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U Baumgartner

Publications and source records attributed to U Baumgartner.

41 records · Page 3Linked to original sources

Kupffer cells infiltrate liver tissue early after ischemia-reperfusion and partial hepatectomy.

Kupffer cells, ED2+macrophages of the liver, play an important role in liver damage and regeneration. It is proposed that Kupffer cells are stationary and regenerate after acute liver trauma by local proliferation. We analyzed their kinetics in three surgically relevant murine models of acute liver injury: partial liver resection, ischemia with reperfusion and sepsis. We found an early increase in ED2+cells after 0.5 h and a maximum after 12 h. These results suggest an infiltration of the cells early after the injury and a later local proliferation. These ED2+macrophages are localized predominantly periportally; nearly no macrophages are found pericentrally, except in the sepsis model. Therefore, a shifting of macrophages from portal to central seems to be unlikely, suggesting a hepatic zonation of homing factors.

Animals↗

Chemokines in human colorectal carcinoma.

BACKGROUND: Chemokines (CKs) may promote antitumor immunity in cancer, act as tumor growth factors, influence metastatic spreading or angiogenesis. The purpose of this study was to investigate whether CK expression is altered in colorectal carcinomas compared to normal mucosa and to elucidate its possible clinico-pathological implications. MATERIALS AND METHODS: The levels of CCL2 (MCP-1), CCL4 (MIP-1beta), CCL5 (RANTES), CXCL 1 (GRO-alpha), CXCL 5 (ENA-78) and CXCL 8 (IL-8) were investigated in 10 colorectal carcinomas and their corresponding normal mucosa by the use of ELISA. RESULTS: All CK analyzed, with the exception of CCL5 (RANTES), were expressed at a significantly higher level in malignant tissue. CONCLUSION: Therapeutic studies in colon carcinomas should, therefore, focus more on the neutralization of CKs than on their application.

Adenocarcinoma↗

Hepatocyte proliferation and apoptosis in rat liver after liver injury.

BACKGROUND/AIMS: In this paper the early phase of proliferate response and apoptosis of hepatocytes after partial liver resection, during reperfusion after ischemia and during sepsis is demonstrated. METHODOLOGY: Experiments were conducted in a rat model with regeneration times of 0.5-24 hours after injury. Proliferation was analyzed by Ki-67 immunohistochemistry and confirmed by double staining with CK18 in FACS. Apoptosis was analyzed by TUNEL technique. RESULTS: Periportal hepatocytes enter the cell cycle already 0.5-2 hours after injury in all three models. This early proliferative response is predominant periportally localized. During reperfusion and during sepsis there was a strict pericentral apoptosis of hepatocytes found. CONCLUSIONS: An early periportal proliferation of hepatocytes is a common reaction of the liver to injury. This proliferation takes place much earlier then the main proliferative response 24-72 h after partial resection. This predominant periportal proliferation together with the pericentral apoptosis fit to the concept of the "streaming liver" in liver regeneration.

Animals↗

Aminoterminal propeptide of type III procollagen: a marker of hepatic fibrosis after bile duct obstruction in the monkey.

BACKGROUND/AIMS: In an experimental study in monkeys, liver fibrosis development after segmental bile duct obstruction was investigated and correlated with the aminoterminal propeptide of type III procollagen (PIIINP). MATERIALS AND METHODS: Segmental bile duct obstruction was produced by ligation and section of the left hepatic bile duct in all monkeys. Fibrosis induction was examined by intravenous leukotriene C4 (LTC4, 5 nmol/kg) application, endogenous LT-production stimulated by endotoxin (LPS,salmonella abortus equi, 50 ng/kg), fibrosis inhibition by dexamethasone (1 mg/kg) intramuscularly and subsequent endogenous LT-production stimulation by LPS (50 ng/kg). Ligated and unligated liver lobe biopsies were taken 3, 7 and 12 weeks after ligation. All portal areas were measured morphometrically. PIIINP was measured by a specific radioimmunoassay each week and correlated with the morphometric results. RESULTS: Bile duct obstruction leads to secondary sclerosing cholangitis with bile duct vanishing and subsequent biliary cirrhosis combined with perivenous sclerosis and cavernous transformation of the terminal vein. The collagen concentration increased in the nonligated lobe from mean +/-SEM 1.05 +/- 0.03% to 1.53 +/- 0.19% only after LTC4 and with no difference in the other groups. In the ligated lobe collagen concentration increased significantly in all groups continuously from 1.05 +/- 0.03% up to: controls 6.1 +/- 0.9%, dexamethasone 5.9 +/- 0.8%, LPS 8.2 +/- 0.8%, LTC4 9.075 +/- 1.4%. PIIINP concentration rose within 6 weeks in the controls with hepatic bile duct obstruction from 34.43 +/- 15 ng/ml up to 57 +/- 13.27 ng/ml, after dexamethasone to 48.5 +/- 18.23 ng/ml, after LPS to 57 +/- 13.27 ng/ml, after LTC4 to 80.25 +/- 16.04 ng/ml. After 12 weeks, PIIINP decreased in the controls resp. after dexamethasone to 41.25 +/- 6.94 ng/ml resp. 33.5 +/- 7.72 ng/ml and increased after LPS resp. LTC4 up to 64.25 +/- 17.07 ng/ml resp.104 +/- 22.46 ng/ ml. The correlation of collagen deposition and PIIINP was in the controls r = 0.83, after dexamethasone r = 0.71, after LPS r = 0.83 after LTC4 r = 0.91. CONCLUSION: PIIINP determination after segmental bile duct obstruction correlates with collagen deposition and allows evaluation of hepatic fibrosis activity.

Animals↗

Early detection of graft dysfunction after orthotopic liver transplantation in man by serum and biliary bile acid analysis.

BACKGROUND/AIMS: Several routine parameters are used to monitor the functional state of the liver after orthotopic liver transplantation (OLT). These parameters may not fully mirror hepatic function and even liver biopsy may be unreliable during onset of graft rejection. Additional analytical methods on bile constituents for recognition of early graft dysfunction have been assessed. Conflicting results have prompted discussions about the usefulness of monitoring serum bile acids and biliary lipids after OLT with respect to early recognition of graft dysfunction. MATERIALS AND METHODS: Routine serum liver function tests were compared with serum bile acid (BA) concentrations and output of biliary lipids (BA, phospholipids, cholesterol) over 20-25 days in 12 patients after (OLT) with different postoperative courses. RESULTS: 4 patients had an uneventful postoperative course (group 1); 5 experienced a rejection episode (group 2); 3 demonstrated a poor initial graft function (group 3). In group 1 aspartate-aminotransferase (AST) (<20 U/L), urinary BA excretion (<21 mmoles/day) and normalized bile flow (NBF; 72 +/- 25 ml bile/mmole BA) fell into the normal range within 4 days after OLT; serum BA concentration (<20 mM) was within normal on the first postoperative day. Output of biliary BA, phospholipids, cholesterol and bile production increased continuously during the observation period reaching values of 11.2 +/- 3.3 mmoles/day, 2.7 +/- 0.9 mmoles/day, 1.3 +/- 0.5 mmoles/day and 761 +/- 221 ml/day, respectively. The ratio of taurocholate/glycocholate (TC/GC) decreased from an initial value of 0.45 to 0.11. Group 2 yielded similar values until rejection appeared. At this time serum BA concentration, NBF urinary BA excretion and TC/GC-ratio rose; biliary lipid output and bile flow decreased. In most of the patients these changes occurred at the same day or 1-3 days earlier than that of AST. CONCLUSIONS: The determination of serum BA concentration, TC/GC-ratio, output of biliary lipids and NBF may indicate graft dysfunction 1-3 days earlier than AST and, thus, may provide useful parameters for early recognition of liver graft dysfunction.

Adult↗