When is it safe to resume driving after total hip and total knee arthroplasty? a meta-analysis of literature on post-operative brake reaction times.

AIMS: The aim of this study was to assess the current available evidence about when patients might resume driving after elective, primary total hip (THA) or total knee arthroplasty (TKA) undertaken for osteoarthritis (OA). MATERIALS AND METHODS: In February 2016, EMBASE, MEDLINE, Web of Science, Scopus, Cochrane, PubMed Publisher, CINAHL, EBSCO and Google Scholar were searched for clinical studies reporting on 'THA', 'TKA', 'car driving', 'reaction time' and 'brake response time'. Two researchers (CAV and JJT) independently screened the titles and abstracts for eligibility and assessed the risk of bias. Both fixed and random effects were used to pool data and calculate mean differences (MD) and 95% confidence intervals (CI) between pre- and post-operative total brake response time (TBRT). RESULTS: A total of 19 studies were included. The assessment of the risk of bias showed that one study was at high risk, six studies at moderate risk and 12 studies at low risk. Meta-analysis of TBRT showed a MD decrease of 25.54 ms (95% CI -32.02 to 83.09) two weeks after right-sided THA, and of 18.19 ms (95% CI -6.13 to 42.50) four weeks after a right-sided TKA, when compared with the pre-operative value. CONCLUSION: The TBRT returned to baseline two weeks after a right-sided THA and four weeks after a right-sided TKA. These results may serve as guidelines for orthopaedic surgeons when advising patients when to resume driving. However, the advice should be individualised. Cite this article: Bone Joint J 2017;99-B:566-76.

Characterization and fibrin-binding properties of different molecular forms of pro-urokinase from a monkey kidney cell culture.

Culture fluid of a monkey kidney cell culture was harvested every two days, for a two week period, in order to obtain urokinase in the zymogen form. Pro-urokinase was isolated by immunoadsorption chromatography and gel filtered on Sephadex G-150, which resulted in three peaks with pro-urokinase activity. SDS-polyacrylamide gel electrophoresis showed that the first peak contained 55 kd pro-urokinase, aggregated with high molecular weight contaminants, whereas the second and third peaks consisted of almost pure 55 kd and 30 kd pro-urokinase, respectively. The latter form represented a relatively unknown and inactive precursor of low molecular weight urokinase, which was, like 55 kd pro-urokinase, activatable with plasmin. In comparison with tissue-type plasminogen activator, 55 kd and 30 kd pro-urokinase only bound weakly to purified fibrin clots and fibrin-sepharose columns. The extent of binding of the two pro-urokinases and their plasmin-activated forms to fibrin-sepharose decreased in the following order: 55 kd pro-urokinase 30 kd pro-urokinase 55 kd urokinase 30 kd urokinase. These results indicate that the two precursors exhibited stronger binding to fibrin-sepharose than the corresponding active enzymes, and the two 55 kd forms exhibited stronger binding than the corresponding 30 kd forms. This indicates the importance of both the zymogen nature and an intact NH2-terminal part of the molecules for binding to fibrin.

Circulating antibodies to cysteinyl catecholamines in amyotrophic lateral sclerosis and Parkinson's disease patients.

Amyotrophic lateral sclerosis (ALS) is a degenerative disease of unknown aetiology, affecting motor neurons. Many radical species, such as O(2)(-) NO, and ONOO(-), and lipoperoxidative products are involved, but not all processes have yet been identified. It is known that the oxidation of catecholamines leads to quinone formation. These orthoquinones react with the sulphhydril group of cysteine to produce neurotoxic cysteinyl catecholamine (Cyst-CA) neo-compounds. We synthesised Cyst-CA in order to mimic their endogenous formation. Using the ELISA method, circulating antibodies to Cyst-CA were found in sporadic ALS sera. First, the antibody titres were compared to those of controls and patients with other neurodegenerative diseases. Significant antibody levels were found for Cyst-CA. The G and A isotypes were found but not the M isotype. A second series of experiments showed that A and G titres were elevated, depending on the type of Cyst-CA and the onset of the disease. IgG to Cyst-3,4-dihydroxyphenylalanine (L-DOPA) were present in cases of bulbar and upper limb onsets. IgA to Cyst-homovanillic acid (HVA), Cyst-adrenaline (A), and Cyst-dopamine (DA) were found in lower limb onset. These results indirectly show that: 1) the oxidation of CA and the formation of Cyst-CA may be involved in ALS; 2) these radical processes have different targets depending on the onset of the disease.