Long-term labour-market performance of whiplash claimants

A whiplash is a sudden acceleration–deceleration of the neck and head, typically associated with a rear-end car collision that may produce injuries in the soft tissue. Often there are no objective signs or symptoms of injury, and diagnosing lasting whiplash-associated disorders (WAD) is difficult, in particular for individuals with mild or moderate injuries. This leaves a scope for compensation-seeking behaviour. The medical literature disagrees on the importance of this explanation. In this paper we trace the long-term earnings of a group of Danish individuals with mild to moderate injuries claiming compensation for having permanently lost earnings capacity and investigate if they return to their full pre-whiplash earnings when the insurance claim has been assessed. We find that about half of the claimants, those not granted compensation, return to an earnings level comparable with their pre-whiplash earnings suggesting that these individuals do not have chronic WAD in the sense that their earnings capacity is reduced. The other half, those granted compensation, experience persistent reductions in earnings relative to the case where they had not been exposed to a whiplash, even when they have a strong financial incentive to not reduce earnings. This suggests that moderate injuries tend to be chronic, and that compensation-seeking behaviour is not the main explanation for this group. We find that claimants with chronic WADs used more health care in the year prior to the whiplash than claimants with non-chronic cases. This suggests that lower initial health capital increases the risk that a whiplash causes persistent WAD.     

Prothrombin profragment-1 optical rotatory dispersion and circular dichroism

The circular dichroism and optical rotatory dispersion of profragment-1. (MW 24,000) derived from human prothrombin (MW 72,000) as a function of pH and in the presence and absence of added calcium ions suggests that related conformational changes occur. As pH is increased from 3.0 an ORD trough at 232 nm becomes less negative and beginning near pH 5 a Cotton effect at 225 nm predominates. An ORD Cotton effect near 245 nm decreases in intensity upon addition of calcium ions. Between pH 4.9 and 5.9 profound changes are observed in the CD spectra of profragment-1 over the range from 228 nm to 260 nm. Over this same wavelength range calcium ions added at neutral pH induced changes to a spectrum morphology similar to that evinced by profragment-1 at pH 4.9 in the absence of calcium ions.     

Influence of atropine microinjection into nucleus reticularis thalami on activity of lateral geniculate nucleus neurones in freely moving rats

The influence of the microinjection of atropine into the visual part of the nucleus reticularis thalami (TR) on flash-evoked unit responses of the dorsal lateral geniculate nucleus (dLGN) was investigated in freely moving rats. Atropine induced a significant prolongation and accentuation of the postexcitatory inhibitory phases in water-deprived trained rats, to which light flashes acted as conditioned stimuli and initiated a drinking behaviour. In satiated relaxed rats atropine did not change the unit activity significantly. Acetylcholine injected into TR caused a facilitation of the dLGN transmission. Since the decrease of flash-evoked excitatory response phases in thirsty, trained rats as compared to satiated ones could not be blocked by atropine, not all behaviourally dependent changes are mediated by a disinhibitory action of cholinergic fibres on TR.     

The clinical manifestations of Degos' syndrome

Pathologic mechanisms underlying Degos' syndrome are poorly characterized. Thrombosis, either as a consequence of a postulated vasculitis or as a primary defect, is often a clinical complication of this syndrome. We have studied multiple coagulation parameters, including potential defects in fibrin assembly and other adhesive proteins, in a patient with Degos' syndrome and found no specific abnormality to explain the pathologic features of this syndrome. An extensive literature review as well as detailed biochemical and biophysical coagulation studies are presented. The alternative possibility of Degos' syndrome as a mucinosis is discussed.