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U Maier

Publications and source records attributed to U Maier.

At least 19 recordsLinked to original sources
PubMed2000

Power consumption in shaking flasks on rotary shaking machines: I. Power consumption measurement in unbaffled flasks at low liquid viscosity.

In this first article of a series a new method is introduced that enables the accurate determination of the power consumption in a shaking flask. The method is based on torque measurements in the drive and appropriate compensation of the friction losses. The results for unbaffled shaking flasks at low viscosities are presented after varying shaking frequency, flask size, filling volume, shaking diameter, and surface quality (hydrophilic and hydrophobic) of the inner flask walls. The order of magnitude of the values of power consumption in shaking flasks is equal to, or even higher than, the values typical for agitated tank bioreactors. A physically based model equation for shaking flasks is derived that introduces a modified power number and a resulting constant as the only fitting parameter. With this equation, the measured results are correlated with sufficient accuracy. For the first time, comprehensive data for the power consumption in unbaffled shaking flasks at low viscosity is available, giving a detailed picture of the influences of the different variables.

Biotechnology↗
PubMed2000

Power consumption in shaking flasks on rotary shaking machines: II. Nondimensional description of specific power consumption and flow regimes in unbaffled flasks at elevated liquid viscosity.

This article is the second part of a series presenting and modeling the hydrodynamics and specific power consumption in shaking flasks on rotary (orbital) shaking machines. In part I, a new method was introduced that enables the accurate determination of the specific power consumption in shaking flasks. The method was first applied to investigate unbaffled flasks with a nominal volume of < or =1 L at low viscosity. In part II, the results for the specific power consumption of unbaffled shaking flasks at elevated viscosities are investigated after varying shaking frequency, flask size, filling volume, and shaking diameter. The theory introduced in part I is extended to liquids of elevated viscosities using nondimensional equations. With these results, the specific power consumption in unbaffled shaking flasks can now be fully described. For the first time, the phenomenon of the liquid being "out of phase" is observed and described. This occurs at certain operating conditions and is characterized by an increasing amount of liquid not following the movement of the shaking table, thus reducing the specific power consumption. This, of course, has much relevance for practical work with microbial cultures. The phenomenon of being "out-of-phase" is described in the form of a newly defined nondimensional phase number (Ph) in analogy to a partially filled, rotating horizontal drum. The Ph can be used to determine reasonable operating conditions for shaking flask experiments when using viscous media, avoiding unfavorable "out-of-phase" operation.

Biotechnology↗
PubMed2000

Gbeta 5gamma 2 is a highly selective activator of phospholipid-dependent enzymes.

In this study, Gbeta specificity in the regulation of Gbetagamma-sensitive phosphoinositide 3-kinases (PI3Ks) and phospholipase Cbeta (PLCbeta) isozymes was examined. Recombinant mammalian Gbeta(1-3)gamma(2) complexes purified from Sf9 membranes stimulated PI3Kgamma lipid kinase activity with similar potency (10-30 nm) and efficacy, whereas transducin Gbetagamma was less potent. Functionally active Gbeta(5)gamma(2) dimers were purified from Sf9 cell membranes following coexpression of Gbeta(5) and Ggamma(2-His). This preparation as well as Gbeta(1)gamma(2-His) supported pertussis toxin-mediated ADP-ribosylation of Galpha(i1). Gbeta(1)gamma(2-His) stimulated PI3Kgamma lipid and protein kinase activities at nanomolar concentrations, whereas Gbeta(5)gamma(2-His) had no effect. Accordingly, Gbeta(1)gamma(2-His), but not Gbeta(5)gamma(2-His), significantly stimulated the lipid kinase activity of PI3Kbeta in the presence or absence of tyrosine-phosphorylated peptides derived from the p85-binding domain of the platelet derived-growth factor receptor. Conversely, both preparations were able to stimulate PLCbeta(2) and PLCbeta(1). However, Gbeta(1)gamma(2-His), but not Gbeta(5)gamma(2-His), activated PLCbeta(3). Experimental evidence suggests that the mechanism of Gbeta(5)-dependent effector selectivity may differ between PI3K and PLCbeta. In conclusion, these data indicate that Gbeta subunits are able to discriminate among effectors independently of Galpha due to selective protein-protein interaction.

Enzyme Activation↗
PubMed2000

Comparative study of two different TRUS-guided sextant biopsy techniques in detecting prostate cancer in one biopsy session.

OBJECTIVE: The aim of this study was to compare a transrectal ultrasound (TRUS)-guided sextant biopsy technique, which puts more emphasis on the apical region of the prostate where most prostate carcinomas (PCs) develop, with the standard sextant biopsy technique. METHODS: A total of 280 patients with suspected PC were included in this analysis. Twelve biopsy cores were obtained from all patients. Six biopsy cores were taken within a lateral parasagittal plane from each lobe at the apex, middle and basis, with an angle of approximately 45 degrees (technique A), and 6 further biopsy cores were taken from the left to the right lateral margin always penetrating the prostate in the apex with the same angle (socalled fan-shaped technique, technique B). Technique A predominantly samples in the sagittal and technique B samples more in the transversal plane with emphasis on the apical region where most PCs develop. The sensitivity in detecting PCs for both techniques was calculated and correlated to the serum prostate-specific antigen (PSA) levels. RESULTS: A total of 72 PCs (25.7%) were diagnosed. We subsequently performed subgroup analysis depending on the serum PSA levels: in patients with a PSA of </=10 ng/ml (n = 27) technique A has a PC sensitivity of 88.8% (p = 0.037) and technique B 96.2% (p = 0.326) as compared to our reference standard of 100% by sampling 12 biopsy cores in the same prostate. The number of positive biopsy cores using technique B was superior in 12 cases as compared to 3 cases with technique A (p = 0.04). In 12 patients the number of positive biopsy cores was identically. In patients with a PSA of >10 ng/ml (n = 45) technique A has a PC sensitivity of 93.3% (p = 0.083) and technique B 88.8% (p = 0.023) as compared to our reference standard. The number of positive core biopsies using technique A was superior in 14 cases as compared to 12 with technique B (p = 0.154). In 19 patients the number of positive biopsies was identical. CONCLUSION: Our data suggest that in patients with PSA of </=10 ng/ml technique B bring significant benefit with regard to the number of positive core biopsies, as well as an enhanced PC detection rate which is near the 12-core biopsy. Due to the fact that technique B samples more in the apical region where most cancers develop, it should be performed in suspected early stage cancers of the prostate (PSA</=10 ng/ml).

Adolescent↗
PubMed1999

Roles of non-catalytic subunits in gbetagamma-induced activation of class I phosphoinositide 3-kinase isoforms beta and gamma.

By using purified preparations we show that nanomolar concentrations of Gbetagamma significantly stimulated lipid kinase activity of phosphatidylinositol 3-kinase (PI3K) beta and PI3Kgamma in the presence as well as in the absence of non-catalytic subunits such as p85alpha or p101. Concomitantly, Gbetagamma stimulated autophosphorylation of the catalytic subunit of PI3Kgamma (EC(50), 30 nM; stoichiometry >/=0.6 mol of P(i)/mol of p110gamma), which also occurred in the absence of p101. Surprisingly, we found that p101 affected the lipid substrate preference of PI3Kgamma in its Gbetagamma-stimulated state. With phosphatidylinositol as substrate, p110gamma but not p101/p110gamma was significantly stimulated by Gbetagamma to form PI-3-phosphate (EC(50), 20 nM). The opposite situation was found when PI-4,5-bisphosphate served as substrate. Gbetagamma efficiently and potently (EC(50), 5 nM) activated the p101/p110gamma heterodimer but negligibly stimulated the p110gamma monomer to form PI-3,4,5-trisphosphate. However, this weak stimulatory effect on p110gamma was overcome by excess concentrations of Gbetagamma (EC(50), 100 nM). This finding is in accordance with the in vivo situation, where activated PI3K catalyzes the formation of PI-3,4,5-trisphosphate but not PI-3-phosphate. We conclude that p101 is responsible for PI-4, 5-bisphosphate substrate selectivity of PI3Kgamma by sensitizing p110gamma toward Gbetagamma in the presence of PI-4,5-P(2).

Androstadienes↗
PubMed1999

Differential distribution of G-protein beta-subunits in brain: an immunocytochemical analysis.

Heterotrimeric G proteins play central roles in signal transduction of neurons and other cells. The variety of their alpha-, beta-, and gamma-subunits allows numerous combinations thereby confering specificity to receptor-G-protein-effector interactions. Using antisera against individual G-protein beta-subunits we here present a regional and subcellular distribution of Gbeta1, Gbeta2, and Gbeta5 in rat brain. Immunocytochemical specificity of the subtype-specific antisera is revealed in Sf9 cells infected with various G-protein beta-subunits. Since Gbeta-subunits together with a G-protein gamma-subunit affect signal cascades we include a distribution of the neuron-specific Ggamma2- and Ggamma3-subunits in selected brain areas. Gbeta1, Gbeta2, and Gbeta5 are preferentially distributed in the neuropil of hippocampus, cerebellum and spinal cord. Gbeta2 is highly concentrated in the mossy fibres of dentate gyrus neurons ending in the stratum lucidum of hippocampal CA3-area. High amounts of Gbeta2 also occur in interneurons innervating spinal cord alpha-motoneurons. Gbeta5 is differentially distributed in all brain areas studied. It is found in the pyramidal cells of hippocampal CA1-CA3 as well as in the granule cell layer of dentate gyrus and in some interneurons. In the spinal cord Gbeta5 in contrast to Gbeta2 concentrates around alpha-motoneurons. In cultivated mouse hippocampal and hypothalamic neurons Gbeta2 and Gbeta5 are found in different subcellular compartments. Whereas Gbeta5 is restricted to the perikarya, Gbeta2 is also found in processes and synaptic contacts where it partially colocalizes with the synaptic vesicle protein synaptobrevin. An antiserum recognizing Ggamma2 and Ggamma3 reveals that these subunits are less expressed in hippocampus and cerebellum. Presumably this antiserum specifically recognizes Ggamma2 and Ggamma3 in combinations with certain G alphas and/or Gbetas. The widespread but regionally and cellularly rather different distribution of Gbeta- and Ggamma2/3-subunits suggests that region-specific combinations of G-protein subunits mediate signal transduction in the central nervous system. The different subcellular distribution of Gbeta-subunits in cultivated neurons reflects that observed in tissue where Gbeta5 and Gbeta2 associate preferentially with the perikarya and the neuropil, respectively, and suggests an additional association of Gbeta2 with secretory vesicles.

Amino Acid Sequence↗
PubMed1999

Gbetagamma dimers stimulate vascular L-type Ca2+ channels via phosphoinositide 3-kinase.

We have previously reported that, in venous myocytes, Gbetagamma scavengers inhibit angiotensin AT1A receptor-induced stimulation of L-type Ca2+ channels (1). Here, we demonstrate that intracellular infusion of purified Gbetagamma complexes stimulates the L-type Ca2+ channel current in a concentration-dependent manner. Additional intracellular dialysis of GDP-bound inactive Galphao or of a peptide corresponding to the Gbetagamma binding region of the beta-adrenergic receptor kinase completely inhibited the Gbetagamma-induced stimulation of Ca2+ channel currents. The gating properties of the channel were not affected by intracellular application of Gbetagamma, suggesting that Gbetagamma increased the whole-cell calcium conductance. In addition, both the angiotensin AT1A receptor- and the Gbetagamma-induced stimulation of L-type Ca2+ channels were blocked by pretreatment of the cells with wortmannin, at nanomolar concentrations. Correspondingly, intracellular infusion of an enzymatically active purified recombinant Gbetagamma-sensitive phosphoinositide 3-kinase, PI3Kgamma, mimicked Gbetagamma-induced stimulation of Ca2+ channels. Both Gbetagamma- and PI3Kgamma-induced stimulations of Ca2+ channel currents were reduced by protein kinase C inhibitors suggesting that the Gbetagamma/PI3Kgamma-activated transduction pathway involves a protein kinase C. These results indicate for the first time that Gbetagamma dimers stimulate the vascular L-type Ca2+ channels through a Gbetagamma-sensitive PI3K.

Animals↗
PubMed1998

Two-dimensional magnetic particles

Single two-dimensional (2D) atomically thick magnetic particles of cobalt and iron with variable size and shape were fabricated by combining a mask technique with standard molecular beam epitaxy. Reduction of the lateral size of in-plane magnetized 2D cobalt films down to about 100 nanometers did not essentially modify their magnetic properties; although the separation of boundaries decreased greatly, neither domain penetrated the particle, nor was any sizable shape anisotropy observed. The mutual interaction of 2D cobalt particles was negligible, and the magnetic state of a single particle could be switched without modifying the state of the neighbors. Perpendicularly magnetized iron particles did not exhibit such responses. These results suggest that only a few atoms forming a 2D in-plane magnetized dot may provide a stable elementary bit for nanorecording.

Journal Article↗
PubMed1998

Gbetagamma stimulates phosphoinositide 3-kinase-gamma by direct interaction with two domains of the catalytic p110 subunit.

Class I phosphoinositide 3-kinases (PI3Ks) regulate important cellular processes such as mitogenesis, apoptosis, and cytoskeletal functions. They include PI3Kalpha, -beta, and -delta isoforms coupled to receptor tyrosine kinases and a PI3Kgamma isoform activated by receptor-stimulated G proteins. This study examines the direct interaction of purified recombinant PI3Kgamma catalytic subunit (p110gamma) and Gbetagamma complexes. When phosphatidylinositol was used as a substrate, Gbetagamma stimulated p110gamma lipid kinase activity more than 60-fold (EC50, approximately 20 nM). Stimulation was inhibited by Galphao-GDP or wortmannin in a concentration-dependent fashion. Stoichiometric binding of a monoclonal antibody to the putative pleckstrin homology domain of p110gamma did not affect Gbetagamma-mediated enzymatic stimulation, whereas incubation of Gbetagamma with a synthetic peptide resembling a predicted Gbetagamma effector domain of type 2 adenylyl cyclase selectively inhibited activation of p110gamma. Gbetagamma complexes bound to N- as well as C-terminal deletion mutants of p110gamma. Correspondingly, these enzymatically inactive N- and C-terminal mutants inhibited Gbetagamma-mediated activation of wild type p110gamma. Our data suggest that (i) p110gamma directly interacts with Gbetagamma, (ii) the pleckstrin homology domain is not the only region important for Gbetagamma-mediated activation of the lipid kinase, and (iii) Gbetagamma binds to at least two contact sites of p110gamma, one of which is close to or within the catalytic core of the enzyme.

Adenylyl Cyclases↗
PubMed1998

High incidence of nephrogenic adenoma of the bladder after renal transplantation.

BACKGROUND: Tumors of the bladder termed nephrogenic adenomas in kidney allograft recipients are believed to develop as urothelial metaplastic proliferations in response to mechanical trauma, chemical noxae, irradiation, and bacterial or viral pathogens. We report on the incidence of nephrogenic adenoma of the bladder in patients who received renal transplants during a period of 7 years and 3 months at the University Hospital of Vienna. METHODS: Diagnosis was obtained by cystoscopy and histological analysis. Nephrogenic adenoma was treated by transurethral electroresection and administration of antibiotics in case of urinary tract infections. Follow-up consisted of cytological controls of urine and bladder irrigation fluid as well as of cystoscopy every 3 months. RESULTS: In 7 of 1328 renal allograft recipients, nephrogenic adenoma could be detected after 7 to 60 months following renal transplantation. In five patients, recurrence was detected 9 to 23 months after diagnosis of the initial lesion. No evidence of malignant degeneration was observed in any patient. Nephrogenic adenoma was not related to immunosuppressive therapy, cytomegalovirus disease, or gancyclovir therapy. CONCLUSIONS: We suggest that after successful transurethral electroresection of nephrogenic adenomas, cytological controls are adequate every 3 months. Only in renal transplant patients with recurrence of voiding disturbances, macrohematuria, or urinary tract infection are cystoscopy and biopsy indicated in the routine follow-up regimen.

Adenoma↗
PubMed1998

Nephrogenic adenoma in renal transplant recipients: a truly benign lesion?

OBJECTIVES: Nephrogenic adenoma is a benign metaplastic lesion of the urinary bladder, reported to occur as a response to inflammation, trauma, intravesical therapies, and after renal transplantation. The aim of this study was to evaluate on the basis of chromosomal analysis whether nephrogenic adenoma really is benign. METHODS: Twelve renal transplant recipients with histologically verified nephrogenic adenoma were analyzed for numerical aberrations of chromosomes 7, 9, and 17. Results were related to total DNA content, p53 and Ki-67 positivity, and clinical outcome. Ten patients with superficial bladder cancer and 10 healthy renal transplant recipients formed the control groups. RESULTS: All 12 patients with nephrogenic adenoma had monosomy 9 in a mean of 24.3% (range 20% to 30%) of the evaluated cells; 3 patients had an additional trisomy 7 in a mean of 8% (range 6% to 10%) of the counted cells. Chromosome 1 7 was disomic in all patients. DNA histograms were diploid in 11 of the 12 patients and aneuploid in 1 patient. No p53 and Ki-67 positivity was present in this group. All patients with superficial bladder cancer had monosomy 9 in a mean of 79.8% (range 75% to 85%) of the counted cells. Two patients were found to have an additional trisomy 7 in 50% and 65% of the cells, respectively. The latter had an aneuploid histogram; the others had haploid/diploid histograms. p53 was negative in all specimens. Ki-67 positivity was present in 70% of these patients. All healthy transplant recipients had disomic chromosomal patterns according to diploid DNA histograms and negative immunocytochemical results. CONCLUSIONS: Even if in a lower percentage of cells, aberrations of chromosome 7 and 9 were detected in nephrogenic adenoma. It therefore cannot be excluded that nephrogenic adenomas in immunosuppressed renal transplant recipients may develop into malignant lesions.

Adolescent↗
PubMed1998

Phenotypic and functional characterization of mast cells derived from renal tumor tissues.

Mast cells (MCs) originate from multipotent hematopoietic progenitor cells. However, MCs in various organs are heterogenous in terms of mediator or receptor expression and response to diverse stimuli. We characterized the phenotype and functional properties of human renal mast cells (HRMCs). Tissue was obtained from 17 patients suffering from renal tumors (transitional cell carcinoma, n = 4; renal cell carcinoma, n = 13). HRMCs were isolated by collagenase digestion. Double staining with toluidine blue and immunofluorescence using monoclonal antibodies (mAbs) revealed expression of stem cell factor (SCF)-receptor (c-kit/CD117), CD9, CD29, CD33, CD43, CD44, CD54, and CD63 on HRMCs. In contrast, HRMCs were not recognized by mAbs to CD2, CD3, CD4, CD11b, CD14, CD15, CD16, CDw17, CD19, or CD23. HRMCs were also negative for CD116 (granulocyte-macrophage colony-stimulating factor [GM-CSF] receptor alpha), CD123 (interleukin [IL]-3Ralpha), CD121a (IL-1R type I), CD122 (IL-2Rbeta), and CD127 (IL-7R) and were also found to lack C5aR (CD88). Ligand-induced activation of HRMCs through immunoglobulin (Ig)E-R or SCF-R (c-kit) resulted in histamine secretion (control: <10%; alphaIgE, 1 microg/mL: 50.12 +/-5.18%; rhSCF, 100 ng/mL: 29.24 +/- 22.39), whereas recombinant C5a, erythropoietin (EPO), IL-1 through 10, and GM-CSF exerted no effects. As determined by in situ staining, HRMCs contained tryptase, but only low or undetectable amounts of chymase. Electron microscopy confirmed the presence of MCs in renal tissues and revealed a scroll-rich granule population in HRMCs. Together, HRMCs are tryptase+, C5aR- mast cells exhibiting phenotypic and functional properties similar to those of lung MCs.

Adult↗
PubMed1997

Late ureteral obstruction after kidney transplantation. Fibrotic answer to previous rejection?

Today, the incidence of urological complications following renal transplantation is 2%-10%. Most of these complications occur within the 1st year and affect the distal ureter. We report on two patients who developed very late ureteral obstruction, 14 and 18 years after transplantation. Both patients had rejection episodes 1 and 10 months prior to the ureteral stenosis. Histological examination of one resected ureter revealed findings strongly suggestive of a rejection process. Open surgery with antirefluxive reimplantation into the bladder was successful in both patients, with a postoperative observation time of 20 and 8 months, respectively. We conclude that a percutaneous nephrostomy may be required in patients with rising creatinine and incipient hydronephrosis even long after transplantation has been performed.

Adult↗
PubMed1997

[Acromio-humeral distance and acromial shape in 3-dimensional computerized tomography reconstruction. Side comparison in supraspinatus outlet syndrome].

Mechanical irritations of the supraspinatus tendon due to a reduction of the subacromial space are considered to be a potential cause of supraspinatus outlet syndrome. The aim of the current study was, therefore, to provide a method of improved measurement of the acromiohumeral distance and the evaluation of the acromial shape. In seven patients aged 50-60 years with unilateral supraspinatus outlet syndrome, imaging with standardized, high-resolution computed tomography (CT) was performed in order to demonstrate the acromion and the subacromial space three-dimensionally. The acromiohumeral distance was measured in three reconstructed frontal sections, and the two sides of each patient were directly compared. The acromial shape was compared with the classification of Bigliani as derived from conventional radiography. Whereas the Constant Score was found to be significantly reduced in the diseased shoulders (p < 0.01), the acromiohumeral distance was not significantly lower in three standardized frontal sections. In five cases the classification of the acromial form from the conventional radiograph was confirmed by 3D CT, whereas in two cases it was shown to be different. Our results suggest that primary or secondary changes of the acromial form can be more accurately evaluated with 3D CT than with conventional radiography. A direct comparison of the two sides in patients with supraspinatus syndrome does not suggest a reduction of acromiohumeral distance in the diseased shoulder.

Female↗