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Biomedical subjects

U R Fölsch

Publications and source records attributed to U R Fölsch.

At least 37 records · Page 2Linked to original sources
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↗
PubMed2002

Unusual course of colonic tattooing with India ink.

We here report the successful but unusual course of colonic tattooing in a patient with a carcinoma in situ in a polyp. A 70-year-old woman was admitted for persistent diarrhea, occult fecal blood, and anemia. During colonoscopy, a pedunculated large polyp in the sigmoid colon occluding the lumen was removed successfully. Histopathological examination revealed a carcinoma in situ with a resection of the peduncle in sano. At the second sigmoidoscopy, the polypectomy site was marked with India ink to facilitate the recovery of the polypectomy site in follow-up endoscopies. Three months later, the India ink had spread in the submucosal layer and a segment measuring 15 cm was colored dark blue. At the original polypectomy site, an uncolored flat mucosal proliferation was found above the dark colonic wall. After mucosectomy, the tissue was classified as hyperplastic. Six weeks later, a second control sigmoidoscopy did not show any suspicious mucosal alterations.

Adenoma, Villous↗
PubMed2002

Functional anatomy of the papilla Vateri: biomechanical aspects and impact of difficult endoscopic intubation.

BACKGROUND: Problems with intubation of the ampulla Vateri during diagnostic and therapeutic endoscopic maneuvers are a well-known feature. The ampulla Vateri was analyzed three-dimensionally to determine whether these difficulties have a structural background. METHODS: Thirty-five human greater duodenal papillae were examined by light and scanning electron microscopy as well as immunohistochemically. RESULTS: Histologically, highly vascularized finger-like mucosal folds project far into the lumen of the ampulla Vateri. The excretory ducts of seromucous glands containing many lysozyme-secreting Paneth cells open close to the base of the mucosal folds. Scanning electron microscopy revealed large mucosal folds inside the ampulla that continued into the pancreatic and bile duct, comparable to valves arranged in a row. CONCLUSIONS: Mucosal folds form pocket-like valves in the lumen of the ampulla Vateri. They allow a unidirectional flow of secretions into the duodenum and prevent reflux from the duodenum into the ampulla Vateri. Subepithelial mucous gland secretions functionally clean the valvular crypts and protect the epithelium. The arrangement of pocket-like mucosal folds may explain endoscopic difficulties experienced when attempting to penetrate the papilla of Vater during endoscopic retrograde cholangiopancreaticographic procedures.

Aged↗
PubMed2002

Pharmacogenetic investigation of the TNF/TNF-receptor system in patients with chronic active Crohn's disease treated with infliximab.

Infliximab (anti-TNF-alpha monoclonal antibody) induces remission in 30-40% of Crohn's disease patients. Treatment response is a stable trait. Two cohorts from independent, prospective clinical trials of infliximab in Crohn's disease were studied. Hypotheses were generated in an exploratory cohort (n = 90) and then tested in a confirmatory cohort (n = 444), using a statistical design, which is stable against type 1 and type 2 errors. In the exploratory cohort, the mutant 196Arg allele of TNFR-II (exon 6 polymorphism) and a novel silent polymorphism in exon 2 of TNFR-II were associated with lack of response to infliximab (83.3% in homozygote mutant 196 Arg patients vs 36.9% in heterozygotes and wild-type homozygotes (P = 0.036) and 85.7% in homozygote mutant exon 2 patients vs 36.1% (P = 0.01), respectively). None of the homozygote mutant individuals (0/6) achieved clinical remission, whereas the remission rate was 35.7% (30/84) in wild-type homozygotes and heterozygotes. In the large second cohort, the observed genotype-phenotype associations were not replicated. Other polymorphisms (TNF-alpha promoter -238, -308, -376, -857, -1031, TNF-R-I -609, +36 (exon 1), TNF-R-II 1663, 1690 (3'-UTR)) were not associated with treatment response in both cohorts (P > 0.5). None of the polymorphisms was associated with refractory Crohn's disease itself when compared to healthy controls. In a two-cohort study, a series of polymorphisms in the TNF, the TNF-R-I and in the TNF-R-II genes could be thoroughly excluded as pharmacogenetic markers for a treatment response to infliximab and as etiologic factors for Crohn's disease, respectively. The discrepancy between the two cohorts observed for the TNF-R-II exon 6 and exon 2 polymorphism may point to a weak effect on treatment response but also serves to illustrate the need for a sequential exploratory/confirmatory design in pharmacogenetic studies.

Adolescent↗
PubMed2002

[Recurrent sanguineous and mucous diarrhea and spasms in a 46-year-old woman--manifestation of endometriosis in the colon sigmoideum].

Intestinal endometriosis is the most frequent extragenital manifestation of this disease. Sometimes patients even present with acute bowel obstruction. We report on a 46-year-old woman complaining about recurrent sanguineous and mucous diarrhea and spasms for several years. Colonoscopy showed a stenosis in the sigmoid colon without macroscopically visible alterations of the mucosa. Computertomography, ultrasound and barium contrast enema did not provide us with further information about the origin of the stenosis. Biopsies out of the mucosa at the stenosis showed typical endometriosis tissue. After starting a conservative therapy with GnRH-agonist gosereline the patient became completely free of symptoms. The coincidence of endometriosis and M. Crohn has to be taken into consideration. Therapy planning should include a close co-operation with gynaecologists and surgeons to transfer the patient to surgical intervention when needed.

Colon, Sigmoid↗
PubMed2002

[High plasma levels of factor VIII and von Willebrand factor in a patient with portal vein thrombosis].

In portal vein thrombosis, various hypercoagulable conditions and inherited or acquired thrombophilias have already been described as predisposing factors. In a 33-year-old man admitted to a hospital with upper abdominal pain, a partial portal vein and upper mesenteric vein thrombosis, respectively, and a complete splenic vein thrombosis were diagnosed. Further diagnostic procedures showed no evidence for local precipitating factors or any underlying infectious, paraneoplastic or inflammatory disease. Thrombophilia screening demonstrated elevated factor VIII levels (206 %) and von Willebrand factor levels (> 440 %). An acute-phase reaction was excluded. Oral anticoagulant therapy with phenprocoumon was started. Factor VIII and von Willebrand factor were reproducibly elevated to high activity levels over a period of 12 months in absence of acute or chronic inflammatory reaction. Increased levels of factor VIII and von Willebrand factor may play a pathogenetic role in the development of portal, splenic, and mesenteric thrombosis.

Adult↗
PubMed2002

Activation of signal transducer and activator of transcription (STAT) 1 in human chronic inflammatory bowel disease.

BACKGROUND: Increased expression of proinflammatory cytokines, including tumour necrosis factor alpha, interleukin 6, and interferon gamma, as well as activation of proinflammatory signalling molecules such as nuclear factor kappa B, is characteristic of inflammatory bowel disease (IBD). AIMS: To investigate expression and activation of signal transducer and activator of transcription (STAT) 1 in patients with IBD. PATIENTS: Patients with active IBD (n=42), disease specificity controls (n=8), and normal controls (n=12) were investigated. METHODS: Expression and activation of STAT1 were assessed by western blotting and electrophoretic mobility shift assays in extracts of endoscopic colonic biopsies. Cellular localisation was determined by immunohistochemistry. RESULTS: Western blots and immunohistochemical staining revealed an increase in STAT1 expression and activation in mucosal samples from ulcerative colitis and to a lesser extend in Crohn's disease patients. High levels of suppressor of cytokine signalling (SOCS)-3 expression, an inhibitor of STAT activation, were observed in Crohn's disease patients and normal controls in western blot experiments whereas no differences were observed for SOCS-1 expression. Phosphorylated (p) STAT1 was mainly detected in monocytic cells and neutrophils in the inflamed mucosa. Induction of remission by systemic glucocorticoids led to a decrease in levels of pSTAT1. In vitro studies indicated a direct effect of steroid treatment on STAT1 activation. CONCLUSIONS: Expression and activation of STAT1 are predominantly heightened in ulcerative colitis and may therefore play an important role in the pathophysiology of colonic inflammation.

Anti-Inflammatory Agents↗