Search PubMed⌕ Search

Biomedical subjects

G Heinemann

Publications and source records attributed to G Heinemann.

At least 19 recordsLinked to original sources
PubMed2006

[Managing the side effects of angiogenetic inhibitors in metastatic renal cell carcinoma].

Sunitinib and Sorafenib are both effective angiogenetic inhibitors for the treatment of renal cell carcinoma. With these drugs of a new class of chronic therapy is performed. During chronic treatment, the inherent side effects may necessitate stopping the application of these drugs thus preventing the required effective therapy. Most of the effects can be avoided or attenuated by prophylaxis. In this paper the published data are reviewed and added with our experience in 138 patients over up to two and a half years.

Adult↗
PubMed2000

Vanadium-contaminated perioperatively administered infusion solutions and drugs.

Vanadium was determined in 51 solutions and drugs for intravenous administration and in 6 salt components of a multitrace element solution using electrothermal atomic absorption spectrometry. The highest V contaminations were found in albumin solutions showing values of more than 600 microg/L V. Two heparines contained 14.3 and 122 microg/L V, respectively. In the ultratrace element solution, 14.8 microg/L vanadium were determined. The most contaminated salt of this solution was Mn(II)-DL-aspartate (12.8 microg V/g). The concentrations of unbound V (Vf) in the albumin solutions were between 0.31 and 299 microg/L. The manufacturing process is the reason for V contamination. The biological half-life of V administered intravenously by albumin solutions in man was about 125 h.

Albumins↗
PubMed2000

The effect of vanadium-contaminated commercially available albumin solutions on renal tubular function.

We report our findings in a patient with coronary heart disease who received an intravenous albumin solution that contained a significant level of vanadium on the first day after elective primary coronary revascularization. Six patients who underwent similar surgical procedures without albumin infusion were taken as a control group. After administration of the V-contaminated albumin solution, the urinary excretion rates of alpha-glutathione S-transferase, a marker of proximal tubular damage, showed a several-fold elevation above the reference value, and the mean excretion rate was significantly different from that of the control group (p < 0.05). pi-Glutathione S-transferase, a marker of distal tubular damage, only marginally exceeded the upper reference limit in two urine samples from this patient. In all urine samples from the control group the excretion rates of pi-GST were below the detection limit. No significant differences in the excretion rates of alpha1-microglobulin and N-acetyl-beta-D-glucosaminidase were found between the patient treated with the albumin infusion and the patients of the control group. The biological half-life of intravenously administered V was approximately 125 h. All commercially available albumin solutions contain traces of vanadium with the concentration varying between 1.1 and 677 microg/l. The free V fraction in the albumin solutions increased with total V concentration, the highest concentration of free V found being 299 microg/l. The data suggest that the use of albumin solutions containing high levels of vanadium can lead to renal injuries, especially in patients with existing impaired renal function, as is the case with extracorporal circulation. The contamination is believed to be a result of the commercial isolation process.

Albumins↗
PubMed1997

Comparative study of CD26 as a Th1-like and CD30 as a potential Th2-like operational marker in leprosy.

In the last years we have been able to establish CD26 as an operational marker for a human Th1-like reaction in various granulomatous diseases. Recently, CD30 was described as a marker for a Th2-type reaction, where CD30 is preferentially expressed and its soluble form released by human T cell clones producing Th2-type cytokines. To evaluate the possibility of CD30 as an eventual operational marker for a human Th2-like reaction in vivo, we performed immunohistological stainings on frozen sections of skin biopsies from patients with lepromatous and tuberculoid leprosy. A maximum of three to four CD30-positive cells was found per section, and there was no difference in the accumulation of CD30-positive cells between the tuberculoid and the lepromatous form of leprosy. With respect to CD26-positive cells, a high number was found in tuberculoid leprosy in contrast to a greatly reduced expression of CD26 in lepromatous leprosy. We conclude that, while CD26 was confirmed as an operational marker for a Th1-like reaction in leprosy, CD30 does not represent an operational Th2 marker in this disease.

Biomarkers↗
PubMed1996

Quantification of vanadium in serum by electrothermal atomic absorption spectrometry.

We describe an ultrasensitive and reliable method for determining vanadium in human serum by electrothermal atomic absorption spectrometry. After lyophilization, the serum is digested in acid at high pressure, and the digests are evaporated to a small volume. Vanadium in the digests is complexed with cupferron, extracted, and dried. The residue is redissolved in formic acid, where it is 15-fold more concentrated than in the original serum sample. To enhance the furnace sensitivity, we injected six 40-microL aliquots (total, 240 microL) of the concentrated extract. The median concentration of vanadium in 108 persons was 50 ng/L, in good agreement with previously reported results by neutron activation analysis. The characteristic mass obtained (the mass required to give a signal of 0.0044A. s) was 28 pg, the limit of detection 11 ng/L, the limit of quantification 17 ng/L, and the total imprecision (CV) 5.5% at 1.54 micrograms/L. In two assays of Standard Reference Material 1577a (certified vanadium content 99 +/- 8 ng/g), we obtained values of 94.1 and 97 ng/g.

Adult↗
PubMed1994

A new substitution, gamma 358 Ser-->Cys, in fibrinogen Milano VII causes defective fibrin polymerization.

Fibrinogen Milano VII is a hereditary fibrinogen variant detected in a woman with no clinical symptoms of bleeding or thrombosis. Thrombin and reptilase clotting times were prolonged in six family members from three generations. Release of fibrinopeptides A and B was normal. Fibrin polymerization was strongly delayed both in the presence and in the absence of calcium. The structural defect was determined by sequence analysis of a 290-bp fragment of genomic DNA amplified by polymerase chain reaction and cloned in M13mp19. The triplet TCT coding for the amino acid residue gamma 358 was found to be replaced by TGT, resulting in the substitution gamma 358 Ser-->Cys. Immunoblot analysis demonstrated the presence of covalently linked fibrinogen albumin and fibrinogen (albumin)2 complexes. Albumin was released from fibrinogen Milano VII by limited reduction with 2-mercaptoethanol. Fibrin polymerization was not normalized after removal of albumin from fibrinogen Milano VII, suggesting that the delayed clot formation is not due to steric hindrance caused by bound albumin but by substitution of gamma 358 Ser by Cys itself. Our results indicate that the residue gamma 358 Ser is essential for normal expression of the carboxy terminal polymerization site on the fibrinogen gamma-chain.

Adult↗
PubMed1994

Fibrinogen Milano V: a congenital dysfibrinogenaemia with a gamma 275 Arg-->Cys substitution.

An abnormal fibrinogen was discovered in a clinically asymptomatic woman from Italy. Routine coagulation studies revealed prolonged thrombin and reptilase clotting times and a discrepancy between the plasma fibrinogen levels determined by the clotting assay and electroimmunoassay. Release of fibrinopeptides A and B from fibrinogen Milano V by thrombin was normal. Fibrin polymerization was strongly delayed in the presence of EDTA and was partially corrected at physiological calcium concentration. Normal migration of mercaptolysed polypeptide chains was observed in polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulphate. Moreover, there was no apparent abnormality in the charge of the reduced chains of the variant fibrinogen, as judged by two-dimensional gel electrophoresis. A fragment of the gamma-chain gene coding for the amino acids 259-350 was amplified and cloned. The amino acid gamma 275 arginine was found to be substituted by cysteine. Immunoblotting analysis with a rabbit antiserum against human serum albumin indicated that albumin was not linked to the odd sulphydryl group of fibrinogen Milano V. Treatment of fibrinogen Milano V with cysteamine, that is surmised to convert the mutant cysteine to a positively charged lysine analogue, did not improve the clotting properties of fibrinogen Milano V.

Afibrinogenemia↗
PubMed1993

Fibrinogen Bern I: substitution gamma 337 Asn-->Lys is responsible for defective fibrin monomer polymerization.

An inherited fibrinogen variant, fibrinogen Bern I, was isolated from plasma of an asymptomatic woman. Routine coagulation studies showed prolonged thrombin and reptilase clotting times. Fibrinogen concentration was diminished when determined by a functional assay, but was normal by the heat precipitation method. The release of fibrinopeptides A and B was not delayed. Two-dimensional gel electrophoresis of mercaptolyzed fragments D of fibrinogen, obtained by digestion with plasmin, showed an abnormal electrophoretic mobility in the gamma-chain remnants of fragments D1 and D2 from fibrinogen Bern I, whereas conversion of D2 to D3 by plasmin resulted in the loss of the abnormal charge, suggesting that the structural abnormality in this variant is located in the region gamma 303 through 356. The molecular defect in fibrinogen Bern I was identified by sequence analysis of genomic DNA amplified by polymerase chain reaction and cloned in M13mp19. The triplet AAC coding for asparagine at position gamma 337 was found to be substituted by AAA coding for lysine. We conclude that the substitution gamma 337 Asn-->Lys in fibrinogen Bern I is responsible for defective polymerization of fibrin monomers and for impaired protection by calcium against plasmic degradation.

Adult↗
PubMed1990

Determinants of left ventricular hypertrophy in arterial hypertension.

A long term study (2-7 years, mean 3.6 years) monitoring 112 clinical and echocardiographic pattern in 593 hypertensives and 156 normotensives was performed in order to find associations to left ventricular hypertrophy (LVH) developing later. 49% of the hypertensives developed echocardiographic signs of LVH (wall thickness of 12 mm and more), in contrast to 5.1% of normotensive persons. Multivariate analysis revealed the following parameters examined at entry were associated with LVH on follow-up: male sex, prolonged hypertensive history, higher diastolic blood pressure, frequent lipid-metabolism disturbances, uncharacteristic chest pain and less effective antihypertensive treatment. Thus, LVH development can be regarded as a multifactorial process.

Cardiac Volume↗
PubMed1990

Combined Doppler and M-mode analysis of diastolic filling behaviour in arterial hypertension with and without left ventricular hypertrophy.

The authors analysed Doppler and M-mode derived diastolic parameters of left ventricular filling in patients with arterial hypertension with and without left ventricular hypertrophy (LVH) and with hypertrophic nonobstructive cardiomyopathy (HNCM). In hypertrophied hearts they demonstrated that the transmitral flow during rapid filling phase was significantly reduced. The lower early diastolic flow is compensated by an augmentation of atrial systole. Diastolic filling anomalies are the consequence of an impaired ventricular relaxation due to LVH as could been proved by the M-mode derived retraction constant Te. Diastolic filling anomalies significantly depend on the extent of left ventricular hypertrophy. Impaired diastolic function was found in hypertensive patients without LVH. In this case, diastolic disorders indicate an early involvement of the heart in the hypertensive process.

Adult↗
PubMed1988

Human carbonyl reductase. Nucleotide sequence analysis of a cDNA and amino acid sequence of the encoded protein.

Carbonyl reductase (EC 1.1.1.184) is one of several monomeric, NADPH-dependent oxidoreductases having wide specificity for carbonyl compounds that are generally referred to as the aldoketoreductases. The grouping of the enzyme into the family has been proposed on the basis of functional similarities and in the absence of structural data. Here, we describe the isolation and characterization of a cDNA clone complementary to human carbonyl reductase mRNA from a human placenta cDNA library constructed in phage lambda gt11. The cDNA consists of 1199 base pairs and contains an open reading frame encoding a protein comprised of 277 amino acids with a Mr of 30,375. The predicted amino acid sequence was confirmed by partial sequence analysis of the carbonyl reductase protein. Comparison of the protein sequence with the primary structures of other aldoketoreductases revealed no significant homologies. A possible homology, on the other hand, exists between carbonyl reductase and "short" subunit alcohol/polyol dehydrogenases.

Alcohol Oxidoreductases↗
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↗
PubMed1987

Highly significant negative correlations between erythrocyte aggregation value and serum concentration of high density lipoprotein cholesterol in a sample from a normal population and in patients with coronary heart disease.

In a previous clinical study it was found that patients with coronary heart disease and diabetics with peripheral artery disease often have an elevated erythrocyte aggregation value (AW) and that there is a positive correlation between AW and the number of risk factors found in a subject. In the present investigation we studied the relationship between AW and the serum concentration of high density lipoprotein cholesterol (HDL-C), which is known to be inversely associated with coronary heart disease (CHD) incidence. We found highly significant negative correlations between AW and HDL-C both in a subsample of the study population of a cross-sectional epidemiologic study on CHD risk factors (First Survey of the MONICA Project Augsburg) and in male patients with angiographically confirmed CHD. Correlation coefficients were -0.233 for normal men (P less than 0.01, n = 136), -0.261 for normal women (P less than 0.01, n = 117), and -0.745 for CHD patients (P less than 0.01, n = 14). The results support the concept that the erythrocyte aggregation value as an indicator of cardiovascular risk is consistent with established risk factor associations.

Adult↗
PubMed1987

Gold colitis induced by auranofin treatment of rheumatoid arthritis: case report and review of the literature.

A case of ulcerative colitis occurred during treatment of rheumatoid arthritis with the new oral gold preparation auranofin after a cumulative dose of 2160 mg. A barium enema showed loss of mucosal pattern and a rectal biopsy disclosed deep erosions, mucosal inflammation, and crypt abscesses. Precipitates of gold were seen in the periglandular stroma. On electron microscopy the gold deposits seemed to be identical to granules described in gold nephropathy. As the extrapolated serum gold level was within the normal range at the onset of the complication, the morphological findings suggested a local toxicity of the drug. The patient recovered within 14 days of withdrawal of auranofin and the start of therapy with sulphasalazine and steroids. A review of the published work shows that the previously reported mortality in gold colitis of 40% has decreased in recent years. The causes of this decrease may be both the earlier diagnosis of gold colitis and the improved intensive care of its severe complications.

Arthritis, Rheumatoid↗