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Notes: Summary The effects of orally-administered myo-inositol have been compared with those of an aldose reductase inhibitor on acute neurological defects in experimentally diabetic rats. Three groups of streptozotocin-treated diabetic rats (50mg/kg, IP) together with three groups of age-matched controls (saline, IP) were compared. One pair of groups (control and diabetic) were untreated for 3 weeks, another pair of groups received daily oral myo-inositol (667 mg/kg) and the third pair received an aldose reductase inhibitor (ICI 105552; 50 mg·kg-1·day-1, orally). The untreated diabetic group showed statistically significant deficits in accumulation, proximal to 24 h sciatic nerve constrictions, of choline acetyltransferase activity by comparison with untreated controls (2.8±0.4 versus 5.1±0.4nmol acetylcholine ·h-1·nerve-1; p〈0.001). The untreated diabetic rats also showed a fall in motor nerve conduction velocity of 6.2±0.7 m/s which was statistically significant (p〈0.001). Treatment of the diabetic group with myo-inositol prevented the development of both defects of axonal transport and conduction velocity; both measurements were similar to those of the myo-inositol treated control rats. Likewise the diabetic rats which received aldose reductase inhibitor showed prevention of both defects. Nerves from untreated diabetic rats showed marked sorbitol accumulation and a statistically significant reduction in myo inositol content by comparison with the untreated controls (sorbitol, 1.56 ±0.22 versus 0.8±0.01 and myo-inositol, 1.47±0.10 versus 2.3±0.10 nmol/mg; p〈0.001). Treatment of the diabetic rats with myo-inositol elevated the myo-inositol levels in nerve (3.05±0.22 nmol/mg) without affecting nerve sorbitol levels. Treatment of diabetic rats with aldose reductase inhibitor also normalised nerve myo-inositol (2.75±0.20 nmol/mg) and reduced nerve sorbitol (0.08±0.01 nmol/mg). These findings are consistent with the suggestion that both treatments prevent the development of the two functional defects by normalising the nerve myo-inositol content.

Notes: Summary The effects of a low dose of alloxan on the blood glucose, islet beta cell granulation, body weight, insulin resistance, glucose tolerance, and responses to fasting and growth hormone were studied inob/ob mice, which respond to a single low dose of alloxan with a rapid (24 h) and long-term (108 day) significant decrease in blood glucose levels, and increase in islet beta cell granulation. Three weeks after alloxan administration, insulin resistance is ameliorated in alloxan-treated obese mice whose body weight is not significantly different from their obese controls. A low dose of alloxan has a therapeutic influence on glucose management inob/ob mice: reduced glycemia, improved glucose tolerance, and increased tolerance to fasting. Growth hormone induces a similar hyperglycemic response in alloxan-treated and control

Notes: Summary The present study reports on polysomnographic findings of sleep apnea syndrome in a representative sample of otherwise healthy middle-aged blue collar workers (age 45.7±8.5) with normal to borderline blood pressure (systolic 135.5±16.1; diastolic: 88.3±10.2), mild overweight (Broca 114.9±14.7) and with reported nocturnal sleep disturbances. The prevalence of sleep apnea in this sample (N=20 out of a total of 78 workers with reported sleep disturbances) is 40%. Mean frequency of apnoeic episodes during night was 97.6±42.7 in the apnea-positive group as compared to 27.1±19.9 in the apnea-negative group (T=5.0;p〈0.0001), with an apnea index of 13.3±6.2 as compared to 3.5±2.3 (T=7.2,p〈0.0001). Left ventricular hypertrophy (mean diameter of end diastolic left ventricle: 64.0±9.5 mm) was found in individuals with apnea although manifest hypertension was absent in most individuals.

Notes: Summary The pulmonary artery pressure values of 65 patients with sleep apnea syndrome were measured at rest and during ergometer exercise up to 100 W. Pulmonary hypertension at rest was found in 13, and during exercise in 31 more patients. Only 8 patients with pathological pressure findings suffered from pulmonary hypertension in combination with a pulmonary or cardiac disease. In the other 36 patients, no indication of a primary cause of pulmonary hypertension apart from sleep apnea syndrome could be found. Out of the 65 patients, 11 with a finding of more than 20 apnea episodes per hour's sleep underwent polysomnographic recordings in the sleep laboratory. The hemodynamic parameters were continuously measured. All 11 patients had a finding of severe sleep apnea with more than 300 apnea episodes during the night of recording. In 6 patients, the appearance of apnea episodes was accompanied by only moderate changes in pulmonary artery pressure. In 5 patients, there were critical increases in pulmonary artery pressure, which went along with increases in cardiac output and in pulmonary capillary wedge pressure. Increases in pulmonary vascular resistance were established in 3 out of these 5 patients, and a slight decrease in 2. The mechanism of hypoxic vasoconstriction of the pulmonary arteries may account for the pressure increases in 3 of our patients, but fails to explain the findings in the other 2 patients. Nocturnal changes in pulmonary artery pressure in patients with sleep apnea may therefore have different causes. Pulmonary hypertension constitutes a severe complication in patients with sleep apnea. As 55% of all sleep apnea patients were found to suffer from pulmonary hypertension without any indication of a primary pulmonary or cardiac disease, the possibility that pulmonary hypertension results should not be underestimated in patients with suspected sleep apnea syndrome. Measurements of the pulmonary artery pressure must therefore be included in the examination regimen of such patients.

Notes: Abstract A sedimentological study of the early Proterozoic Black Reef Quartzite Formation in the south-western parts of the Transvaal province of South Africa was undertaken with the primary aim of examining the sedimentological controls of gold mineralization in the Black Reef placer, which occurs at the base of this Formation. A second aim of the study was to investigate the early history of the basin in which the Transvaal Sequence of South Africa was deposited. The thin, siliciclastic Black Reef Quartzite Formation, which is informally subdivided into a lower Conglomerate Unit and an upper Quartzite Unit, is underlain by Archaean rocks belonging to the basement complex and the Witwatersrand and Ventersdorp Supergroups, and is overlain by a thick succession of carbonate rocks of the Malmani Subgroup. The pre-Transvaal palaeosurface is characterised by elongated northeast to southwest trending grabens and partly-eroded horst blocks. The Black Reef Quartzite Formation, which has a maximum thickness of about 30 m in the study area, typically comprises a succession of interbedded arenites and mudstones, with a sporadically-developed basal Conglomerate Unit. Thickness trends are similar to the dominant structural trend of the pre-Transvaal palaeosurface. At localities where the Conglomerate Unit is absent, the Formation invariably overlies quartzites of the Witwatersrand Supergroup directly. The palaeocurrent distribution of the Conglomerate Unit is unimodal, with modes towards the southwest in the southern parts of the study area and towards the north in the northern regions. Most of the palaeocurrent distributions of the Quartzite Unit are unimodal, too, but bimodal distributions were found at three localities. Pebble size of the Black Reef placer is largest in the northeastern parts of the study area, but no orderly lateral size variation was found. Pebble roundness, too, varies greatly and apparently randomly. The composition of the pebble assemblage is not constant, but no systematic lateral change could be detected. A petrographic study of the arenites of the Formation reveals a remarkable textural and mineralogical maturity, especially for the upper beds. It is concluded that the pre-Transvaal palaeosurface had a palaeorelief of up to 30 m and that the topography of the palaeo-landscape was the dominant factor controlling early sedimentation in the basin. The palaeo-grabens probably constituted the valleys of shallow braided stream systems that drained south-westwards and northwards from a palaeo-drainage divide in the northern parts of the study area. Sediment, including detrital gold, was derived from erosion of Witwatersrand rocks and fed to the graben valleys via several alluvial fans. During a subsequent transgression, the fluvial systems became drowned and transgressive estuarine conditions ensued. During the final stages of siliciclastic sedimentation, the upper quartzite beds of the Formation were probably reworked by shallow marine processes before carbonate precipitation commenced. The cause of the marine transgression is not known beyond doubt. It is suggested, however, that lithospheric rifting, which initiated the extrusion of the underlying Ventersdorp lavas, resumed during early Transvaal times, resulting in complete severing of the continental crust and the creation of a linear sea.

Notes: Abstract Extended lattice damage created by implantation of 3.6 MeV Au2+ ions has been investigated using transmission electron microscopy (TEM) and Rutherford backscattering spectrometry (RBS). Systematic observations of damage for Au2+ ions implanted with varying doses into silicon are explained in terms of a model. The origin of two distinct bands of extended defects is explained in terms of annealing of the central region of implant-damage, during the course of the implantation. Two distinct bands of Au precipitates are observed in high-dose implanted samples. This observation is explained as being the result, in part, of segregation of gold in front of a recrystallizing front, and in part, of gettering of dopant-atoms to nodes in a dislocation network. The network arises as a result of dynamic annealing of damaged crystalline silicon.

Notes: Abstract The structure of Si implanted with high doses of yttrium has been investigated by varying implantation doses and energies. As implantation doses increase into the low 1017 cm−2 range, silicide precipitates form. The precipitates are thin and long and lie parallel to {111} planes in the Si matrix. As dopant concentrations increase, the precipitates themselves become more equiaxed, aspect ratios decrease, and precipitates densities increase until the precipitates coalesce to form a continuous buried layer of yttrium silicide within the Si matrix. The layer thickness is relatively uneven. As implant doses increase to ∼ 4×1017 cm−2, the layer thicknesses become more uniform although there are still defects present. As the implant doses increase further, the precipitate bands on either side of the continuous layer decrease due to gettering of yttrium to the layer. As the energy of the implant is increased, the appearance of the sample is similar to that of the lower energy implants except that the layer is buried deeper in the Si matrix. Observations of the silicide are consistent with its having the AlB2 structure with ordered vacancies on the Si sublattice.

Notes: Summary During cell multiplication of the Bacterium bifidum in media, that contain sugars or sugar alcohols, propionic acid is produced. The highest propionic acid concentrations have been found in sorbitol containing solutions.

Notes: Summary Strains No. 8 and Tissier of Bacterium bifidum (B. b.) were incubated in Tomarelli's solution. From this medium, thiamine, riboflavin, pyridoxine, calcium pantothenate and nicotinic acid amide were withheld respectively or altogether in the performance of different experiments. Growth of the cells was estimated after each passage by evulation of the packed volume. In general, the propagation of cells is impaired by the withdrawal of the vitamines from the Tomarelli solution. In the absence of all five vitamines, the rate of multiplication was the smallest one. Pantothenic acid seems to be of outstanding importance for the increase of a B. b. culture. The role of B. b. as a supplier of vitamines is not sufficienly defined as yet and needs further investigation.

Notes: Abstract Two bioavailability studies of S(+)-ibuprofen (dexibuprofen) were conducted in healthy volunteers to define the relationship between the bioavailability of the drug after administration of dexibuprofen alone or as part of ibuprofen racemate. Enantioselective plasma drug analysis was used throughout. In the first study, the bioavailability of dexibuprofen from a 400 mg tablet formulation was compared with that from 400 mg in aqueous solution. The tablet formulation did not influence the bioavailability of the drug and dexibuprofen was well absorbed from the gastro-intestinal tract. The second study was divided into three identical parts. Bioavailability of dexibuprofen 200, 400 and 600 mg was compared with its bioavailability from ibuprofen racemate 400, 800 and 1200 mg. The second study showed that the mean relative bioavailability of dexibuprofen to ibuprofen racemate was 0.66, thus enabling the estimation of clinically useful dexibuprofen doses from the usual doses of the racemate. The 95% confidence interval limits did not include 0.5, leading to the conclusion that administering half of the racemate dose would not provide patients with an adequate amount of therapeutically active drug.