PubMed Health⌕ Search

Biomedical subjects

U R Fölsch

Publications and source records attributed to U R Fölsch.

At least 19 recordsLinked to original sources
PubMed2005

[Pharmacologic therapy for inflammatory bowel diseases: hopes, disappointments].

Because the etiology of inflammatory bowel diseases is unclear, no causative therapy is available. However, pathophysiology of the disease offers a lot of possibilities to disrupt the inflammatory cascade that maintains the inflammatory process. The aim of every therapy is to maintain remission as long as possible and to amend the natural course of the disease. Pharmacotherapy includes 5-Aminosalicylates, glucocorticoids, immunosupressants (methotrexate, azathioprine) as well as specific pharmacologic interventions like monoclonal antibodies directed against TNF-alpha (Infliximab). Important supportive tools are available to improve symptoms like diarrhea and pain. Dietetic treatment and surgical procedures represent important alternatives or supplement pharmacotherapeutic interventions.

Anti-Inflammatory Agents↗
PubMed2005

Matrix metalloproteinase-9 in bronchiolitis obliterans syndrome after lung transplantation.

Bronchiolitis obliterans syndrome (BOS) is a severe complication after lung transplantation (LTX). In a retrospective cohort study 12 stable healthy recipients (non-BOS) and eight patients with BOS were enrolled after LTX and matrix metalloproteinases (MMP)-9, TIMP-1 and cell characteristics in bronchoalveolar lavage (BAL) samples (n = 145) were analysed. BALs from patients with BOS were further divided according to whether they were obtained before (pre-BOS) or after manifestation of BOS (BOS group). The MMP-9/TIMP-1 ratio was significantly increased in the BOS group compared with non-BOS or pre-BOS; furthermore, the ratio was negatively correlated with forced expiratory volume in one second. In zymography, the active form of MMP-9 was detected predominantly in the BOS group. In addition, zymography showed the banding pattern of neutrophil-derived MMP-9, indicating that polymorphonuclear neutrophils (PMNs) were the main source of MMP-9. According to that, MMP-9 was significantly correlated with the number of PMN. In immunocytochemistry, MMP-9 was also associated predominantly with PMN. This is the first study to evaluate the expression of matrix metalloproteinase-9 and tissue inhibitors of metalloproteinases-1 over time during manifestation of a fibroproliferative lung disease in patients. It demonstrates development of bronchiolitis obliterans syndrome after lung transplantation is associated with an imbalance of matrix metalloproteinases-9/tissue inhibitors of metalloproteinase-1 ratio.

Adult↗
PubMed2004

[Diagnosis of acute splenic infarction by echo-signal-enhanced ultrasound].

HISTORY AND CLINICAL FINDINGS: A 35-year-old patient with known mitral valve endocarditis presented with a stabbing pain in the left upper abdomen (patient 1). A 79-year-old patient with a history of chronic lymphocytic leukaemia (CLL) and aortic valve replacement presented with acute left upper quadrant, chest pain and impaired vision (patient 2). INVESTIGATIONS: An abdominal ultrasound revealed nonhomogeneous hypoechoic splenic lesions in both patients, which were classified as extended splenic infarctions by echo enhancer studies. The diagnosis was confirmed by computed tomography. Transesophageal echocardiography showed extensive mitral valve vegetations in patient 1. Patient 2 had a progression of the CLL without evidence of endocarditis. Magnetic resonance imaging of the brain showed infarction of the posterior cerebral artery area. DIAGNOSIS, TREATMENT AND COURSE: Patient 1: Mitral valve endocarditis with embolic splenic infarction. Patient 2: Progressive CLL with thrombotic splenic and brain infarction. In patient 1, mitral valve replacement was performed. In patient 2, chemotherapy was initiated and she was started on low molecular weight heparin s. c. and aspirin. No further embolic or thrombotic complications occurred. No splenectomy was performed. CONCLUSION: A splenic infarction is a complication pointing towards an underlying serious disorder. Echo-enhanced ultrasound is as sensitive as computed tomography for early diagnosis. Splenic infarction should trigger urgent treatment of the underlying condition.

Acute Disease↗
PubMed2004

[Chronic inflammatory bowel diseases competence network ].

Inflammatory bowel diseases (IBD) are intermittently appearing, often chronic diseases mostly affecting young people between 20-30 years of age influencing their quality of life and socioeconomic efficiency. The triggering factors for the development of IBD are not completely understood: besides environmental factors there is clear evidence for additional genetic factors influencing the risk of disease and the pattern of gut inflammation in Crohn's disease. Pathopysiological discoveries are leading to new therapeutic opportunities which are conducted in large clinical studies with main participation of the competence network IBD. The disseminated structure of the network comprising universitary and nonuniversitary hospitals and labs, the self-help-organization DCCV and its vertical cooperation with general practitioners nationwide gives opportunity to describe the diseases from the point of view of the scientist and the physician simultaneously. Therefore the competence network IBD yields the basis for the standardized integration of patient information, for the development of guidelines and the establishment of a quality management system thus leading to an improvement of scientific and clinical research.

Biomedical Research↗
PubMed2004

The expression of immediate early gene X-1 (IEX-1) is differentially induced by retinoic acids in NB4 and KG1 cells: possible implication in the distinct phenotype of retinoic acid-responsive and -resistant leukemic cells.

In a cell-type- and stimulus-dependent fashion, the early response gene immediate early gene X-1 (IEX-1) is involved in growth control and modulation of apoptosis. The present study demonstrates that, in the two acute promyelocytic leukemia (APL) cell lines NB4 and KG1, exhibiting distinct responsiveness to retinoic acids (RAs), IEX-1 expression is rapidly (30-60 min) induced by all-trans- or cis-RA and independently of other signal transduction mediators, such as TNFalpha, NF-kappaB or MAP kinases. In NB4 cells (expressing PML-RARalpha), this increase is transient and completely reversible, along with a cell cycle arrest, ongoing differentiation and lower sensitivity to anti-cancer-drug-induced apoptosis. In contrast, the RA-induced IEX-1 expression in KG1 cells (expressing PLZF-RARalpha) persists over days, along with continued cell cycle progression and increased apoptotic sensitivity. Furthermore, two functional RA-response elements in the IEX-1 promoter were identified by gel shift and luciferase reporter gene assays. IEX-1 might be a rather unique transcriptional target of the two X-RARalpha fusion receptors exhibiting distinct responsiveness to RAs. Following a different time course of direct transcriptional induction by PML-RARalpha and PLZF-RARalpha in NB4 and KG1 cells, respectively, IEX-1 expression may be involved in the modified actions of these receptors and the distinct phenotypes of APL cells.

Antineoplastic Agents↗
PubMed2004

Expression of leptin and leptin receptor during the development of liver fibrosis and cirrhosis.

Leptin is involved in the regulation of food intake and is mainly secreted by adipocytes. Major secretagogues are cytokines such as TNF-alpha or IL-1. Leptin in turn upregulates inflammatory immune responses. Elevated leptin serum levels have been detected in patients with liver cirrhosis, a disease frequently associated with elevated levels of circulating cytokines as well as hypermetabolism and altered body weight. Recently, leptin has been detected in activated hepatic stellate cells in vitro and an involvement of leptin in liver fibrogenisis has been suggested. The current study was designed to further clarify the role of leptin in liver disease by characterizing leptin and leptin receptor expression in the development and onset of experimental liver fibrosis. Liver fibrosis and cirrhosis was induced in rats by use of phenobarbitone and increasing doses of CCl (4). Leptin and leptin receptor mRNA expression was determined by semiquantitative RT-PCR, protein expression by Western blot analysis and localization of leptin and its receptor by immunohistochemistry. Normal liver tissue does not express leptin, but leptin receptor mRNA. Increasing levels of leptin mRNA were detected in fibrotic and cirrhotic livers correlated to the degree of fibrosis. Leptin receptor mRNA expression was not significantly altered in damaged livers. Increasing levels of leptin were detected in fibrotic and cirrhotic livers, whereas protein expression of the receptor remained unchanged. Throughout different stages of liver fibrosis, leptin immunoreactivity was localized in activated hepatic stellate cells only, whereas immunoreactivity for the receptor was mainly seen on hepatocytes. In conclusion, leptin is expressed at increasing levels in activated hepatic stellate cells in vivo, which may therefore be a source of increased leptin tissue and serum levels contributing to the pathophysiology and morphological changes of chronic liver disease.

Animals↗
PubMed2004

Reduction in diversity of the colonic mucosa associated bacterial microflora in patients with active inflammatory bowel disease.

BACKGROUND AND AIMS: The intestinal bacterial microflora plays an important role in the aetiology of inflammatory bowel disease (IBD). As most of the colonic bacteria cannot be identified by culture techniques, genomic technology can be used for analysis of the composition of the microflora. PATIENTS AND METHODS: The mucosa associated colonic microflora of 57 patients with active inflammatory bowel disease and 46 controls was investigated using 16S rDNA based single strand conformation polymorphism (SSCP) fingerprint, cloning experiments, and real time polymerase chain reaction (PCR). RESULTS: Full length sequencing of 1019 clones from 16S rDNA libraries (n = 3) revealed an overall bacterial diversity of 83 non-redundant sequences-among them, only 49 known bacterial species. Molecular epidemiology of the composition of the colonic microflora was investigated by SSCP. Diversity of the microflora in Crohn's disease was reduced to 50% compared with controls (21.7 v 50.4; p<0.0001) and to 30% in ulcerative colitis (17.2 v 50.4; p<0.0001). The reduction in diversity in inflammatory bowel disease was due to loss of normal anaerobic bacteria such as Bacteroides species, Eubacterium species, and Lactobacillus species, as revealed by direct sequencing of variable bands and confirmed by real time PCR. Bacterial diversity in the Crohn's group showed no association with CARD15/NOD2 status. CONCLUSIONS: Mucosal inflammation in inflammatory bowel disease is associated with loss of normal anaerobic bacteria. This effect is independent of NOD2/CARD15 status of patients.

Adolescent↗