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Biomedical subjects

I Fodor

Publications and source records attributed to I Fodor.

At least 73 records · Page 4Linked to original sources
PubMed1979

Synthesis of proteins coded by plasmid vectors of pCV series (Apr, Tcr) and their recombinant derivatives (pDm) in E. coli minicells.

Polypeptide synthesis directed by vector plasmids of pCV series conferring ampicillin and tetracycline resistance (Apr, Tcr) and by recombinant plasmids (pDm) have been analyzed using the minicell system. It has been found that a polypeptide of 34 000 daltons is responsible for the Tcr phenotype and regulated from the promoter near the HindIII site. Cloning of DNA fragments into HindIII site allowed to conclude that DNA from Drosophila melanogaster contains nucleotide sequences which may act as promoters for a 34 000 dalton polypeptide gene. beta-Lactamase is expressed as five proteins of 24 000, 26 5000, 27 000, 28 500 and 29 500 daltons. Insertion of DNA fragments into PstI site prevents the synthesis of all five polypeptides. Recombinant clones Dm39 and Dm187 produce additional proteins of 19 000, 23 000, 24 000 and 27 000 daltons.

Chromosome Mapping↗
PubMed1978

Location of the cleavage sites on the SV 40 DNA map produced by the restriction endonucleases Pst 1 and Bam 1.

Restriction endonucleases from Providencia stuartii (Pst 1) and Bacillus amyloliquefaciens H (Bam 1) cleave SV 40 DNA at two and one specific sites, respectively. Using EcoRI and Hind III endonuclease restriction sites as reference, the two Pst I sites were mapped at 0.050; 0.265 and the Bam I site was mapped at 0.170 of the genome length, clockwise, from the single EcoRI cleavage site.

DNA Restriction Enzymes↗
PubMed1978

Physical mapping of cleavage sites recognized by restriction endonucleases on the genome of bacteriophage T5.

The DNA of bacteriophage T5 has been treated with restriction endonucleases EcoRI, HindIII, BamI, SmaI, PstI, SalI, KpnI and the electrophoretic pattern obtained in agarose gel has been analyzed in order to localize the specific cleavage sites on the T5 DNA. The localization of cleavage sites has been reduced from the electrophoretic pattern of double and partial digests, the digests of isolated restriction fragments and the digests of deletion mutant T5st(o) DNA. Four BamI cleavage sites have been found and localized on the physical map of T5 DNA at 0.21, 0.225, 0.685 and 0.725 fractional length. Endonuclease SmaI cleaves at 0.39, 0.59 and 0.69 fractional length. Endonuclease PstI cuts T5 DNA at 11 sites: 0.090, 0.210, 0.320, 0.510, 0.635, 0.670, 0.705, 0.770, 0.815, 0.840, 0.875 fractional length. Six KpnI cleavage sites have been mapped at 0.170, 0.215, 0.525, 0.755, 0.830, 0.850 fractional length. A complete cleavage map of the phage genome is presented for seven restriction enzymes.

Chromosome Mapping↗
PubMed1977

Histogenesis of beryllium-induced bone tumours.

In response to beryllium treatment, irregular bone formation starts mainly in the marrow cavity of long bones, preceding neoplastic growth. Irregular medullary bone formation may be connected with the endosteum, but usually it develops in the bone marrow, independently of the endosteum. Osteogenesis in the bone marrow may be preceded by fibrosis but irregular bone may be formed also without any previous histological changes in the bone marrow. The tumour develops directly from the medullary bone. The prolonged irritation causes abnormal osteogenesis, which ultimately turns into neoplastic proliferation. Thus, the beryllium-induced bone sarcoma is, from histogenesis point of view, a hyperplaseogenic tumour. Irregular bone formation is considered a preblastomatous change, because it is closely connected with the development of the tumour and precedes it in time. The multiplicity of the tumour is explained by the "neoplastic field" theory of WILLIS.

Animals↗
PubMed1976

Immune complexes in chronic hepatitis.

Rheumatoid factors were present in 33.2%, crioglobulins in 47.6%, and anticomplementary assay in 34.2% of cases with chronic active hepatitis. No statistically significant loss of total complement was observed, but its components especially C1 and C3, exhibited lowered titers in 48.6% and respectively 45.7% of 160 cases. The origin, significance and pathogenicity of these factors are discussed in connection with the presence and possible role of the immunologic complexes to the development of chronic liver injury.

Antigen-Antibody Complex↗
PubMed1975

Glucagon treatment of experimental acute pancreatitis.

CFY male rats anaesthetized with pentobarbital were used in different groups for inducing acute pancreatitis by the retrograde injection either of 1 mg elastase, 5 mg trypsin, 4 mg lysolecithin, 10 mg Na-taurocholate in 0.2 ml volume or of 0.3 m. sunflower oil. In each group laparatomized animals served for control. The animals with pancreatitis were treated either with 15 mug/b.w.kg/hour glucagon or with physiological saline for 72 hours. Twenty-four and 72 hours after inducing pancreatitis glucagon did not influence the significant fall in blood pressure elicited by the intraductal injection of trypsin or elastase or in the plasma calcium level in pancreatitis induced by trypsin or sunflower oil. Neither did glucagon affect the significant increase of plasma lipase activity in pancreatitis induced by trypsin or taurocholate. It also failed to reduce the 24-hour mortality rate and the extension of fat tissue necrosis in the abdominal cavity of pancreatitic animals. In contrast, glucagon treatment significantly reduced the amount of abdominal exudate associated with bile salt induced pancreatitis and, probably due to its pancreatic blood flow increasing effect, seemed to moderate the degree of tissue damage elicited in the pancreas by detergents such as taurocholate or lysolecithin.

Acute Disease↗