[Steatohepatitis after chemotherapy for colorectal liver metastases (CASH)]. / Steatohepatitis bei der Chemotherapie kolorektaler Lebermetastasen (CASH).

Neoadjuvant chemotherapy provides an important treatment option for patients who, as a consequence of colorectal cancer, have developed liver metastases. Regression of metastases prior to surgery may substantially improve prognosis. However, chemotherapeutics may harm non-tumorous liver tissue, particularly if this is already impaired prior to chemotherapy. The present article discusses the risks of chemotherapeutics for liver tissue-including sinusoidal obstruction syndrome, nodular regenerative hyperplasia, and chemotherapy-associated steatohepatitis, amongst others-which should be borne in mind when selecting therapy.

[Histopathological diagnose of non-alcoholic and alcoholic fatty liver disease]. / Histopathologische Diagnose der nicht alkoholischen und alkoholischen Fettlebererkrankung.

Alcoholic fatty liver (AFL) as well as non-alcoholic fatty liver (NAFL) are characterised by deposition of lipids into hepatocytes. The diagnosis of steatosis is made if lipid deposition exceeds 5 % of hepatocytes, in case of more than 50 % it is called "fatty liver". An additional inflammatory reaction, with ballooning of hepatocytes, leads to alcoholic steatohepatitis (ASH) or non-alcoholic steatohepatitis (NASH). Both ASH or NASH may lead to fibrosis or cirrhosis. To date in clinical practice it is not possible to differentiate between steatosis and steatohepatitis just on the basis of non-invasive tests. Steatohepatitis is present if, along with steatosis, both inflammatory infiltrates of mixed cells in the small liver lobules and liver cell injury in terms of ballooning can be detected. Liver biopsy represents the "gold standard" for confirming the diagnosis and to determine inflammatory activity and potential fibrosis of fatty liver disease. Indications for biopsy should take into account the possible information and its consequences as compared to expense and complication rate and therefore should be assessed in the clinical context.

[Histopathological diagnosis of non-alcoholic and alcoholic fatty liver disease. Grade 2 consensus-based guidelines]. / Histopathologische Diagnose der nichtalkoholischen und alkoholischen Fettlebererkrankung. Konsensusbasierte Leitlinie der Stufe 2.

Both alcoholic (AFL) and non-alcoholic fatty liver (NAFL) are characterized by lipid deposition in hepatocytes. The diagnosis of steatosis is made when lipid deposition exceeds 5% of hepatocytes, while involvement of more than 50% is called "fatty liver ". An additional inflammatory reaction leads to alcoholic (ASH) or non-alcoholic steatohepatitis (NASH). Steatohepatitis is present when both inflammatory infiltrates of mixed cells in the small liver lobules as well as liver cell injury in terms of ballooning can be detected.Liver biopsy represents the "gold standard" for confirming diagnosis and determining inflammatory activity and potential fibrosis of fatty liver disease.The differential diagnosis of ASH-NASH cannot be made on the basis of histological criteria alone. Steatosis, inflammatory changes and hepatocytic injury can be semiquantified as a "Brunt Score" or "NAS" (NAFLD activity score), providing the basis on which to decide whether or not steatohepatitis is present.People at increased risk of developing a fatty liver possess an increased risk of developing chemotherapy-associated steatohepatitis (CASH).Histologically, pediatric NASH differs from adult NASH and is often only clinically manifest through a mild if persistent elevation in transaminases.

bFGF induces its own gene expression in astrocytic and hippocampal cell cultures.

Basic FGF mRNA induction by bFGF was investigated in cell cultures from rat brain, i.e. postnatal day 2 cortex and embryonic day 18 hippocampus. In situ hybridization shows that after bFGF treatment (10(-10) M) for 14 h neurones and glial cells show a remarkable increase in bFGF mRNA production. Incubation of astrocytes with antisense bFGF phosphorothioate oligodeoxynucleotides (bFGF-PTOs) resulted in an inhibition of both bFGF induced and serum induced proliferation. The results indicate that bFGF is capable of inducing its own mRNA production. This induction, i.e. new synthesis of bFGF mRNA, seems to be essential for the mitogenic effect of both bFGF and serum components.

Homocysteic and homocysteine sulphinic acid exhibit excitotoxicity in organotypic cultures from rat brain.

UNLABELLED: The excitotoxic action of homocysteine and related sulphur-containing metabolites was investigated in organotpyic cultures derived from rat brain cortex and hippocampus by inhibition experiments using antagonists selective for different glutamate receptor subtypes. In addition the direct interaction of these metabolites with glutamate receptors expressed in frog oocytes was tested by conventional two electrode voltage clamp techniques. CONCLUSION: Neurodegeneration and epilepsy observed in homocystinuria may be mediated by L-homocysteic and L-homocysteine sulphinic acid. Both metabolites exhibit excitotoxic potency by interaction with different glutamate receptor subtypes.

Glutaric aciduria type I: pathomechanisms of neurodegeneration.

In organotypic corticostriatal and hippocampal slice cultures from rat brain, 3-hydroxyglutaric acid but not glutaric and glutaconic acids induced neurodegeneration by activation of NMDA receptors. Electrophysiological investigations (Xenopus laevis oocytes expressing glutamate receptors; rat mixed cortex culture) revealed no direct interaction of 3-hydroxyglutaric acid with glutamate receptors. We speculate that 3-hydroxyglutaric acid induces a mild energy deprivation that interferes with the voltage-dependent Mg(2+)-block of NMDA receptors.