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Biomedical subjects

S Bauer

Publications and source records attributed to S Bauer.

At least 181 records · Page 10Linked to original sources
PubMed1989

Protection of rhesus monkeys from fatal Lassa fever by vaccination with a recombinant vaccinia virus containing the Lassa virus glycoprotein gene.

Lassa fever is an acute febrile disease of West Africa, where there are as many as 300,000 infections a year and an estimated 3000 deaths. As control of the rodent host is impracticable at present, the best immediate prospect is vaccination. We tested as potential vaccines in rhesus monkeys a closely related virus, Mopeia virus (two monkeys), and a recombinant vaccinia virus containing the Lassa virus glycoprotein gene, V-LSGPC (four monkeys). Two monkeys vaccinated with the New York Board of Health strain of vaccinia virus as controls died after challenge with Lassa virus. The two monkeys vaccinated with Mopeia virus developed antibodies measurable by radioimmunoprecipitation prior to challenge, and they survived challenge by Lassa virus with minimal physical or physiologic disturbances. However, both showed a transient, low-titer Lassa viremia. Two of the four animals vaccinated with V-LSGPC had antibodies to both Lassa glycoproteins, as determined by radioimmunoprecipitation. All four animals survived a challenge of Lassa virus but experienced a transient febrile illness and moderate physiologic changes following challenge. Virus was recoverable from each of these animals, but at low titer and only during a brief period, as observed for the Mopeia-protected animals. We conclude that V-LSGPC can protect rhesus monkeys against death from Lassa fever.

Animals↗
PubMed1988

Demographic study on the family planning behaviour of the German population: the importance of natural methods.

A total of 1,267 women in the F.R.G., aged from 15 to 45 years, were interviewed about their family planning behavior and the importance of natural methods of family planning (NFP) in a representative demographic study. It was found that 19.6% of the respondents were not sexually active. The others used various methods, as follows: pill, 38.4%; IUD, 10.3%; condom, 5.9%; diaphragm, 2.1%; spermicides, 0.8%; withdrawal, 3.4%; NFP methods, 3.9%. The main reason for rejecting a method was a possible medical risk. Of the responding women, 73% had some previous knowledge about NFP; 47% of them found such methods to be interesting, and approximately 20% indicated a high probability of the use of NFP methods in the future.

Adolescent↗
PubMed1987

Altered expression of beta-globin, transferrin receptor, and ornithine decarboxylase in Friend murine erythroleukemia cells inhibited by alpha-difluoromethylornithine.

alpha-Difluoromethylornithine (DFMO) is an irreversible inhibitor of ornithine decarboxylase (ODC) and restricts the proliferation and differentiation of Friend murine erythroleukemia cells. We have studied the effect of this compound on the expression of ODC, transferrin receptor (TFR), and beta-globin during normal cellular proliferation and dimethylsulfoxide-induced terminal differentiation. Elevated RNA levels for ODC were observed during both normal Friend murine erythroleukemia cell division and replication associated with terminal differentiation, but these transcripts decreased as the cells ceased proliferating. However, in the presence of DFMO the levels of ODC remained elevated even when the cells had stopped dividing; this appears to be a feedback mechanism to overcome the effects of the inhibitor. TFR expression paralleled regular cell division and was curtailed when replication was reduced by DFMO. However, the inhibitor was unable to prevent the differentiation associated maintenance of TFR levels, well after proliferation terminated. While DFMO was able to restrict differentiation and hemoglobin synthesis, it did not inhibit the dimethylsulfoxide-induced expression of beta-globin RNA. We concluded that the block in differentiation caused by DFMO occurs along some pathway(s) other than the activation of beta-globin or TFR.

Animals↗
PubMed1987

Vesicoureteral reflux in asymptomatic siblings of patients with known reflux: radionuclide cystography.

The familial nature of vesicoureteral reflux among siblings of patients with vesicoureteral reflux has been reported to be from 8% to 32%. These included both symptomatic and asymptomatic siblings. The incidence of vesicoureteral reflux in asymptomatic siblings, however, has not been studied extensively. Sixty asymptomatic siblings of patients known to have vesicoureteral reflux were studied with radionuclide voiding cystography. Their ages ranged from 2 months to 15 years (mean, 4.2 years). Vesicoureteral reflux was detected in 27 of 60 (45%) of the siblings. Vesicoureteral reflux was unilateral in 15 and bilateral in 12 of the siblings. Radionuclide cystography is more sensitive than radiographic cystography and results in a very low radiation dose to the patient. The gonadal dose with radionuclide cystography is only 1.0 to 2.0 mrads. Because of these features, radionuclide cystography is a nearly ideal technique for the diagnosis of vesicoureteral reflux in siblings of patients with known vesicoureteral reflux. All siblings (symptomatic or asymptomatic) of patients with known vesicoureteral reflux should have a screening radionuclide cystography.

Child↗
PubMed1986

Demonstration of cGMP-dependent protein kinase and cGMP-dependent phosphorylation in cell-free extracts of platelets.

Homogenates, membranes and cytosol of rat and human platelets were found to contain cGMP-dependent protein kinase immunoreactivity. Specific cGMP-dependent protein kinase immunoreactivity was about 1.7 pmol protein kinase/mg protein for homogenates of human platelets and 0.7 pmol/mg for homogenates of rat platelets; the majority appeared to be associated with the membrane fraction. In membranes of platelets low concentrations of cAMP (0.5-2 microM) stimulated the phosphorylation of five major proteins with apparent relative molecular masses, Mr, of 240 000, 130 000, 50 000, 42 000 and 22 000 while low concentrations of cGMP (0.5-2 microM) stimulated the phosphorylation of three major proteins with apparent Mr of 130 000, 50 000 and 46 000. An affinity-purified antibody against the cGMP-dependent protein kinase was prepared which specifically inhibited the activity of cGMP-dependent protein kinase. In membranes of human platelets this affinity-purified antibody inhibited the cGMP-stimulated phosphorylation of the three proteins with Mr of 130 000, 50 000 and 46 000 while it had no effect on the cAMP-dependent and cyclic-nucleotide-independent protein phosphorylation. The results demonstrate that platelets contain a cGMP-dependent protein kinase and at least three specific substrates for this enzyme. Two of these substrates, the proteins with apparent molecular Mr of 130 000 and 50 000, are substrates for both cAMP- and cGMP-dependent protein kinase. The protein with apparent Mr of 130 000 appears to be closely related to an intrinsic plasma membrane protein of vascular smooth muscle cells which is a substrate for a membrane-associated cGMP-dependent protein kinase. Therefore, cGMP-dependent protein kinase and cGMP-regulated phosphoproteins may mediate in platelets the intracellular effects of those hormones, vasodilators and drugs which elevate the level of cGMP and inhibit platelet aggregation.

Animals↗
PubMed1986

Phorbol ester treatment impairs hormone- but not stable GTP analog-induced inhibition of adenylate cyclase.

Treatment of intact human platelets and S49 lymphoma cyc- cells with the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate, impairs GTP-dependent and hormone-induced inhibition of adenylate cyclase, an action mediated by the inhibitory coupling protein Ni. In contrast, receptor-independent activation of Ni with subsequent adenylate cyclase inhibition induced by the stable GTP analog, guanosine 5'-[gamma-thio]triphosphate, was affected in neither the potency nor onset of Ni activation by the stable GTP analog, in both membrane systems studied. The data indicate that modification of Ni following phorbol ester treatment does not impair its activation by stable GTP analogs.

Adenosine Diphosphate Ribose↗
PubMed1986

Activity of phagocytic granulocytes in patients with prostatic cancer.

Chemilumenescence (CL) occurs due to the phagocytosis of bacteria and of tumor cells by polymorphonuclear neutrophils (PMN). Levels of CL were measured in patients with prostatic cancer and from normal subjects. Patients with advanced disease (stage C, D) showed no elevated CL levels as compared to healthy individuals or patients with minimal disease (stage A, B). Following external radiation therapy in patients with stage A-C prostatic carcinoma high levels of CL were recorded. Estrogen medication also resulted in increased CL levels, while estramustine did not affect phagocytic activity. Intradermal BCG vaccination caused increased PMN activity. Progressive prostatic cancer in hormone treated patients was associated with increased CL as compared to patients with stable or regressive disease.

Antineoplastic Agents↗
PubMed1986

Interactions between the hormone-sensitive adenylate cyclase system and the phosphoinositide-metabolizing pathway in human platelets.

At least two signal-generating systems are involved in the actions of various hormonal factors in human platelets--the adenylate cyclase system and the phosphoinositide-metabolizing pathway. The formation of cyclic AMP (cAMP) by the adenylate cyclase system--consisting of the catalyst itself, the Ns and Ni proteins, and various hormone receptors--is stimulated by prostaglandins and adenosine, and is inhibited by alpha 2-adrenergic agonists, ADP, vasopressin, platelet-activating factor, and thrombin. On the other hand, the formation of inositol trisphosphate and diacylglycerol by the phosphoinositide-metabolizing pathway is stimulated by some of the latter agents, particularly by thrombin. There are apparently several mutual interactions between these two signal-generating systems. On the one hand, increases in the level of cAMP inhibit the formation of inositol phosphates and diacylglycerol. It is presently unclear whether this inhibitory effect of cAMP is due to a direct action at the phospholipase C itself or to an indirect mechanism, for example, a depletion of the substrate of the enzyme. On the other hand, protein kinase C, which is activated by diacylglycerol, largely interferes with the adenylate cyclase system. This kinase, when activated by diacylglycerol or phorbol esters, apparently phosphorylates the guanine nucleotide-binding alpha-subunit of Ni, which results in an impairment or loss of the inhibitory hormonal signal transduction to the adenylate cyclase. Thus, available evidence indicates that the two signal-generating systems present in platelet membranes are not completely separated, and furthermore suggests that they may even be causally related to each other.

Adenylyl Cyclases↗
PubMed1986

Diltiazem inhibits transferrin receptor expression and causes G1 arrest in normal and neoplastic T cells.

Transferrin receptor expression is essential for the proliferation of both normal and malignant T cells. While transferrin receptor expression in normal T cells is tightly coupled to interleukin-2 receptor expression, transferrin receptor expression in malignant cells is usually constitutive and is released from this constraint. Temporally, the appearance of these membrane receptors is preceded by changes in the expression of the proto-oncogenes c-myc and c-myb. In addition, although an increase in the level of intracellular free calcium occurs early in the sequence of T-cell activation, the activation events dependent on this calcium flux have not been resolved. In the present study we report that diltiazem, an ion channel-blocking agent that inhibits calcium influx, arrested the growth in vitro of both normal and malignant human T cells in the G1 phase of the cell cycle. However, diltiazem did not inhibit the expression of c-myc or interleukin-2 receptor mRNA and protein in normal mitogen-activated T cells or the constitutive expression of c-myc and c-myb mRNA in malignant T cells (T acute lymphoblastic leukemia cells). In contrast, diltiazem prevented the induction of transferrin receptor (mRNA and protein) in normal T cells and caused a progressive loss of transferrin receptor (mRNA and protein) in malignant T cells. These data demonstrate that diltiazem can dissociate several growth-related processes normally occurring in G1 and thereby disrupt the biochemical cascade leading to cell proliferation.

Cell Cycle↗
PubMed1985

Protein kinase C interferes with Ni-mediated inhibition of human platelet adenylate cyclase.

Addition of phorbol ester-activated, partially purified protein kinase C to membranes of human platelets had no effect on forskolin stimulation of the adenylate cyclase and increased stimulation by prostaglandin E1 only at high GTP concentrations by preventing inhibition by GTP. Hormonal inhibition of the platelet adenylate cyclase by epinephrine was eliminated or largely impaired. At low GTP concentrations, epinephrine even caused a small increase in cyclase activity. The data suggest that activated protein kinase C interferes with GTP- and hormone-induced adenylate cyclase inhibition probably by phosphorylating the inhibitory guanine nucleotide-binding regulatory component Ni.

Adenylyl Cyclase Inhibitors↗
PubMed1985

Modulation of adenylate cyclase of human platelets by phorbol ester. Impairment of the hormone-sensitive inhibitory pathway.

The influence of the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), a direct activator of the Ca2+-activated, phospholipid-dependent protein kinase (protein kinase C), was studied on regulation of human platelet adenylate cyclase. Intact platelets were pretreated with the phorbol ester and, thereafter, membranes were prepared and the regulation of the hormone-sensitive adenylate cyclase in these membranes was studied. The following data were obtained: The TPA treatment applied had apparently no effect on the activity of the catalytic moiety of the platelet adenylate cyclase nor on the stimulatory NS protein nor on stimulatory hormone receptors (prostaglandin E1) and the mutual interactions of these components of the stimulatory hormone-sensitive pathway. However, the TPA treatment of intact platelets largely impaired the GTP-dependent, hormone-sensitive inhibitory pathway to the adenylate cyclase, involving the inhibitory Ni protein. The pretreatment led to a large reduction or loss of adenylate cyclase inhibition by GTP itself and by the inhibitory agonists, epinephrine and thrombin, inhibiting the untreated enzyme via separate receptors by an Ni-mediated process. In contrast, platelet adenylate cyclase inhibition not involving the Ni protein was not affected by the TPA treatment. The observed effects of TPA were very rapid in onset and were not shared by a derivative of TPA which did not activate protein kinase C. The data obtained suggest than protein kinase C activated by the phorbol ester interferes with the platelet adenylate cyclase system, leading to a specific alteration of the Ni-protein-mediated signal transduction to the adenylate cyclase.

Adenylyl Cyclase Inhibitors↗
PubMed1985

Protein kinase C phosphorylates the inhibitory guanine-nucleotide-binding regulatory component and apparently suppresses its function in hormonal inhibition of adenylate cyclase.

Human platelet membrane proteins were phosphorylated by exogenous, partially purified Ca2+-activated phospholipid-dependent protein kinase (protein kinase C). The phosphorylation of one of the major substrates for protein kinase C (Mr = 41 000) was specifically suppressed by the beta subunit of the inhibitory guanine-nucleotide-binding regulatory component (Gi, Ni) of adenylate cyclase. The free alpha subunit of Gi (Mr = 41 000) also served as an excellent substrate for the kinase (greater than 0.5 mol phosphate incorporated per mol of subunit), but the Gi oligomer (alpha X beta X gamma) did not. Treatment of cyc- S49 lymphoma cells, which are deficient in Gs/Ns (the stimulatory component) but contain functional Gi/Ni, with the phorbol ester, 12-O-tetradecanoylphorbol 13-acetate, a potent activator of protein kinase C, did not alter stimulation of adenylate cyclase catalytic activity by forskolin, whereas the Gi/Ni-mediated inhibition of the cyclase by the hormone, somatostatin, was impaired in these membranes. The results suggest that the alpha subunit of the inhibitory guanine-nucleotide-binding regulatory component of adenylate cyclase may be a physiological substrate for protein kinase C and that the function of the component in transducing inhibitory hormonal signals to adenylate cyclase is altered by its phosphorylation.

Adenylyl Cyclase Inhibitors↗
PubMed1985

Testicular torsion in children: scintigraphic assessment.

Seventy-five patients with suspected testicular torsion who had scintiscans and adequate clinical follow-up were analyzed retrospectively. The scintiscans diagnosed 12/13 cases of surgically proven missed torsion and 3/3 cases of surgically proven acute complete torsion. The scintiscans successfully distinguished all 35 cases of epididymo-orchitis, 14 cases of torsion of the appendix testes and 8 other miscellaneous conditions from testicular torsion. The incidence of testicular torsion in our patients undergoing scrotal scintigraphy was approximately 24%.

Adolescent↗
PubMed1984

Characterization of artefacts produced by treatment of organic acids with diazomethane.

When alpha, beta-unsaturated acids and alpha-keto acids react with diazomethane not only are the corresponding methylates produced, but also diazomethane is added to the C = C double bond or to the oxo group. The gas chromatographic and mass spectral behaviour of these undesired products and some further artefacts produced in the hot inlet lines of a gas chromatograph are described. The mass spectra and retention indices allowed the structural assignment of several "unknown" compounds found previously in the methylated acid fraction of urine. A detailed analysis of the reaction of alpha-oxo acids with diazomethane revealed that, besides the already known oxirane methyl esters, homologous esters are also produced by an insertion reaction.

Body Fluids↗