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Biomedical subjects

J Svoboda

Publications and source records attributed to J Svoboda.

At least 73 records · Page 4Linked to original sources
PubMed1991

[Takayasu's disease. Detection of the early systemic stage of the disease in a pregnant woman].

The authors describe the case of Takayasu's disease detected in the non-obliterating systemic stage. The disease developed in a 24-year-old woman in the 8th month of gestation and was associated with severe pain of the back and upper extremities, subfebrile temperatures, later fever and tachycardia. The authors describe the difficult diagnosis of the disease and discuss the relationship of the case with so-called fever of unknown aetiology and the development of the disease during pregnancy.

Adult↗
PubMed1990

[Immunocomplex vasculitis].

The clinician suspects immunocomplex vasculitis when he cannot find a common denominator for the concurrent affection of various neighbouring organs and tissues. These affections result from the inflammatory response of the organism to the deposition of non-phagocytized circulating immunocomplex into the vascular wall. Despite the delicacy of attempts to classify them, the author tried to differentiate them into non-progressing immunocomplexes vasculitis, which recedes, and progressing immunocomplex vasculitis which may be either primary or secondary. Among primary ones he includes nodose polyarteritis and its granulomatous variant, Churg-Strauss' disease, Henoch-Schönlein anaphylactoid purpura and granulomatous vasculitis of the Wegener granulomatosis type, Horton's temporal arteritis, Takayasu's pulseless disease and Winiwarter-Buerger's obliterating thromboangiitis, which may be of the peripheral or more rarely the visceral type. Secondary progressing vasculitis is encountered in so-called "collagenoses" (e.g. systemic lupus erythematodes), where the clinical picture is to a considerable extent conditioned by vasculitis. The clinical picture is due to the generalized affection of the microcirculation. Symptoms of ischaemic affection of all organs and tissues may be encountered. A typical feature are different types of damage of the same adjoining system, e.g. a combination of asymmetric central and peripheral pareses in affections of the nervous system. The author discusses the most frequent clinical pictures, the importance of different examination procedures and therapeutic possibilities. Assessment of the diagnosis of immunocomplex or autoaggressive systemic disease is very difficult, as a typical picture corresponding clearly to a defined nosological unit is encountered rarely.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigen-Antibody Complex↗
PubMed1990

Extracellular alkaline-acid-alkaline transients in the rat spinal cord evoked by peripheral stimulation.

Regional differences in extracellular pH (pHe) were found in unstimulated rat spinal cord using double-barrel pH-sensitive microelectrodes. The pHe in the lower dorsal horn (laminae III-VII) was about 7.15, i.e. by about 0.2 pH units lower than that measured in the cerebrospinal fluid. Transient acid shifts in pHe by 0.01-0.05 pH units were found when acute nociceptive stimuli (pinch, press, heat) were applied to the hind paw. Chemical or thermal injury evoked by subcutaneous injection of turpentine or by application of 1-3 ml of hot oil onto the hindpaw produced a long-term decrease in pHe base line in the lower dorsal horn by about 0.05-0.1 pH units. The decrease in pHe began 2-10 min after injury and persisted for more than 2 h. Electrical nerve stimulation (10-100 Hz, 20-60 s) elicited biphasic (acid-alkaline) or triphasic (alkaline-acid-alkaline) changes in pHe which have a similar depth profile as the concomitantly recorded increase in [K+]e. An initial alkaline shift by about 0.005 pH units was found to be significantly decreased by La3+, an H+ channel blocker. The dominating acid shift by about 0.1-0.2 pH units was accelerated and increased by acetazolamide (carbonic anhydrase inhibitor) showing that the high buffering capacity of the extracellular fluid may hamper the resolution of acid perturbations. Stimulation-evoked acid shifts were blocked by amiloride, SITS, DIDS and La3+ and therefore have a complex mechanism which includes Na+/H+ exchange, Cl-/HCO3- cotransport and/or Na+/Cl-/H+/HCO3- antiport and H+ efflux through voltage-sensitive H+ channels. The poststimulation alkaline shift (alkaline undershoot) was blocked by ouabain and reflects coupled clearance of K+ and H+ by active transport processes.

Acetazolamide↗
PubMed1990

Activity-related rise in extracellular potassium concentration in the brain of 1-3-day-old chicks.

The concentration of K+ [( K+]) was measured in the cerebrospinal fluid (CSF) and in the extracellular fluid [( K+]e) in the medial forebrain of two-day-old chicks by means of K(+)-sensitive microelectrodes (K-ISM). The K-ISM potential in the CSF was compared with that in artificial CSF with 3, 4 or 6 mmol/l of [K+]. The [K+] found in CSF was 3.79 +/- 0.57 (n = 8), in the hyperstriatum accessorium (HA) 3.70 +/- 0.32 (n = 13) and in the neostriatum (N) 3.51 +/- 0.32 (n = 13; mmol/l; mean +/- SEM). Trains of local electrical stimuli (10-100 Hz, 30 sec) applied to the surface of the forebrain increased [K+]e in both HA and N by 11-13 mmol/l. Increases in [K+]e in the ectostriatum (E) of 5-6 mmol/l was found in response to electrical stimulation (30-100 Hz, 5-10 sec) of the contralateral optic nerve, and of about 2 mmol/l by applying pressure to the bulb. In chicks adapted to the dark, stimulation of the contralateral eye or both eyes with bright light flashes (1-2 Hz) or with continuous light resulted in an increase in [K+]e of 0.5-1.0 mmol/l. Smaller increases in [K+]e of 0.15-1.25 mmol/l were found in HV and N after the application of a small quantity (0.1 ml) of the chemical taste aversant methylanthranilate (MeA) or the electrical stimulation of the beak by two needle electrodes inserted into the palatum or into the tongue. After application of MeA the increase in [K+]e began 3-4 min after application and persisted for 20 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Ducks: a new experimental host system for studying persistent infection with avian leukaemia retroviruses.

Long-term persistence of the avian leukosis virus (ALV), the transformation-defective mutant of Prague strain Rous sarcoma virus subgroup C (td PR-C) was established in heterologous duck hosts after infection in mid-embryogenesis. Transient viraemia was observed for about 4 weeks after hatching and was lost in most of the infected ducks by about 6 months. Loss of viraemia was accompanied by the increasing synthesis of virus-neutralizing antibodies. In spite of strong virus-neutralizing antibodies, virus was detected by the cocultivation assay in duck tissues throughout the observation period up to 5 years. In the viraemic phase of infection, we found integrated proviruses in various tissues, preferentially in stomach muscle tissue and in the thymus. The long-term persistence of virus was frequently accompanied by liver necrosis and neoplastic diseases. Injection of td PR-C virus into early embryos resulted in more pronounced infection accompanied by an increased copy number of viral DNA per cell, high mortality and remarkable atrophy of thymus tissue in infected ducklings.

Animals↗
PubMed1990

A transformation-competent recombinant between v-src and Rous-associated virus RAV-1.

The LTR, v-src, LTR provirus, which arose by the reverse transcription and integration of src mRNA in the H-19 hamster tumor, has been successfully rescued by fusion with chicken fibroblasts infected with Rous-associated virus RAV-1. One rescued virus, E6, acquired 1 kilobase of the 5' end of the gag gene structure. Recombination took place in the region of 15-nucleotide homology exactly between v-src exon (position 7054) and gag (position 1417). This recombination resulted in the alteration of src splice acceptor site sequences, but this site is maintained as a functional splice acceptor site. The nucleotide structure of the long terminal repeat of recombinant E6 virus suggests that it arose by the intermolecular jump of reverse transcription from RAV-1 to src mRNA and then the switch of templates between already depicted regions of homology. The second jump of reverse transcription was apparently an intramolecular event. The acquisition of 1 kilobase of the 5' gag by E6 resulted in maintaining the balance of unspliced and spliced E6 RNAs and assured the replication advantage of rescued E6 virus over rescued F6 virus, the genome of which corresponds to that present in ancestral H-19 cells.

Animals↗
PubMed1989

The LTR, v-src, LTR provirus generated in the mammalian genome by src mRNA reverse transcription and integration.

Different types of altered proviruses of Rous sarcoma virus (RSV) have been detected in mammalian tumor cell lines. We cloned and sequenced one of these altered proviruses with the structure LTR, v-src, LTR. The presence of an intact viral splice junction, as well as duplications of the chromosomal sequence GCGGGG flanking the two 2-base-pair-deleted LTRs, demonstrated reverse transcription and normal retroviral integration of src mRNA in mammalian cells. In addition, a 1-nucleotide deletion 2 bases upstream from the AAUAAA polyadenylation signal is suspected to be responsible for the absence of a poly(A) track in the src mRNA present in virions of rescued viruses.

Animals↗
PubMed1989

Transduction of the cellular src gene and 3' adjacent sequences in avian sarcoma virus PR2257.

When injected into chickens, a transformation-defective mutant of the Prague C strain of Rous sarcoma virus induced tumors at low incidence and after a long latency. One such tumor released a replication-defective virus designated PR2257. We molecularly cloned and sequenced the proviral DNA from quail fibroblasts transformed by PR2257. Comparison of PR2257 sequence with that of Prague C, cellular src, and 3' adjacent cellular DNA showed that the spliced version of the c-src gene and about 950 base pairs (bp) of 3'-flanking cellular DNA were transduced into PR2257. This transduction eliminated nearly all replicative genes, since the gag gene splice donor site was linked to the splice acceptor site of the src gene and, on the 3' side, recombination occurred in the end of env gene. Insertion of two extra cytosines 23 bp before and 19 bp after the c-src stop codon resulted in an extension of the coding portion up to 587 amino acids, divergence of sequences after Pro-525 and replacement of Tyr-527 by a valine residue. In addition, it appears that the 5' and 3' untranslated regions of PR2257 result from multiple recombinations between exogenous and endogenous virus genomes. Limited digestion of p66src encoded by PR2257 with Staphylococcus aureus V8 protease yielded a V2 peptide (C-terminal moiety) with an apparent molecular mass of 31 kilodaltons, consistent with the 5.7-kilodalton increase expected from the DNA sequence. The structure of PR2257 suggests that the first step in the capture of c-src gene by avian lymphomatosis viruses is the trans splicing of the viral leader mRNA to exon 1 of c-src.

Amino Acid Sequence↗
PubMed1989

Structural analysis of proviruses in additional hamster tumour cell lines transformed by provirus II rescued from XC cells and definition of a new cell line harbouring amplified proviruses.

Additional 18 Syrian hamster tumour cell lines induced independently with the virus rescued from XC cells (provirus type II) have been analysed by restriction mapping. Taking into account the already published results of an analysis of other six tumour cell lines, altogether 24 tumour cell lines were characterized. In 62.5% of these lines a complete proviral unit has been integrated; 20.8% of the lines harbour altered proviral structures where the 3' end of the gag gene and the entire pol gene had been deleted; 8.3% of the lines carry both such a deleted provirus and a complete provirus. Apart from the already published cryptic provirus found in H-19 cells, no such provirus has been found in another cell line. Therefore the appearance of the cryptic provirus represents an infrequent event (4.16%). Similarly, the significant amplification of proviruses accompanied with a rearrangement in the env gene was found only in one tumour cell line. H-42, in the genome of which five proviral units are accommodated. The probable arrangement of amplified proviruses and the mechanism of their genesis are discussed.

Animals↗
PubMed1988

Increase in extracellular potassium level in rat spinal dorsal horn induced by noxious stimulation and peripheral injury.

Changes in extracellular K+ concentration ([K+]e) in dorsal horn were studied by means of double-barrel K+-sensitive microelectrodes in rats anesthetized with Nembutal. Acute nociceptive stimuli (pinch, press, heat) applied to the hind paw induced a transient increase in [K+]e of about 0.1-0.5 mM which persisted for 5-30 s. Regional variations in [K+]e were found in unstimulated rat spinal cords. The K+ level in the lower dorsal horn (laminae III-V) was by about 0.4 +/- 0.06 mM higher than that in more superficial laminae and in the ventral horn. Chemical or thermal injury was evoked by: s.c. injection of 0.1-0.5 ml formalin or turpentine into the hind paw, by application of mustard oil onto the skin, or by thermal injury of the hind paw. These produced a long-term increase in [K+]e in the lower dorsal horn by 0.3-3.0 mM in 75% of animals (n = 27). The increase in [K+]e began 5-15 min after injury and persisted for more than 2 h. In the rest of the animals, occasional elevation in [K+]e of 0.1-0.3 mM were observed. The K+ increases evoked by acute nociceptive stimuli as well as by injury were blocked by preinjecting the hind paw with 1% procaine. However, when procaine was applied 20 min or later after injury, the evoked long-term rise in [K+]e was not affected. This shows that the long-term K+ accumulation results from self-sustained abnormal neuronal firing induced in the dorsal horn by injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗