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CePtSi is a known heavy-fermion compound with no magnetic ordering. It forms in a tetragonal non-centrosymmetric crystal structure. Pronounced Kondo features at elevated temperatures originate from magnetic Ce+3 ions. Towards low temperatures coherence develops in the electronic scattering and a Kondo lattice forms below 30 K. At the same temperature scale the electronic specific heat steeply escalates to CP/ T ≃ 0.7 J mol−1 K−2. Considerable effort has been devoted in previous studies to find the origin for the observed low-temperature divergences in thermal properties in CePtSi and in particular for the putative non-Fermi-liquid behaviour. To date however, a coherent description of the physics of CePtSi remains to be found. In this work we present low-temperature results of χ( T), CP( T), and ρ( T). A picture of the low-temperature nature of this compound is forwarded that is consistent across the thermal properties. We illustrate how a non-Fermi-liquid state intervenes between the high-temperature incoherent Kondo region and Kondo lattice ground state of CePtSi. The non-Fermi-liquid region effectively mediates a crossover from the high-temperature paramagnetic state in CePtSi to its Fermi-liquid ground state. We argue that magnetic ordering is avoided through a small but intrinsic dissimilarity between nearest-neighbour Ce atoms. [ABSTRACT FROM AUTHOR]

The tendency of unpaired meiotic chromosomes to undergo centric misdivision was exploited to translocate leaf rust and stripe rust resistance genes from an Aegilops kotschyi addition chromosome to a group 2 chromosome of wheat. Monosomic and telosomic analyses showed that the translocation occurred to wheat chromosome arm 2DL. The introgressed region did not pair with the corresponding wheat 2DL telosome during meiosis suggesting that a whole arm may have been transferred. Female transmission of the resistance was about 55% whereas male transmission was strongly preferential (96%). The symbols Lr54 and Yr37 are proposed to designate the new resistance genes. [ABSTRACT FROM AUTHOR]

1. The foreshortened 2 h method of measuring liquid gastric emptying (i.e. the proportional cumulative area under the curve of paracetamol) was utilized in diabetic patients in order to detect both gastroparesis and the influence of metoclopramide, a known prokinetic drug, on this condition. 2. Metoclopramide, 10 mg intravenously, caused a significant increase in the median PCAUC from 20 min onwards. 3. In this study delayed gastric emptying was defined as a %PCAUC without pretreatment lower than the 5% percentile at 40, 60 and 90 min for normal volunteers. According to this criterion seven of the 10 patients with clinical symptoms of gastroparesis and/or peripheral neuropathy had delayed gastric emptying. 4. The PCAUC method would therefore seem to be a reliable model for investigating gastric emptying in diabetics and the effects of various prokinetic drugs on this condition.

1. The effects of the anticholinergic agent, propantheline, the opiate, codeine, and the prokinetic agent, metoclopramide, on oral-caecal transit time and on the absorption of theophylline from a sustained-release formulation were examined in six healthy male volunteers. 2. A cross-over randomised sequence design was followed, allowing at least 2 weeks interval between studies. On each occasion 500 mg theophylline in a sustained-release formulation was taken simultaneously with 2 g sulphasalazine at zero time. On three of the four occasions one of the following treatments was given concurrently at -0.5 h, +3.5 h, and +7.5 h: 30 mg codeine phosphate, 30 mg propantheline bromide, or 10 mg metoclopramide monohydrochloride. 3. The appearance of sulphapyridine in the plasma was used to assess oral-caecal transit time and the mean fraction absorbed-time profile of theophylline was calculated from serial serum theophylline concentration measurements using the Wagner-Nelson method. 4. Codeine increased the mean (s.d.) oral-caecal time (h) significantly (5.14 +/- 0.94) compared with the control value (3.78 +/- 0.34). Propantheline inhibited peristaltic contractions to such an extent that the oral-caecal transit time in five of the volunteers was between 9 and 25 h, while sulphapyridine appeared in the 9 h serum sample of the sixth. Metoclopramide did not significantly alter the oral-caecal transit time. 5. Despite the observed changes in oral-caecal transit time the rate and extent of theophylline absorption was similar with all regimens.

1. To test the hypothesis that the in vivo inhibition of angiotensin converting enzyme in a patient who presents atopy, results in a significant increase in cutaneous bradykinin and prostaglandin production, the effect of enalapril on the cutaneous hypersensitivity reaction was examined in 10 atopic volunteers. 2. A crossover study design was used and volunteers were randomly allocated to treatment with either enalapril (10 mg) alone, or in combination with indomethacin (75 mg), with and without ketotifen (1 mg). Drugs were administered twice daily for 2 days. 3. Allergen (Southern Grass Mix) was administered intradermally 2 h after last drug dosage and the surface areas of the immediate wheal-and-flare-reactions were measured 15 min later. The late phase of the cutaneous response was evaluated 6 h later by determining skinfold thickness and surface area. 4. Enalapril alone had no effect on any of the parameters measured. 5. The cutaneous hypersensitivity reaction was significantly reduced with regard to both immediate and late cutaneous responses when the indomethacin and ketotifen combination was added to enalapril therapy. 6. When only indomethacin was added to enalapril pretreatment the flare reaction was significantly reduced, but whealing was unaffected. 7. This study presents further evidence that mast cell mediators other than prostaglandins are involved in the cutaneous hypersensitivity reaction. Furthermore, that endogenous bradykinin production after enalapril pretreatment either never reaches the supraphysiological concentrations used in previous experiments, or that bradykinin is rapidly and effectively broken down to inactive peptides by other carboxypeptidase enzymes.

The in vivo pharmacological effects of cimetidine on delayed hypersensitivity reactions in healthy volunteers were studied using the tuberculin skin test as parameter. Cimetidine clearly enhanced this reaction when it was administered well before antigenic stimulation.