique, were able to find fungi in 96% of patients with chronic rhinosinusitis. Immunoglobulin E-mediated hypersensitivity to fungal allergens was not evident in the majority of their patients. Because the presence of eosinophils in the allergic mucin, not a type I hypersensitivity, is probably the common denominator in the pathophysiology of allergic fungal sinusitis, the Mayo Clinic group proposed a change in terminology from allergic fungal sinusitis to eosinophilic fungal rhinosinusitis. Using new techniques of culturing fungi from nasal secretion, as well as preservation and histological examination of mucus, we investigated the incidence of "eosinophilic fungal rhinosinusitis" in our patient population. STUDY DESIGN METHODS: In an open prospective study nasal mucus from patients with chronic rhinosinusitis as well as from healthy volunteers was cultured for fungi. In patients, who underwent functional endoscopic sinus surgery, nasal mucus was investigated histologically to detect fungi and eosinophils within the mucus. RESULTS: Fungal cultures were positive in 84 of 92 patients with chronic rhinosinusitis (91.3%). In all, 290 positive cultures grew 33 different genera, with 3.2 species per patient, on average. Fungal cultures from a control group of healthy volunteers yielded positive results in 21 of 23 (91.3%). Histologically, fungal elements were found in 28 of 37 patients (75.5%) and eosinophilic mucin in 35 of 37 patients (94.6%). Neither fungi nor eosinophils were present in 2 of 37 patients (5.4%). CONCLUSIONS: Our data show that the postulated criteria of allergic fungal sinusitis are present in the majority of patients with chronic rhinosinusitis. Either those criteria will be found to be invalid and need to be changed or, indeed, "eosinophilic fungal rhinosinusitis" exists in the majority of patients with chronic rhinosinusitis. Based on our results, fungi and eosinophilic mucin appear to be a standard component of nasal mucus in patients with chronic rhinosinusitis.\n\nBraun, Hannes\n\nBuzina, Walter\n\n\n"
        },
        {
            "text": "\n6779\nDiscrepancies in current practice of pathological evaluation of sentinel lymph nodes in breast cancer. Results of a questionnaire based survey by the European Working Group for Breast Screening Pathology.\n\nCserni, G\n\nAmendoeira, I\n\nApostolikas, N\n\nBellocq, JP\n\nBianchi, S\n\nBoecker, W\n\nBorisch, B\n\nConnolly, CE\n\nDecker, T\n\nDervan, P\n\nDrijkoningen, M\n\nEllis, IO\n\nElston, CW\n\nEusebi, V\n\nFaverly, D\n\nHeikkila, P\n\nHolland, R\n\nKerner, H\n\nKulka, J\n\nJacquemier, J\n\nLacerda M, Martinez-Penuela J, De Miguel C, Peterse JL, Rank F, Regitnig P, Reiner A, Sapino A, Sigal-Zafrani B, Tanous AM, Thorstenson S, Zozaya E, Fejes G, Wells CA\n\nBeiträge in Fachzeitschriften\nISI:000222268000005\n15220360.0\n10.1136/jcp.2003.013599\nPMC1770358\nAIMS: To evaluate aspects of the current practice of sentinel lymph node (SLN) pathology in breast cancer via a questionnaire based survey, to recognise major issues that the European guidelines for mammography screening should address in the next revision. METHODS: A questionnaire was circulated by mail or electronically by the authors in their respective countries. Replies from pathology units dealing with SLN specimens were evaluated further. RESULTS: Of the 382 respondents, 240 European pathology units were dealing with SLN specimens. Sixty per cent of these units carried out intraoperative assessment, most commonly consisting of frozen sections. Most units slice larger SLNs into pieces and only 12% assess these slices on a single haematoxylin and eosin (HE) stained slide. Seventy one per cent of the units routinely use immunohistochemistry in all cases negative by HE. The terms micrometastasis, submicrometastasis, and isolated tumour cells (ITCs) are used in 93%, 22%, and 71% of units, respectively, but have a rather heterogeneous interpretation. Molecular SLN staging was reported by only 10 units (4%). Most institutions have their own guidelines for SLN processing, but some countries also have well recognised national guidelines. CONCLUSIONS: Pathological examination of SLNs throughout Europe varies considerably and is not standardised. The European guidelines should focus on standardising examination. They should recommend techniques that identify metastases > 2 mm as a minimum standard. Uniform reporting of additional findings may also be important, because micrometastases and ITCs may in the future be shown to have clinical relevance.\n\nRegitnig, Peter\n\n\n"
        },
        {
            "text": "\n61834\nFrom pneumonic infiltration to parapneumonic effusion--from effusion to pleural empyema: internal medicine aspects of parapneumonic effusion development and pleural empyema\n\nDomej, W\n\nWenisch, C\n\nDemel, U\n\nTilz, GP\n\nBeiträge in Fachzeitschriften\nNone\n13677257.0\nNone\nNone\nInfectious processes cause the majority part of all clinically relevant pleural effusions which frequently complicate the course of pneumonia. The assessment of an inflammatory effusion requires a careful history, physical examination, imaging techniques and clinical workup. The presence of polymorphonuclear leukocytes, high LDH-activity (> 200 U/L) and protein level (> 3 g/dL) in a pleural effusion indicates acute inflammation. An effusion is usually called empyema, when large numbers of neutrophils form thick, turbid exudates within preexisting body cavities. A thoracic empyema may occur as a result of primary or secondary pleural pathologies and in most cases involves infection with bacteria, frequently provided by progressing pneumonia. There are several therapeutic options for treatment of parapneumonic effusions and of thoracic empyemata, respectively. Optimal therapeutic management and antimicrobial medication to the infected pleural space depend in part on the stage of the empyema at presentation. Treatment can vary from a conservative medical approach in uncomplicated or small parapneumonic effusions to invasive surgical interventions in fibroprulent or organizational stages of empyema. Empyemata usually progress from a parapneumonic exudative stage (stage I), when the fluid is still sterile, with low leukocyte counts, low LDH, physiological pH, and normal glucose, to the fibropurulent [figures: see text] stage (stage II) with high leukocyte counts, high LDH activity, low pH, and low glucose, and finally to the organizational stage (stage III), in which fibroblasts convert fibrin strands into inelastic membranes. Pleural peels and pockets may compartmentalize the viscous empyematous fluid and can cause serious restrictive ventilatory impairment. Each patient must be individually evaluated to determine the nature of the exudate and the stage of the pleural space infection. Due to its high mortality rate (5%) a thoracic empyema requires prompt treatment. Diagnostic thoracentesis and withdrawal of liquid for the microbiological, cytological and biochemical analysis is urgently recommended in all cases to assess severity of the disease and the likelihood of a complicated or uncomplicated course, and to select the most appropriate treatment option.\n\nDemel, Ulrike\n\nDomej, Wolfgang\n\nTilz, Gernot\n\n\n"
        },
        {
            "text": "\n112370\nComparative analysis of immunohistochemistry, polymerase chain reaction and focus-floating microscopy for the detection of Treponema pallidum in mucocutaneous lesions of primary, secondary and tertiary syphilis.\n\nMuller, H\n\nEisendle, K\n\nBrauninger, W\n\nKutzner, H\n\nCerroni, L\n\nZelger, B\n\nBeiträge in Fachzeitschriften\nISI:000292111200010\n21410678.0\n10.1111/j.1365-2133.2011.10314.x\nNone\nBackground The incidence of syphilis is increasing in many parts of the world including a re-emergence in Western Europe and North America. Depending on the disease stage, direct detection of Treponema pallidum in mucocutaneous lesions of syphilis may be difficult and histopathological findings are not always straightforward. Thus, the correct histological diagnosis may be challenging. Objectives Comparatively to evaluate the evidence for infection with T. pallidum by immunohistochemistry (IHC), polymerase chain reaction (PCR) and focus-floating microscopy (FFM). Methods A series of 86 paraffin-embedded skin biopsy samples from patients with primary, secondary or tertiary syphilis was assessed for detection of T. pallidum by IHC and FFM; 45 specimens were also investigated by a T. pallidum-specific PCR analysis. Histopathological reaction patterns and number and distribution of treponemes were studied, and all data were re-evaluated by clinicopathological correlation. Results Using a polyclonal antibody directed against T. pallidum, we detected the presence of T. pallidum by IHC in 42/86 (49%) samples [6/9 (67%) primary, 34/62 (55%) secondary and 2/15 (13%) tertiary syphilis]. T. pallidum-specific DNA was detected in 31/45 (69%) specimens [4/4 (100%) primary, 26/34 (76%) secondary and 1/7 (14%) tertiary syphilis]. In comparison, FFM analysis resulted in an overall detection rate of 82/86 (95%) [9/9 (100%) primary, 60/62 (97%) secondary and 13/15 (87%) tertiary syphilis]. Significant differences were observed concerning amount and distribution of organisms (epitheliotropic vs. endotheliotropic) in correlation to the three disease stages and to histopathological reaction patterns. Conclusions FFM is a highly sensitive and specific method to detect T. pallidum in tissue from mucocutaneous syphilis lesions. Our results indicate that a combination of PCR and FFM, as the most sensitive approach, could provide an additional benefit for the histopathological diagnosis of (late) secondary and tertiary syphilis and may be helpful in cases where serological testing of T. pallidum antibodies has failed, but the clinical suspicion for syphilis remains.\n\nCerroni, Lorenzo\n\n\n"
        }
    ]
}