[Study on cefotaxime in respiratory surgery: transfer to lung tissue and kinetics in serum].

Cefotaxime (CTX) was intravenously administered in a dose of 1 g to patients just prior to lung surgery. Lung tissue specimens were collected at 1, 2 and 3 hours after the CTX administration, and the concentration of CTX in each specimen was determined. At the same time, the concentration of CTX in the serum was also measured.

Interleukin 2 promotes expression of an interleukin 2 receptor and proliferation of T cells stimulated with non-mitogenic dose of concanavalin A.

Interleukin 2 (IL-2) initiated proliferation of the cells of T-enriched population stimulated with non-mitogenic dose of concanavalin A (Con A), whereas it could not induce proliferation of the cells treated with non-mitogenic lectin wheat germ agglutinin (WGA). Use of monoclonal antibody (MAb) directed against interleukin 2 receptor (IL-2R) showed that IL-2 significantly increased expression of IL-2R on the cells of T-enriched population stimulated with Con A, whereas it could not cause any significant enhancement of expression of IL-2R on the cells treated with WGA. We concluded that IL-2 activated T cells in combination with non-mitogenic does of Con A, and induced both expression of IL-2R and proliferation.

Persistent hyperkalaemia in vitamin B12 unresponsive methylmalonic acidaemia.

Persistent hyperkalaemia was found in a patient with vitamin B12 unresponsive methylmalonic acidaemia associated with hyperuricaemia. At 3 years and 8 months of age, a serum potassium level of 6.8 mmol L-1 was found when blood gas measurement was normal.

DNA damage induced by ascorbate in the presence of Cu2+.

DNA damage induced by ascorbate in the presence of Cu2+ was investigated by use of bacteriophage phi X174 double-stranded supercoiled DNA and linear restriction fragments as substrates. Single-strand cleavage was induced when supercoiled DNA was incubated with 5 microM-10 mM ascorbate and 50 microM Cu2+ at 37 degrees C for 10 min. The induced DNA damage was analyzed by sequencing of fragments singly labeled at their 5'- or 3'-end.

Hypocarnitinemia in the handicapped individuals who receive a polypharmacy of antiepileptic drugs.

Decrease in the serum concentrations of total and free carnitine were found in patients who had received multiple doses of antiepileptic drugs, either including or excluding sodium valproate. These concentrations were more depressed in a former patient group. In all patients there were no abnormal losses of carnitine in urine.

Sequence-specific modification of DNA by 6-hydroxybenzo[a]pyrene.

6-Hydroxybenzo[a]pyrene cleaved phi X174 supercoiled DNA to open circular DNA in the presence of heavy metal ions. It induced an alkali-labile modification in DNA via an oxygen-radical-mediated reaction; the most frequent alkali-labile sites were on the 3' side of the pyrimidine residues of the pyrimidine cluster.

Sequence-specific alkali-labile lesions in DNA caused by D-isoglucosamine.

The site-specific induction of DNA damage by 1-amino-1-deoxy-D-fructose (D-isoglucosamine) was investigated. When 32P-end-labeled DNA restriction fragments of known sequence were reacted with D-isoglucosamine in the presence of Cu2+, and the DNA products were analyzed on high-resolution denaturing polyacrylamide gels after treatment with aqueous piperidine (1 M) at 90 degrees C for 30 min, the DNA strands were cleaved at pyrimidine residues at a statistically significant frequency, and 80.5% of the extensively damaged sites were induced at pyrimidine residues in dinucleotide sequences of pyrimidine-purine (5'----3').

Effect of kallikrein-kinin system on calcium-vitamin D3 metabolism.

Kallikrein has been reported to stimulate callus formation and cell proliferation. It is well-known that vitamin D3 play an role on the metabolism of calcium. However, the relation between vitamin D3 and kallikrein are still poorly understood.

Site-specific DNA damage caused by lipid peroxidation products.

DNA damage induced by autoxidized lipids was investigated using covalently closed circular (supercoiled) DNA and DNA fragments of defined sequence. DNA-strand-breaking substances accumulated during autoxidation of methyl linolenate, and strand breakage was measured with samples taken at different times. The DNA-strand-breaking activity reached its maximum a little after the peak value of peroxide and decreased upon further autoxidation.

Sequence specific damage of DNA induced by reducing sugars.

Reducing sugars induced alkali-labile sites in DNA. The DNA reacted with D-fructose 6-phosphate or D-fructose in the presence of Cu2+ was cleaved by the treatment with aqueous piperidine at 90 degrees C for 30 min. Alkali-labile sites were induced frequently at the pyrimidine residues, especially at the pyrimidine residues in pyrimidine-purine (5'----3') sequences.

Sequence specificity of heat-labile sites in DNA induced by mitomycin C.

The sequence specificity of the mitomycin C-DNA interaction was directly determined by using DNA sequencing techniques and by using 3'- or 5'-end-labeled DNA fragments of defined sequence as substrates. Mitomycin C reduced with sodium borohydride induced heat-labile sites in DNA preferentially at specific sequences. The heat-labile sites were induced most preferentially at the dinucleotide sequence G-T ( especially Pu G-T), which was determined by scanning autoradiograms with a microdensitometer after gel electrophoresis.

Identification of a membrane protein induced concurrently with cell filamentation by cyclic AMP in an Escherichia coli K-12 fic mutant.

A membrane protein with a molecular weight of 40,000 (40K protein) was induced concurrently with cell filamentation by cyclic AMP (cAMP) in a fic mutant. In the crp mutant and the wild-type strain, cell filamentation by cAMP was not observed, and the 40K protein was not induced. Induction of the 40K protein is regulated by the cAMP-cAMP receptor protein complex and is closely related to cell filamentation by cAMP in the fic mutant.

Aclacinomycin A-inhibition of phage phi X174 DNA synthesis in vitro.

Aclacinomycin A inhibited the in vitro conversion of phage phi X174 single-stranded DNA to the replicative form DNA. DNA synthesis was inhibited by 50% in the presence of 15 microM aclacinomycin A. The inhibition was competitive with respect to template DNA (Ki = 13 microM) and was reversed by addition of Escherichia coli cell extracts.

Reduced mitomycin C induces heat-labile sites in DNA at specific sequences.

We have investigated the sequence specificity of DNA damage induced by mitomycin C reduced with NaBH4, by using 3'- or 5'-end labeled DNA fragments of defined sequence. Mitomycin C reduced with NaBH4 induced heat-labile sites in DNA preferentially at specific sequences. The most preferred trinucleotide sequence for induction of heat-labile sites was GGT, followed by GGG, AGT, GAG, GGC and AGG.

Phage inactivation and DNA strand scission activities of 7-N-(p-hydroxyphenyl)mitomycin C.

A new derivative of mitomycin C (MMC), 7-N-(p-hydroxyphenyl)mitomycin C (M-83), had higher phage inactivation activity against phages phiX174 and PM2 than MMC, and also higher DNA strand scission activity against their single- and double-stranded DNAs. M-83, at one third to one sixth concentration of MMC, showed the same level of phage inactivation and DNA strand scission activities. The mechanism of phage inactivation and DNA strand scission by M-83 were similar to those of MMC: (1) Reduction of M-83 was required for its action.

In vitro conversion of S13 viral DNA in phage particles to the double-stranded DNA.

The conversion of single-stranded DNA in S13 intact phage particles to the double-stranded replicative form DNA was observed in cell extracts prepared from Escherichia coli H560 (S13s, polA, endA) cells lysed with lysozyme and the non-ionic detergent, Brij 58. The DNA product, which associated with a rapidly sedimenting component, was identified as RFII-DNA with a gap by sedimentation analysis. The conversion was inhibited by N-ethylmaleimide, but not by rifampicin, nicotinamide mononucleotide or polymyxin B.

Induction of single strand scission in bacteriophage phi X174 replicative form I DNA by mitomycin C.

The action of mitomycin C on double-stranded replicative form I DNA (RF I DNA; supercoiled, covalently closed, circular duplex DNA) of bacteriophage phi X174 was investigated using the technique of agarose gel electrophoresis. Mitomycin C reduced with sodium hydrosulfite (sodium dithionite, Na2S2O4) caused single strand scission in phi X174 RF I DNA in the presence of Cu2+. Cu2+ was essential for this DNA cleave action, and other transition metal ions such as Fe2+, Fe3+, Mn2+, Co2+ and Zn2+ were of no effect.

Process of attachment of phi X174 parental DNA to the host cell membrane.

The phi X174-DNA membrane complex was isolated from Escherichia coli infected with phi X174 am3 by isopycnic sucrose gradient centrifugation followed by zone electrophoresis. The phi X174 DNA-membrane complex banded at two positions, intermediate density membrane fraction and cytoplasmic membrane fraction, having bouyant densities of 1.195 and 1.

Inactivation of bacteriophage phi X174 by mitomycin C in the presence of sodium hydrosulfite and cupric ions.

Bacteriophage phi X174 was inactivated by mitomycin C reduced with sodium hydrosulfite in the presence of cupric ions (Cu2+). 99% of the phage particles lost their plaque-forming abilities when incubated with 1.5 .

Purification and some properties of a neutral muscle pyrophosphatase.

In the water-soluble fraction of rabbit skeletal muscle, at least two types of inorganic pyro phosphatase (PPase) are distinguishable on ion exchange column chromatography. One of them, pyrophosphatase-A (PPase-A), was isolated in an electrophoretically homogeneous form. This enzyme catalyzed the hydrolysis of PPi but not that of other phosphate esters.

Inactivation of infectivity of phiX174 DNA by menadione and reduced menadione.

Interaction of menadione and reduced menadione with phage phiX174 DNA was investigated. A concentration of 2-10(-4) M menadione inactivated 60% of the infectivity of phiX174 DNA to spheroplasts of Escherichia coli, while reduced menadione inactivated 97% of the infectivity of phiX174 DNA at the same concentration. Alkaline sucrose gradient centrifugation revealed 2-10(-5) M reduced menadione caused approximately 24% of phiX174 DNA to produce strand break under the condition of 80% lethanlity.