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Biomedical subjects

B Lauer

Publications and source records attributed to B Lauer.

At least 55 records · Page 3Linked to original sources
PubMed1997

[Comparative studies of the rate of restenosis after implantation of Palmaz-Schatz and AVE-Micro stents].

Late results of interventional procedures utilizing coronary stents are largely determined by the rate of restenosis. So far few data are available addressing the effect of stent design, implantation pressure and morphologic factors on this crucial variable. Therefore we analyzed the coronary angiograms obtained in 259 patients before, immediately after and at 3 to 6 months following stent implantation for obstructive coronary disease. A total of 196 AVE-Micro-Stents and 142 Palmaz-Schatz-Stents were implanted into 307 stenoses. In 126 stenoses there were implanted only Palmaz-Schatz-Stents, in 170 only AVE-Micro-Stents and in 11 stenoses there were implanted Palmaz-Schatz- as well as Micro-Stents. Restenosis was defined as an over 50% stenosis at follow up. No significant difference was detected with regard to global restenosis rate at an average of 4 months following implantation (Palmaz-Schatz 33%, Micro-Stent 27%). If results were analyzed according to implantation pressure however, there was a significantly lower restenosis rate for AVE-Micro-Stents implanted with > 10 atm (17%) as compared to < or = 10 atm (35%, p < 0.02) and as compared to Palmaz-Schatz-Stents (34%, p < 0.02), which were also implanted with high pressure over 10 atm. In addition to implantation pressure, vessel segment and morphology of stenosis proved to be important determinants of late results. In this series of patients the AVE-Micro-Stent compared favourably to the Palmaz-Schatz-Stent not only with respect to a significantly lower restenosis rate, when implanted with pressures > 10 atm, but also with regard to its superior flexibility and handling characteristics.

Aged↗
PubMed1997

Detection of mRNA and immunoreactive proteins for acidic and basic fibroblast growth factor and expression of the fibroblast growth factor receptors in the bovine oviduct.

The heparin-binding acidic and basic fibroblast growth factors (aFGF, bFGF) and their receptors in the bovine oviduct are described. By means of western blot analysis one 18 kDa aFGF and two bFGF proteins (16 and 18 kDa, respectively) were detected in oviductal flushings. Different concentrations of these two growth factors could be measured in oviductal flushings during the oestrous cycle: concentrations of aFGF protein were significantly higher at ovulation (mean +/- SEM; 5.3 +/- 0.5 ng ml-1) than during the luteal phase (3.0 +/- 0.3 ng ml-1); concentrations of bFGF were higher at the preovulatory stage (3.5 +/- 0.7 ng ml-1) than at the post-ovulatory stage (1.3 +/- 0.15 ng ml-1). Immunohistochemical studies using a/bFGF-specific antibodies indicated that these growth factors were localized mainly in oviduct epithelial cells. The sequence of the bovine FGF receptor (FGFR) was partly determined. Quantification of mRNAs by an RNase-protection assay (RPA) showed that expression of aFGF and bFGF was different during the oestrous cycle, indicating that the regulation of aFGF is separate from that of bFGF. Only mRNA encoding bFGF and FGFR could be detected in cumulus-oocyte complexes by reverse transcription PCR. In summary, the components of the FGF system were found in the bovine oviduct suggesting an autocrine or paracrine regulation involving oviduct cells and cumulus-oocyte complexes.

Animals↗
PubMed1995

[Recurrent immune thrombocytopenia: a rare complication after contrast medium injection].

HISTORY AND CLINICAL FINDINGS: In a 66-year-old woman with unstable angina, treated with 20,000 IU heparin daily for 6 days, platelet count fell dramatically from 310,000 to 1000/microliters 8 hours after injection of 90 ml of contrast medium (Iopromide) during coronary angiography. In addition to a marked tendency towards spontaneous bleeding she developed a large haematoma at the site of the arterial puncture, with a fall in haemoglobin to 9 g/dl, and acute renal failure. TREATMENT AND COURSE: Red blood cell and platelet infusions were given, together with cortisone, 1000 mg, and immunoglobulins. Platelet count returned to within normal limits after 8 days. Two haemodialyses initiated polyuria, followed by rapid normalization of kidney function. No antibodies against iopromide, iopamidol, heparin or heparinoids were found. At an emergency coronary balloon angioplasty 3 weeks later iopamidol was injected (45 ml). Again there was a profound fall in platelets to 1000/microliters, associated with acute renal failure. Treatment identical to that after the first episode brought about complete normalization. CONCLUSION: The reported reactions were most likely due to immune thrombocytopenia after administration of contrast medium.

Acute Kidney Injury↗
PubMed1995

[Autoantibodies against cardiac myosin in patients with myocarditis and dilated cardiomyopathy].

Evidence accumulated in recent years indicates that autoimmunologic mechanisms may play an important role in the pathogenesis of myocarditis and dilated cardiomyopathy. In animal studies with Coxsackie B3-virus-induced murine myocarditis circulating autoantibodies against cardiac myosin have been detected. The present study investigates whether in patients with myocarditis and dilated cardiomyopathy antimyosin-autoantibodies can be detected. Patients with other cardiac diseases and healthy blood donors were used as controls. In 30 of 62 (48.4%) patients with myocarditis antimyosin-antibodies could be detected, whereas in patients with dilated cardiomyopathy only 10 of 41 (24.4%) sera contained antimyosin-antibodies (p < 0.05). In patients with other cardiac diseases, 9 of 43 (21%) sera showed antimyosin-autoantibodies (p < 0.05 vs myocarditis, not significant vs DCM). In healthy blood donors, antimyosin-autoantibodies could only be detected in 1 of 39 (2.5%) sera. In Western-blot tests, the antimyosin-antibodies in patients with myocarditis bound to the myosin heavy chain. Protein A-Sepharose chromatography showed that the antimyosin-autoantibodies are of the IgG-type. No organ-specificity of the antibodies for cardiac myosin could be detected, and the antimyosin-autoantibodies bind equally to myosin prepared from either cardiac or skeletal muscle, respectively.

Autoantibodies↗
PubMed1994

Food restriction eliminates preneoplastic cells through apoptosis and antagonizes carcinogenesis in rat liver.

Restriction of dietary calories reduces cancer formation in experimental animals and probably also in humans. This effect is generally attributed to the inhibitory effect of fasting on cell proliferation. Here we studied the effect of fasting on physiological cell death through apoptosis by using rat liver as a model. (i) In normal liver, involution of hyperplasia by apoptosis was reinforced by food withdrawal and suppressed by feeding. Complete food withdrawal for 8 days or food reduction by 40% for 3 months eliminated 20-30% of normal liver cells through apoptosis. (ii) Putative preneoplastic liver foci exhibited severalfold higher rates of DNA replication and apoptosis than unaltered liver. Food restriction lowered DNA replication but increased apoptosis, which reduced the number and volume of putative preneoplastic liver foci by 85% within 3 months. Subsequent return to ad libitum feeding normalized cell replication and apoptosis but clear differences in the volume and number of putative preneoplastic liver foci persisted throughout the following 17 months. Treatment of animals after food restriction with nafenopin, a peroxisome proliferator and potent tumor promoter, produced only half as many hepatocellular adenomas and carcinomas as in animals fed unrestrictedly throughout their lifetime. This indicates that food restriction had actually eliminated a part of the initiated cells. This study demonstrates that food restriction preferentially enhances apoptosis of preneoplastic cells. This effect in combination with lowered cell replication provides protection from carcinogenesis.

Animals↗
PubMed1994

Autoantibodies against human ventricular myosin in sera of patients with acute and chronic myocarditis.

OBJECTIVES: The present study investigated the presence of antimyosin autoantibodies in sera of patients with myocarditis and in three control groups: healthy blood donors, patients with alcoholic cardiomyopathy and patients with other cardiac diseases. BACKGROUND: An increasing body of evidence indicates that in the course of myocarditis, autoimmunologic mechanisms may play a pathogenetic role. Animal studies with Coxsackie B3 virus-induced murine myocarditis could demonstrate the appearance of circulating autoantibodies against cardiac myosin. METHODS: Sera were analyzed by enzyme-linked immunosorbent assay (ELISA) and Western blot with human left ventricular myosin as antigen. RESULTS: Seventeen (42%) of 40 serum samples from patients with myocarditis showed antibody-binding against myosin, whereas only 1 (2.5%) of 39 samples from healthy blood donors and 9 (21%) of 43 samples from patients with other cardiac diseases showed autoantibodies against myosin (p < 0.05 vs. myocarditis). In sera from patients with alcoholic cardiomyopathy (n = 12), no antibodies against human ventricular myosin could be detected. In Western blots, the antimyosin antibodies in patients with myocarditis bound to the myosin heavy chain. Using protein-A sepharose chromatography, it could be shown that the antimyosin autoantibodies are of the immunoglobulin G (IgG) type. In ELISA, the antimyosin autoantibodies bind equally to myosin prepared from either cardiac or skeletal muscle, respectively. CONCLUSIONS: These results demonstrate the presence of autoantibodies against human ventricular myosin in patients with myocarditis. The prevalence of these autoantibodies is significantly higher in patients with myocarditis than in patients with other cardiac diseases. No organ specificity of the autoantibodies could be detected.

Acute Disease↗
PubMed1994

Genetic identification of a new Puumala virus strain causing severe hemorrhagic fever with renal syndrome in Germany.

A severe case of suspected hemorrhagic fever with renal syndrome (HFRS) was recently identified in northwestern Germany. A genetic detection assay was designed that identified hantavirus-specific RNA in the patient's clinical specimens by reverse transcriptase-polymerase chain reaction amplification of virus S and M genome segments. Phylogenetic analysis of the nucleotide sequences demonstrated that this virus belonged to the Puumala (PUU) group, with the closest relationship to a PUU isolate from Finland. Within the group, this virus formed a separate lineage. This finding represents the first genetic characterization of a hantavirus causing severe HFRS in Germany. The data suggest that PUU viruses circulating in western European countries are genetically distinct from their northeastern counterparts. Comparison of deduced amino acid sequences demonstrated a loss of a potential N-glycosylation site in the G2 protein compared with other PUU viruses.

Amino Acid Sequence↗
PubMed1992

[Malignant hemangioendotheliosarcoma in the area of the right coronary artery: imaging by selective coronary angiography].

We report on a case of a malignant hemangioendotheliosarcoma in the right coronary artery. The first manifestation was a pericardial tamponade from a hemorrhagic pericardial effusion. The diagnosis was established only by selective coronary angiography of the right coronary artery, other imaging procedures did not lead to the diagnosis. During follow-up, multiple angiosarcoma developed in the liver, the spleen and, finally, in the lungs. Despite multichemotherapy, the patient died 7 months after the first manifestation.

Biopsy↗
PubMed1990

Serum IgG subclass antibody responses in children vaccinated with influenza virus antigens by live attenuated or inactivated vaccines.

To ascertain whether live attenuated or inactivated vaccines can be considered equivalent, we examined the primary antibody response of children following vaccination with influenza virus antigens in three different formulations. Nine children received cold recombinant vaccine (CRV) containing A/Korea/82 (H3N2) and A/Dunedin/83 (H1N1) variants. Eight of these children responded to HA of the H3N2 subtype and the major portion of the elicited antibody was in the IgG1 subclass. Antibody of low titer in the IgG2 and IgG3 subclasses was detected in two and six serum specimens, respectively. Six of the nine children administered with CRV responded to the H1 antigen and only IgG1 antibody was detected. Serum specimens from eight children less than one year of age (5 less than 6 months of age) who had developed an antibody response to trivalent inactivated vaccine (TIV) vaccination were examined. High levels of IgG1 antibody to purified H3 were detected in all eight children. Low titers of antibody in IgG2 and IgG3 subclasses were detected in two and five children, respectively. Antibody responses to purified H1 showed a similar subclass distribution. In order to examine secondary response, eight children primed by immunization with TIV vaccine were subsequently given a single booster dose of purified hemagglutinin (HA) conjugated to diphtheria toxoid (HA-D). In 6/8 specimens antibody rises were detected to purified H3 and H1 antigens. Prior to the HA-D immunization, low levels of HA specific IgG1 antibody were detected in all serum specimens and vaccine induced responses were primarily of the IgG1 subclass.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

ATPase activity of the cross-linked complex between cardiac myosin subfragment 1 and actin in several models of chronic overloading. A new approach to the biochemistry of contractility.

Myosin ATPase activity is usually considered to reflect the contractile capacity of a given muscle since it correlates with the maximum initial speed of shortening of the unloaded muscle (Vmax). There are several exceptions to this scheme, and it was the goal of this study to determine if the Mg2+-ATPase activity of the covalently bound actomyosin S1 is a more physiological index of contractility. On polyacrylamide gels, the complex obtained after condensation of fast skeletal myosin S1 to skeletal actin is identical to that obtained with myosin S1 from the ventricles of different species, including rat, guinea pig, and human, cross-linked to cardiac or skeletal actin. In every condition, the ATPase activity of the complex is 700-fold higher than that of myosin S1. It correlates linearly with the Vmax both in phylogeny and in conditions in which an isomyosin shift has been reported, such as hypothyroidism and chronic cardiac overload. Such a relation indicates that, in species that already have a low Vmax, a small change in myosin ATPase may induce dramatic consequences in the shortening velocity. Cardiac hypertrophy in humans, where the drop in Vmax is not associated with a myosin change, does not fit into this scheme. The enzymatic activity of the complex is also unmodified in this condition, which shows that, in humans, the myosin ATPase is not a determinant of Vmax and suggests that other mechanisms may be involved. Measurement of this type of ATPase activity provides a new tool to explore contractility biochemically, which is more reproducible and, from a technical point of view, easier to perform than a kinetic assay. It also correlates better with mechanical data obtained with skinned fibers than with those measured on fresh papillary muscles.

Actins↗
PubMed1988

Striated muscle overload.

In response to increasing demand, cardiac muscle develops several adaptational mechanisms. Gene expression is modified: the heart hypertrophies and its structure changes in order to improve the efficiency of the contraction. The sarcomere modifications are both species and tissue specific. An isoenzymic shift of myosin from the high ATPase activity form V1 to the slow activity form V3 occurs in all conditions where V1 is initially predominant, i.e. rat (and also rabbit) ventricles and the atria of other species, including humans. The isoenzymic shift was not observed in conditions where V3 is predominant, as in human (and also cat and pig) ventricles. Similar changes are observed in skeletal muscle suggesting that the primary determinant of these modifications is not dependent on the innervation but only on the mechanical activity.

Adult↗
PubMed1987

Adaptational changes of sarcomere and sarcolemma during chronic cardiac overloading in rats and in humans.

In response to increasing demand, the cardiac muscle has developed several adaptational mechanisms. Gene expression is modified in a quantitative and a qualitative way since the heart hypertrophies and since its structure changes to improve the efficiency of the contraction. The sarcomere modifications are both species- and tissue-specific. An isoenzymic shift of myosin from high adenosine triphosphatase (ATPase) activity form V-1 to low activity form V-3 occurs in all conditions in which V-1 is initially predominant, i.e., in rat (and also rabbit) ventricles and the atria of other species, including humans. It was not observed in conditions in which V-3 was predominant, as in human ventricles (and also in those of cats and pigs). Another shift from creatine kinase (CK) monomer M to CK B, the form that predominates in the fetal heart, is also observed. The sarcolemma is also modified, at least in rats. The digitalis receptor was characterized by studying the inotropic effect of the drug on an isolated heart preparation and on a purified preparation of sarcolemma with a high Na+,K(+)-ATPase activity by binding [3H]ouabain and ouabain-induced inhibition of the enzymatic activity. In hypertrophied heart, both the recovery of normal contractility after ouabain infusion and the release of previously bound ouabain infusion and the release of previously bound ouabain were slowed, as for fetal hearts. Changes in other inotropic receptors have also been reported. From a practical point of view, this means that screening of new inotropic agents has to be done on hypertrophied hearts and not, as usual, on normal tissue.

Adult↗
PubMed1985

Quantitative histological and histochemical studies on the occurrence and stages of controlled cell death (apoptosis) during regression of rat liver hyperplasia.

Hyperplasia of the rat liver can be induced by cyproterone acetate (CPA). The fate of this hyperplasia after cessation of CPA treatment has been studied and the following findings were obtained: Liver DNA content decreased by about 25% within a few days after CPA withdrawal. In histological sections some hepatocytes showed degenerative changes. Among these, small membrane bounded bodies ("apoptotic bodies"; ABs) with or without chromatin were most numerous. Their incidence coincided with the phase of DNA elimination. Inflammatory reactions were not observed. Their small size and occurrence in clusters suggests that many of these ABs are formed by fragmentation of dying hepatocytes. Liver DNA was prelabelled with 3H-thymidine. Autoradiographic evaluation showed that many hepatocytes contained labelled nuclei, but unlabelled ABs. This finding strongly suggests that ABs, after the fragmentation stage, can be phagocytized by intact hepatocytes. About 80% of all ABs were found within hepatocytes. Extracellular ABs (early stage) contained no or very few active lysosomes. Intracellular ABs were sometimes surrounded by lysosomes, while others were in various stages of digestion. These observations suggest that the lysosomes of the phagocytizing hepatocytes degrade intracellular ABs, whereas intraapoptotic lysosomes seem to be inactive until the late stages of this degradation. Hepatocytes that did not replicate during CPA-induced liver growth appear to die off preferentially after CPA withdrawal. Retreatment with CPA greatly reduced the number of ABs within 4 h. Phenobarbital, another stimulus of liver growth, had the same effect. These findings suggest that the present type of cell death can be inhibited by growth stimuli and is therefore a controlled event serving to eliminate an excess of cells, rather than a manifestation of toxic injury to hepatocytes. The findings also suggest that this type of cell death and elimination is a rapid process completed within a few hours. It is concluded that cell death under the present experimental conditions probably occurs through apoptosis.

Animals↗
PubMed1984

Controlled death (apoptosis) of normal and putative preneoplastic cells in rat liver following withdrawal of tumor promoters.

Numerous drugs, hormones and environmental pollutants induce liver growth by hypertrophy and/or hyperplasia, and promote preferential growth of putative preneoplastic foci in the liver. In the present study the regression of hyperplasia after cessation of inducer/promoter treatment was studied in normal liver and in liver foci. High doses of cyproterone acetate (CPA), a synthetic sex steroid, were administered to rats and produced a doubling of liver size; after cessation of treatment liver size declined, and 27% of the total liver DNA disappeared within 6 days. In histological sections from the involuting liver no necroses, but numerous apoptotic bodies (ABs) were found; retreatment with CPA interrupted the formation of ABs. These findings suggest that elimination of excess liver DNA after cessation of CPA treatment is due to controlled cell death by apoptosis. In a further series of experiments putative preneoplastic foci were produced by a single dose of N-nitrosomorpholine and subsequently stimulated to grow by 10 or 28 weeks of phenobarbital (PB) treatment. After withdrawal of PB numerous ABs were present in normal liver and in the foci; in both, retreatment with PB decreased the appearance of ABs. It appears that inhibition of cell death by PB may contribute to tumour promotion. Under all conditions tested more ABs were found in the foci than in non-focal parts of the liver, suggesting an enhanced cell turnover in foci. The apparent sensitivity of foci to mechanisms controlling cell death might eventually provide a means for elimination of preneoplastic lesions.

Animals↗
PubMed1975

[The serum and uterine muscle concentrations of Cephradin and Cephalothin].

On the day of operation 2 grams of Cephradin was given intravenously to 33 patient and 2 grams of Cephalothin was given intravenously to 31 patients. At various time intervals, uterine tissue and serum was removed. The mean serum concentrations of Cephradin were 3 times higher and the mean tissue concentrations of Cephradin were 7-8 times higher than the corresponding concentrations of Cephalothin. Because of the difference in protein binding of the examined cephalosporins (Cephradin 6%, Cephalothin 60-65%) the difference for the antimicrobially active portion (Protein free portion) is even more favorable for Cephradin. The significance of these pharmacokinetic differences for the treatment are obvious.

Adult↗