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Sonstige beteiligte Institutionen
Hautmann, Christopher ; Döpfner, Manfred ; Katzmann, Josepha ; Schürmann, Stephanie ; Wolff Metternich-Kaizman, Tanja ; Jaite, Charlotte ; Kappel, Viola ; Geissler, Julia ; Warnke, Andreas ; Jacob, Christian ; Hennighausen, Klaus ; Haack-Dees, Barbara ; Schneider-Momm, Katja ; Philipsen, Alexandra ; Matthies, Swantje ; Rösler, Michael ; Retz, Wolfgang ; Gontard, Alexander von ; Sobanski, Esther ; Alm, Barbara ; Hohmann, Sarah ; Häge, Alexander ; Poustka, Luise ; Colla, Michael ; Gentschow, Laura ; Freitag, Christine M. ; Becker, Katja ; Jans, Thomas
Background
The efficacy of parent-child training (PCT) regarding child symptoms may be reduced if the mother has attention-deficit/hyperactivity disorder (ADHD). The AIMAC study (ADHD in Mothers and Children) aimed to compensate for the deteriorating effect of parental psychopathology by treating the mother (Step 1) before the beginning of PCT (Step 2). This secondary analysis was particularly concerned with the additional effect of the Step 2 PCT on child symptoms after the Step 1 treatment.
Methods
The analysis included 143 mothers and children (aged 6–12 years) both diagnosed with ADHD. The study design was a two-stage, two-arm parallel group trial (Step 1 treatment group [TG]: intensive treatment of the mother including psychotherapy and pharmacotherapy; Step 1 control group [CG]: supportive counseling only for mother; Step 2 TG and CG: PCT). Single- and multi-group analyses with piecewise linear latent growth curve models were applied to test for the effects of group and phase. Child symptoms (e.g., ADHD symptoms, disruptive behavior) were rated by three informants (blinded clinician, mother, teacher).
Results
Children in the TG showed a stronger improvement of their disruptive behavior as rated by mothers than those in the CG during Step 1 (Step 1: TG vs. CG). In the CG, according to reports of the blinded clinician and the mother, the reduction of children’s disruptive behavior was stronger during Step 2 than during Step 1 (CG: Step 1 vs. Step 2). In the TG, improvement of child outcome did not differ across treatment steps (TG: Step 1 vs. Step 2).
Conclusions
Intensive treatment of the mother including pharmacotherapy and psychotherapy may have small positive effects on the child’s disruptive behavior. PCT may be a valid treatment option for children with ADHD regarding disruptive behavior, even if mothers are not intensively treated beforehand.
Trial registration
ISRCTN registry ISRCTN73911400. Registered 29 March 2007.
Kollikowski, Alexander M. ; Pham, Mirko ; März, Alexander G. ; Papp, Lena ; Nieswandt, Bernhard ; Stoll, Guido ; Schuhmann, Michael K.
Experimental evidence has emerged that local platelet activation contributes to inflammation and infarct formation in acute ischemic stroke (AIS) which awaits confirmation in human studies. We conducted a prospective observational study on 258 consecutive patients undergoing mechanical thrombectomy (MT) due to large-vessel-occlusion stroke of the anterior circulation (08/2018-05/2020). Intraprocedural microcatheter aspiration of 1 ml of local (occlusion condition) and systemic arterial blood samples (self-control) was performed according to a prespecified protocol. The samples were analyzed for differential leukocyte counts, platelet counts, and plasma levels of the platelet-derived neutrophil-activating chemokine C-X-C-motif ligand (CXCL) 4 (PF-4), the neutrophil attractant CXCL7 (NAP-2), and myeloperoxidase (MPO). The clinical-biological relevance of these variables was corroborated by specific associations with molecular-cellular, structural-radiological, hemodynamic, and clinical-functional parameters. Seventy consecutive patients fulfilling all predefined criteria entered analysis. Mean local CXCL4 (+ 39%: 571 vs 410 ng/ml, P = .0095) and CXCL7 (+ 9%: 693 vs 636 ng/ml, P = .013) concentrations were higher compared with self-controls. Local platelet counts were lower (- 10%: 347,582 vs 383,284/µl, P = .0052), whereas neutrophil counts were elevated (+ 10%: 6022 vs 5485/µl, P = 0.0027). Correlation analyses revealed associations between local platelet and neutrophil counts (r = 0.27, P = .034), and between CXCL7 and MPO (r = 0.24, P = .048). Local CXCL4 was associated with the angiographic degree of reperfusion following recanalization (r = - 0.2523, P = .0479). Functional outcome at discharge correlated with local MPO concentrations (r = 0.3832, P = .0014) and platelet counts (r = 0.288, P = .0181). This study provides human evidence of cerebral platelet activation and platelet-neutrophil interactions during AIS and points to the relevance of per-ischemic thrombo-inflammatory mechanisms to impaired reperfusion and worse functional outcome following recanalization.
Mencacci, Niccoló E. ; Isaias, Ioannis U. ; Reich, Martin M. ; Ganos, Christos ; Plagnol, Vincent ; Polke, James M. ; Bras, Jose ; Hersheson, Joshua ; Stamelou, Maria ; Pittman, Alan M. ; Noyce, Alastair J. ; Mok, Kin Y. ; Opladen, Thomas ; Kunstmann, Erdmute ; Hodecker, Sybille ; Münchau, Alexander ; Volkmann, Jens ; Samnick, Samuel ; Sidle, Katie ; Nanji, Tina ; Sweeney, Mary G. ; Houlden, Henry ; Batla, Amit ; Zecchinelli, Anna L. ; Pezzoli, Gianni ; Marotta, Giorgio ; Lees, Andrew ; Alegria, Paulo ; Krack, Paul ; Cormier-Dequaire, Florence ; Lesage, Suzanne ; Brice, Alexis ; Heutink, Peter ; Gasser, Thomas ; Lubbe, Steven J. ; Morris, Huw R. ; Taba, Pille ; Koks, Sulev ; Majounie, Elisa ; Gibbs, J. Raphael ; Singleton, Andrew ; Hardy, John ; Klebe, Stephan ; Bhatia, Kailash P. ; Wood, Nicholas W.
GTP cyclohydrolase 1, encoded by the GCH1 gene, is an essential enzyme for dopamine production in nigrostriatal cells. Loss-of-function mutations in GCH1 result in severe reduction of dopamine synthesis in nigrostriatal cells and are the most common cause of DOPA-responsive dystonia, a rare disease that classically presents in childhood with generalized dystonia and a dramatic long-lasting response to levodopa. We describe clinical, genetic and nigrostriatal dopaminergic imaging ([(123)I]N-ω-fluoropropyl-2β-carbomethoxy-3β-(4-iodophenyl) tropane single photon computed tomography) findings of four unrelated pedigrees with DOPA-responsive dystonia in which pathogenic GCH1 variants were identified in family members with adult-onset parkinsonism. Dopamine transporter imaging was abnormal in all parkinsonian patients, indicating Parkinson's disease-like nigrostriatal dopaminergic denervation. We subsequently explored the possibility that pathogenic GCH1 variants could contribute to the risk of developing Parkinson's disease, even in the absence of a family history for DOPA-responsive dystonia. The frequency of GCH1 variants was evaluated in whole-exome sequencing data of 1318 cases with Parkinson's disease and 5935 control subjects. Combining cases and controls, we identified a total of 11 different heterozygous GCH1 variants, all at low frequency. This list includes four pathogenic variants previously associated with DOPA-responsive dystonia (Q110X, V204I, K224R and M230I) and seven of undetermined clinical relevance (Q110E, T112A, A120S, D134G, I154V, R198Q and G217V). The frequency of GCH1 variants was significantly higher (Fisher's exact test P-value 0.0001) in cases (10/1318 = 0.75%) than in controls (6/5935 = 0.1%; odds ratio 7.5; 95% confidence interval 2.4-25.3). Our results show that rare GCH1 variants are associated with an increased risk for Parkinson's disease. These findings expand the clinical and biological relevance of GTP cycloydrolase 1 deficiency, suggesting that it not only leads to biochemical striatal dopamine depletion and DOPA-responsive dystonia, but also predisposes to nigrostriatal cell loss. Further insight into GCH1-associated pathogenetic mechanisms will shed light on the role of dopamine metabolism in nigral degeneration and Parkinson's disease.
Carsten A., Böger ; Gorski, Mathias ; Li, Man ; Hoffmann, Michael M. ; Huang, Chunmei ; Yang, Qiong ; Teumer, Alexander ; Krane, Vera ; O'Seaghdha, Conall M. ; Kutalik, Zoltán ; Wichmann, H.-Erich ; Haak, Thomas ; Boes, Eva ; Coassin, Stefan ; Coresh, Josef ; Kollerits, Barbara ; Haun, Margot ; Paulweber, Bernhard ; Köttgen, Anna ; Li, Guo ; Shlipak, Michael G. ; Powe, Neil ; Hwang, Shih-Jen ; Dehghan, Abbas ; Rivadeneira, Fernando ; Uitterlinden, André ; Hofman, Albert ; Beckmann, Jacques S. ; Krämer, Bernhard K. ; Witteman, Jacqueline ; Bochud, Murielle ; Siscovick, David ; Rettig, Rainer ; Kronenberg, Florian ; Wanner, Christoph ; Thadhani, Ravi I. ; Heid, Iris M. ; Fox, Caroline S. ; Kao, W.H.
Family studies suggest a genetic component to the etiology of chronic kidney disease (CKD) and end stage renal disease (ESRD). Previously, we identified 16 loci for eGFR in genome-wide association studies, but the associations of these single nucleotide polymorphisms (SNPs) for incident CKD or ESRD are unknown. We thus investigated the association of these loci with incident CKD in 26,308 individuals of European ancestry free of CKD at baseline drawn from eight population-based cohorts followed for a median of 7.2 years (including 2,122 incident CKD cases defined as eGFR < 60ml/min/1.73m(2) at follow-up) and with ESRD in four case-control studies in subjects of European ancestry (3,775 cases, 4,577 controls). SNPs at 11 of the 16 loci (UMOD, PRKAG2, ANXA9, DAB2, SHROOM3, DACH1, STC1, SLC34A1, ALMS1/NAT8, UBE2Q2, and GCKR) were associated with incident CKD; p-values ranged from p = 4.1e-9 in UMOD to p = 0.03 in GCKR. After adjusting for baseline eGFR, six of these loci remained significantly associated with incident CKD (UMOD, PRKAG2, ANXA9, DAB2, DACH1, and STC1). SNPs in UMOD (OR = 0.92, p = 0.04) and GCKR (OR = 0.93, p = 0.03) were nominally associated with ESRD. In summary, the majority of eGFR-related loci are either associated or show a strong trend towards association with incident CKD, but have modest associations with ESRD in individuals of European descent. Additional work is required to characterize the association of genetic determinants of CKD and ESRD at different stages of disease progression.
Leyh, Catherine ; Ehmer, Ursula ; Roessler, Daniel ; Philipp, Alexander B. ; Reiter, Florian P. ; Jeliazkova, Petia ; Jochheim, Leonie S. ; Jeschke, Matthias ; Hammig, Janina ; Ludwig, Johannes M. ; Theysohn, Jens M. ; Geier, Andreas ; Lange, Christian M.
The optimal treatment sequence of tyrosine kinase inhibitor (TKI)-based therapy in patients with hepatocellular carcinoma (HCC) remains unclear. Therefore, sequential systemic therapy after first-line therapy with sorafenib or lenvatinib was compared in a retrospective real-world cohort. In total, 164 patients with HCC were included. Child B cirrhosis was present in 26 patients (16.5%), whereas 132 patients (83.5%) had preserved liver function. In total, 72 patients (44%) discontinued systemic therapy after first-line therapy while 51 (31%) and 31 (19%) patients received 2 or more treatment lines. Most notably, median overall survival (mOS) was influenced by liver functional status and patient performance status at the beginning of first-line therapy. Patients receiving a sequential therapy regimen had significantly longer mOS compared to patients that discontinued systemic therapy after omitting first-line treatment. The choice of the initial TKI did not impact mOS. A clear deterioration of liver function could be observed during the course of TKI-based treatment.
Kleinschnitz, Christoph ; Grund, Henrike ; Wingler, Kirstin ; Armitage, Melanie E. ; Jones, Emma ; Mittal, Manish ; Barit, David ; Schwarz, Tobias ; Geis, Christian ; Kraft, Peter ; Barthel, Konstanze ; Schuhmann, Michael K. ; Herrmann, Alexander M. ; Meuth, Sven G. ; Stoll, Guido ; Meurer, Sabine ; Schrewe, Anja ; Becker, Lore ; Gailus-Durner, Valerie ; Fuchs, Helmut ; Klopstock, Thomas ; de Angelis, Martin Hrabe ; Jandeleit-Dahm, Karin ; Shah, Ajay M. ; Weissmann, Norbert ; Schmidt, Harald H. H. W.
Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90% of the patients. This medical need contrasts with a high failure rate of more than 1,000 pre-clinical drug candidates for stroke therapies. Thus, there is a need for translatable mechanisms of neuroprotection and more rigid thresholds of relevance in pre-clinical stroke models. One such candidate mechanism is oxidative stress. However, antioxidant approaches have failed in clinical trials, and the significant sources of oxidative stress in stroke are unknown. We here identify NADPH oxidase type 4 (NOX4) as a major source of oxidative stress and an effective therapeutic target in acute stroke. Upon ischemia, NOX4 was induced in human and mouse brain. Mice deficient in NOX4 (Nox42/2) of either sex, but not those deficient for NOX1 or NOX2, were largely protected from oxidative stress, blood-brain-barrier leakage, and neuronal apoptosis, after both transient and permanent cerebral ischemia. This effect was independent of age, as elderly mice were equally protected. Restoration of oxidative stress reversed the stroke-protective phenotype in Nox42/2 mice. Application of the only validated low-molecular-weight pharmacological NADPH oxidase inhibitor, VAS2870, several hours after ischemia was as protective as deleting NOX4. The extent of neuroprotection was exceptional, resulting in significantly improved long-term neurological functions and reduced mortality. NOX4 therefore represents a major source of oxidative stress and novel class of drug target for stroke therapy.
Fiedler, Mascha O. ; Muellenbach, Ralf M. ; Rolfes, Caroline ; Lotz, Christopher ; Nickel, Felix ; Müller-Stich, Beat P. ; Supady, Alexander ; Lepper, Philipp M. ; Weigand, Markus A. ; Meybohm, Patrick ; Kalenka, Armin ; Reyher, Christian
Background: Extracorporeal hemadsorption eliminates proinflammatory mediators in critically ill patients with hyperinflammation. The use of a pumpless extracorporeal hemadsorption technique allows its early usage prior to organ failure and the need for an additional medical device. In our animal model, we investigated the feasibility of pumpless extracorporeal hemadsorption over a wide range of mean arterial pressures (MAP). Methods: An arteriovenous shunt between the femoral artery and femoral vein was established in eight pigs. The hemadsorption devices were inserted into the shunt circulation; four pigs received CytoSorb\(^®\) and four Oxiris\(^®\) hemadsorbers. Extracorporeal blood flow was measured in a range between mean arterial pressures of 45–85 mmHg. Mean arterial pressures were preset using intravenous infusions of noradrenaline, urapidil, or increased sedatives. Results: Extracorporeal blood flows remained well above the minimum flows recommended by the manufacturers throughout all MAP steps for both devices. Linear regression resulted in CytoSorb\(^®\) blood flow [mL/min] = 4.226 × MAP [mmHg] − 3.496 (R-square 0.8133) and Oxiris\(^®\) blood flow [mL/min] = 3.267 × MAP [mmHg] + 57.63 (R-square 0.8708), respectively. Conclusion: Arteriovenous pumpless extracorporeal hemadsorption resulted in sufficient blood flows through both the CytoSorb\(^®\) and Oxiris\(^®\) devices over a wide range of mean arterial blood pressures and is likely an intriguing therapeutic option in the early phase of septic shock or hyperinflammatory syndromes.
Munz, Matthias ; Richter, Gesa M. ; Loos, Bruno G. ; Jepsen, Søren ; Divaris, Kimon ; Offenbacher, Steven ; Teumer, Alexander ; Holtfreter, Birte ; Kocher, Thomas ; Bruckmann, Corinna ; Jockel-Schneider, Yvonne ; Graetz, Christian ; Munoz, Loreto ; Bhandari, Anita ; Tennstedt, Stephanie ; Staufenbiel, Ingmar ; van der Velde, Nathalie ; Uitterlinden, André G. ; de Groot, Lisette C. P. G. M. ; Wellmann, Jürgen ; Berger, Klaus ; Krone, Bastian ; Hoffmann, Per ; Laudes, Matthias ; Lieb, Wolfgang ; Andre, Franke ; Dommisch, Henrik ; Erdmann, Jeanette ; Schaefer, Arne S.
Evidence for a shared genetic basis of association between coronary artery disease (CAD) and periodontitis (PD) exists. To explore the joint genetic basis, we performed a GWAS meta-analysis. In the discovery stage, we used a German aggressive periodontitis sample (AgP-Ger; 680 cases vs 3,973 controls) and the CARDIoGRAMplusC4D CAD meta-analysis dataset (60,801 cases vs 123,504 controls). Two SNPs at the known CAD risk loci ADAMTS7 (rs11634042) and VAMP8 (rs1561198) passed the pre-assigned selection criteria (PAgP-Ger < 0.05; PCAD < 5 × 10−8; concordant effect direction) and were replicated in an independent GWAS meta-analysis dataset of PD (4,415 cases vs 5,935 controls). SNP rs1561198 showed significant association (PD[Replication]: P = 0.008 OR = 1.09, 95% CI = [1.02–1.16]; PD [Discovery + Replication]: P = 0.0002, OR = 1.11, 95% CI = [1.05–1.17]). For the associated haplotype block, allele specific cis-effects on VAMP8 expression were reported. Our data adds to the shared genetic basis of CAD and PD and indicate that the observed association of the two disease conditions cannot be solely explained by shared environmental risk factors. We conclude that the molecular pathway shared by CAD and PD involves VAMP8 function, which has a role in membrane vesicular trafficking, and is manipulated by pathogens to corrupt host immune defense.
López, Cristina ; Kleinheinz, Kortine ; Aukema, Sietse M. ; Rohde, Marius ; Bernhart, Stephan H. ; Hübschmann, Daniel ; Wagener, Rabea ; Toprak, Umut H. ; Raimondi, Francesco ; Kreuz, Markus ; Waszak, Sebastian M. ; Huang, Zhiqin ; Sieverling, Lina ; Paramasivam, Nagarajan ; Seufert, Julian ; Sungalee, Stephanie ; Russell, Robert B. ; Bausinger, Julia ; Kretzmer, Helene ; Ammerpohl, Ole ; Bergmann, Anke K. ; Binder, Hans ; Borkhardt, Arndt ; Brors, Benedikt ; Claviez, Alexander ; Doose, Gero ; Feuerbach, Lars ; Haake, Andrea ; Hansmann, Martin-Leo ; Hoell, Jessica ; Hummel, Michael ; Korbel, Jan O. ; Lawerenz, Chris ; Lenze, Dido ; Radlwimmer, Bernhard ; Richter, Julia ; Rosenstiel, Philip ; Rosenwald, Andreas ; Schilhabel, Markus B. ; Stein, Harald ; Stilgenbauer, Stephan ; Stadler, Peter F. ; Szczepanowski, Monika ; Weniger, Marc A. ; Zapatka, Marc ; Eils, Roland ; Lichter, Peter ; Loeffler, Markus ; Möller, Peter ; Trümper, Lorenz ; Klapper, Wolfram ; Hoffmann, Steve ; Küppers, Ralf ; Burkhardt, Birgit ; Schlesner, Matthias ; Siebert, Reiner
Burkitt lymphoma (BL) is the most common B-cell lymphoma in children. Within the International Cancer Genome Consortium (ICGC), we performed whole genome and transcriptome sequencing of 39 sporadic BL. Here, we unravel interaction of structural, mutational, and transcriptional changes, which contribute to MYC oncogene dysregulation together with the pathognomonic IG-MYC translocation. Moreover, by mapping IGH translocation breakpoints, we provide evidence that the precursor of at least a subset of BL is a B-cell poised to express IGHA. We describe the landscape of mutations, structural variants, and mutational processes, and identified a series of driver genes in the pathogenesis of BL, which can be targeted by various mechanisms, including IG-non MYC translocations, germline and somatic mutations, fusion transcripts, and alternative splicing.
Functional and structural characterization of axonal opioid receptors as targets for analgesia
(2016)
Mambretti, Egle M. ; Kistner, Katrin ; Mayer, Stefanie ; Massotte, Dominique ; Kieffer, Brigitte L. ; Hoffmann, Carsten ; Reeh, Peter W. ; Brack, Alexander ; Asan, Esther ; Rittner, Heike L.
Background
Opioids are the gold standard for the treatment of acute pain despite serious side effects in the central and enteric nervous system. µ-opioid receptors (MOPs) are expressed and functional at the terminals of sensory axons, when activated by exogenous or endogenous ligands. However, the presence and function of MOP along nociceptive axons remains controversial particularly in naïve animals. Here, we characterized axonal MOPs by immunofluorescence, ultrastructural, and functional analyses. Furthermore, we evaluated hypertonic saline as a possible enhancer of opioid receptor function.
Results
Comparative immunolabeling showed that, among several tested antibodies, which all provided specific MOP detection in the rat central nervous system (CNS), only one monoclonal MOP-antibody yielded specificity and reproducibility for MOP detection in the rat peripheral nervous system including the sciatic nerve. Double immunolabeling documented that MOP immunoreactivity was confined to calcitonin gene-related peptide (CGRP) positive fibers and fiber bundles. Almost identical labeling and double labeling patterns were found using mcherry-immunolabeling on sciatic nerves of mice producing a MOP-mcherry fusion protein (MOP-mcherry knock-in mice). Preembedding immunogold electron microscopy on MOP-mcherry knock-in sciatic nerves indicated presence of MOP in cytoplasm and at membranes of unmyelinated axons. Application of [D-Ala\(^2\), N-MePhe\(^4\), Gly-ol]-enkephalin (DAMGO) or fentanyl dose-dependently inhibited depolarization-induced CGRP release from rat sciatic nerve axons ex vivo, which was blocked by naloxone. When the lipophilic opioid fentanyl was applied perisciatically in naïve Wistar rats, mechanical nociceptive thresholds increased. Subthreshold doses of fentanyl or the hydrophilic opioid DAMGO were only effective if injected together with hypertonic saline. In vitro, using β-arrestin-2/MOP double-transfected human embryonic kidney cells, DAMGO as well as fentanyl lead to a recruitment of β-arrestin-2 to the membrane followed by a β-arrestin-2 reappearance in the cytosol and MOP internalization. Pretreatment with hypertonic saline prevented MOP internalization.
Conclusion
MOPs are present and functional in the axonal membrane from naïve animals. Hypertonic saline acutely decreases ligand-induced internalization of MOP and thereby might improve MOP function. Further studies should explore potential clinical applications of opioids together with enhancers for regional analgesia.