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Notes: Summary Type 2 (non-insulin-dependent) diabetes mellitus may originate through impaired development in fetal life. Both insulin deficiency and resistance to the action of insulin are thought to be important in its pathogenesis. Although there is evidence that impaired fetal development may result in insulin deficiency, it is not known whether insulin resistance could also be a consequence of reduced early growth. Insulin resistance was therefore measured in 81 normoglycaemic subjects, and 22 subjects with impaired glucose tolerance, who were born in Preston, UK, between 1935 and 1943. Their birth measurements had been recorded in detail. Insulin resistance was measured by the insulin tolerance test which uses the rate of fall in blood glucose concentrations after intravenous injection of insulin as an index of insulin resistance. Men and women who were thin at birth, as measured by a low ponderal index, were more insulin resistant. The association was statistically significant (p =0.01) and independent of duration of gestation, adult body mass index and waist to hip ratio and of confounding variables including social class at birth or currently. Thinness at birth and in adult life has opposing effects such that resistance fell with increasing ponderal index at birth but rose with increasing adult body mass index. It is concluded that insulin resistance is associated with impaired development in fetal life. [Diabetologia (1994) 37: 150–154]

Notes: Summary Recent studies suggest that NIDDM is linked with reduced fetal and infant growth. Observations on malnourished infants and studies of experimental animals exposed to protein energy or protein deficiency in fetal or early neonatal life suggest that the basis of this link could lie in the detrimental effects of poor early nutrition on the development of the beta cells of the islets of Langerhans. To test this hypothesis we have measured insulin secretion following an IVGTT in a sample of 82 normoglycaemic and 23 glucose intolerant subjects who were born in Preston, England, and whose birthweight and body size had been recorded at birth. The subjects with impaired glucose tolerance had lower first phase insulin secretion than the normoglycaemic subjects (mean plasma insulin concentrations 3 min after intravenous glucose 416 vs 564 pmol/l, p =0.04). Insulin secretion was higher in men than women (601 vs 457 pmol/l, p =0.02) and correlated with fasting insulin level (p =0.04). However, there was no relationship between insulin secretion and the measurements of prenatal growth in either the normoglycaemic or glucose intolerant subjects. These results argue against a major role for defective insulin secretion as a cause of glucose intolerance in adults who were growth retarded in prenatal life. [Diabetologia (1994) 37: 592–596]

Notes: Summary Recent studies suggest that NIDDM is linked with reduced fetal and infant growth. Observations on malnourished infants and studies of experimental animals exposed to protein energy or protein deficiency in fetal or early neonatal life suggest that the basis of this link could lie in the detrimental effects of poor early nutrition on the development of the beta cells of the islets of Langerhans. To test this hypothesis we have measured insulin secretion following an IVGTT in a sample of 82 normoglycaemic and 23 glucose intolerant subjects who were born in Preston, England, and whose birthweight and body size had been recorded at birth. The subjects with impaired glucose tolerance had lower first phase insulin secretion than the normoglycaemic subjects (mean plasma insulin concentrations 3 min after intravenous glucose 416 vs 564 pmol/l, p=0.04). Insulin secretion was higher in men than women (601 vs 457 pmol/l, P=0.02) and correlated with fasting insulin level (p=0.04). However, there was no relationship between insulin secretion and the measurements of prenatal growth in either the normoglycaemic or glucose intolerant subjects. These results argue against a major role for defective insulin secretion as a cause of glucose intolerance in adults who were growth retarded in pre-natal life.

Notes: Summary Certain flavonoids released from plants regulate activities of soil microbes at micromolar and nanomolar concentrations. Processes affected by these compounds include induction of nodulation gene transcription in rhizobial bacteria, promotion of chemotaxis in rhizobia, increase in growth rate of several bacterial species, and enhancement of Glomus spore germination and hyphal growth. Data on the amount and identity of flavonoids released from several crop plant species form a new basis for molecular genetic and ecological studies of the rhizosphere.

Notes: Abstract The tonotopicity of the cat's primary auditory cortex (AI) is thought to provide the framework for frequency-specific processing in that field. This study was designed to assess this postulate by examining the spatial distribution of neurons within AI that are activated by a single tonal frequency delivered to the contralateral ear. Distributions obtained at each of several stimulus levels were then compared to assess the influence of stimulus amplitude on the spatial representation of a given stimulus frequency in AI. Data were obtained from 308 single units in AI of four adult, barbiturate-anesthetized cats, using extracellular recording methods. Stimuli were 40-ms tone pulses presented through calibrated, sealed stimulating systems. In each animal, the CF (stimulus frequency to which the unit is most sensitive), threshold at CF, response/level function at CF, and binaural interactions were determined for isolated neurons (usually one per track) in 60–90 electrode tracks. For each unit, regardless of its CF, responses to 40 repetitions of contralateral tones of a single frequency, presented at each of four or five sound pressure levels (SPLs) in the range from 10 to 80 dB were obtained. Different test frequencies were used in each of four cats (1.6, 8.0, 11.0, and 16.0 kHz). For tones of each SPL, we generated maps of the response rates across the cortical surface. These maps were then superimposed on the more traditional maps of threshold CF. All units whose CF was equal to the test frequency could be driven at some SPL, given an appropriate monaural or binaural configuration of the stimulus. There was a clear spatial segregation of neurons according to the shapes of their CF tone response/level functions. Patches of cortex, often occupying more than 2 mm2, seemed to contain only monotonic or only nonmonotonic units. In three cortices, a patch of nonmonotonic cells was bounded ventrally by a patch of monotonie cells, and in one of these cases, a second patch of monotonic cells was found dorsal to the nonmonotonic patch. Contralateral tones of any given SPL evoked excitatory responses in discontinuous cortical territories. At low SPLs (10, 20 dB), small foci of activity occurred along the isofrequency line representing the test frequency. Many of these cells had nonmonotonic response/level functions. At mid- and high SPLs, the CFs of neurons activated by a pure tone varied across 3 octaves. At the highest SPL used (80 dB), most of the neurons with nonmonotonic response/level functions were inactive, or responded poorly; the active neurons were widely spread across the cortex, and the distribution of activity had a pattern bearing little relationship to the threshold CF contour map. These data indicate that only isolated patches of units within the relevant isofrequency contour are activated by a given suprathreshold contralateral tone. At suprathreshold stimulus levels, the region of cortex containing active patches extends widely beyond the threshold isofrequency contour region corresponding to the test stimulus frequency. The spatial representation of a stimulus delivered to the contralateral ear appears, therefore, to be highly level dependent and discontinuous. These observations suggest that in the cat's AI, tonotopicity and isofrequency contours are abstractions which bear little resemblance to the spatial representation of tonal signals.

Notes: Pod rot and stem canker, caused by Phytophthora palmivora, are serious diseases of cocoa causing pod losses of up to 63% and the death of up to 10% of trees annually on Kar Kar Island. Papua New Guinea. Trials were conducted on commercial cocoa plantations to compare the effectiveness of potassium phosphonate when applied as trunk injections, trunk paints and foliar sprays, and trunk injections of Aliette CA and of Ridomil 250EC, with conventional Ridomil-based spray programmes. The results show that, in trials conducted over 5 years, injections of potassium phosphonate give the highest healthy pod yield and lowest incidence of Phytophthora pod rot and stem canker when compared with Ridomil-based spray programmes or trunk injections of Ridomil 250EC or Aliette CA. The increase in ripe healthy pod yields was due to both pod rot and stem canker control. The level of control is independent of the seasonal timing of injection. Optimum control was achieved with annual injections of 15 g a. i. per tree, and varied with tree size and disease severity. Injections of phosphonate will, under the range of conditions found in our trials. provide the most cost-effective control of Phytophthora diseases.

Notes: It is shown that in the vicinity of 77 K beryllium has a superior specific conductance compared with the nominally excellent metallic conductors aluminum and copper. It is concluded that beryllium should be considered for some conduction applications, despite its well known toxicity problems.