PubMed Health⌕ Search

Biomedical subjects

G Wittmann

Publications and source records attributed to G Wittmann.

At least 55 records · Page 3Linked to original sources

Formation of cysteinyl-containing leukotrienes by human arterial tissues.

Human arterial rings incubated in modified Tyrode solution released small amounts of leukotriene (LT) C4-like material spontaneously and larger amounts upon stimulation with the ionophore A23187 as determined by radioimmunoassay. By reversed phase high pressure liquid chromatography (HPLC) LTC4-like material was found to comigrate with authentic LTC4, LTD4 and LTE4. Nordihydroguaiaretic acid (NDGA) significantly inhibited the ionophore A23187-induced release of LTC4-like material, while indomethacin was without effect. Simultaneously the arterial rings released much larger amounts of 6-keto-prostaglandin (PG) F1 alpha, which were significantly decreased by indomethacin. The results demonstrate that human arterial tissue has the capacity to synthesize cysteinyl-containing LT from endogenous arachidonic acid.

Adult↗

Herpesvirus (pseudorabies virus) latency in swine: occurrence and physical state of viral DNA in neural tissues.

The occurrence of the pseudorabies virus (PRV, herpes suis 1) genome in various neural tissues of latently infected pigs was investigated. During the latent phase of infection, between 7 and 52 weeks p.i., the average amount of PRV DNA ranged between 0.3 and 0.05 genome copies per cell. The results obtained by in situ cytohybridization and reassociation kinetic experiments indicated that each latently infected cell harbored at least 30 viral genome copies. PRV DNA could be demonstrated in similar frequencies (about 30% of cases) in the trigeminal ganglia, the olfactory bulb, and the medulla oblongata, and less frequently in the brain stem and the spinal cord. Southern blot analysis showed that in general the physical state of the latent genome was linear and nonintegrated. Only in 2 of 15 animals could the presence of circular or concatemeric viral DNA be observed. Thus, we could show that over a period of 13 months after infection the PRV genome persisted both qualitatively and quantitatively in a stable state in different areas of both the peripheral and the central nervous system.

Animals↗

Pharmacological modification of leukotriene release and coronary constrictor effect in cardiac anaphylaxis.

The modification of anaphylactic release of leukotriene (LT) C4-like immunoreactivity from isolated guinea pig hearts and of LT-induced coronary constriction by the muscarinic receptor against methacholine and by various exogenous prostaglandins (PG) was investigated. The vasodilators PGI2 and PGE2 as well as the vasoconstrictors PGD2, PGF2alpha, and 11,9-epoxymethano-PGH2, a PG endoperoxide analogue with biological properties similar to thromboxane (TX) A2, inhibited the anaphylactic coronary constriction without affecting release of LTC4-like immunoreactivity. On the other hand, the increased anaphylactic LT release in the presence of methacholine was not paralleled by more pronounced coronary constriction after challenge. The results suggest that the coronary constrictor effect of endogenous LT is modified by the drugs used by direct vascular effects and/or effects on other anaphylactic mediators.

Anaphylaxis↗

Occurrence and reactivation of latent Aujeszky's disease virus following challenge in previously vaccinated pigs.

Pigs which were vaccinated with an inactivated ADV vaccine developed a latent ADV infection up to 18 months after ADV challenge. Up to 6.5 months p.i. latent virus could be demonstrated by co-cultivation of different organ tissues (lungs, tonsils, olfactory bulb, brain stem, medulla). Afterwards, reactivation of latent virus was only achieved by immunosuppression of the animals. Immunosuppression led to a limited virus replication in nasal mucosa, tonsils, lymph nodes and central nervous system. In addition ADV was detected in the nasal secretions., Humoral and cellular immunity was investigated before and after immunosuppression of the animals. Before immunosuppression most of the animals displayed SCC, ADV-ADCC and ADV-LYST, and all animals had medium to high titres of neutralizing serum antibodies. After immunosuppression the number of pigs reacting in SCC and ADV-LYST, assays was distinctly reduced, but the number of animals reacting in ADV-ADCC assays remained unaltered. A significant reduction of serum antibody titres occurred only in 2 of 12 animals one day after the end of immunosuppression.

Animals↗

Multiplication and distribution of Aujeszky's disease (pseudorabies) virus in vaccinated and non-vaccinated pigs after intranasal infection.

The primary sites of Aujeszky's disease virus (ADV) multiplication in intranasally (i.n.) infected pigs were found to be in the nasopharyngeal, tracheal and pulmonary regions. From the second day post infection (DPI) onward ADV invaded the central nervous system and other organs. The virus was isolated from the nasopharyngeal region for at least 2 weeks. In serum ADV was present with low levels from DPI 1 to DPI 7. In pigs vaccinated with an inactivated vaccine and then challenged the distribution of ADV was rather similar to that in non-vaccinated animals, in spite of the presence of neutralizing antibodies. The virus titres in the organs generally were lower than in non-vaccinated animals up to DPI 7. Thereafter, titre differences were no longer significant. Virus was isolated from the tonsils and the lungs for at least 2 weeks. Interferon production in vaccinated infected pigs was significantly lower than in non-vaccinated infected pigs. Though multiplication and dissemination of ADV occurred, vaccinated pigs did not show clinical symptoms of Aujeszky's disease. Traces of ADV were detected in a small percentage of white blood cells (WBC) of non-vaccinated infected pigs. ADV was isolated from the lymphocyte-enriched and polymorphnuclear leukocyte-enriched fractions, but not from the monocyte-enriched fractions, apparently on account of the small cell number. Multiplication of ADV was demonstrated in cultured WBC from some of the vaccinated and non-vaccinated infected animals.

Animals↗