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Biomedical subjects

W Vogt

Publications and source records attributed to W Vogt.

At least 73 records · Page 4Linked to original sources
PubMed1990

The use of cluster analysis in clinical chemical diagnosis of liver diseases.

Diagnostic judgement is usually based on recognition of patterns. Unfortunately more than three quantitative data cannot be judged simultaneously without help of mathematical methods. Working on laboratory reports, a clinician usually goes linearly through the columns and reduces quantitative to qualitative data. Therefore the medical decision process should be improved if data reduction is performed with the aid of mathematical methods for pattern recognition. A total of 191 consecutive outpatients with a tentative or proven diagnosis of hepatobiliary disease were examined clinically, clinically chemically and partly histologically. Nineteen clinical chemical parameters were determined. Prior to pattern cognition, a principal component analysis was performed. Using six factors, accounting for 72.4% of total variance, cluster analysis was done, applying a hierarchical algorithm for ascertaining a starting partition, followed by the k-means algorithm. The validity of the solution was scrutinized, and a stable structure was found with nine clusters. Patients with a rejected suspect of liver disease were mainly located in clusters 1, 6 and 7. Cluster 1 also contains patients with compensated cirrhosis without inflammation, idiopathic hyperbilirubinaemia, focal nodular hyperplasia and haemangioma of the liver. In contrast, one third of cirrhoses, all with inflammatory activity were assigned to cluster 5. Patients with primary biliary disease were distributed among clusters 2, 3 and 4. All malignant neoplasias were assigned to cluster 9. More than 50% of fatty livers were classified to cluster 7. Cluster 2 and 8 contain only one patient with primary biliary cirrhosis (cluster 2) and fatty liver hepatitis (cluster 8). The follow-up of 66 patients also showed clinically meaningful changes of cluster assignment.

Cluster Analysis↗
PubMed1989

Non-enzymic activation of the fifth component of human complement, by oxygen radicals. Some properties of the activation product, C5b-like C5.

Purified human C5 was converted non-enzymically to an activated form as defined by its ability to participate in reactive lysis. This conversion occurred following exposure to systems that generate oxygen radicals, namely addition of H2O2 in the presence of ascorbic acid and iron or the addition of xanthine oxidase, acetaldehyde and iron. The conversion of C5 to a functionally active species was iron-dependent and inhibited by hydroxyl radical scavengers such as DMSO. The findings suggest that OH. is the active oxygen species that converts C5. The conversion product of C5, termed C5(H2O2), is C5b-like due to its ability to bind C6 and cause reactive lysis. C5(H2O2) is much more stable than C5b obtained by complement convertases. Although C5(H2O2) has lost the binding site of native C5 for C3b it can be cleaved by complement-derived convertases; the cleavage is, however, less efficient than in the case of native C5. The resulting cleavage product, which is C5a-like, is chemotactic although C5(H2O2) is not chemotactic. C5(H2O2) serves as a better substrate for plasma kallikrein than native C5, resulting in the generation of a C5a-like chemotactic product. These data indicate that oxygen radicals can bring about a conformational change in C5, causing it to behave as a functionally activated molecule of the complement system. This may have implications for the role of complement and its activation in the inflammatory response.

Complement Activation↗
PubMed1989

Release of glutamate and of free fatty acids in vasogenic brain edema.

The pathophysiological potential of mediator substances in manifestations of secondary brain damage is attracting increased attention. This is particularly true of the excitatory transmitters glutamate and arachidonic acid. Noxious properties of these compounds in central nervous tissue have been demonstrated. The current study was performed to determine whether glutamate and arachidonate are released in brain tissue secondary to focal trauma. For this purpose, a cold injury of exposed cerebral cortex was induced in cats. Marked accumulation of glutamate was observed in interstitially drained edema fluid, reaching 10 to 15 times the level that was assessed in normal cerebrospinal fluid (CSF) prior to trauma. The extracellular release of glutamate was further dramatically enhanced by a critical decrease of the cerebral perfusion pressure due to a malignant increase of intracranial pressure. Under these conditions, glutamate concentrations 1000 to 1500 times normal levels accumulated in vasogenic edema fluid, demonstrating a relationship between the extent of the release of glutamate in damaged brain and the severity of the insult. Although under normal conditions glutamate concentrations in plasma were considerably higher than in the interstitial fluid, the pronounced increase of glutamate in this compartment due to trauma cannot be explained by transport of the compound together with the plasma-like edema from the intravascular space. Corresponding findings were obtained for free fatty acid concentrations in edema fluid. Almost all fatty acids that were studied had a significantly higher concentration in edema fluid than in normal CSF obtained as a control prior to trauma. However, contrary to the findings for glutamate, fatty acid concentrations in edema fluid were lower than in plasma. Accumulation of fatty acids in vasogenic edema fluid might, therefore, have resulted from uptake of the material together with edema fluid through the breached blood-brain barrier. Arachidonic acid was an exception. Its concentrations were significantly higher in edema fluid than in plasma, suggesting that it was released from cerebral parenchyma as the underlying mechanism of its extracellular accumulation. The current observations provide further support for a mediator function of glutamate and arachidonic acid in acute traumatic lesions of the brain. Quantitative assessment of the release of highly active mediator substances in brain tissue may facilitate analysis of the therapeutic efficiency of specific treatment aimed at interfering with the release or pathological function of mediators of secondary brain damage.

Animals↗
PubMed1989

[Sufentanil-N2O2/O2 or halothane-N2O/O2 anesthesia in surgery of infants and children with congenital heart defects. Hemodynamics and plasma catecholamines].

Sufentanil-nitrous oxide/oxygen anesthesia was compared to halothane-nitrous oxide/oxygen anesthesia in 44 infants and children undergoing cardiac surgery. Patients were randomly assigned to one of the two techniques studied, with 22 patients in each group. The mean weight was 8.3 (4.4-15.8) kg in the sufentanil (S) group and 11.7 (5.2-18) kg in the halothane (H) group. All patients were premedicated with IM atropine 0.01 mg/kg, morphine 0.2 mg/kg, and flunitrazepam 0.04 mg/kg. In the S group 1 micrograms/kg S was given intravenously for induction, followed by a cumulative dose of 4 micrograms/kg S until the beginning of surgery. In the H group anesthesia was induced with H 0.5-1.0 vol.% and for deepening of anesthesia increasing H concentrations of 0.5-1.0-1.5 vol.% were applied. Following intubation all patients were ventilated with nitrous oxide/oxygen (1:1). There were no significant differences between the two groups in systolic, diastolic and mean arterial blood pressures or in heart-rate response to induction and intubation. Peripheral arterial oxygen saturation increased significantly in cyanotic patients in both groups following induction. There were dose-dependent decreases in heart rate and small but significant decreases in mean and diastolic arterial pressure in the S group during deepening of anesthesia. There was a significantly greater decrease in systolic, diastolic and mean blood pressures during the same period in the H group whereas the reduction in heart rate was minimal. In addition, in 5 of 22 patients receiving H there were episodes of nodal rhythms with dramatic decreases in systemic arterial pressure and peripheral arterial oxygen saturation in cyanotic patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1989

[Suture of the Achilles tendon with a reinforcing-plasty--experiences with 30 primary sutures of Achilles tendon ruptures].

We analysed 32 patients with fresh Achilles tendon rupture. 30 operations with a special primary suture and plasty of the fascia triceps muscle. Most of the patients were content with the operative treatment and the functional result. We saw one wound infection and one wound rand necrosis. The objective controls of OSG foot function and the muscle activity is good.

Achilles Tendon↗
PubMed1988

The determination of bilirubin with a new enzymatic method (Dri-STAT bilirubin) using the Hitachi 704 selective analyzer.

A new enzymatic method for the determination of bilirubin in serum and plasma by means of a Hitachi 704 selective analyzer was evaluated. This endpoint method (37 degrees C) including a sample blank showed very reliable results. The range of linearity was 0.3 to 437 mumol/l bilirubin. The within-run imprecision of three different bilirubin concentrations (n = 16) was 0.37, 0.44 and 0.76% (coefficient of variation). Between-assay imprecision (n = 15) was 0.51 to 1.76% (coefficient of variation) for five different control materials. Inaccuracy, determined with 5 control sera (assigned values: 19, 23.9, 90.7, 142.0 and 295.6 mumol/l bilirubin), was 0.14 to 4.27%. Recovery rates, determined in two spiked plasma samples, were 97.8% and 99.1%, and in six bilirubin standard solutions between 92 and 99%. The comparison with the routinely used 2.5-dichlorophenyl diazonium salt method as well as with the Jendrassik & Grof [1938) Biochem. Z. 297, 81-89) method as the reference yielded correlation coefficients of r = 0.997 and r = 0.998.

Bilirubin↗
PubMed1988

Modified TDx assay for cyclosporine and metabolites, for use with whole-blood samples.

A recently introduced fluorescence polarization immunoassay (FPIA) for determination of cyclosporine A in serum and plasma is discussed with regard to its use for whole-blood samples, with and without hemolysis before the assay. The performance characteristics of the modified method are highly satisfactory (within-run CVs 2.06 to 5.50% and 1.99 to 3.39%, respectively; long-term between-run CVs under routine conditions 5.73 to 8.95%). The limit of detection is 30 micrograms/L. Results agree well with those obtained with the RIAs compared, but the modified FPIA is more convenient and faster.

Cyclosporins↗
PubMed1987

High-performance liquid chromatographic determination of hormonal peptides and their fluorenylmethoxycarbonyl derivatives.

Reference methods for the quantitation of peptide and protein hormones in blood are urgently needed and high-performance liquid chromatography (HPLC) is potentially applicable. Owing to the low concentrations of these substances in body fluids, very low detection limits have to be achieved. This can be done on the one hand by reducing the diameter of the separation column and increasing the number of theoretical plates, and on the other by derivatization. Angiotensin II was chosen as a model compound. Reduction of the inner diameter from 4 to 2 mm increased the peak height by a factor of 3.4 (theoretical value 4.0). The peptide was derivatized with 9-fluorenyl methylchloroformate in lithium carbonate-sodium hydrogencarbonate or sodium borate buffer at different pH values. The precision (coefficient of variation) was 10.4%, the linear range 1:40 (r = 0.998) and the detection limit 500 fmol of derivative on-column. The volume injected was 2 microliter. However, this is not sufficiently sensitive for the quantitation of most peptide hormones using an acceptable maximum specimen volume of 5 ml of serum or plasma.

Angiotensin II↗
PubMed1986

Role of the N-terminal regions of hog C3a, C5a and C5a-desArg in their biological activities.

The N-terminal regions of the complement peptides C3a, C5a and C5a-desArg (purified from yeast-activated hog serum) were gradually shortened by incubation with leucine amino peptidase. This treatment led to the following changes in the biological activities of these peptides: the potencies of C5a and C5a-desArg in aggregation of human polymorphonuclear leukocytes and of guinea-pig platelets, and their ability to deactivate these cells were gradually diminished; the chemotactic effect of C5a-desArg on human leukocytes was similarly lowered, while the chemotactic potency of C5a was even increased up to the loss of the first 12 N-terminal amino acids. However, after removal of the whole N-terminal region (i.e. 20 amino acids distal of the first disulfide bridge) the potency of both peptides was decreased to a few percent. In contrast, C3a totally lost its platelet-aggregating as well as deactivating activity already after cleavage of 10-15 N-terminal amino acids by LAP. On leukocytes, on the other hand, C3a retained some activity even after the loss of the whole N-terminal region. These results indicate that the N-terminal regions play an important role for biological activities of the three complement peptides, possibly by stabilizing the optimal conformation of their C-terminal regions which contain the receptor-activating domains.

Animals↗
PubMed1986

Complement activation in human lymph: modulation by the contact activation system and by leukocytes.

Complement components, their activation and the generation of C3a and C5a peptides were studied in human lymph used as a model of tissue fluid. Both, classical and alternative pathways could be activated by suitable agents such as immune aggregates or zymosan. C3 activation and C3a formation were marked while only 10-15% of the anyway low amount of C5 were converted during complement activation, yielding very low concentrations of C5a. Carboxypeptidase N activity was present in lymph and converted the peptides to their less (C5a) or not at all (C3a) active desArg derivatives. Contact activation of Hageman factor and kallikrein enhanced activation of the classical pathway up to C3 conversion. The search for additional processes apt to create efficient concentrations of C5a (desArg) in lymph led to the discovery that the presence of leukocytes in lymph greatly increases the release of C5a activity upon complement activation. This suggests a physiological role of leukocytes resident in tissues for the induction of inflammatory reactions.

Anaphylatoxins↗
PubMed1986

Anaphylatoxins: possible roles in disease.

Anaphylatoxins, in particular C3a and C5a, have various biological activities which suggest a role as mediators of inflammatory reactions: they cause contraction of smooth muscle, histamine release, increase in capillary permeability, adhesion of leukocytes to vascular endothelium, leukocyte chemotaxis, and aggregation of platelets and leukocytes. Most of these effects are supported by the cooperation of other mediators, in particular arachidonic acid derivatives which may be produced by anaphylatoxin-stimulated cells, e.g. leukocytes or endothelium. In vivo effects of the complement peptides depend very much on the site of their generation: intravascular release in the general circulation leads to adverse symptoms such as adult respiratory distress syndrome and shock lung, mainly due to leukocyte activation, aggregation and their accumulation in lung vessels. Intravascular release may be induced by certain drugs, and by contact of blood with the surfaces of bypass or dialysis apparatus. Induction of local inflammatory and defense reactions requires release of anaphylatoxins in tissue spaces. Tissue fluid differs quantitatively from blood plasma in its concentration of complement components. This raises some problems of how efficient concentrations of C3a and C5a can be attained at the site of a lesion to generate a chemotactic gradient capable of attracting blood leukocytes.

Anaphylatoxins↗
PubMed1985

Mechanisms of complement activation by crystalline cholesterol.

The mechanism by which cholesterol crystals activate complement in human serum has been studied. Crystals treated with serum and washed with buffer contain a fixed C3/C5 convertase. Its generation is dependent on the presence of divalent cations (and of factor B). The cholesterol-fixed convertase is subject to decay and can be regenerated by factors B and D. C2 in combination with C1 is not essential but enhances the convertase formation. These findings indicate that it is predominantly the alternative C3/C5 convertase C3bBb(P) that assembles on cholesterol during exposure to human serum. By the use of different antisera and immunofluorescence a C3 fragment, probably C3b, was demonstrated on serum-treated crystals. Its fixation is resistant to washing with urea, and with buffers of differing pH: by hydroxylaminolysis the C3 fragment dissociates from the crystals. This indicates a covalent ester bond linking the labile binding site of activated C3 to the hydroxyl group of cholesterol. Cholesterol acetate does not fix C3 nor acquire a C3-cleaving activity upon contact with serum. In addition, cholesterol crystals bind factor I (C3b inactivator) and in this way may facilitate fixation and amplification of the alternative C3/C5 convertase.

Cholesterol↗
PubMed1985

Generation of anaphylatoxin activity related to C3a, by treatment of human serum with the nitrogen nucleophile N2H4 or the chaotrope KSCN.

The present study is concerned with the proteolytic processing of complement component C3 in normal human serum treated with N2H4 or KSCN in the presence of EDTA. Upon incubation with these agents, C3 is first converted to the thiolester-cleaved form (C3i) and thereafter fragmented by factor I. In consecutive, relatively slow steps, spasmogenic and platelet-aggregating activity is released. The active principle shows characteristics of C3a. First, the pretreated sera deactivate guinea pig ileum and platelets towards the action of C3ahog, but not C5a-desArghog. Second, the activity is only stable under conditions causing inhibition of serum carboxypeptidase N, such as in the presence of EDTA or of MERGETPA (DL-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid). Third, the molecular weight determined by gel filtration is in agreement with that of C3a. The release of C3a activity requires conversion of C3 to C3i, as well as the complement-independent generation of proteolytic activity in the pretreated sera. The enzyme releasing C3a activity is a serine esterase probably identical with Hageman factor, kallikrein, or another protease related to the contact system.

Anaphylatoxins↗