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H W Weber

Publications and source records attributed to H W Weber.

At least 19 recordsLinked to original sources
PubMed2003

Current percolation and anisotropy in polycrystalline MgB(2).

The influence of anisotropy on the transport current in MgB(2) polycrystalline bulk samples and wires is discussed. A model for the critical current density is proposed, which is based on anisotropic London theory, grain boundary pinning, and percolation theory. The calculated currents agree convincingly with experimental data, and the fit parameters, especially the anisotropy, obtained from percolation theory agree with experiment or theoretical predictions.

Journal Article↗
PubMed1993

In vivo regulation of rRNA transcription occurs rapidly in nondividing and dividing Drosophila cells in response to a phorbol ester and serum.

The synthesis of ribosomes is an essential cellular process which requires the transcription of the rRNA genes by RNA polymerase I (Pol I). The regulation of rRNA synthesis is known to be coupled to growth regulation. In nongrowing, slowly growing, and rapidly growing Drosophila cells, exposure to the tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) increases the synthesis of precursor and mature rRNAs. Using nuclear run-on assays, we show that TPA enhances transcription of the rRNA genes. These results suggest that TPA regulates expression of RNA genes transcribed by Pol I, irrespective of the growth state of the cells. In slowly dividing Drosophila cells, increasing the serum concentration rapidly alters the accumulation of rRNA by enhancing rDNA transcription within 1 h. Thus, TPA and serum are each able to rapidly regulate rRNA gene expression in Drosophila cells. These results indicate that the RNA Pol I transcription system can be regulated by agents which have previously been shown to effect specific genes transcribed by the RNA Pol II system.

Animals↗
PubMed1986

Insulin stimulation of cyclic AMP phosphodiesterase is independent from the G-protein pathways involved in adenylate cyclase regulation.

The intact rat adipocyte was used to investigate the possibility of common intermediates in the insulin stimulation of cyclic AMP phosphodiesterase and the beta-adrenergic/adenosine regulation of adenylate cyclase. A five minute incubation of the isolated adipocytes with insulin produced a 50-100% increase in the phosphodiesterase activity found in the particulate fraction of homogenates. The insulin stimulation was not impaired by the presence of either agonist or antagonists of the inhibitory adenosine receptor which acts on adenylate cyclase. Phosphodiesterase activation by insulin was also observable above the level of stimulation produced by the beta-adrenergic agent isoproterenol and forskolin. The validity of the enzyme activity measurements was supported by measurements of the hormonal actions on cyclic AMP levels within the cells. Possible crossover between the adenylate cyclase and phosphodiesterase regulation systems at a post-receptor site was investigated using adipocytes exposed to bacterial toxins specific for the modification of guanine nucleotide binding proteins. Both cholera toxin, which irreversibly activates Gs and pertussis toxin which inactivates Gi caused some stimulation of the phosphodiesterase activity and suppressed activation by isoproterenol, but neither toxin prevented the insulin stimulation of cyclic AMP phosphodiesterase. These results suggest, while common components may participate in the beta-adrenergic stimulation of both adenylate cyclase and phosphodiesterase, the mechanism of insulin activation of the phosphodiesterase does not involve the components of adenylate cyclase regulation.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1985

Extensive but reversible depletion of ATP via adenylate cyclase in rat adipocytes.

In adipocytes, adenylate cyclase is positively regulated by beta-adrenergic agents and negatively regulated by adenosine. Incubation of adipocytes with adenosine deaminase relieves the inhibition of adenylate cyclase by destroying the adenosine that the cells release into the medium. When adipocytes are incubated with adenosine deaminase and the beta-adrenergic agent isoproterenol, most of their ATP is converted to AMP in 5 min. Either isoproterenol or adenosine deaminase alone has little or no effect. In the additional presence of the phosphodiesterase inhibitor 4-(3-butoxy-4-methoxybenzyl)imidazolidin-2-one (Ro 20-1724) cAMP accumulates instead of AMP. Under these conditions, cAMP represents 40-50% of the total intracellular adenine nucleotides, and ATP only 5%. N6-(L-2-phenylisopropyl)adenosine, a deaminase-resistant adenosine agonist, prevents beta-adrenergic stimulation. 8-(p-Sulfophenyl)theophylline and 3-isobutyl-1-methylxanthine are both adenosine antagonists that can replace the deaminase in permitting beta-adrenergic stimulation of adenylate cyclase, but only the latter also inhibits the phosphodiesterase and causes accumulation of cAMP. When the ATP-depleted adipocytes are washed with fresh medium, the nucleoside triphosphate level can be restored within 5 min. The ATP-restored adipocytes can respond rapidly to a second dose of isoproterenol and adenosine antagonist. These findings point out the important role of adenosine in controlling adenylate cyclase activity and the possible involvement of adenylate cyclase in the control of energy flow in rat adipocytes.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗
PubMed1982

Insulin-dependent and insulin-independent low Km cyclic AMP phosphodiesterase from rat adipose tissue.

Chromatographic analysis of a soluble extract of rat adipose tissue on DEAE-Sephacel resolves four distinct peaks of 3':5'-nucleotide phosphodiesterase (EC 3.1.4.17) activity. Kinetic investigation indicates that two of these fractions have a high affinity for cyclic AMP and show negative cooperative kinetic behavior at high substrate concentration. They differ in the degree of inhibition by cyclic GMP and in their response to insulin. If rat epididymal fat pads are incubated with insulin prior to homogenization, only one of the low Km cyclic AMP phosphodiesterase forms is stimulated.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1979

Effect of 5-bromodeoxyuridine on heterogeneous nuclear RNA in rat hepatoma cells.

Heterogeneous nuclear RNA HnRNA) was isolated from untreated and 5-bromodeoxyuridine (BrdUrd) treated hepatoma tissue culture (HTC) cells. analysis of this RNA by either electrophoresis on polyacrylamide-agarose gels or centrifugation in sucrose gradients demonstrated that BrdUrd caused a shift in the labeled HnRNA population toward a smaller size distribution. This effect was produced by concentrations of BrdUrd which specifically lower the level of the differentiated enzyme tyrosine aminotransferase, but do not greatly affect cell growth. Differential binding to oligo(dT) cellulose was used to fractionate HnRNA further into classes containing poly(A) (alpha), oligo(A) (beta) or neither category of A-rich sequences (gamma). BrdUrd did not alter the relative rates of uridine incorporation into the three classes. The shift in the labeled HnRNA population due to BrdUrd was observed in all three subclasses of HnRNA.

Animals↗
PubMed1978

Induction of intracisternal type A particles by 5-bromo-2'-deoxyuridine in rat hepatoma cells.

Electron microscopic examination of hepatoma tissue culture (HTC) cells revealed low numbers of intracisternal type A particles (IAP) and type C viruses. Exposure of HTC cells to either 10(-4) or 10(-5) M5-bromo-2'-deoxyuridine (BUdR) caused a more than 50-fold increase in the number of IAP observed with the electron microscope. The number of IAP increased after only 2 days of growth in 10(-5) M BUdR, whereas 3 days of growth in 10(-4) m BUdR were necessary to observe an increase. A 2-day pulse of 10(-4) M BUdR was also sufficient to cause the increase in type A particles, provided the cells were continued in culture for another 2 days. Unlike many other cell lines, HTC cells treated with BUdR did not show an increase in type C viruses. This conclusion was based on the observations that BUdR treatment caused no detectable increase in extracellular particulate viral reverse transcriptase or in viral RNA complementary to a DNA probe made to a rat endogenous type C virus (RaLV).

Animals↗
PubMed1975

Cardiomyopathy in crowded rabbits.

Rabbits were crowded 4 to a cage for 2 weeks, then released for 1 week, crowded again for 2 weeks, and so on. Of 44 rabbits subjected to intermittent crowding, only 9 survived for longer than 10 months, 20 died during the 1st month, and 15 died between the 2nd and 9th month of the experiment. Histological sections of the myocardium showed myocytolysis, intersititial edema, and an increased amount of acid mucopoly saccharides in rabbits surviving for 2 weeks and more. The accumulations of acid mucopolysaccharides were apparently unrelated to necrotic foci. Long-term survivors frequently showed myocardial fibrosis and endocardial fibroelastosis, as well as basophilic degeneration of myocardial fibers. The lesions observed were similar to those described in idiopathic endomyocardiopathy in Southern Africa. Therefore, the rabbit may be of some value for research in cardiomyopathies.

Animals↗