[Wernicke's encephalopathy on CT and MR].
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Biomedical subjects
Publications and source records attributed to E Hofmann.
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The kinetics of PFK-2 and FBPase-2 from rat liver were investigated with respect to the substrates and the effector sn-glycerol 3-phosphate. PFK-2 exhibits a hyperbolic response with respect to its substrates Fru 6-P and ATP. The inhibition of the activity of PFK-2 by sn-glycerol 3-phosphate could be described by assuming competition with Fru 6-P at the catalytic site. sn-Glycerol 3-phosphate activates the FBPase-2 and is capable of reversing partially the inhibition of the enzyme by Fru 6-P. The dynamics of the PFK-2/FBPase-2 cycle has been investigated in an enzyme system composed of PFK-2/FBPase-2, creatine kinase and creatine phosphate. sn-Glycerol 3-phosphate was found to decrease the quasi-stationary concentration of Fru 2,6-P2. The control of the PFK-2/FBPase-2 cycle by sn-glycerol 3-phosphate turned out most efficient at high concentrations of both sn-glycerol 3-phosphate and Fru 6-P. In addition, sn-glycerol 3-phosphate was found to increase the concentration control coefficient of Fru 2,6-P2 with respect to Fru 6-P.
Binding of Fru-2,6-P2 to yeast phosphofructokinase was investigated by ultrafiltration technique. Per mol of subunit of phosphofructokinase (M = 100,000) 0.5 moles of Fru-2,6-P2 are bound. The binding curve proceeds cooperatively (nH = 1.8 +/- 0.2). The apparent affinity constant of Fru-2,6-P2 amounts to about 2.25 +/- 0.12 microM. Fru-1,6-P2 decreases the affinity of yeast phosphofructokinase to Fru-2,6-P2. The data can be described by assuming either competition of Fru-2,6-P2 and Fru-1,6-P2 for the same binding site or conformationally mediated interactions.
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Marked portosystemic venous anastomosis of the parumbilical veins is referred to as the Cruveilhier-Baumgarten syndrome. Opening of these vessels has been described mainly in the sonographic literature. In this case report CT and MR findings are presented, which have been confirmed by angiography. This paper is intended to draw the radiologist's attention to dilatation of the parumbilical veins, which is a highly specific sign of portal hypertension resulting from intrahepatic blockage.
Fat-storing cells and other non-parenchymal cells (endothelial and Kupffer cells) were isolated from rat liver by a combined pronase-collagenase procedure and subsequent Visotrast-370 density gradient centrifugation. The lactate dehydrogenase isoenzyme pattern of fat-storing cells was found different from that of other non-parenchymal liver cells. Fat-storing cells contain LDH-4 as the main isoenzyme and do not contain LDH-1, whereas the other non-parenchymal cells have all five lactate dehydrogenase isoenzymes, among which LDH-5 is dominating. All non-parenchymal liver cell populations contain the M-type pyruvate kinase. The alkaline phosphatase of fat-storing cells has the same electrophoretic mobility as that of the other non-parenchymal cells.
Quantitative estimates of M- and L-type phosphorylase subunits in adult and developing rat tissues have been obtained by immunotitration of tissue extracts with subunit-specific antibodies. It has been shown that M-type subunits occur in all studied tissues with exception of adult liver and placenta. L-type subunits account for most of the total phosphorylase activity in liver and bone marrow but are present also in a variety of other adult and in most of the fetal tissues examined. During maturation, selective increases in the expression of phosphorylase isozymes occur in certain tissues such as liver, brain, heart and skeletal muscle. The hitherto unknown hybrid LM has been produced by in vitro hybridization of M- and L-subunits.
In rat liver, alkaline phosphatase is shown to exist in several distinct molecular forms originating from different cell types. The alkaline phosphatases of isolated hepatocytes and non-parenchymal liver cells were characterized with respect to electrophoretic mobility, thermostability, and sensitivity to treatment with neuraminidase in order to define the cellular distribution of the different enzyme forms within the liver. The major form of liver alkaline phosphatase could be attributed to the hepatocytic enzyme, whereas the properties of the minor form were found to be identical with those of the non-parenchymal cell enzyme. In contrast to the hepatocytic enzyme, that of the non-parenchymal cells revealed heterogeneity after desialylation.
Fructose-2,6-bisphosphatase was purified from yeast and separated from 6-phosphofructo-2-kinase and alkaline phosphatase. The enzyme released Pi from the 2-position of fructose 2,6-bisphosphate and formed fructose 6-phosphate in stoichiometric amounts. The enzyme displays hyperbolic kinetics towards fructose 2,6-bisphosphate, with a Km value of 0.3 microM. It is strongly inhibited by fructose 6-phosphate. The inhibition is counteracted by L-glycerol 3-phosphate. Phosphorylation of the enzyme by cyclic-AMP-dependent protein kinase causes inactivation, which is reversible by the action of protein phosphatase 2A.
Stationary states of the fructose 6-phosphate/fructose 2,6-bisphosphate cycle were investigated in relation to the input concentration of fructose 6-phosphate. Below a critical input concentration of fructose 6-phosphate very low levels of fructose 2,6-bisphosphate were obtained. Above this point the fructose 2,6-bisphosphate changes in direct proportion to the input of fructose 6-phosphate. Phosphorylation of the enzyme causes an increase of the critical input concentration of fructose 6-phosphate. The control coefficients for fructose 2,6-bisphosphate have their maximum at the critical input concentration of fructose 6-phosphate.
Conventional plain film roentgenography is the basic examination of bone tumors. Modern digital roentgenography offers technical innovations but no fundamental new diagnostic dimensions. Computerized and magnetic resonance-tomography allow a far better delineation of the tumor spread (staging). These new imaging methods together with ultrasound have revolutionized the diagnosis of soft tissue neoplasms, not visible on plain film roentgenograms except lipomas and calcifications.
In the liver of suckling rats, the synthesis of hepatic tyrosine aminotransferase, serine dehydratase, and phosphofructokinase 2 as well as of renal beta-glucosidase is controlled by the circulating concentrations of adrenal and pancreatic hormones. Glucagon is capable of stimulating enzyme synthesis only in the presence of a steroid hormone. Dexamethasone and estradiol have been found to exert a permissive function on the inducibility of the studied enzymes by glucagon. Between the hormones of the adrenal medulla and glucagon antagonistic effects in enzyme induction were observed. Obviously, this antagonism is mediated by the alpha 1-adrenergic signal transferring system. A characteristic age dependence of enzyme induction by dexamethasone has been established. This might be correlated to alterations in the degree of methylation of the respective promoters. The methylation inhibitor 5-azacytidine influences significantly the enzyme induction by glucocorticoid hormones.
Tinnitus is a familiar symptom in diseases of the central nervous system. Its aetiology being of a varied nature, the type of tinnitus is a pointer to the pathoanatomic findings that are responsible for the disease. The causes of tinnitus are often found in the borderline areas between various neighbouring disciplines, such as otology, neurology and neurosurgery, whereas the final identification of the real causes is mainly within the scope of radiological diagnosis, in which computed tomography and superselective angiography play an essential role. In addition to arteriovenous fistulas near the petrous bone and glomus tumours, which are well known, there are a few other aetiologies of pulse-synchronous tinnitus that are being discussed in this paper. In recent years there has been substantial therapeutical progress owing to the introduction of new techniques and the development of improved materials for embolisation in interventional neuroradiology. Their application is discussed in connection with various patient groups.
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The alpha-1-adrenergic receptor system in liver plasma membranes purified from rats of different ages were quantified by means of the [3H]prazosin binding assay. Maximum binding was found to increase with age. The binding constant, however, does not change significantly. Coupling of the receptor to the nucleotide-binding protein was studied by competitive displacement analysis of [3H]prazosin binding with norepinephrine (NE) in the presence and in the absence of guanyl-5'-yl-imidodiphosphate (GppNHp). GppNHp induced a shift in the NE-displacement curves to lower affinities in membranes of adult rat livers, but not in liver membranes prepared from 12-day-old rats. Computer analysis showed that in the adult liver the displacement curves fit a two site binding model in the absence of GppNHp and in its presence a one site model. In liver membranes of adult rats more than 70% of the alpha-1-receptor population are apparently in the high affinity form, whereas in 12-days old rats the percentage is only 30%. Protease inhibitors were found without effect on the displacement curves. The phorbol ester 4 beta-phorbol 12-myristate 13-acetate (PMA) blocks the stimulation of glycogenolysis by alpha-1-agonists in hepatocytes of adult rats without changing their binding capacity for [3H]prazosin. The liver of newborn rats strongly responds towards exogenous stimulation by alpha-1-agonists.
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Tinnitus synchronous with the pulse is usually caused by vascular anomalies. In our own patient group we found the most frequent cause to be highly vascularised tumours related to the pretrous bone, the most common being glomus tumours. Pulsatile tinnitus however also is a main symptom of dural arterio-venous malformations with shunts into the transverse and sigmoid sinus. Finally pulsatile tinnitus may be caused by venous deformities, possibly combined with anomalies of the bulb of the jugular vein. While clinical methods give valuable clues to the type of pathological findings, subtle radiological investigations are necessary for the final diagnosis, such as high resolution computer tomography and super-selective angiography. There has been substantial progress in recent years due to technical developments leading to improved diagnosis and treatment by interventional radiology.