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Biomedical subjects

A Schmidt

Publications and source records attributed to A Schmidt.

At least 451 records · Page 25Linked to original sources
PubMed1991

Influenza A virus infects macrophages and stimulates release of tumor necrosis factor-alpha.

The clinical picture of influenza A virus infections indicates that release of tumor necrosis factor-alpha (TNF-alpha) may be involved. In the present study we exposed the murine macrophage line PU5-1.8 to influenza A virus and observed a productive infection which was followed by subsequent cell death. Infection of macrophages was accompanied by TNF-alpha mRNA accumulation and TNF-alpha release. TNF-alpha production could only be induced by live virus whereas interferon release was also stimulated by inactivated virus. When virus-infected macrophages were exposed to low amounts of lipopolysaccharide (LPS; 1-10 ng/ml) TNF-alpha production was strongly potentiated. These data show that low LPS concentrations could readily trigger a high TNF-alpha release from influenza-A-virus-infected macrophages which could, at least partially, explain the serious complications of combined influenza A virus and bacterial infections.

Animals↗
PubMed1991

Inhibition of voltage-dependent Ca2+ currents and activation of pertussis toxin-sensitive G-proteins via muscarinic receptors in GH3 cells.

In the rat pituitary cell line GH3, carbachol inhibits PRL secretion in a pertussis toxin-sensitive manner. For elucidation of the underlying mechanisms, we studied the effect of carbachol on voltage-dependent Ca2+ currents. Under voltage-clamp conditions, carbachol inhibited whole-cell Ca2+ currents by about 25%. This inhibitory action of carbachol was not observed in cells treated with pertussis toxin, indicating the involvement of a pertussis toxin-sensitive G-protein. In membranes of GH3 cells, carbachol stimulated a pertussis toxin-sensitive high-affinity GTPase. In immunoblot experiments with peptide antisera, we identified two forms of the Gi alpha-subunit (41 and 40 kDa) and two forms of the Go alpha-subunit (40 and 39 kDa). The 40-kDa Gi alpha-subunit was recognized by an antibody specific for the Gi2 alpha-subunit, and the 39-kDa Go alpha-subunit was detected by an antibody specific for the Go2 alpha-subunit. Incubation of membranes with the photoreactive GTP analog [alpha-32P]GTP azidoanilide resulted in photo-labelling of 40- and 39-kDa pertussis toxin substrates comigrating with G-protein alpha-subunits of the corresponding molecular masses. Carbachol dose-dependently stimulated incorporation of the photoreactive GTP analog into the 39-kDa pertussis toxin substrate and, to a lesser extent, into 40-kDa pertussis toxin substrates. The data indicate that muscarinic receptors of GH3 cells couple preferentially to Go, which is likely to be involved in the inhibition of secretion, possibly by conferring an inhibitory effect to voltage-dependent Ca2+ channels.

Affinity Labels↗
PubMed1991

Urologic experience with the Dornier multipurpose lithotripter MPL 9000.

From March, 1988 until October, 1989, 502 patients with 603 stones were treated with the Dornier multipurpose lithotripter MPL 9000. Sixty-six percent of the stones were situated in the calix, 29.6% in the renal pelvis, 3% in the upper, and 1% in the distal ureter; 18.4% of the stones were radiolucent. Multiple MPL treatments were performed in 8.6%. In 6.1% fragments post-ESWL treatment were larger than 5 mm. In 58.6% of the treatments were performed without using analgesia or anesthesia. Intravenous anesthesia was used in 22.3%, analgesia and sedation in 16.9%, general anesthesia in 1.4%, and epidural anesthesia in 0.8%. After 3 months follow-up 73.1% were stone-free. Residual fragments were found in the upper calix in 1.1%, in the middle calix in 5.2%, in the lower calix in 13.4%, in the renal pelvis in 5.9%, and in the ureter in 1%. The MPL 9000 has been proven to be as effective for the treatment of renal stones, while difficulties in localizing ureteral stones were noted. The major number of treatments were performed without any analgesia or anesthesia. No major complications were encountered.

Adult↗
PubMed1991

Potassium channel activation, hyperpolarization, and vascular relaxation.

1) Numerous compounds and changes in physical state functions shift the membrane potential of vascular smooth muscle to more negative values. The consequence is a vasodilatation because Ca2+ channels are closed. K+ channel opening frequently causes the hyperpolarization. 2) Acidification of the blood substitute solution, a fall in O2 partial pressure, and an increase in blood flow dilate arterial vessels. Acidosis is associated with a rise in K+ permeability and a simultaneous fall in Na+ permeability. Prostacyclin has a 20-30% share, and EDHF a 70-80% share in hypoxic vasodilatation. Experiments with iloprost (PGI2 analogue) confirmed the K+ channel opening properties of this drug. A voltage-dependent K+ channel and a Ca(2+)-activated K+ channel, via the influence of cA-PK or cG-PK, are responsible for the hyperpolarization with iloprost and with oxygen deficiency. 3) With 23Na+ nuclear magnetic resonance techniques, it has been demonstrated that with flow-dependent vasodilatation, proteoheparan sulphate integrated in the membrane of endothelial cells possibly served as a "flow sensor". With an external strain, such a compound can go from a randomly coiled state to an oriented state. Based on these viscoelastic properties, heparan sulphate proteoglycan is present as a random coil under "no flow" conditions and as an unfurled filament structure with increasing flow. This conformational change produces additional anionic binding sites to which Na+ ions of the blood are bound. A membrane hyperpolarization could be directly initiated by this Na+ binding via the protein fraction within the macromolecule or via a change in zeta-potential. Therefore, these ions can trigger the signal transduction for a vasodilatory vessel reaction. Decrease in flow is followed by a structural change of the macromolecule towards coil conformation, a release of Na+ ions and, thus, an interruption of the signal chain. 4) Cicletanine, aqueous garlic extract, and ajoene cause a concentration-dependent membrane hyperpolarization and are potent vasodilators. A cicletanine concentration, which is attained by the dosage given to patients, is sufficient to produce these effects. Under noradrenaline, the cicletanine effect is amplified. Aqueous garlic extract and ajoene exert a hyperpolarizing and vasodilating influence even in a concentration which may occur in the extracellular space by the administration of a single garlic clove. 5) The stationary activation curve "developed force vs. membrane potential" satisfactorily explains the effects of K+ channel openers. The tight electromechanical coupling expressed by this curve comprises a 50% vasorelaxation for a 2.5 mV hyperpolarization. In the linear part of the curve, the coupling ratio is 5.1 mV/g.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Biliary obstruction secondary to shrapnel.

Foreign bodies of the biliary tree represent infrequent causes of obstructive jaundice. We report a patient who developed biliary obstruction from metal shrapnel, 44 yr after a war injury. From our review of the literature, the syndrome of shrapnel-induced obstructive jaundice may occur many years after the initial injury. In the majority of patients, the missile lodges in the liver parenchyma, and migrates to the common bile duct. Complications from this injury include cholangitis, pancreatitis, and liver abscesses. As demonstrated by this case, computed tomography scan and endoscopic retrograde cholangio-pancreatogram may reliably detect this infrequent occurrence. With the development of therapeutic biliary procedures, many foreign bodies can be removed endoscopically. Thus, one should consider shrapnel-induced biliary obstruction in those patients with obstructive jaundice and prior combat injury.

Cholangiopancreatography, Endoscopic Retrograde↗
PubMed1990

Variations in the activity of glutathione reductase and the cellular glutathione content in relation to sensitivity to methylviologen in Escherichia coli.

To study the function of glutathione reductase and glutathione in Escherichia coli the coding sequence of the bacterial glutathione reductase gene (gor gene) was cloned into the vector pBR322, and the gor gene was expressed under the control of the promoter of the tetracycline-resistance gene (tet gene) in different Escherichia coli strains. Cells of the gor-mutant strain SG5 containing the vector pBR322 (SG5:pBR322) had no detectable glutathione reductase activity and a significantly lower total glutathione (GSH + GSSG) content relative to control cells of the strain JM101 (JM101: pBR322). The gor mutant cells were less sensitive to inhibition by methylviologen (as defined by changes in growth) than cells of the strain JM101. Elevated levels of both glutathione reductase activity and the total glutathione content (GSH + GSSG) were found when the gor gene was expressed in cells of the gor-mutant strain SG5 (SG5:pJIK1). Thus the activity of glutathione reductase is essential in order to maintain a high glutathione content. Furthermore, cells of the strain SG5: pJIK1 showed an increased sensitivity to methylviologen compared to cells of the gor mutant containing the vector pBR322 alone without the cloned gor gene insert (SG5:pBR322). In all experiments, the glutathione pool (GSH + GSSG) of bacterial cells was 90% reduced. In methylviologen-sensitive sodB mutant cells lacking iron superoxide dismutase activity (QC773:pBR322) overexpression of the cloned gor gene resulted in an elevated level of glutathione reductase activity which partially protected sodB mutant cells (QC773:pJIK1) against methylviologen toxicity. In sodB mutant cells expressing the gor gene (QC773:pJIK1) protection by glutathione reductase was, however, less effective than protection provided by expression of the iron superoxide dismutase gene (sodB gene) in these mutant cells (QC773:pJIK2). In sodA mutant cells lacking manganese superoxide dismutase activity but expressing the cloned gor gene (QC772:pJIK1) increased cellular glutathione reductase activity did not provide protection against methylviologen.

Cloning, Molecular↗
PubMed1990

[Relationship of the left ventricular wall thickness to the degree of late microvascular complications in diabetes mellitus type I].

Left-ventricular wall thickness, measured by echocardiography, was determined in 111 normotensive diabetics (63 men and 48 women; mean age 26 +/- 9 years; diabetes duration 13.5 +/- 6.2 years) and 91 comparable control subjects. The interventricular septum was significantly thicker in diabetics than in controls: systolic 13.3 +/- 2.3 mm, diastolic 9.2 +/- 2.2 mm vs. systolic 12.5 +/- 2.1 mm and diastolic 8.9 +/- 1.7 mm (P less than 0.05). Posterior wall thickness measurements were: systolic 15.8 +/- 2.2 mm vs 14.6 +/- 2.0 mm (P less than 0.001), diastolic 9.5 +/- 1.8 mm vs 8.4 +/- 1.3 mm (P less than 0.01). Left-ventricular wall thickness increased stepwise with increasing severity of microvascular complications (retinopathy, nephropathy, neuropathy). There was a moderately close correlation between blood pressure values and the degree of microvascular complications (r = 0.49, P less than 0.01). These correlations indicate that increases in wall thickness are diabetes specific, but may be influenced by the level of blood pressure.

Adult↗
PubMed1990

Tumor necrosis factor-alpha production of influenza A virus-infected macrophages and potentiating effect of lipopolysaccharides.

Influenza A virus infections are commonly associated with symptoms that suggest involvement of TNF-alpha. In this study, we exposed human monocytes, rat alveolar macrophages, and murine PU5-1.8 macrophages to influenza A virus, strain Puerto Rico 8. We observed a productive infection that was accompanied by TNF-alpha mRNA accumulation, TNF-alpha release and subsequent cell death. TNF-alpha production was dependent on exposure to live virus, in contrast to IFN release that was also induced by UV-inactivated virus. Most strikingly, low amounts of LPS (1 to 10 ng/ml) from Escherichia coli or Haemophilus influenzae were capable of strongly potentiating TNF-alpha production from virus-infected macrophages. The potentiating effect of LPS was neither due to increased survival of macrophages nor to altered virus multiplication, enhanced TNF-alpha gene expression, discharge of intracellular TNF-alpha stores, or shifts in the kinetics of TNF-alpha release. Thus, low amounts of LPS, which could easily be present in vivo, may serve as a potent trigger signal for TNF-alpha production from macrophages that have been primed by influenza A virus infection. These data suggest that the frequently observed serious complications of combined influenza A virus and bacterial infections may be partially due to a high TNF-alpha production.

Blotting, Northern↗