Effects of the transciption inhibitory protein, TF1, on phage SP01 promoter complex formation and stability.

The uptake of a homologous single-stranded fragment by superhelical DNA produces a complex that contains a stable displacement loop. When the circular DNA was relaxed by the random action of pancreatic DNAase, complexes dissociated by a process which requires that the single-stranded arm of the D-loop be intact. We attribute the dissociation to branch migration, the exchange of like strands at a branch point. The kinetics of dissociation were biphasic. A fraction of the nicked complexes dissociated in a few seconds, the rest dissociated much more slowly. The fraction of molecules that dissociated slowly was directly related to the length of the third strand, and inversely related to temperature. Salt also inhibited dissociation. Under physiological conditions, 37 °C and 0.15 m-NaCl, more than half of complexes containing a third strand of 1000-nucleotide residues survived for at least one minute. These observations provide a guide to handling certain natural or synthetic branched derivatives of DNA. Analyzing our data by the method of Thompson et al. (1976), we have estimated that the time for the exchange of one nucleotide for another at a single-stranded branch is 12 microseconds; but the calculated value depends strongly upon the assumption that single-strand branch migration occurs by a random walk.     

CARBOHYDRATE AND ENERGY METABOLISM IN PERINATAL RAT BRAIN: RELATION TO SURVIVAL IN ANOXIA

The ability of rats of different ages to survive exposure to anoxia was correlated with rates of high energy phosphate consumption (metabolic rates) of the fore-brain. Fetal rats at term, delivered by hysterotomy following maternal decapitation, survived in nitrogen at 37°C twice as long as 1-day-old neo-nates, 5 times longer than 7-day-old rats, and 45 times longer than adults. During ischemia induced by decapitation, the cerebral concentrations of the labile energy reserves (ATP, ADP, P-creatine, glucose and glycogen) and of lactate were determined in fetuses, 1- and 7-day post-natal animals. From the changes, the cerebral energy use rates were calculated to be 1·57 mmol/kg/min in fetuses, 1·33 mmol/kg/min in 1-day-olds and 2·58 mmol/kg/min in 7-day-olds. Maximal rates of lactate accumulation during ischemia, as a measure of glycolytic capacity, were comparable in fetuses and neonates, but were about twice as great in 7-day-old rats. It is concluded that in post-natal animals survival in anoxia and cerebral energy consumption are inversely, and nearly quantitatively, related. However, the reduced cerebral energy requirement cannot entirely account for the greater anoxic resistance of fetuses.     

Idioms of distress: Somatic responses to distress in everyday life

In-depth interviews were conducted among 50 subjects residing in the industrial town of Newcastle, Australia. Half of these subjects were from the general population and half were currently seeking counselling for personal/family problems. None of the subjects were receiving any medical care at the time of interview, though seven had done so during the episode of distress they were discussing. The study shows that while the subjects psychologized their problems, members of both groups tended to somatize at a rate proportional to the level of distress. Subjects were unaware of any relationship between the distress they were experiencing and their physical complaints. The results of this study support previous research which argues that those experiencing distress and those who tend to introspect are also those who are likely to amplify somatic symptoms. At the same time these results depart from findings in the United States which suggest that in the West, people learn to express social and personal distress in psychological terms,, thereby reducing the level of somatization. Though not representative of the population as a whole, the findings raised questions warranting further study.     

Suppression of postprandial glucose, insulin, C-peptide, and glucose-dependent insulinotropic peptide (GIP) in man by oral administration of a prostaglandin analogue (enprostil)

Enprostil, a long-acting, orally active dehydroprostaglandin E2 with cytoprotective and gastric antisecretory properties, is a potent inhibitor of meal-stimulated gastrin release. Recent data have suggested suppression of additional other gastrointestinal peptide hormones following single doses of enprostil. The current investigation was conducted to further clarify the effects of enprostil administration on gastrointestinal hormones and glucose metabolism under physiologic conditions and to determine whether these effects were present following multiple doses of the agent. Enprostil 70 mcg/d and its placebo were each administered for 7 1/2 days to eight normal male subjects in a study of crossover design, each treatment period lasting 7 1/2 days and separated by a 7 day washout period. Subjects received a test meal on days 1 and 8 and an oral glucose challenge on day 3 of each treatment period following enprostil or its placebo. Following the test meal, there was a delay and suppression of the maximum measured serum glucose levels. Mean overall peak glucose concentrations were lower during the enprostil phase compared to placebo (112 vs. 121 mg/dd, P = 0.025) with a trend toward delay in the time to achievement of peak glucose concentrations. Mean overall peak levels for insulin, C-peptide, and glucose-dependent insulinotropic peptide (GIP) were significantly suppressed by 36%, 16% and 60%, respectively by enprostil when compared to placebo. The overall integrated postprandial responses for insulin, C-peptide, and GIP were significantly reduced by 42%, 39% and 90%, respectively while that for glucose above baseline was reduced by 44% (P = 0.098). Similar effects were present following the oral glucose challenge.(ABSTRACT TRUNCATED AT 250 WORDS)     

Murine Toxicity of Agrobacterium tumefaciens

Eleven strains of the crown gall organism, Agrobacterium tumefaciens, tested by intraperitoneal injection into mice, were lethal within 48 hr. Five other species had some lethal strains. The lethal effect of A. tumefaciens appeared to be the result of a toxic rather than an infectious process, since histopathological anomalies were not found in mice injected with live cultures and since heat-killed cultures were lethal. The murine toxin disappeared when A. tumefaciens was grown at 36 C and reappeared when the organism was subsequently incubated below 30 C. The murine toxin itself was not inactivated by exposure to 100 C for 30 min. The toxin was associated with the cells and was not excreted into the medium. Centrifugal fractionation revealed that the toxin was associated with the smaller cells in 3-day stationary-phase cultures. These data suggested a possible relationship between toxin production and the production of the agents responsible for the initiation of plant tumors.