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Search Results: 1 - 10 of 219502 matches for " Loddenkemper C "
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Ein kombinierter Operationsansatz zur Therapie der rektovaginalen Endometriose auf der Basis histologischer Befunde
K?hler C,Mangler M,Loddenkemper C,Lanowska M
Journal für Gyn?kologische Endokrinologie , 2008,
Abstract: Einleitung: Eine Endometriose des Septum rectovaginale kann oberfl chlich dem Darm aufliegen oder die Darmwand infiltrieren. Durch bildgebende Verfahren kann jedoch pr operativ eine Infiltration des Darms weder hinreichend best tigt noch ausgeschlossen werden, was zu einem therapeutischen Dilemma führt, da nur die Darmwand eindeutig infiltrierende Endometrioseprozesse durch eine Darmresektion behandelt werden sollten. Wir m chten ein neues Operationsverfahren vorstellen, das eine intraoperative Differenzierung zwischen einer oberfl chlichen und einer infiltrativen Darmendometriose erlaubt. Patienten und Methodik: 70 Patientinnen mit rektovaginaler Endometriose wurden nach einem neu entwickelten kombinierten vaginal-laparoskopisch-abdominalen Verfahren operiert. Diese Operationsmethode wird Schritt für Schritt vorgestellt. Die Entscheidung zur Darmresektion wurde dabei allein aufgrund der intraoperativen Befunde und nicht aufgrund der pr operativen bildgebenden Diagnostik getroffen. Alle Resektate wurden standardisiert histologisch aufgearbeitet. Ergebnisse: Ob eine Darmresektion notwendig war, lie sich intraoperativ anhand der Pr paration des rektovaginalen Septums entscheiden. Daher wurden nur bei Patientinnen mit gesichertem infiltrativem Darmbefall Darmresektionen unter Erhalt des Mesointestinums durchgeführt. Weder intraoperative noch postoperative Komplikationen wie Anastomoseninsuffizienzen oder Restharnmengen traten auf. Diskussion: Die vorgestellte Operationsmethode zur Therapie der rektovaginalen Endometriose erlaubt eine exakte Diagnosestellung und pr zise Therapieentscheidung bei minimaler Morbidit t. Die Resektion des Darmschlauches ohne Mesoresektion ist ausreichend, da sich die Endometrioseknoten wie histologisch bewiesen wurde nur im ventralen Darmbereich befinden. Durch die Mesoerhaltung werden die vegetativen Funktionen des kleinen Beckens nicht beeintr chtigt.
In situ analysis of FOXP3+ regulatory T cells in human colorectal cancer
Christoph Loddenkemper, Martin Schernus, Michel Noutsias, Harald Stein, Eckhard Thiel, Dirk Nagorsen
Journal of Translational Medicine , 2006, DOI: 10.1186/1479-5876-4-52
Abstract: In the last years, immunotherapy of malignant diseases and the understanding of underlying mechanisms have made rapid progress despite limited clinical response [1]. T cells directed against tumor antigens are believed to play a crucial role in mediating anti-tumor effects. Even without prior immunotherapy, spontaneous T cell responses against tumor antigens have been described in a variety of malignant diseases [2]. Colorectal cancer (CRC) has been intensely studied for interactions with the immune system. Although the colon is considered a rather tolerogenic organ, spontaneous T cell responses against several tumor-associated antigens (TAA) have been detected in the peripheral blood of CRC patients, particularly in metastatic disease [3,4]. However, patients with peripheral TAA-directed T cell response showed no benefit in a first survival analysis with a limited number of CRC patients [5]. Interestingly, active specific immunotherapy of metastatic CRC only causes a clinical response in less than 1% of patients despite the successful induction of immunological responses [6]. Multiple factors like the immune system, tumor stroma, and tumor cells influence the induction and modulation of tumor-directed immune responses [7]. Limited anti-tumor activity of antigen-specific T cells at a clinical level may be limited in CRC patients for various reasons. One major reason for the clinical failure of tumor-directed immune responses might be the immunosuppressive effect of tumor-infiltrating regulatory T cells.The immune system is potentially able to develop immune responses against self antigens and tumor-associated antigens. Regulatory T cells (Tregs) play a crucial role in regulating the balance between the attack and tolerance of such antigens. Regulatory CD4+ CD25+ FOXP3+ T cells are a subset of T cells mediating immunological tolerance by suppressing the activation of autoreactive T cells. Tregs not only inhibit the development of autoimmune-mediated diseases such as
Tumor-infiltrating macrophages and dendritic cells in human colorectal cancer: relation to local regulatory T cells, systemic T-cell response against tumor-associated antigens and survival
Dirk Nagorsen, Sabine Voigt, Erika Berg, Harald Stein, Eckhard Thiel, Christoph Loddenkemper
Journal of Translational Medicine , 2007, DOI: 10.1186/1479-5876-5-62
Abstract: Immunohistological staining was performed with nine markers for macrophages and DC (CD68, CD163, S100, CD11c, CD208, CD209, CD123, CD1a, Langerin) in 40 colorectal cancer samples from patients, in whom the state of systemic T-cell responses against tumor-associated antigens (TAA) and Treg infiltration had previously been determined.All specimens contained cells positive for CD68, CD163, S100 and CD1a in epithelial tumor tissue and tumor stroma. Only a very few (less than median 3/HPF) CD123+, CD1a+, CD11c+, CD 208+, CD209+, or Langerin+ cells were detected in the specimens. Overall, we found a trend towards increased infiltration by S100-positive DC and a significantly increased number of stromal S100-positive DC in patients without T-cell response. There was an increase of stromal S100 DC and CD163 macrophages in limited disease (S100: 11.1/HPF vs. 7.3/HPF, p = 0.046; CD163: 11.0/HPF vs. 8.1/HPF, p = 0.06). We found a significant, positive correlation between S100-positive DC and FOXP3-positive Tregs. Survival in patients with high DC infiltration was significantly better than that in those with low DC infiltration (p < 0.05). Furthermore, we found a trend towards better survival for increased infiltration with CD163-positive macrophages (p = 0.07).The present in situ study adds new data to the discussion on the interaction between the innate and adoptive immune system. Our data strongly support the hypothesis that tumor-infiltrating DC are a key factor at the interface between innate and adaptive immune response in malignant disease. Tumor infiltrating S100-positive DC show an inverse relationship with the systemic antigen-specific T-cell response, a positive correlation with regulatory T cells, and a positive association with survival in CRC. These data put tumor-infiltrating DC at the center of the relevant immune response in CRC.Colorectal cancer (CRC) is a common malignant disease, which has been intensely studied for tumor-immune interactions to develop succe
Risk Factors Associated with Death in In-Hospital Pediatric Convulsive Status Epilepticus
Tobias Loddenkemper, Tanvir U. Syed, Sriram Ramgopal, Deepak Gulati, Sikawat Thanaviratananich, Sanjeev V. Kothare, Amer Alshekhlee, Mohamad Z. Koubeissi
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0047474
Abstract: Objective To evaluate in-patient mortality and predictors of death associated with convulsive status epilepticus (SE) in a large, multi-center, pediatric cohort. Patients and Methods We identified our cohort from the KID Inpatient Database for the years 1997, 2000, 2003 and 2006. We queried the database for convulsive SE, associated diagnoses, and for inpatient death. Univariate logistic testing was used to screen for potential risk factors. These risk factors were then entered into a stepwise backwards conditional multivariable logistic regression procedure. P-values less than 0.05 were taken as significant. Results We identified 12,365 (5,541 female) patients with convulsive SE aged 0–20 years (mean age 6.2 years, standard deviation 5.5 years, median 5 years) among 14,965,571 pediatric inpatients (0.08%). Of these, 117 died while in the hospital (0.9%). The most frequent additional admission ICD-9 code diagnoses in addition to SE were cerebral palsy, pneumonia, and respiratory failure. Independent risk factors for death in patients with SE, assessed by multivariate calculation, included near drowning (Odds ratio [OR] 43.2; Confidence Interval [CI] 4.4–426.8), hemorrhagic shock (OR 17.83; CI 6.5–49.1), sepsis (OR 10.14; CI 4.0–25.6), massive aspiration (OR 9.1; CI 1.8–47), mechanical ventilation >96 hours (OR9; 5.6–14.6), transfusion (OR 8.25; CI 4.3–15.8), structural brain lesion (OR7.0; CI 3.1–16), hypoglycemia (OR5.8; CI 1.75–19.2), sepsis with liver failure (OR 14.4; CI 5–41.9), and admission in December (OR3.4; CI 1.6–4.1). African American ethnicity (OR 0.4; CI 0.2–0.8) was associated with a decreased risk of death in SE. Conclusion Pediatric convulsive SE occurs in up to 0.08% of pediatric inpatient admissions with a mortality of up to 1%. There appear to be several risk factors that can predict mortality. These may warrant additional monitoring and aggressive management.
Analysis of IL-17+ cells in facet joints of patients with spondyloarthritis suggests that the innate immune pathway might be of greater relevance than the Th17-mediated adaptive immune response
Heiner Appel, René Maier, Peihua Wu, Rebecca Scheer, Axel Hempfing, Ralph Kayser, Andreas Thiel, Andreas Radbruch, Christoph Loddenkemper, Joachim Sieper
Arthritis Research & Therapy , 2011, DOI: 10.1186/ar3370
Abstract: Immunohistochemical analysis of IL-17+ cells was performed in facet joints of 33 ankylosing spondylitis (AS) patients and compared with data from 20 osteoarthritis (OA) patients. The frequency of IL-17+CD4+ T cells in PB and SF of SpA patients (PB n = 30, SF n = 11), rheumatoid arthritis (RA) patients (PB n = 14, SF n = 7), OA patients (PB n = 10) and healthy controls (PB n = 12) was analysed after stimulation with Staphylococcus aureus Enterotoxin B and phorbol 12-myristate 13-acetate/ionomycin and quantified by flow cytometry.In AS facet joints, the frequency of IL-17-secreting cells was significantly higher than in samples obtained from OA patients (P < 0.001), with a slight predominance of IL-17+ cells among the mononuclear cells (61.5% ± 14.9%) compared to cells with polysegmental nuclei. Immunofluorescence microscopy revealed that the majority of IL-17+ cells were myeloperoxidase-positive (35.84 ± 13.06/high-power field (HPF) and CD15+ neutrophils (24.25 ± 10.36/HPF), while CD3+ T cells (0.51 ± 0.49/HPF) and AA-1+ mast cells (2.28 ± 1.96/HPF) were less often IL-17-positive. The frequency of IL-17+CD4+ T cells in the PB and SF of SpA patients did not differ significantly compared to RA patients, OA patients or healthy controls.Our data suggest an important role for IL-17 in the inflammatory processes in AS. However, the innate immune pathway might be of greater relevance than the Th17-mediated adaptive immune response.Spondyloarthritis (SpA) comprises ankylosing spondylitis (AS), reactive arthritis, arthritis/spondylitis with inflammatory bowel disease and arthritis/spondylitis with psoriasis. Inflammatory back pain, a similar pattern of peripheral joint involvement with an asymmetrical arthritis predominantly of the lower limbs and the possible occurrence of sacroiliitis, spondylitis, enthesitis and uveitis are typical clinical features in this group of diseases [1]. SpA can be split into two categories, SpA with predominant axial involvement and SpA with pred
Continuous Spikes and Waves during Sleep: Electroclinical Presentation and Suggestions for Management
Iván Sánchez Fernández,Kevin E. Chapman,Jurriaan M. Peters,Chellamani Harini,Alexander Rotenberg,Tobias Loddenkemper
Epilepsy Research and Treatment , 2013, DOI: 10.1155/2013/583531
Abstract: Continuous spikes and waves during sleep (CSWS) is an epileptic encephalopathy characterized in most patients by (1) difficult to control seizures, (2) interictal epileptiform activity that becomes prominent during sleep leading to an electroencephalogram (EEG) pattern of electrical status epilepticus in sleep (ESES), and (3) neurocognitive regression. In this paper, we will summarize current epidemiological, clinical, and EEG knowledge on CSWS and will provide suggestions for treatment. CSWS typically presents with seizures around 2–4 years of age. Neurocognitive regression occurs around 5-6 years of age, and it is accompanied by subacute worsening of EEG abnormalities and seizures. At approximately 6–9 years of age, there is a gradual resolution of seizures and EEG abnormalities, but the neurocognitive deficits persist in most patients. The cause of CSWS is unknown, but early developmental lesions play a major role in approximately half of the patients, and genetic associations have recently been described. High-dose benzodiazepines and corticosteroids have been successfully used to treat clinical and electroencephalographic features. Corticosteroids are often reserved for refractory disease because of adverse events. Valproate, ethosuximide, levetiracetam, sulthiame, and lamotrigine have been also used with some success. Epilepsy surgery may be considered in a few selected patients. 1. Introduction Continuous spikes and waves during sleep (CSWS) is an epileptic encephalopathy, that is, a condition in which the epileptic processes themselves are thought to contribute to the disturbance in cerebral function. CSWS is characterized by (1) seizures, (2) neurocognitive regression, and (3) an electroencephalography (EEG) pattern of electrical status epilepticus during sleep (ESES) [1–6]. ESES is characterized by marked sleep potentiation of epileptiform activity in the transition from wakefulness to sleep that leads to near-continuous bilateral (or occasionally lateralized) slow spikes and waves that occupy a significant proportion of nonrapid eye movement (non-REM) sleep [2, 4]. In this review, we summarize epidemiological, etiological, clinical, and EEG features in CSWS based on available data. We also suggest an approach to manage this syndrome and present it in the framework of a more general childhood seizure susceptibility syndrome. 2. Definitions The terms “ESES,” “CSWS,” and “Landau-Kleffner syndrome” have been used interchangeably in the literature to refer to the EEG pattern of frequent spike-waves or to the associated epileptic encephalopathy
Helicobacter pylori Induced Gastric Immunopathology Is Associated with Distinct Microbiota Changes in the Large Intestines of Long-Term Infected Mongolian Gerbils
Markus M. Heimesaat, André Fischer, Rita Plickert, Tobias Wiedemann, Christoph Loddenkemper, Ulf B. G?bel, Stefan Bereswill, Gabriele Rieder
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0100362
Abstract: Background Gastrointestinal (GI) inflammation in mice and men are frequently accompanied by distinct changes of the GI microbiota composition at sites of inflammation. Helicobacter (H.) pylori infection results in gastric immunopathology accompanied by colonization of stomachs with bacterial species, which are usually restricted to the lower intestine. Potential microbiota shifts distal to the inflammatory process following long-term H. pylori infection, however, have not been studied so far. Methodology/Principal Findings For the first time, we investigated microbiota changes along the entire GI tract of Mongolian gerbils after 14 months of infection with H. pylori B8 wildtype (WT) or its isogenic ΔcagY mutant (MUT) strain which is defective in the type IV secretion system and thus unable to modulate specific host pathways. Comprehensive cultural analyses revealed that severe gastric diseases such as atrophic pangastritis and precancerous transformations were accompanied by elevated luminal loads of E. coli and enterococci in the caecum and together with Bacteroides/Prevotella spp. in the colon of H. pylori WT, but not MUT infected gerbils as compared to na?ve animals. Strikingly, molecular analyses revealed that Akkermansia, an uncultivable species involved in mucus degradation, was exclusively abundant in large intestines of H. pylori WT, but not MUT infected nor na?ve gerbils. Conclusion/Significance Taken together, long-term infection of Mongolian gerbils with a H. pylori WT strain displaying an intact type IV secretion system leads to distinct shifts of the microbiota composition in the distal uninflamed, but not proximal inflamed GI tract. Hence, H. pylori induced immunopathogenesis of the stomach, including hypochlorhydria and hypergastrinemia, might trigger large intestinal microbiota changes whereas the exact underlying mechanisms need to be further unraveled.
Comprehensive Postmortem Analyses of Intestinal Microbiota Changes and Bacterial Translocation in Human Flora Associated Mice
Markus M. Heimesaat, Silvia Boelke, André Fischer, Lea-Maxie Haag, Christoph Loddenkemper, Anja A. Kühl, Ulf B. G?bel, Stefan Bereswill
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0040758
Abstract: Background Postmortem microbiological examinations are performed in forensic and medical pathology for defining uncertain causes of deaths and for screening of deceased tissue donors. Interpretation of bacteriological data, however, is hampered by false-positive results due to agonal spread of microorganisms, postmortem bacterial translocation, and environmental contamination. Methodology/Principal Findings We performed a kinetic survey of naturally occurring postmortem gut flora changes in the small and large intestines of conventional and gnotobiotic mice associated with a human microbiota (hfa) applying cultural and molecular methods. Sacrificed mice were kept under ambient conditions for up to 72 hours postmortem. Intestinal microbiota changes were most pronounced in the ileal lumen where enterobacteria and enterococci increased by 3–5 orders of magnitude in conventional and hfa mice. Interestingly, comparable intestinal overgrowth was shown in acute and chronic intestinal inflammation in mice and men. In hfa mice, ileal overgrowth with enterococci and enterobacteria started 3 and 24 hours postmortem, respectively. Strikingly, intestinal bacteria translocated to extra-intestinal compartments such as mesenteric lymphnodes, spleen, liver, kidney, and cardiac blood as early as 5 min after death. Furthermore, intestinal tissue destruction was characterized by increased numbers of apoptotic cells and neutrophils within 3 hours postmortem, whereas counts of proliferative cells as well as T- and B-lymphocytes and regulatory T-cells decreased between 3 and 12 hours postmortem. Conclusions/Significance We conclude that kinetics of ileal overgrowth with enterobacteria and enterococci in hfa mice can be used as an indicator for compromized intestinal functionality and for more precisely defining the time point of death under defined ambient conditions. The rapid translocation of intestinal bacteria starting within a few minutes after death will help to distinguish between relevant bacteria and secondary contaminants thus providing important informations for routine applications and future studies in applied microbiology, forensic pathology, and criminal medicine.
Anti-Inflammatory Effects of Resveratrol, Curcumin and Simvastatin in Acute Small Intestinal Inflammation
Stefan Bereswill,Melba Mu?oz,André Fischer,Rita Plickert,Lea-Maxie Haag,Bettina Otto,Anja A. Kühl,Christoph Loddenkemper,Ulf B. G?bel,Markus M. Heimesaat
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0015099
Abstract: The health beneficial effects of Resveratrol, Curcumin and Simvastatin have been demonstrated in various experimental models of inflammation. We investigated the potential anti-inflammatory and immunomodulatory mechanisms of the above mentioned compounds in a murine model of hyper-acute Th1-type ileitis following peroral infection with Toxoplasma gondii.
Characterization of Chromosomal Instability in Murine Colitis-Associated Colorectal Cancer
Marco Gerling,Rainer Glauben,Jens K. Habermann,Anja A. Kühl,Christoph Loddenkemper,Hans-Anton Lehr,Martin Zeitz,Britta Siegmund
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0022114
Abstract: Patients suffering from ulcerative colitis (UC) bear an increased risk for colorectal cancer. Due to the sparsity of colitis-associated cancer (CAC) and the long duration between UC initiation and overt carcinoma, elucidating mechanisms of inflammation-associated carcinogenesis in the gut is particularly challenging. Adequate murine models are thus highly desirable. For human CACs a high frequency of chromosomal instability (CIN) reflected by aneuploidy could be shown, exceeding that of sporadic carcinomas. The aim of this study was to analyze mouse models of CAC with regard to CIN. Additionally, protein expression of p53, beta-catenin and Ki67 was measured to further characterize murine tumor development in comparison to UC-associated carcinogenesis in men.
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