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Biomedical subjects

H Wolf

Publications and source records attributed to H Wolf.

At least 595 records · Page 33Linked to original sources
PubMed1982

Kirromycin-resistant elongation factor Tu from wild-type of Lactobacillus brevis.

Properties of the elongation factor Tu from Lactobacillus brevis which is naturally insensitive to kirromycin are described. The protein is characterized by an unusual nucleotide-binding site with increased affinity for GTP and extreme heat stability. EF-Tu is sensitive to pulvomycin in the assay of polyphenylalanine synthesis. However, the failure of the protein to display pulvomycin-dependent GDP-binding and GTPase activity indicates that pulvomycin action in L. brevis differs from that in E. coli.

Aminoglycosides↗
PubMed1982

The antibiotics kirromycin and pulvomycin bind to different sites on the elongation factor Tu from Escherichia coli.

Pulvomycin and kirromycin, two antibiotics which inhibit protein biosynthesis in Escherichia coli by complex formation with the elongation factor Tu (EF-Tu), bind to different sites on the protein. While only one molecule of kirromycin can be bound to one molecule of EF-Tu, more than one molecule of pulvomycin interacts with a molecule of EF-Tu. This has been deduced from experiments in which the aminoacyl-tRNA binding and the GTPase activity of EF-Tu were measured in the presence of varying amounts of both antibiotics. These experiments are interpreted to mean that pulvomycin but not kirromycin can replace the other antibiotic in its respective site. Our conclusions are supported by circular dichroism spectroscopy.

Aminoglycosides↗
PubMed1982

Increased pulmonary vascular resistance and permeability due to arachidonate metabolism in isolated rabbit lungs.

Liberation and metabolism of arachidonic acid may be the common final pathway of different stimuli on the pulmonary vascular bed. In a model of isolated, ventilated rabbit lungs, perfused with Krebs Henseleit albumin buffer in a recirculating system, changes of pulmonary vascular resistance and of vascular permeability are monitored continuously. The addition of free arachidonic acid or of the Ca-ionophore A 23187 to the perfusion fluid consistently evokes a biphasic increase in vascular resistance as well as an initially reversible increase in vascular permeability, followed by pulmonary edema. Both phases of increased vascular resistance are completely suppressed by inhibition of the cyclooxygenase, decreased to a large degree by inhibitors of thromboxane synthetase, and markedly augmented by short preincubation of arachidonic acid with ram seminal vesicular microsomes and by sulfhydryl reagents. The increased pulmonary vascular permeability is augmented by inhibition of cyclooxygenase and reduced by simultaneous lipoxygenase inhibition. Antagonists of histamine, serotonin and sympathic or parasympathic activity do not have any influence. PG F2alpha., TxB2, PG E2 and PG I2 alter the pulmonary vascular resistance, but do not increase vascular permeability. In conclusion, increased availability of free arachidonic acid evokes a rise in pulmonary vascular resistance, which can be ascribed to cyclooxygenase products, especially to thromboxane, and causes a rise in vascular permeability which can be ascribed to lipoxygenase products. The findings may be related to acute pulmonary lesions with increase in vascular resistance and with vascular leakage.

Animals↗
PubMed1982

Influence of tocopherol, its chromane compound, phytyl chains and superoxide dismutase on increased vascular resistance and permeability due to arachidonate metabolism in isolated rabbit lung.

In the model of isolated, ventilated rabbit lungs, perfused with isoionic and isooncotic fluid, the addition of arachidonic acid to the perfusion fluid or the liberation of arachidonic acid by the Ca-ionophore A 23187 result in an increase in pulmonary vascular resistance and permeability. The former can be ascribed to cyclooxygenase products, the latter to lipoxygenase products of arachidonic acid. The effect of alpha-tocopherol, its chromane compound, alpha-tocopherolquinone, phytol, 2-methyl-1,4-naphthoquinone, 2-methyl-3-phytyl-1,4-naphthoquinone and of superoxide dismutase (SOD) on the increase in pulmonary vascular resistance and permeability was investigated. A membrane effect of the phytyl side chain and an antioxidative effect of the chromane compound can be distinguished: phytol increase the arachidonate-induced rise of pulmonary vascular resistance and permeability, whereas the chromane compound decreases both to a large degree. Methyl-phytyl-naphthoquinone and methyl-naphthoquinone gave equivalent results. SOD decreases the enhanced vascular resistance and the vascular leakage. The possibility of antioxidative therapy in acute pulmonary lesions with vascular leakage and increased vascular resistance is discussed.

Animals↗
PubMed1982

Carnitine blood concentrations and fat utilization in parenterally alimented premature newborn infants.

To investigate the relationships among carnitine intake, carnitine blood concentrations, and the ability to utilize exogenous fat, total carnitine, free carnitine, acylcarnitine, beta-hydroxybutyrate, free fatty acid and triglyceride plasma concentrations were measured in 26 parenterally alimented appropriate-for-gestational-age premature infants before and at the end of a four-hour infusion of Intralipid, 1 gm/kg body weight. There was an increase in plasma levels of AC, BOB, FFA, and TG, but a decrease of FC, TC was unaffected by the infusion, but strongly correlated with calculated carnitine intake. At the end of the fat infusion, AC and BOB were positively correlated, and FFA negatively correlated with TC. The results demonstrate the proportion of AC to FC to be an additional indicator of fatty acid utilization and suggest that decreased carnitine intake in premature infants may impair fatty acid oxidation and ketogenesis.

3-Hydroxybutyric Acid↗
PubMed1982

Lymphocyte-dose response relationship in spontaneous lymphocyte mediated cytotoxicity (SLMC) measured by microcytotoxicity assay.

Titrations of spontaneous lymphocyte-mediated cytotoxicity (SLMC) in a 44-hour microcytotoxicity assay (MA) by serial dilutions of effector lymphocytes were performed to characterize the lymphocyte-dose response relationship, and to investigate the methodological basis for comparative cytotoxicity studies. The following lymphocyte fractions were used: unseparated, E rosetting, non-E rosetting, EA rosetting, and non-EA rosetting. Assays were performed against target cell lines from normal and malignant urothelium with high or low sensitivity to SLMC in allogeneic and autologous combinations, and against an osteosarcoma cell line. Analysis of SLMC titration curves showed that two different mathematical models could be used to describe the relationship between lymphocyte concentration and SLMC, I: linear relationship (log lymphocytes, CI) with exclusion of both high and low CI values, and II: sigmoid relationship (log lymphocytes, CI) which was transformed to linear relationship (log lymphocytes, log CI/100 - CI), including also high and low values. It is pointed out that perfect quantitative comparisons of SLMC in different combinations were complicated by statistically significant differences between the curve slopes. However, estimations based on experimental results in a range close to 50% cytotoxicity index (CI) may be acceptable, as the differences between slopes were small.

Carcinoma, Transitional Cell↗
PubMed1982

Effect of the arginine analog canavanine on the synthesis of Epstein-Barr virus-induced proteins in superinfected Raji cells.

The addition of canavanine to cultures of superinfected Raji cells in the absence of arginine prevented the appearance of early antigens as defined by immunofluorescent staining. Addition of various amounts of arginine permitted the identification of at least three groups of proteins, each responding differently to the various concentrations of arginine-canavanine.

Antigens, Viral↗
PubMed1982

[Antibodies against viruses of the herpes group in cerebrospinal fluid in idiopathic facial paralysis. Enzyme immuno-serologic studies].

In a prospective study, paired CSF samples and sera of 12 patients suffering from Bell's palsy were examined for IgG and IgM antibodies against Herpes simplex virus (HSV), Varicella-zoster virus (VZV) and Cytomegalovirus (CMV). For determination of antibodies an enzyme-linked immunosorbent assay was carried out. CSF- and serum samples were taken within one week after Bell's palsy had been diagnosed and were compared with further CSF- and serum samples taken 2 weeks later. The results are discussed.

Adult↗
PubMed1982

[Should splenic tissue be re-implanted after splenectomy due to birth trauma?].

Splenectomy results in loss of about 1/4 of the reticulo-endothelial system and 1/3 of the lymphatic tissue. Reduced phagocytosis and "clearing" capacity are reflected in the appearance of Howell Jolly bodies, thrombocytosis and decreased circulating immune-complexes. Reduction of IgM and compensatory increase of IgG and IgA levels further indicate immunological impairment. Transitory reduction of complement activity and the number of T-lymphocytes in the first weeks post-splenectomy constitute a significant limitation of immunological function and are accompanied by low serum tuftsin levels. These factors help explain the increased susceptibility to overwhelming infection seen in splenectomized patients. The lethality rate due to sepsis has been reported to be as high as 50%. Patients with hematological disorders, with systemic malignancies and children under 4 years of age who undergo splenectomy because of abdominal trauma are at especially high risk. The most common infectious agents are Haemophilus influenzae and Pneumococcus. The present report describes 2 infants who underwent splenectomy for the treatment of splenic rupture due to birth trauma. In one case, splenic tissue was homogenized and re-implanted; in the second case, splenectomy was followed by penicillin prophylaxis. The clinical course in the latter patient was complicated by Candida meningitis.

Bacterial Infections↗
PubMed1981

[Increase of pulmonary vascular resistance and permeability due to the metabolism of free arachidonic acid (author's transl)].

Release and metabolism of arachidonic acid are supposed to form the common final pathway of different stimuli on the pulmonary vascular endothelium. In a model of isolated, ventilated and perfused rabbit lungs we investigated the influence of increased availability of free arachidonic acid on pulmonary vascular resistance and permeability. Addition of arachidonic acid to the perfusion fluid or release of arachidonic acid by Ca-ionophore A 23187 regularly produces a characteristic biphasic increase of the pulmonary vascular resistance as well as a continuous increase in permeability, followed by pulmonary edema. Inhibition of cyclooxygenase by indomethacin prevents the augmentation of vascular resistance, the increase of vascular permeability however is enhanced. thus the raise in pulmonary vascular resistance can be ascribed to cyclooxygenase products, the increased pulmonary vascular permeability to lipoxygenase products of arachidonic acid.

Animals↗
PubMed1981

[The antioxidative chromane structure of alpha-tocopherol protects against the consequences of arachidonic acid release in the pulmonary vascular bed (author's transl)].

In the model of isolated, ventilated and perfused rabbit lungs release of arachidonic acid results in an increase of pulmonary vascular resistance and permeability. The former can be ascribed to cyclooxygenase products, the latter to lipoxygenase products of arachidonic acid. The effect of alpha-tocopherol on the increase of pulmonary vascular resistance and permeability either after the addition of arachidonic acid to the perfusion fluid or after stimulation of arachidonic acid liberation by Ca-ionophore A 23187 was investigated. It is possible to distinguish a membrane effect of the phytol side chain of alpha-tocopherol and an antioxidative effect of its chromane structure: Phytol augments the increase of pulmonary vascular resistance and permeability, whereas the chromane-structure decreases both to a large degree. The possibility of antioxidative therapy in disturbances of pulmonary vascular permeability is discussed.

Animals↗