A deoxyribonucleic acid-replication intermediate in the growing mosquito

The arrangement of 18-S rRNA and 28-S rRNA within their 40-S common precursor molecule (pre-rRNA) of Xenopus laevis was investigated by electron microscopic analysis of secondary structure of nascent pre-rRNA chains of oocytes, and by 5'-end analysis of 18-S rRNA and 28-S rRNA hybridized to the EcoRI fragment of rDNA cloned as plasmid pCD42. Secondary structure mapping of phenol-extracted RNA from nucleolar cores revealed complete pre-rRNA chains or molecules at various stages of processing and pre-rRNA molecules apparently lacking one end. In this latter group, which was regarded as representing nascent chains, more than 90% of the molecules had no 28-S rRNA REGION. This shows that the 28-S rRNA sequence is transcribed after the 18-S rRNA region and hence must be located nearer to the 3' end of the pre-rRNA molecule. For 5' end-group determination [3H]uridine-labelled 18-S rRNA and 28-S rRNA were hybridized, as fragments of about 200 nucleotides, to the plasmid pCD42 containing coding sequences for four-fifths of the 18-S rRNA sequence, the external transcribed spacer, the non-transcribed spacer and a tenth of the 28-S rRNA sequence. The RNA was recovered from the hybrids and analyzed for uridine 3',5'-bisphosphate (pUp) after alkaline hydrolysis. The pUp content of the hybridized 18-S rRNA fragments was 20-fold higher than in those of 28-S rRNA, THUS DEMONSTRATING THAT THE 5' END OF THE 18-S rRNA is located next to the external spacer region. From these results it is concluded that the 18-S rRNA is located close to the 5' end of the 40-S pre-rRNA molecule.     

Operant autonomic conditioning and rod-and-frame test performance

Forty subjects were administered the portable rod-and-frame test (RFT) before and after operant autonomic conditioning training or control experiences. Ten subjects were assigned to each of four groups: a heart rate conditioning group; a false heart rate feedback group; a galvanic skin-response conditioning group; and a control group. Half of the subjects in the three experimental groups were informed of the response-reinforcement contingencies, and half were not informed. Informed subjects in the conditioning groups exhibited significantly lower portable RFT scores after conditioning. The results suggest that awareness of and control over autonomic functioning may be an important determinant of RFT performance.     

Initial experience of clinical pharmacology and clinical pharmacy interactions in a clinical pharmacokinetics consultation service

International statistics indicate that there is a close correlation between the consumption of saturated fats (dairy fats and meat fats) and the mortality from coronary heart disease (CHD), and this conception has been confirmed by many epidemiological studies. Such studies alone, however, cannot prove the existence of a cause-and-effect relationship between these two variables; dietary intervention trials are needed. The Finnish Mental Hospital Study was such a trial, conducted in two hospitals near Helsinki in 1959--1971. Practically total replacement of dairy fats by vegetable oils in the diets of these hospitals was followed by a substantial reduction in the mortality of men from CHD. Total mortality also appeared to be reduced. As to the causes of death other than CHD, none was significantly influenced by dietary change. This was also true for malignant neoplasms. To alleviate the burden of CHD on public health, many investigators have recommended important changes in the quantity and quality of dietary fats.     

Acute pretreatment with pyrazole and ethanol: effects on glucose-induced changes in insulin and glucagon

Ethanol suppressed, in a dose-related manner, glucose-induced insulin (IRI) release and thus delayed the disappearance of glucose from the blood of rats. Pretreatment with pyrazole, an alcohol dehydrogenase inhibitor, exacerbated the effect of ethanol on IRI release, glucose tolerance and glucagon (IRG) release. These results suggest that ethanol produces glucose intolerance by inhibiting glucose-induced IRI release and by augmenting IRG release. Moreover, these findings indicate that ethanol does not have to be metabolized completely in order to produce these effects.