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J Svoboda

Publications and source records attributed to J Svoboda.

At least 91 records · Page 5Linked to original sources
PubMed1988

[Cryoglobulinemia].

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Cryoglobulinemia↗
PubMed1988

Extracellular pH and stimulated neurons.

The use of ion-sensitive microelectrodes enabled us to follow the dynamic changes in extracellular pH (pHe) together with those in the extracellular concentration of some biologically important ions, particularly K+ and Ca2+. Activity-related changes in pHe were studied in isolated spinal cords of frogs and in spinal cords of rats in vivo. Repetitive electrical stimulation of an afferent input led either to triphasic alkaline-acid-acid changes (90% of frogs) or to triphasic alkaline-acid-alkaline changes (10% of frogs and rats) with the greatest changes in the lower dorsal horns. The transient acid shift by as much as 0.15-0.25 pH units is dominant and builds up during the stimulation. The changes in pHe were also found in response to various adequate stimuli applied to the skin on the hind limb. Using specific inhibitors of Na+/H+ exchange, K+-Cl- co-transport, Cl-/HCO3- exchange, the Na+/K+ pump and carbonic anhydrase, we found pHe homeostasis to be impaired and stimulation-induced changes in pHe decreased. We conclude that the pHe changes evoked by electrical or adequate stimulation of an afferent input are not determined by changes in extracellular strong ion concentration differences due to accumulation of lactate, since we found no effect of NaF, a metabolic blocker of lactate production. However, lactate accumulation has been demonstrated during seizures, spreading depression and anoxia. Recently, it has been recognized that the observed pHe changes can affect permeability of membrane ionic channels, neuronal excitability and glial cell function.

Acid-Base Equilibrium↗
PubMed1988

Genome structure of a new avian sarcoma virus PR2257 determined by restriction analysis.

The genome structure of a new avian src-containing acute transforming virus, designated PR2257, was studied by restriction analysis. PR2257 was isolated from a sarcoma grown in a 155-day-old chick inoculated intraembryonally with a transformation-defective mutant of daPR-C retaining no src sequences. The 4.4-kb genome of PR2257 consists of the following regions: 5' LTR--spliced version of chicken c-src--incomplete env gene--3' LTR. This structure clearly indicates that PR2257 was generated by recombination between a td daPR-C and chicken c-src.

Animals↗
PubMed1987

Restriction analysis of additional "non-producing" cell clones obtained after transformation of Japanese quail fibroblasts with viruses rescued from cryptovirogenic H-19 cells.

The proviral structure of two transforming viruses rescued from cryptovirogenic H-19 hamster cells harbouring the LTR, v-src, LTR proviral structure was analysed by restriction mapping. It was established that the rescued G8 virus keeps the same restriction pattern as that observed in the cryptic H-19 provirus and that it is integrated into the cell genome at a different position characteristic of each "non-producing" (NP) cell clone. In these features it corresponds to the previously described F6 rescued virus. In studying the E6 rescued virus we found again that it is integrated at a position characteristic of the NP cell line studied. Using a series of restriction enzymes it was specified that the E6 proviral unit acquired at least 0.25 kb from the left part of the gag gene and 0.85 kb of an unidentified DNA. Because this DNA structure was not digested with the enzymes employed that cut in RSV provirus and did not hybridize with the viral gene probes, it might be of cellular origin. The recombinational events involved in E6 virus genesis, the nature of an additional DNA structure, and the functional significance of the acquired part of the gag gene are discussed.

Animals↗
PubMed1987

Haematological and pathomorphological studies on chickens inoculated with transformation-defective sarcoma virus.

A transformation-defective mutant of Rous sarcoma virus (td PR-RSV-C) inoculated into chicken embryos caused a number of pathological changes in chickens after hatching. Disturbances in haematopoiesis were manifested by anaemia of different degree and by the presence of immature blood elements in the peripheral blood. The haematological picture of erythroblastosis was confirmed histologically. In addition to erythroblastosis, lymphoid leukosis and a proliferative lymphosarcoma-like tumour were demonstrated histologically.

Animals↗
PubMed1986

Transmission of (LTR, v-src, LTR) without recombination with a helper virus.

We have analyzed transmission of (LTR, v-src, LTR) cryptic structure integrated in the H-19 mammalian tumor cell line. From this cell line different isolates of transforming virus were rescued in heterokaryons produced by fusion with chicken fibroblasts infected by replication-competent avian leukosis virus RAV-1. One of them (F6) was used for the transformation of avian cells in the absence of the helper virus. In four transformed cell lines studied, the (LTR, v-src, LTR) structure was again integrated at a unique position in the cell DNA of each line. This indicated that the (LTR, v-src, LTR) structure is transmitted by the helper virus without recombination. This point has been further supported by the finding that a src-containing species corresponding in size to the nonpolyadenylated src mRNA is present in the RNA isolated from the rescued F6 transforming virus which might serve as template for the synthesis of (LTR, v-src, LTR) structure by the reverse transcriptase provided by RAV-1.

Animals↗
PubMed1986

Characterization of transforming viruses rescued from a hamster tumour cell line harbouring the v-src gene flanked by long terminal repeats.

The organization of proviruses derived from infecting transforming viruses rescued from hamster tumour cells was studied. Southern blot analysis indicated that the provirus from the F6 cell line was organized as long terminal repeat (LTR)-src-LTR, and S1 mapping experiments suggested that it was probably derived by reverse transcription of src mRNA followed by integration. In the E6 cell line, the provirus unit was arranged as LTR-delta gag-src-LTR, indicating a recombination event between the rescued transforming virus and the helper virus. These results suggest that transforming defective viruses containing only the src gene can be rescued from nonpermissive mammalian cells.

Animals↗
PubMed1985

Biologically active proviral clone of myeloblastosis-associated virus type 1: implications for the genesis of avian myeloblastosis virus.

A biologically active myeloblastosis-associated virus (MAV) provirus was cloned from a bacteriophage recombinant library constructed from leukemic chicken myeloblast DNA. The restriction endonuclease map of this clone was consistent with that of a type 1 MAV (MAV-1). Interference assays of virus recovered from cultured chicken embryo fibroblasts after DNA transfection established that the provirus was infectious and confirmed that it belonged to avian retrovirus subgroup A (type 1). Antipeptide antibodies raised against the env-encoded carboxyl terminus of p48myb, the transforming protein of avian myeloblastosis virus, specifically immunoprecipitated the gp37env from quail cells transfected with MAV-1 proviral DNA but not from cells infected with MAV-2. This suggests that MAV-1 rather than MAV-2 is the progenitor helper virus from which avian myeloblastosis virus arose by the transduction of cellular proto-oncogene sequences.

Animals↗
PubMed1985

Isolation of two transforming viruses from sarcomas obtained in chickens inoculated intraembryonally with a transformation defective mutant of Prague strain Rous sarcoma virus.

Sarcomas appeared after long latency with a frequency of about 2% in Brown Leghorn and (CB X IC)F1 chickens after intraembryonic and neonatal inoculation of transformation-defective mutants of ASVs subgroup C. Only the freshly isolated td mutants, td daPR-C and td daPR-C morphf, exhibited the tumorigenic activity, whereas the standard td mutants induced no sarcomas. Two (862 and 2257) out of four tumours could be transplanted in young chickens and produced low titres of transforming virus. The other two tumours were not transplantable and devoid of any transforming virus. Viruses 862 and 2257 are clearly defective in replication, virus 2257 cannot be complemented efficiently by any helper virus in vitro. The low titre of virus 2257 is not caused by interference with a helper virus of the same subgroup specificity. Both viruses are highly tumorigenic in vivo.

Animals↗
PubMed1985

Identification of transformation-specific proteins synthesized in cryptovirogenic mammalian cells.

The cryptovirogenic PR-RSH-19 (H-19) hamster cell line, derived originally from a tumour induced by the virus rescued from XC cells by transfection, was studied. The pp60v-src protein was detected by immunoprecipitation with sera from tumour-bearing rabbits (TBR sera) from lysates of H-19 cells. A closely related protein p60 was precipitated by antiserum obtained from hamsters with tumours induced by H-19 cells. The pp60v-src of H-19 cells possesses an associated kinase activity. These results are consistent with the notion that the detected pp60v-src protein is a product of the cryptic sequences in H-19 cells.

Animals↗