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Biomedical subjects

G Lindahl

Publications and source records attributed to G Lindahl.

At least 91 records · Page 5Linked to original sources
PubMed1985

Epithelial HLA-DR expression and T lymphocyte subsets in salivary glands in Sjögren's syndrome.

Salivary glands obtained at biopsy from patients with Sjögren's syndrome and controls were studied with regard to phenotype of infiltrating and residing cells, by means of a double immunoenzymatic staining technique. The infiltrating lymphocytes, which were sparse or absent in the control group in contrast to their abundant presence in the Sjögren patients, consisted in both groups mainly of T lymphocytes, the majority of which were T helper cells. In the controls, the glandular epithelial cells were HLA-DR- whereas in the Sjögren patients HLA-DR+ epithelial cells were found, mainly confined to areas, where the epithelial cells were seen in close proximity to the periphery of dense lymphocytic infiltrates. The data are in accordance with recent findings of HLA-DR expressing residing cells in the target organs of various chronic inflammatory diseases and might indicate the induction of HLA-DR expression in nonlymphocytic cells of target organs in which a cellular infiltration dominated by cells of the T helper phenotype is found.

Adult↗
PubMed1984

Initiation of DNA replication in Escherichia coli: RNase H-deficient mutants do not require the dnaA function.

A series of temperature-resistant revertants were isolated from strains of Escherichia coli K12 carrying a temperature-sensitive mutation in the dnaA gene. Four independent revertants were found which still carry the original ts mutation. The ability of these strains to grow at high temperature is due to a suppressor mutation, called sin. All four sin mutations are located between the genes metD and proA on the genetic map of E. coli, which suggests that they all affect the same gene. The sin suppressors, which were isolated for their ability to suppress one dnaA mutation, are also able to suppress three other temperature-sensitive dnaA mutations, but they are not able to suppress mutations in either of the two genes dnaB or dnaC. The sin suppressors alone do not confer any particular phenotype on bacteria, but they are deficient in the enzyme RNase H. On the basis of these findings we propose that the function of the dnaA protein is to protect a DNA-RNA hybrid at the origin of replication against RNase H.

Bacterial Proteins↗
PubMed1983

Phenotypic characterization of cells within subcutaneous rheumatoid nodules.

An immunohistochemical double-staining technique was applied to frozen sections of biopsies from subcutaneous rheumatoid nodules. Material within the central necrosis reacted with anti-immunoglobulin and anti-HLA-DR antibodies. Cells within the palisading layer were "macrophage-like," as indicated by staining for anti-HLA-DR and OKM1, and showed a high proliferative activity as seen by OKT9 reactivity. The granulation zone contained many (alpha Leu-1+) T cells in close contact with HLA-DR-expressing non-T cells.

Antibodies, Monoclonal↗
PubMed1977

Genetic control of alpha-fetoprotein synthesis in the mouse.

To approach the genetic mechanism that turns off the synthesis of alpha-fetoprotein (AFP) after birth, we assumed that a change in this mechanism might affect the low basal level of AFP that can be detected in the adult organism. The concentration of AFP was therefore determined for serum from adult mice of 27 different inbred strains. With one exception, this basal level was between 34 and 173 ng/ml, which is about 10(5)-fold less than the serum concentration at birth. In one strain, BALB/c/J, the AFP level was found to be considerably increased; it was about 10-fold higher than in other strains at 9-10 wk of age. Two other substrains of BALF/c mice showed normally low AFP levels. Kinetic studies show that the rate with which AFP disappears from serum after birth is reduced in BALB/c/J mice as compared to other strains. The increased AFP level of BALB/c/J mice appears to be due to an increased rate of synthesis of AFP, since the rate of catabolism of AFP was found to be normal in these mice. Genetic analysis was performed by crossing BALB/c/J mice with mice having an ordinary AFP level, followed by determination of AFP levels in mice of the F1 and F2 generations as well as in back-cross mice. The results clearly indicate that the increased AFP level in BALB/c/J mice is controlled by a single recessive Mendelian gene, which has been named Raf (for regulation of alphafetoprotein). The Raf gene could be directly involved in the regulation of AFP synthesis, but it may also control AFP levels only indirectly, e.g., by regulating the synthesis of a hormone that controls AFP synthesis.

Age Factors↗
PubMed1971

On the process of cellular division in Escherichia coli: replication of the bacterial chromosome under control of prophage P2.

The temperature-sensitive mutant CRT46 of Escherichia coli K12 is unable to initiate new rounds of DNA replication at 42 degrees C. Mutants of bacteriophage P2 have been isolated, which, in the prophage state, allow mutant CRT46 to grow at 42 degrees C. The lysogenic bacteria that grow at 42 degrees C are apparently replicating under the control of prophage P2, which substitutes for the bacterial initiation system. The ability of prophage P2 cause this suppression phenomenon depends on the position of the prophage on the bacterial chromosome. Those lysogenic strains that are able to grow at 42 degrees C all carry the prophage close to metE. The P2 mutants that allow CRT46 to grow at 42 degrees C have insertions in the early region of the P2 genome. The suppression requires the cis-acting protein formed by gene A of P2.

Cell Division↗
PubMed1970

Bacteriophage lambda; abortive infection of bacteria lysogenic for phage P2.

The efficiency of plating of wild-type lambda on a host lysogenic for P2 is less than 10(-6), and only a small number of infected cells produce progeny phage. Lambda can adsorb and inject its DNA normally in such cells; the DNA can circularize and is not nicked or degraded, but replication is severely impaired. Mutants of P2, which as prophages no longer interfere with lambda, have been isolated and found to be recessive to wild type, implying that P2 prophage codes for a diffusible product involved in lambda interference. The P2 gene product responsible for preventing lambda growth also kills recombination-deficient bacteria of the recB and recC classes under conditions where P2 does not normally kill the host. Mutants of lambda that are resistant to interference are recessive to wild-type lambda. Thus lambda actively participates in its own interference. The lambda-mutants that are resistant to interference are unable to synthesize at least two nonessential proteins. In addition, they are unable to grow on recombination-deficient bacteria of the recA class, but they can grow on recA recB double mutants.

Carbon Isotopes↗