The patient with an acute brain injury requiring renal replacement therapy presents a major problem in that conventional intermittent hemodialysis may exacerbate the injury by compromising cerebral perfusion pressure, either after a reduction in cerebral perfusion or because of increased cerebral edema. Compared with standard intermittent hemodialysis, the continuous forms of renal replacement therapy (CRRT) provide an effective therapy in terms of solute clearance, coupled with improved cardiovascular and intracranial stability. The disadvantage of CRRT is that anticoagulation may be required, and anticoagulants with systemic effects may provoke intracerebral hemorrhage, either at the site of damage or around the intracranial pressure monitoring device. Although peritoneal dialysis does not require anticoagulation, the clearances achieved are often less than those of CRRT, and sudden changes in intraperitoneal volume may provoke cardiovascular and thus intracranial instability.
Synesthesia is a rare condition in which one property of a stimulus (e.g., shape) triggers a secondary percept (e.g., color) not typically associated with the first. Work on synesthesia has predominantly focused on confirming the authenticity of synesthetic experience, but much less research has been conducted to examine the extent to which synesthesia is linked to broader perceptual differences. In the research reported here, we examined whether synesthesia is associated with differences in color and motion processing by comparing these abilities in synesthetes who experience color as their evoked sensation with nonsynesthetic participants. We show that synesthesia for color is linked to facilitated color sensitivity but decreased motion sensitivity. These findings are discussed in relation to the neurocognitive mechanisms of synesthesia and interactions between color and motion processing in typical adults.
We describe four renal dialysis patients from our hospital who, over a 6-month period, developed erythematous, thickened, indurated dermal plaques. The plaques were limited to the limbs and in three patients there were associated flexion contractures. The clinical features most resembled scleromyxoedema. All patients had previously received at least one renal transplant. Histopathology of the plaques showed features of scleromyxoedema in two patients, whereas the other two showed a different picture, more suggestive of a morphoea-like process. There are important differences between our patients and classical scleromyxoedema. All four patients had normal immunoglobulins and no paraprotein was detected. Almost all cases of classical scleromyxoedema are associated with an IgGlambda paraproteinaemia. We have not yet identified an underlying cause for this cluster of cases in our hospital. It is possible that the skin changes seen may have been precipitated by an environmental agent, such as in 'toxic oil syndrome' and vinyl chloride-induced scleroderma. We discuss the differences between our patients and those with scleromyxoedema, localized or generalized morphoea and environmentally induced scleroderma. We feel that our patients show a constellation of features similar, but not identical, to scleromyxoedema. There has been only one previous report of similar patients. We believe this to be a new and distinct phenomenon.
Aims/hypothesis Lipolytic breakdown of endogenous lipid pools in pancreatic beta cells contributes to glucosestimulated insulin secretion (GSIS) and is thought to be mediated by acute activation of neutral lipases in the amplification pathway. Recently it has been shown in other cell types that endogenous lipid can be metabolised by autophagy, and this lipophagy is catalysed by lysosomal acid lipase (LAL). This study aimed to elucidate a role for LAL and lipophagy in pancreatic beta cells. Methods We employed pharmacological and/or genetic inhibition of autophagy and LAL in MIN6 cells and primary islets. Insulin secretion following inhibition was measured using RIA. Lipid accumulation was assessed by MS and confocal microscopy (to visualise lipid droplets) and autophagic flux was analysed by western blot. Results Insulin secretion was increased following chronic (≥8 h) inhibition of LAL. This was more pronounced with glucose than with non-nutrient stimuli and was accompanied by augmentation of neutral lipid species. Similarly, following inhibition of autophagy in MIN6 cells, the number of lipid droplets was increased and GSIS was potentiated. Inhibition of LAL or autophagy in primary islets also increased insulin secretion. This augmentation of GSIS following LAL or autophagy inhibition was dependent on the acute activation of neutral lipases. Conclusions/interpretation Our data suggest that lysosomal lipid degradation, using LAL and potentially lipophagy, contributes to neutral lipid turnover in beta cells. It also serves as a constitutive negative regulator of GSIS by depletion of substrate for the non-lysosomal neutral lipases that are activated acutely by glucose.
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