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S Bergström

Publications and source records attributed to S Bergström.

At least 235 records · Page 13Linked to original sources

ampC beta-lactamase hyperproduction in Escherichia coli: natural ampicillin resistance generated by horizontal chromosomal DNA transfer from Shigella.

Six ampicillin-resistant clinical isolates of Escherichia coli that hyperproduced the chromosomal ampC beta-lactamase were studied. By DNA sequence analysis, we found that five of them were identical over an entire 449-base-pair sequence and carried a novel strong ampC promoter [Olsson, O., Bergström, S. & Normark, S. (1982) EMBO J. 1, 1411-1416]. Except for one base pair this sequence was identical to that of a low beta-lactamase-producing clinical isolate of Shigella sonnei. Spontaneous one-step mutants of S. sonnei that overproduced the ampC beta-lactamase by 45-fold were characterized and found to be mutated at the single base that distinguishes S. sonnei from the five E. coli hyperproducers. The most likely explanation for this result is that chromosomal DNA was transferred in vivo from Shigella to E. coli across the species barrier.

Ampicillin↗

Hyperplasia and growth of the true mesentery in the diabetic rat.

The true mesentery was studied in rats 4 weeks after they had been rendered diabetic with streptozotocin. The diabetic animals showed elongation and enlargement of the small intestine despite reduced body growth compared with controls of the same age. The mesentery in diabetic animals showed increased total area and contained an increased number of "windows", but the increment of total protein, DNA, and histamine (a marker of mast cells) was non-uniform and less than the increase in area. There appeared to be a close relationship between hyperplasia of the small intestine and its mesentery. The number of mast cells yielded by peritoneal lavage was increased in the diabetics. We suggest that our observation of the hyperplastic mesenteric reaction in diabetic rats may make a useful model for the study of growth, profiferation, and function of the mesentery available.

Animals↗

Comparison of the overlapping frd and ampC operons of Escherichia coli with the corresponding DNA sequences in other gram-negative bacteria.

Specific DNA probes from Escherichia coli K-12 were used to analyze the sequence divergence of the frd and ampC operons in various species of gram-negative bacteria. These operons code for the fumarate reductase complex and the chromosomal beta-lactamase, respectively. We demonstrate that the two operons show the same general pattern of divergence, although the frd operon is considerably more conserved than is the ampC operon. The major exception is Salmonella typhimurium LT2, which shows a strong homology to the E. coli frd probe but none to the E. coli ampC probe. The operons from Citrobacter freundii and Shigella sonnei were cloned and characterized by physical mapping, Southern hybridization, and protein synthesis in minicells. In S. sonnei, as in E. coli K-12, the frd and ampC operons overlap (T. Grundström and B. Jaurin, Proc. Natl. Acad. Sci. U.S.A. 79:1111-1115, 1982). Only minor discrepancies between the two operons were found over the entire frd-ampC region. In C. freundii, the ampC and frd operons do not overlap, being separated by about 1,100 base pairs. Presumably the inducible property of the C. freundii chromosomal beta-lactamase is encoded by this 1,100-base-pair DNA segment.

Base Sequence↗

Overlapping genes.

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Base Sequence↗

Identification of a novel ampC beta-lactamase promoter in a clinical isolate of Escherichia coli.

A clinical strain of Escherichia coli, C16, that overproduces the ampC beta-lactamase was isolated. A 203-bp DNA segment from this strain, including the promoter and attenuator region of the ampC structural gene, was sequenced. A comparison with the corresponding sequence of E. coli K12 revealed four base pair differences between the ampC segments from these strains. DNA sequence data and in vitro transcription indicated that the ampC promoter in the clinical isolate was displaced 5 bp upstream of the promotor defined in the E. coli K12 strain. Like the ampC gene of E. coli K12, the ampC gene from the clinical isolate was metabolically regulated. However, the increase in the specific amount of beta-lactamase relative to the increase in specific growth rate was much higher in the clinical isolate. These data imply that the growth rate-dependent anti-termination acting on the ampC attenuator in vivo is more pronounced in the clinical E. coli isolate than in E. coli K12. A possible molecular mechanism for this is discussed.

Base Sequence↗

Plasma levels of 9-deoxo-16,16-dimethyl-9-methylene-PGE2 in connection with its development as an abortifacient.

Gaschromatographic-mass spectrometric quantitation of 9-deoxo-16,16-dimethyl-9-methylene-PGE2 in plasma samples obtained during constant intravenous infusion of the drug revealed that a plasma level of about 20 ng/ml was associated with high enough uterine contractility for induction of second trimester abortions. This level was therefore aimed for during the development of formulations and dose schedules for interruption of pregnancy with this drug. For the first time it was possible to induce second trimester abortions through oral administration of a prostaglandin analog, although the plasma levels were low giving a moderate success rate (about 50%) within 25 hours. Rectal administration of 20 mg of the drug at 6 hours intervals resulted in high enough plasma levels for second trimester abortions. Highly efficient dose schedules for interruption of early first trimester ("menses induction") and second trimester pregnancies through vaginal administration were developed. The frequency of side effects in the early first trimester were so low that "home treatment" was possible. Formulations suitable for 3, 6 or 12 hours preoperative dilatation of the cervix were also developed.

16,16-Dimethylprostaglandin E2↗

Common evolutionary origin of chromosomal beta-lactamase genes in enterobacteria.

A 32P-labeled fragment of DNA, encoding the major part of the chromosomal ampC beta-lactamase gene of Escherichia coli K-12, was used as a hybridization probe for homologous DNA sequences in colonies of Neisseria gonorrhoeae, Pseudomonas aeruginosa, and different enterobacterial species. The ampC probe detected the presence of homologous DNA sequences in clinical isolates of E. coli, Shigella flexneri, Shigella sonnei, Klebsiella pneumoniae, Salmonella typhimurium, Serratia marcescens, and P. aeruginosa. No hybridization was found with N. gonorrhoeae colonies. In Southern blotting experiments the ampC probe hybridized to chromosomal DNA fragments of the same size in all enterobacterial species tested. However, the degree of hybridization differed with DNA from different species. DNA from the Shigella species strongly hybridized to the ampC probe. Furthermore, antibodies raised against purified E. coli K-12 ampC beta-lactamase precipitated beta-lactamases from the Shigella species, suggesting extensive sequence similarities between the ampC genes of these genera. The production of chromosomal beta-lactamase in S. sonnei increased with increasing growth rate similar to E. coli K-12. This growth rate response was abolished in two beta-lactamase-hyperproducing S. sonnei mutants, which thus seem similar to E. coli K-12 attenuator mutants. We propose that both the structure and regulation of the chromosomal beta-lactamase genes are very similar in E. coli and in S. sonnei.

Base Sequence↗

Prostaglandin and protection of the gastroduodenal mucosa.

The prostaglandins, PGs, are formed mainly from arachidonic acid by all nucleated cell populations in the human body. The biosynthesis is easily initiated by unspecific stimulation and is influenced by hormonal, neural and local factors. Human gastroduodenal tissue produces mainly PGE2 and PGF2; an atraumatic approach to follow local production is to identify luminal PGs and their metabolites. In the gastrointestinal tract, the most studied biological action of exogenous PGs is inhibition of the basal and stimulated gastric acid secretion. In addition, PGs stimulate the gastric and duodenal bicarbonate secretion and the production and release of mucus glycoproteins and may have trophic effects on the gastric mucosa. Thus, PGs seem capable of mobilizing all recognized mucosal defense factors. The ability of small amounts of orally administered PGs to protect the gastric mucosa against the gross damage produced by necrotizing agents in experimental animals and to prevent and heal gastroduodenal lesions in man is called "cytoprotection" and is independent of acid inhibition. Cytoprotection may be connected to stimulation of the defensive bicarbonate-mucus barrier or result from yet unidentified mechanisms. --Evidence suggesting a role for the locally biosynthesized PGs in the regulation of the gastric parietal and nonparietal secretions is indirect and based on studies with blocking of the PG-biosynthesis by antiphlogistic compounds. The possible importance of endogenous PGs in the pathophysiology of gastroduodenal disease has been insufficiently examined. --Analogues of PGE2, produced by total synthesis, combine acid antisecretory and cytoprotective properties at dose levels without side effects or systemic actions and are now being tested in clinical trials to confirm effectiveness in the prevention and treatment of peptic ulcer and other gastroduodenal lesions.

Animals↗

Light and electron microscopic correlation of human amniotic fluid cells in late pregnancy.

Cytologic examination of oxazone-stained (nile blue) samples of amniotic fluid has become increasingly accepted as a reliable, inexpensive, and simple method of assessing fetal maturity. The present study focused on the ultrastructure of amniotic fluid cells in late human pregnancy. By means of light microscopy and scanning electron microscopy of the same cell in a series of cells, it was possible to observe the ultrastructural counterpart to the cell pattern indicative of fetal maturity. The type of cell indicating immaturity had a cytoarchitecture different from that of cells indicating maturity. The latter had an amorphous surface and coarse cytoplasmic strands; their oxazone-stainable, orange fat droplets were not found at electron microscopy. It is concluded that cells indicating maturity and those indicating immaturity differ in ultrastructure.

Amniotic Fluid↗

Age-dependent mitogenesis in normal connective tissue cells.

We have previously described ways to use the mesentery for studies of proliferation in intact tissue. Here we have studied a weak and a strong mitogenic response in the mesentery of rats aged 6--42 weeks, induced by a single intraperitoneal injection of saline or the mast-cell-degranulating drug 48/80. Proliferation was measured by the specific DNA activity, the fraction of fibroblast- and mesothelial-like cells in the S+G2 cell-cycle-phases, and the mitotic index. We also counted the relative number of mast cells in the tissue (normalized to 5,000 fibroblast-like and mesothelial-like cells), since this might influence 48/80-induced mast-cell-mediated proliferation. In old animals there was a decline in the proliferative response and the time required to initiate DNA synthesis was prolonged. This appears to be the first report of such an age-dependent proliferation characteristic in the mesentery, and probably in any connective tissue. The normalized number of mast cells in the mesentery also declined with increasing age.

Age Factors↗

Origin of amniotic fluid cells in mid-trimester pregnancies.

Amniotic fluid cells provide important information about the fetus. Studies of the surface ultrastructure of such cells identified four cell populations in mid-gestational fluids. A parallel study of tissue surfaces in contact with or communicating with the amniotic fluid showed that some tissues made no contribution to the cell populations, while others contributed extensively. Two principal cell shedding mechanisms were found in mid-trimester--exfoliation of whole cells and detachment of cellular fragments. The latter mechanism was observed from skin and umbilical cords during a limited period in mid-pregnancy. The majority of cells were derived from exfoliation of squamous epithelia.

Amniotic Fluid↗

A comparison of the amniotic fluid cytology, lecithin/sphingomyelin ratio and creatinine in predicting fetal maturity at term.

The value of three amniotic fluid tests--ratio of lecithin/sphingomyelin, creatine concentration and the Nile blue cytological test for lipid--carrying cells--in predicting fetal maturity at term was investigated. The cytological test was the best individual test, and a combination of all three seemed to accurately diagnose functional immaturity. A sequential approach for maturity testing is suggested. It is also concluded that maturity testing at term is an appropriate means of preventing iatrogenic prematurity.

Amniotic Fluid↗

Surface ultrastructure of amniotic fluid cells and fetal tissues of the Rhesus monkey.

Amniotic fluid cytology is considered to reflect other organ maturity more faithfully than the L/S ratio. In order to assess the origin of amniotic fluid cells a pilot study was undertaken in the Rhesus monkey with the purpose of correlating the surface ultrastructure of amniotic fluid cells and various tissues facing, or communicating with the amniotic cavity. Three distinct cell types were found in the amniotic fluid, out of which two were obviously related to maturational events in fetal skin. The remaining cell type seemed to be derived from umbilical cord, fetal vagina and to some extent oral mucosa. No exfoliation was observed in the urinary bladder, trachea, lungs or amniotic membranes. It is concluded that correlation of cytology and tissue surface morphology in the monkey amniotic fluid compartment may give clues to the origin of amniotic fluid cells in the human.

Amnion↗