Biomedical subjects

F Ernst

Publications and source records attributed to F Ernst.

24 records · Page 2Linked to original sources

PubMed1988

Ceftazidime combined with mecillinam: serum bactericidal titres compared with in-vitro synergy against gram-negative bacilli.

In a study of the possible interaction between mecillinam and ceftazidime against Gram-negative bacilli, ten volunteers received on separate days: ceftazidime 20 mg/kg iv in 15 min, mecillinam 10 mg/kg iv in 15 min, or the combination. Blood samples were obtained before and 1 and 6 h after the end of the infusion. Ten strains each of Klebsiella pneumoniae, Serratia marcescens, Citrobacter freundii, Salmonella spp. and Yersinia spp. and nine strains each of Acinetobacter spp., and Pseudomonas aeruginosa were selected. Most of the strains were resistant to ampicillin and cefazolin. Serum levels of ceftazidime and mecillinam were measured by bioassay. Serum bacteriostatic (SBS) and bactericidal (SBA) titration was done in microtitre plates in cation supplemented Mueller-Hinton broth and 50% human serum. Chequerboard titration was also studied to assess in-vitro synergy between ceftazidime and mecillinam in Mueller-Hinton broth with or without 50% serum. The mean serum concentrations (SD) were for mecillinam: 6.1 (1.7) at 1 h, and less than 0.3 at 6 h and for ceftazidime: 36.3 (5.5) at 1 h and less than 5 at 6 h. Identical concentrations were measured for the combination. By chequerboard titration, no synergy occurred for Acinetobacter spp. and Ps. aeruginosa, whereas it was observed in 37/60 (FIC) and 33/60 (FBC) of the strains of other species in Mueller-Hinton; from the strains showing synergy, 28/37 (FIC) and 30/33 (FBC) showed also synergy in Mueller-Hinton with 50% human serum. In SBS and SBA, on the other hand, the combination of mecillinam with ceftazidime showed an additive effect against most Enterobacteriaceae tested, synergy being shown for only 10-35% of tests.(ABSTRACT TRUNCATED AT 250 WORDS)

Amdinocillin↗

PubMed1987

Determination of the nucleotide sequence flanking the deletion (0.762 to 0.789 map units) in the genome of an intraperitoneally avirulent HSV-1 strain HFEM.

Herpes simplex virus type 1 (HSV-1) strain HFEM which harbours a deletion of 4.1 kbp in its genome (0.762 to 0.789 map units, HpaI DNA fragment P of HSV-1), is apathogenic for mice and tree shrews by the intraperitoneal application route. The exact position of this deletion was determined by DNA sequence analysis. This analysis was performed using the recombinant plasmid pU18HSHF-XmI-B which harbours the flanking genome regions (0.752 to 0.762 and 0.789 to 0.7895 map units) of the deletion in the genome of HSV-1 HFEM, and the recombinant plasmids pU18HSF-XmI-B, pU18HSF-AS, and pHSF-BB-BsH-D, harbouring particular regions of the genome of the virulent HSV-1 strain F at the coordinates 0.752 to 0.761, 0.786 to 0.790, and 0.762 to 0.771, respectively. The comparison of the DNA sequence of this region with the DNA sequences of the corresponding genome regions of the pathogenic HSV-1 strain F and HSV-1 strain 17 showed that the 5' end of the deletion in the genome of HSV-1 HFEM starts at the nucleotide position 3774 of the BamHI DNA fragment B from HSV-1/17. This position is 71 bp upstream of the UL/RL junction of the HSV-1 genome. The 3' terminus of the deletion ends at the nucleotide position 7226 of the BamHI DNA fragment B from HSV-1/17. The position is within the incomplete ninth repetitive box (ACTCC-CACGCACCCCC) and is located 36 bp upstream of the 3' end of the IE 110 mRNA.

Animals↗

PubMed1987

In-vitro activity of two new carbapenems FCE 22101 and CGP 31608 in comparison with imipenem.

The minimum inhibitory concentrations (MICs) of two new penems, CGP 31608 and FCE 22101 were evaluated against 993 aerobic Gram-positive and Gram-negative bacteria and compared with imipenem. FCE 22101 was usually two to eight-fold more active than CGP 31608 except for Pseudomonas aeruginosa against which FCE 22101 was inactive. Both new penems were less active than imipenem. MBCs were equal to 1-2 X MICs. The effects of inocula, cations and serum were minimal. The MICs and MBCs were higher at pH 8 than at pH 6 or 7. Synergy between the new penems and amikacin was detected in 30% of the strains studied. Antagonism occurred with some Gram-positive bacteria.

Anti-Bacterial Agents↗

PubMed1986

Replacement of the deletion in the genome (0.762-0.789 mu) of avirulent HSV-1 HFEM using cloned MluI DNA fragment (0.7615-0.796 mu) of virulent HSV-1 F leads to generation of virulent intratypic recombinant.

The HFEM strain of HSV-1 is apathogenic for the tree shrew by the intraperitoneal (i.p.) route because of a deletion in the genome coordinates 0.762-0.789. Insertion of the MluI DNA fragment (coordinates 0.7615-0.789) cloned from HSV-1 strain F, which is pathogenic for the tree shrew, restored the i.p. pathogenicity to strain HFEM. The recombinant designated R-M1-C1 was highly pathogenic for the tree shrew, but slightly virulent for inbred mouse strain A. It thus appears that the viral DNA sequence involved in the i.p. pathogenicity of HSV-1 is located within the genome coordinates 0.761-0.796. This sequence is recognized differently by the cellular elements involved in HSV-1 infection in the tree shrew and the mouse.

Animals↗

PubMed1985

Binding in vitro of vasoactive intestinal peptide on isolated acini of rat parotid glands.

Binding of 125I-labelled vasoactive intestinal peptide (VIP) to rat parotid acini was saturable, temperature-dependent and reversible, and reflected interaction with a single class of binding sites. Parotid glands possessed approx. 400 fmol binding sites per mg protein and binding of the tracer to these sites could be inhibited by VIP [concentration for half-maximal effect (KD), 24 nM], by the peptide histidine isoleucine (KD, 140 nM), by secretin (KD, 470 nM) and by the human pancreatic growth hormone-releasing factor (hpGRF; KD, 3200 nM). In the same acini preparation, 10 microM VIP also stimulated amylase release 4-fold and increased cyclic AMP 11-fold. Thus, VIP might be a neurotransmitter in the rat parotid gland.

Amylases↗

PubMedDate not supplied

Gas-phase sorption-desorption of propargyl bromide and 1,3-dichloropropene on plastic materials.

The goal of this research was to provide information for choosing appropriate materials for studying gas-phase concentrations of propargyl bromide (3BP) and 1,3-dichloropropene (1,3-D) in laboratory experiments. Several materials were tested and found to sorb both gas-phase chemicals in the following order: stainless steel (SS) < Teflon polytetrafluoroethylene (PTFE-FEP) approximately flexible polyvinyl chloride (PVC) approximately acrylic < low-density polyethylene (PE) < vinyl approximately silicone < polyurethane foam (PUF). Sorption of SS was insignificant and PUF sorbed all the fumigant that was applied. For the other materials, linear sorption coefficients (Kd) for 3BP ranged from 3.0 cm3 g(-1) for PVC to 215 cm3 g(-1) for silicone. Freundlich sorption coefficients for 1,3-D ranged from 11.5 to 371 cm3 g(-1). First-order desorption rate constants in an open system ranged from 0.05 to 1.38 h(-1) for 3BP and from 0.07 to 1.73 h(-1) for 1,3-D. In a closed system, less than 2% of sorbed fumigant desorbed from vinyl while up to 99% desorbed from PVC within 24 h when equilibrated at the highest headspace concentration. Sorption of both fumigants was linearly related to the square root of time except for vinyl and silicone. This may indicate non-fickian diffusion of fumigant into the polymer matrix. Vinyl, silicone, PE, and PUF should be avoided for quantitative study of organic gases, except possibly as a trapping medium. Use of PTFE, PVC, and acrylic may require correction for sorption-desorption and diffusion.

Adsorption↗