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Biomedical subjects

W H Siede

Publications and source records attributed to W H Siede.

16 recordsLinked to original sources
PubMed2000

Interpreting complex urinary patterns with MDI LABLINK: a statistical evaluation.

The measurement of urinary marker proteins is not a generally accepted laboratory practice because the results are difficult to interpret. MDI-LABLINK is software for classifying patterns of specific urinary marker proteins. The interpretations are completely user definable thanks to a specific 'pattern definition database'. Our interpretation set is based on Hofmann and Guder's work in measuring and interpreting single urinary proteins. We include additional marker proteins in order to adapt Boesken's SDS-PAGE classification. During the last 3 years, 1905 patterns were fully differentiated and identically interpreted. Firstly, the samples were classified into three patterns: normal (25.8%), predominantly glomerular (27.2%, selective, unselective, mixed, and with additional tubular proteins) and predominantly tubular (36.9%, complete/incomplete form, with additional glomerular proteins); 8.9% showed postrenal proteinuria. Secondly, glomerular selectivity measured by using urinary transferrin/IgG ratio alone correlates well with the established SI index (the ratio between IgG and transferrin clearances). Thirdly, the creatinine concentration substantiates the validity of the sample. The quality of the preanalytical phase can be improved through the ongoing education of the medical staff. Finally, measurement of urinary albumin and alpha-1-microglobulin is mandatory where kidney disease is suspected, has to be ruled out, or requires close monitoring, even when the total protein concentration is normal.

Adolescent↗
PubMed1996

Computer assisted interpretation of laboratory test data with 'MDI-LabLink'.

Physicians have to confront an enormous output of laboratory data. Normally, only a few experts manually perform the interpretation of highly specialised laboratory tests. PC Windows based 'MDI-LabLink' automates interpretation and expands traditional rule-based expert systems with flexibility and graphic illustrations of complex laboratory data. The laboratory can adjust the interpretation database to its specific needs, maintaining full control over program output. The structured input that 'MDI-LabLink' requires, supports dynamic test scheduling. It can be used to train personnel in the interpretation of laboratory test results. The program provides the clinician with a report that visualises the defect of the evaluated organ system with bitmap pictures and 3-dimensional graphics. Patient follow-ups present in tabular and graphical form. Changes in the severity of the pathobiochemical defect, induced, for example, by therapy, are monitored automatically. Applications available include interpretations of isoenzyme patterns, diagnosis of urinary proteinuria and cerebrospinal fluid analysis.

Chemistry, Clinical↗
PubMed1989

Endoprotease in human liver transforming multiple forms of alkaline phosphatase.

Two forms of alkaline phosphatase, extracted from human liver and named API1 and API3, are of high molecular mass, but API3 is the larger molecule and is membrane-bound while API1 is smaller and soluble. Enzyme kinetics are identical. It is suggested that API1 is produced from API3 by an endoprotease. We demonstrated the action of an endoprotease in human liver homogenate converting API3 into API1. In the absence of this enzyme no conversion occurred. This enzyme is active at an acidic pH (less than 6.5) in the presence of Ca.. or Mg.. -ions. It is inhibited by traces of EDTA. It is insensitive to diisopropyl fluoro-phosphate, to leupeptin and to reducing or oxidizing chemicals. At alkaline pH (8.6) its activity is rapidly destroyed. The enzyme is stable in acidic buffer. We conclude that API1 is indeed formed from API3 in the living cell by enzymatic conversion.

Alkaline Phosphatase↗
PubMed1989

Alkaline phosphatase isoenzymes in rheumatic diseases.

Serum alkaline phosphatase isoenzymes were determined quantitatively by electrophoresis on cellulose acetate in 168 patients with rheumatic diseases subgrouped for disease activity. Median values of total alkaline phosphatase and bone isoenzyme activity, as well as frequency of patients showing pathological values, increased gradually and significantly corresponding to disease activity in rheumatoid arthritis and ankylosing spondylitis, from 0% in inactive to 90% in very active forms. Bone isoenzyme was much more sensitive than total alkaline phosphatase in moderate disease activity and was also correlated to the number of involved extravertebral joints and pain in ankylosing spondylitis. No correlation was found with stage or duration of disease, age, sex, and erythrocyte sedimentation rate. Additional to bone isoenzyme, liver isoenzymes were elevated in some patients, but with only a weak correlation with disease activity. The intestinal isoenzymes were always normal. We conclude that quantitative determination of serum alkaline phosphatase bone isoenzyme activity is a major indicator for the assessment of disease activity and therapeutic monitoring in rheumatoid arthritis and ankylosing spondylitis.

Alkaline Phosphatase↗
PubMed1986

Effect of hypometabolism on cell injury.

Rats were given galactosamine 1 g/kg i.p. Pretreatment with propylthiouracil 14 days prior to intoxication and surgical thyroidectomy 10 days prior to intoxication significantly reduced the elevation of SGOT and GLDH activities and protected against hepatocellular necrosis 28 h after intoxication. T3 and T4 levels decreased significantly within the first 2 days in patients with acute myocardial infarction, while rT3 levels were found to be elevated within this period. TRH and TSH decreased during the first 2 days of the observation period and increased in course of time. The protective role of the "hypometabolic" state is discussed.

Animals↗
PubMed1986

[Effect of captopril in chronic aortic insufficiency].

In 16 patients with chronic aortic regurgitation, we studied the acute hormonal and hemodynamic effects of 12.5 to 25 mg captopril; in 12 patients the changes after a 4 to 8 week treatment period (mean 6.3 +/- 2 weeks; doses: 3 times 12.5 to 3 times 25 mg/day) were investigated. The following baseline variables were evaluated: the radionuclide left ventricular ejection fraction (EF) at rest and during exercise, left ventricular end-diastolic volume (EDV), regurgitant blood volume (RBV); and plasma renin activity (PRA). Repeated determinations of EF, EDV and RPA were carried out 90 minutes after application of the drug. In patients with chronic therapy, EF at rest and during exercise, EDV, RBV and PRA were reinvestigated at the end of the study. Acute administration of captopril was followed by an increase of EF (from 49 +/- 12 to 55 +/- 12%, p less than 0.001) and a slight decrease of EDV (from 389 +/- 160 to 376 +/- 146 ml, p less than 0.05). PRA significantly increased (from 1.6 to 3.1 ng/ml/h, p less than 0.05). Chronic therapy resulted in a moderate decrease of systolic and diastolic blood pressure (from 156/70 +/- 31/15 to 140/63 +/- 23/15 mm Hg, p less than 0.01). However, no significant changes were observed in EF at rest and during exercise (51 +/- 9 vs. 53 +/- 10% and 45 +/- 14 vs. 47 +/- 14%), EDV (433 +/- 179 vs. 422 +/- 179 ml) and RBV (136 +/- 81 vs. 129 +/- 77 ml). PRA was significantly increased (6.3 ng/ml/h, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve Insufficiency↗
PubMed1984

Multiple forms of alkaline phosphatases in human liver tissue.

Alkaline phosphatases (AP) extracted in the presence of n-butanol from human liver are separated by affinity chromatography on phenylsepharose Cl-4B into two fractions named APII and APIIII. By repeated chromatography, APII was purified to a single enzyme entity with a specific activity of 1,684 kU/g protein. APIIII was purified to a specific activity of 535 kU/g protein. It consisted of only APIIII enzyme activity, but still contained gamma-glutamyltransferase activity. These two forms of AP are different in chromatographic and electrophoretic behaviour, APIIII being a larger molecule than APII. APII and APIIII are very similar in enzyme kinetic behavior, such as substrate activity, thermolability and sensitivity to different inhibitors. It is concluded from these experiments that multiple forms of AP in liver bear identical active centres, the difference is due to a modification of protein residue. It is possible that both are modified forms of one enzyme. Both are different from the AP isoenzyme that appears in serum in cholestatic patients.

Alkaline Phosphatase↗
PubMed1981

Beneficial effect of somatostatin in phalloidin-intoxicated rats. Influence on survival rate, biochemical and morphological data, and 3H-demethylphalloin absorption rate by the liver.

The effect of somatostatin in phalloidin-intoxicated rats was studied. Animals were given phalloidin i.p. 1.2 mg/kg (LD 90-100). Somatostatin, 250 microgram/animal, was administered i.p. in saline 5 min prior and s.c. in protamine-sulphate/ZnCl2 suspension 30 min prior and 30 min after intoxication, unless stated otherwise. In vivo and in vitro uptake studies of the toxin were performed. Liver enzymes (GPT, GLDH) and kallikrein-like activities were determined in blood obtained by orbital venipuncture. Light and electron microscopy was carried out. Somatostatin treatment led to an increase in survival rate. Of the 20 treated rats six died whereas of the 20 untreated animals 18 died. A dose dependency was proven effective when half of the initial dose of somatostatin was given. In vivo and in vitro uptake studies of the toxin demonstrate that somatostatin does not alter uptake rate by rat livers. Liver enzymes remained elevated in treated and control rats. Kallikrein-like activities showed a 61% decline in treated animals whereas they rose up to 120% in controls as compared to pretreatment conditions. Light and electron microscopy reveals less severe lesions in somatostatin-treated animals. A possible interaction of somatostatin in shock development is discussed, phalloidin seems to be a suitable tool for further investigations concerning cell protection by somatostatin.

Alanine Transaminase↗
PubMed1981

Alkaline phosphatase isoenzymes in serum of rats during cholestasis.

Alkaline phosphatase isoenzymes (API) in serum of rats during cholestasis are investigated. For comparison different membrane systems in liver are damaged. Proliferation of bile canaliculi, sinusoidal area, and endoplasmic reticulum, respectively, is induced by different toxic conditions. It is found that in cholestasis an API5 in serum arises which is not present in serum of normal rats, but can be detected in normal rat liver. Thus, it is not a de novo synthesis of this API. Under the condition connected with a proliferation of bile canaliculi we find this API5 in serum. Under different conditions without proliferation of bile canaliculi we do not find an increase of this API5. We assume, therefore, that API5 in cholestasis is produced by cells of the bile canaliculi rather than by liver parenchymal cells in the sinusoidal area. No difference is found in intra- or extrahepatic cholestasis.

Alkaline Phosphatase↗
PubMed1980

Stauffer's syndrome in renal cell carcinoma evidence for intravascular coagulation.

In 40 patients with non-metastasising (n = 31) and metastasising (n = 9) renal cell carcinoma, evidence of Stauffer's syndrome (increase in alkaline serum phosphatase and prolongation of prothrombin time) was found in 18 patients. Prolongation of prothrombin time was not due to depletion of vitamin K-dependent coagulation factors or manifest fibrinolysis, but due to the presence of circulating fibrinogen fibrinmonomer-FDP complexes. Ethanol gelation test was found to be positive in 28/40 subjects and soluble fibrin monomer complexes were increased in 38/40 patients. The resulting disturbance of fibrinogen-fibrin conversion was reflected by an increase in thrombin coagulase time and reptilase time. These findings suggests a state of latent compensated intravascular coagulation (presumably triggered within the vascular tumor). For diagnostic purposes the most sensitive indicator is thrombin coagulase time. Thrombin coagulase time normalised after tumor resection and was positive in patients with recurrent metastases. The increase in alkaline serum phosphatase was due to an increase in the hepatic isoenzyme. Such an increase was much more common than the elevation of total alkaline serum phosphatase. Regan's isoenzyme was only found in 1 subject. In parallel, gamma-GT was elevated in 24 patients. The study shows that Stauffer's syndrome occurs more frequently than commonly assumed when thrombin coagulase time, gamma-GT and the hepatic isoenzyme of alkaline serum phosphatase are determined in patients with renal cell carcinoma. DIC and low grade fibrinolysis may account for the coagulation abnormalities of the syndrome.

Adenocarcinoma↗
PubMed1980

Alkaline phosphatase bone isoenzyme activity in serum in various degrees of micromorphometrically assessed renal osteopathy.

Alkaline phosphatase bone isoenzyme activity in serum correlates significantly to micromorphometrically assessed parameters of bone apposition as well as resorption. Though as both processes appear to be coupled in renal osteopathy, bone isoenzyme activity seems to reflect mainly hyperosteoid states. The detection of abnormal findings is impressively better by bone isoenzyme analysis as compared with total alkaline phosphatase activity; pathological values are found even at the initial phase of osteopathy in early renal failure. The determination of alkaline phosphatase bone isoenzyme activity in serum is a sensitive and reliable diagnostic tool in assessing the beginning and degree of metabolic bone disease.

Adult↗
PubMed1977

Quantitative alkaline phosphatase isoenzyme determination by electrophoresis on cellulose acetate membranes.

We present a new method for quantitative determination of alkaline phosphatase isoenzymes. This method consists of electrophoretic separation on cellulose acetate membranes, special fixation technique to avoid elution and diffusion of enzyme protein during incubation, specific staining, and quantitative evaluation by densitometric measurement. We highly recommend the precedure for routine clinical laboratory use. In all normal individuals we observe two isoenzymes of hepatic origin and one isoenzyme each of osseous, intestinal, and biliary origin. Quantitative normal values are presented. Precision of the method is calculated, the CV being less than 10%. The exactness of densitometric quantification is proved by comparison with kinetic assay of alkaline phosphatase isoenzymes by use of an elution method. Clinical implications of alkaline phosphatase isoenzymograms are reported and discussed in detail.

Alkaline Phosphatase↗