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Experiments are described in which the threshold conditions for sediment entrainment are measured for uniform and mixed sand beds beneath both steady and combined steady/oscillatory¯ows. Derived critical shear stresses are compared with the mixed bed entrainment model of Wiberg & Smith (1987). As predicted by the model, coarser grains within a sand mixture are entrained at lower bed shear stresses than progressively ®ner grains. Entrainment occurs generally at lower shear stresses than predicted by the model, especially under unidirectional¯ows. This may be the result of grains resting in unusually unstable positions during the experiments because the beds are`unworked' at the start of the experiments.The model of Wiberg and Smith predicts threshold conditions more accurately for the mixed beds if the bed pivoting angle is correctly de®ned. The pivoting angles of the beds used here are measured using a new technique designed speci®cally for comparison with the threshold data. The measured angles repeat the ®nding that the coarse grains are more mobile than the ®ner fractions of a mixture. The results are poorly described by the pivoting angle model presented by Wiberg & Smith (1987) and are better represented by a model of the form F aD c (D i /D 50 ) b (after Li & Komar, 1986), where a, c and b are empirical constants. The threshold model is found to be more effective using the improved pivoting relationship.The entrainment of grains is found to be easier beneath unidirectional¯ows than combined¯ows, in accordance with previous authors' ®ndings. A suggestion that this result is caused by a change in the erosion mechanism beneath wave¯ows is made. Wave boundary layers may act as an extended laminar sublayer over bed grains and reduce the erosive ef®ciency of the overlying current¯ow. The results of the experiment have implications for the natural sorting mechanisms of sediment beds being deposited in near-threshold¯ows.

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Diabetic hyperglycaemia creates biochemical alterations in nerve that lead to Wallerian degeneration, resulting in the modification of the Schwann cell phenotype. This suggests that the peripheral neuroglia could play a crucial role in diabetes‐induced peripheral neuropathy. Hyperglycaemia‐induced cellular stresses result in up‐regulation of aldose reductase (AR) protein expression. This study aimed to determine whether activation of mitogen‐activated protein kinases (MAPK) in Schwann cells in vitro might represent an early step in the transduction of hyperglycaemia to diabetes‐induced increased AR protein expression. We observed MAPK activation (Western blots for JNK and p38) in response to raised glucose and MAPK responses were expressed as the ratio of phosphorylated to total form. Neonatal rat Schwann cell cultures were treated with glucose (50, 200mM) for up to 24 hours. Mannitol (45, 195mM) was used as an osmotic control. Glucose for 1 hour (200mM) caused transient activation of both p38 (1.9 fold) and JNK (p < 0.01 for p56 and p46) versus controls (5.6mM glucose). Similar results were seen for JNK in response to mannitol. The mannitol‐induced p38 activation was sustained from 1 to 8 hours of treatment (p < 0.01 versus controls and p < 0.05 versus glucose treatment). Similarly, we observed a significant increase of AR content (p < 0.01 and p < 0.05 in response to glucose and mannitol, respectively). However, the maximum response occurred at 24 hours of treatment. Immunocytochemistry studies showed that activated JNK was located both in cytoplasm and nucleus, while accumulation of AR was mainly restricted to the cytoplasm surrounding the nucleus. These results suggest that JNK and/or p38 could transduce increased AR expression in response to high glucose, at least under in vitro conditions.

Diabetic autonomic neuropathy results in significant morbidity and mortality. Both diabetic humans and experimental animals show neuroaxonal dystrophy of autonomic nerve terminals, particularly in the prevertebral superior mesenteric ganglia (SMG) and celiac ganglia (CG) which innervate the hyperplastic/hypertrophic diabetic small intestine. Previously, investigators suggested that disturbances in ganglionic nerve growth factor (NGF) content or transport might play a pathogenetic role in diabetic autonomic pathology. To test this hypothesis, we measured NGF content and NGF receptor expression, p75(NTR) (low affinity neurotrophin receptor) and trkA (high affinity NGF receptor), in control and diabetic rat SMG, CG and superior cervical ganglia (SCG). Surprisingly, rather than a decrease, we observed an approximate doubling of NGF content in the diabetic SMG and CG, a result which reflects increased NGF content in the hyperplastic diabetic alimentary tract. No change in NGF content was detected in the diabetic SCG which is relatively spared in experimental diabetic autonomic neuropathy. NGF receptor expression was not consistently altered in any of the autonomic ganglia. These observations suggest that increased NGF content in sympathetic ganglia innervating the diabetic alimentary tract coupled with intact receptor expression may produce aberrant axonal sprouting and neuroaxonal dystrophy.