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Biomedical subjects

P Pfeiffer

Publications and source records attributed to P Pfeiffer.

At least 181 records · Page 10Linked to original sources
PubMed1983

In vitro premature termination in SV40 late transcription.

Nuclear extracts and viral transcribing minichromosomes were prepared from SV40-infected cells and incubated in vitro with [alpha-32P]UTP under conditions which allow the elongation of preinitiated RNA chains. Sucrose gradient lysis of the transcription mixtures revealed two populations of SV40-specific RNA: elongating chains that remain associated with the viral minichromosomes, and, at the top of the gradient, small free RNA detached from the template and hybridizing exclusively to the promoter-proximal region of SV40 DNA. This free RNA was shown by polyacrylamide gel electrophoresis to comprise essentially a 94 nucleotide species, which could, however, at high UTP concentration, be elongated a further few nucleotides before terminating. These results thus show that the actively transcribing minichromosomes provide a sytem in which the attenuated RNA can be released from the template. Moreover, this is the first demonstration of specific in vitro termination of polymerase B transcription. The conditions which lead to transcription termination are discussed.

Animals↗
PubMed1983

Involvement of reverse transcription in the replication of cauliflower mosaic virus: a detailed model and test of some aspects.

A model is presented according to which cauliflower mosaic virus (CaMV) DNA is replicated via an RNA intermediate. The model explains the typical S1 nuclease-sensitive sites in mature CaMV DNA, the occurrence of the large, terminally redundant transcript, the local separation of CaMV transcription and CaMV assembly, the abundance of knotted CaMV DNA forms, and the high recombination frequency. A site of perfect homology to plant tRNA was detected. Extracts from a mixture of nuclei and inclusion bodies can be separated into fast-sedimenting complexes elongating endogenous CaMV RNA, and slow-sedimenting ones elongating endogenous CaMV DNA. The CaMV DNA synthesis can be partly inhibited both by RNAase and actinomycin D, suggesting the presence of a mixture of RNA- and DNA-templates.

DNA Replication↗
PubMed1983

Genetic dependence of IgE antibody production in mice infected with the nematode Nippostronglyus brasiliensis. I. Modulation of the IgE antibody response in vivo by serum factors.

We investigated the IgE-antibody response in 36 inbred mouse strains during infection with Nippostrongylus brasiliensis. With regard to the N. brasiliensis-specific IgE-antibody activity responder and nonresponder mice were obtained. Mice with the H-2-f haplotype (A.CA, B10.M, A.TFR 5) are high specific responders. It is suggested that one Ir gene for the N. brasiliensis-induced IgE-antibody response is localized within the K to J region of the mouse major histocompatibility complex. To obtain a medium IgE-antibody response it appears that a complementation between two Ir genes is necessary. An additional genetic control beyond the H-2 complex cannot be excluded. As to the total nonspecific serum IgE levels the parasitic infection leads to a 20- to 40-fold increase in high and low specific responder strains as well. Pretreatment of high responder mice (A.TFR 5, B10.M) with sera that were obtained from normal or complete Freund's adjuvant treated low (B10.G) and nonresponder (A.TFR 1) mice led to significant inhibition or enhancement of the N. brasiliensis-specific IgE-antibody response.

Animals↗
PubMed1983

[Biochemical aspects of the pathogenesis of the asthma syndrome].

The induction of asthma is more easily understood by the increasing knowledge of intercellular interactions. It is obvious that a major role for the initiation of extrinsic and mixed form asthma is attributed to IgE-immunoglobulin, which after interaction with the appropriate antigen leads to the release of preformed and newly generated mediators (e.g. leukotriene with chemotactic and spasmogenic [SRS] properties) from mast cells and basophils. The latter mediators are also released from polymorphonuclear neutrophils and macrophages in the course of bacterial adherence, phagocytosis, by bacterial toxins, and via anaphylatoxin dependent mechanisms. It appears likely that the induction of intrinsic asthma might be triggered by these mediators also during viral adsorption and penetration. The interdependency of cellular reactions might be responsible for the complexity of the disease process in asthma.

Anaphylaxis↗
PubMed1983

[Cell biology basis of IgE antibody regulation. Immunotherapeutic approaches].

Recent developments as to the IgE-antibody synthesis in rodents and in the human model are summarized and discussed in reference to our own data. It is by now established that the IgE-antibody response is regulated by interdependent interactions of cellular, humoral and genetic factors. The IgE-bearing B-lymphocyte develops from a surface IgM carrying B-lymphocyte. The transformation into an IgE secreting plasma cell requires T-cell help or soluble T-cell factors. Recent advances in the characterization of human lymphocytes as well as more sophisticated cell biological approaches facilitated the analysis of IgE-antibody synthesis in the human in vitro model. In most of the studies at present available the effect of the polyclonal B-cell mitogen (PWM) was analyzed. PWM either enhanced, suppressed or unlike to other Ig-classes did not affect the IgE-antibody synthesis at all. Immunotherapeutic approaches have to consider to establish the allergen induced in vitro model of IgE-antibody synthesis in humans, to modulate the interactions of T-helper and/or suppressor cells or to generate soluble suppressor factors. In any case the analysis of the IgE-antibody synthesis in humans could be a valuable tool to assess IgE-B-cell memory towards various allergens and to determine the IgE-mediated in patients.

Animals↗
PubMed1983

Accidental visualization of mesenteric lymph nodes by bipedal lymphography.

A case is presented of mesenteric lymph nodes filling accidentally by bipedal lymphography. The radiographs were interpreted erroneously as pathologic; consequently the patient was treated with chemotherapy and radiotherapy. The correct diagnosis was made later by explorative laparotomy.

Diagnostic Errors↗
PubMed1982

[Mediators of allergic reaction (author's transl)].

It is by now well established that allergic and inflammatory reactions interact interdependently. The mediators of inflammation such as histamine, the neutrophil chemotactic factor, the leukotrienes and the platelet aggregating factor are responsible for the cellular infiltration which defines acute, subacute and chronic inflammatory reactions. Thus, new perspectives are opened up as to the pathophysiological disease process "bronchospasm-asthma".

Arachidonic Acid↗
PubMed1981

Modulation of the eosinophil chemotactic factor (ECF) release from various cells and their subcellular components by phospholipids.

An eosinophil chemotactic factor (ECF) can be released from human polymorphonuclear neutrophils (PMN), rat mononuclear and rat mast cells by the calcium ionophore (A23187), during phagocytosis, by arachidonic acid and phospholipase A2. It has been suggested that stimuli such as the ionophore and the phagocytic event lead to phospholipid turnover with the generation of arachidonic acid which is subsequently transformed by a lipoxygenase-like enzyme into ECF. Addition of phospholipids such as phosphatidylethanolamine and phosphatidylinositol during ionophore stimulation of various cells increased the ECF release significantly. ECF activity is also enhanced in the presence of indomethacin at concentrations which inhibit prostaglandin synthesis. With bromphenylacylbromide and eicosatetraynoic acid, ECF generation as well as the chemotaxis of eosinophils is inhibited suggesting that the phospholipase A2-arachidonic acid pathway represents a common link for ECF release as well as for the chemotaxis of eosinophils. From the cytosol of human PMN an ECF-containing enzyme was obtained. Incubation of phospholipase A2 and phospholipids with the ECF-converting enzyme led to potent ECF indicating that addition of phospholipids provides the soluble ECF-generating system with an additional source of arachidonic acid. The data represent a molecular approach to analyze the mechanisms of ECF release from soluble components after immunological triggering of the cells.

Animals↗
PubMed1979

Ultrasonic absorption evidence of structural fluctuations in viral capsids.

When the coat protein of the small icosahedral virus, brome mosaic virus, reassembles into capsids, the ultrasonic absorption of the solution greatly increases. Submitting the solution to an ultrasonic field thus appears to reveal spontaneous molecular motions within a protein assembly. Confirmatory evidence of a dynamics of a protein shell comes from measurements on brome mosaic virus at various degrees of swelling and on tomato bushy stunt virus treated with the crosslinking agent glutaraldehyde. The detected fluctuations may be related either with cooperative deformational motion in the capsid or with more localized structural changes. Such structural changes may help liberate the RNA at an early stage of viral infection.

Mosaic Viruses↗
PubMed1976

RNA viruses: stabilization of brome mosaic virus.

The relative importances of protein-protein and RNA-protein interactions in stabilizing the architecture of brome mosaic virus particles are discussed in the light of the following experimental evidence: (a) disassembly pathways of the virus particles, (b) reassembly of the virus and self-association capacity of the protein moiety, and (c) the role of divalent cations in virus stabilization, and their relevance to localization of the RNA in the virus particles. Evidence is given that the capsid of BMV is primarily stabilized by hydrophobic bonds at low pH, but not around and above neutrality where RNA-protein electrostatic interactions are essential to the integrity of the virus particles. A model is proposed for the structure of BMV in the different configurational states.

Capsid↗