POSSUM, a Physiological and Operative Severity Score for the enUmeration of Mortality and morbidity, is described. This system has been devised from both a retrospective and prospective analysis and the present paper attempts to validate it prospectively. Logistic regression analysis yielded statistically significant equations for both mortality and morbidity (P less than 0.001). When displayed graphically zones of increasing morbidity and mortality rates could be defined which could be of value in surgical audit. The scoring system produced assessments for morbidity and mortality rates which did not significantly differ from observed rates.

The accumulation of α-synuclein aggregates is the hallmark of Parkinson’s disease, and more generally of synucleinopathies. The accumulation of tau aggregates however is classically found in the brains of patients with dementia, and this type of neuropathological feature specifically defines the tauopathies. Nevertheless, in numerous cases α-synuclein positive inclusions are also described in tauopathies and vice versa, suggesting a co-existence or crosstalk of these proteinopathies. Interestingly, α-synuclein and tau share striking common characteristics suggesting that they may work in concord. Tau and α-synuclein are both partially unfolded proteins that can form toxic oligomers and abnormal intracellular aggregates under pathological conditions. Furthermore, mutations in either are responsible for severe dominant familial neurodegeneration. Moreover, tau and α-synuclein appear to promote the fibrillization and solubility of each other in vitro and in vivo. This suggests that interactions between tau and α-synuclein form a deleterious feed-forward loop essential for the development and spreading of neurodegeneration. Here, we review the recent literature with respect to elucidating the possible links between α-synuclein and tau.

Parkinson's disease (PD) is a neurodegenerative disorder characterized by progressive motor disturbances and affects more than 1% of the worldwide population. Despite considerable progress in understanding PD pathophysiology, including genetic and biochemical causes, diagnostic approaches lack accuracy and interventions are restricted to symptomatic treatments. PD is a complex syndrome with different clinical subtypes and a wide variability in disorder course. In order to deliver better clinical management of PD patients and discovery of novel therapies, there is an urgent need to find sensitive, specific, and reliable biomarkers. The development of biomarkers will not only help the scientific community to identify populations at risk, but also facilitate clinical diagnosis. Furthermore, these tools could monitor progression, which could ultimately deliver personalized therapeutic strategies. The field of biomarker discovery in PD has attracted significant attention and there have been numerous contributions in recent years. Although none of the parameters have been validated for clinical practice, some candidates hold promise. This review summarizes recent advances in the development of PD biomarkers and discusses new strategies for their utilization.

POSSUM and APACHE II scores from 117 consecutive admissions to a high-dependency unit after major surgery were correlated with 30-day morbidity and mortality rates. Thirteen patients (11 per cent) died and 59 (50 per cent) developed a postoperative complication. Receiver-operating characteristic curve analysis showed POSSUM to have good predictive value for mortality (area under curve 0.75) and morbidity (area under curve 0.82). APACHE II scores had a significantly inferior predictive value for mortality (area under curve 0.54) (P < 0.002). POSSUM was superior to APACHE II in prediction of mortality in patients admitted to a high-dependency unit after general surgery. Prediction of postoperative complications by POSSUM is accurate and may be useful for audit.