Learning difficulties, including problems with numeracy, are common in Western populations. Many children with learning difficulty are survivors of preterm birth. Although some of these children have neurological disabilities, many are neurologically normal, and the latter group provides us with an important opportunity to investigate the neural bases of learning problems. We have conducted a neuroimaging study of adolescent children who had been born preterm at 30 weeks gestation or less, to investigate the relationship between brain structure and a specific difficulty in arithmetic calculation. Using voxel-based morphometry, we have been able to demonstrate that there is an area in the left parietal lobe where children without a deficit in calculation ability have more grey matter than those who do have this deficit. To our knowledge, this is the first report establishing a structural neural correlate of calculation ability in a group of neurologically normal individuals.

Two-hundred and fifty-eight patients treated with high-activity 131I for thyroid cancer and on prolonged follow-up have been reviewed to determine long-term hazards and their relation to the radiation dose received. The expectation of life of those dying from causes other than cancer was slightly reduced in the female patients. A small, significant excess of deaths from cancer of the bladder and from leukaemia was found which, assuming that these were due to radiation, gave inferred risk-rates respectively of 0.4 and 4.9 deaths per 10(4) PYG (patient-year-grays) to the bladder wall and red marrow. Of 31 younger patients (eight male, 23 female), four of the marriages have been infertile. The fertile marriages produced a total of 44 live births. Considerable gonad irradiation (estimated 0.8-2.7 Gy) was compatible with apparently normal fertility. Despite the high level of irradiation of the salivary glands, no malignancies and only one adenoma was found. Impaired pulmonary function occurred in only one of the patients who had diffuse bilateral metastases. In this patient, tumour in the lung was persistent throughout, so that radiation was probably not alone responsible.

SUMMARY objective We aimed to study the effect of cigarette smoking on the prevalence and severity of Graves’ ophthalmopathy (GO) patients One hundred and fifty‐five newly diagnosed patients with Graves’ disease (GD) were diagnosed clinically and by routine biochemical methods. Twenty‐five per cent (39) were of Asian origin methods Eye signs were classified according to the American Thyroid Association Classification. A detailed smoking questionnaire and data from hospital notes were used to calculate an index of cigarette consumption results Thirty‐four per cent of all patients had Graves’ ophthalmopathy, and the prevalence in males (26%) and females (36%) did not differ significantly. There was a prevalence of 42% among Europeans compared to 7·7% in Asians (P= 0·0002). The overall risk for Europeans for developing Graves’ ophthalmopathy was 6·4 (1·78–22·7 confidence interval) times higher than for Asians. Corrected for the ethnic factor the increased risk from smoking for Europeans was 2·4 (1·12–5·18, 95% confidence interval) times higher. There was a significant dose effect (P= 0·008). conclusions The present findings confirm an effect of cigarette smoking on Graves’ ophthalmopathy and in addition show that Europeans have a substantially greater risk of developing Graves’ ophthalmopathy than have Asians

Measurements of body weight, total body water and total body potassium (*OK) * Measurements periods (in weeks): 1 = 10 to 14; 2 = 24 to 28; 3 = 36 to 38.

Hydrogenase activity and other hydrogenase-related functions can be restored to hydC mutants by the specific addition of nickel salts to the growth medium. These mutants are defective in all three hydrogenase isoenzymes and the restoration is dependent upon protein synthesis. The cellular nickel content of the mutant when grown in LB medium is less than 1% of that of the parental strain. Partial suppression of the hydrogenase phenotype of hydC mutants occurs when growth takes place in a different medium. This correlates with an increased cellular nickel content. The phenotype of the mutant is also fully suppressed by growth in media of very low magnesium content. Such media facilitate nickel uptake via the magnesium transport system, which leads to the acquisition of a normal cellular nickel content. Mutations in the fnr gene, which encodes a transcriptional regulator for several anaerobically expressed enzymes, abolishes hydC expression and gives rise to a defective hydrogenase phenotype. The hydrogenase phenotype of fnr is closely similar to that of hydC in all respects examined. The hydrogenase activity of fnr strains can be restored by the presence of a functional hydC gene on a multicopy plasmid. The hydrogenase phenotype of fnr strains therefore arises indirectly via suppression of hydC, which leads to a low cellular nickel content. Nickel has no influence on fumarate reductase or nitrate reductase activities in fnr strains. The hydrogen-metabolism phenotype of fnr strains is, therefore, dependent upon their ability to acquire nickel from growth media. It is likely that hydC encodes a specific transport system for nickel.

Little research has examined the effect of water consumption on cognition in children. We examined whether drinking water improves performance from baseline to test in 23 6-7 year old children. There were significant interactions between time of test and water group (water/no water), with improvements in the water group on thirst and happiness ratings, visual attention and visual search, but not visual memory or visuomotor performance. These results indicate that even under conditions of mild dehydration, not as a result of exercise, intentional water deprivation or heat exposure, children's cognitive performance can be improved by having a drink of water.

SUMMARY The effect of adrenalectomy on the increase of the transmucosal potential difference (p.d.) of the colon of the rat induced by Na depletion, together with the action of aldosterone on the p.d. and on colonic Na+ and Cl− transport, and K+ and bicarbonate secretion have been investigated. Adrenalectomy increased the Na+ content in the stool, an effect reversed by treatment with aldosterone. When Na+-depleted rats were adrenalectomized and maintained on cortisone, the elevated p.d. fell to levels below those found in normal rats. Aldosterone given intravenously (i.v.) in physiological doses increased the p.d. in normal, adrenalectomized and Na+-depleted adrenalectomized rats after a latency period of 80–110 min., and the p.d. tended to rise further when injections were continued for several days. The p.d. gradient along the colon after treatment with aldosterone was similar to that of Na+-depleted rats, the highest p.d. being at the distal end of the descending colon. Cortisol intravenously increased the p.d. but the effect was small in comparison with that of aldosterone. Measurement of ionic fluxes in the descending colon of adrenalectomized rats showed that treatment with aldosterone produced an increase in Na+ and water absorption, and in K+ secretion, but had no effect on bicarbonate secretion. The effects of aldosterone on the transmucosal p.d. and ion transport were similar to those of Na+ depletion.

Although IQ is thought to remain relatively stable in the normal population, a decline in IQ has been noted in children born preterm. It is not clear, however, to what extent the inclusion of children with clear neurological damage has influenced these findings. We examined IQ scores obtained in childhood and then again in adolescence from a group of children born at 30 weeks gestation or less who had been classified as neurologically normal at 7.5-8 years. They showed a significant decline in mean IQ scores over time. MRI scans obtained from a subset of children at adolescence were read as normal in approximately 50% of cases and, in the others, there were no consistent relationships between radiological abnormalities and IQ results. Such children can, however, have relatively subtle brain abnormalities that are not seen on conventional MRI, and we hypothesized that these would be related to declines in IQ. Voxel-based morphometry (VBM) analyses of the MRI scans revealed that absolute IQ scores were related to areas in both the parietal and temporal lobes. The analyses also showed that frontal and temporal lobe regions were associated with the decline in VIQ, while occipital and temporal lobe regions (including the hippocampi) were associated with the decline in PIQ. Hippocampal volume measurements were consistent with the VBM findings. We concluded that preterm children are at risk of declining IQ over time even if they have not suffered obvious neurological damage and that the decline is associated with specific neural regions. Whether this is true of children born at >30 weeks gestation and what other factors predispose to this decline have yet to be determined.