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SUMMARY Sleep is the most important period for recovery from daily load. Regular physical activity enhances overall sleep quality, but the effects of acute exercise on sleep are not well defined. In sleep hygiene recommendations, intensive exercising is not suggested within the last 3 h before bed time, but this recommendation has not been adequately tested experimentally. Therefore, the effects of vigorous late-night exercise on sleep were examined by measuring polysomnographic, actigraphic and subjective sleep quality, as well as cardiac autonomic activity. Eleven (seven men, four women) physically fit young adults (VO 2max 54 ± 8 mLAEkg )1 AEmin )1 , age 26 ± 3 years) were monitored in a sleep laboratory twice in a counterbalanced order: (1) after vigorous late-night exercise; and (2) after a control day without exercise. The incremental cycle ergometer exercise until voluntary exhaustion started at 21:00 ± 00:28 hours, lasted for 35 ± 3 min, and ended 2:13 ± 00:19 hours before bed time. The proportion of non-rapid eye movement sleep was greater after the exercise day than the control day (P < 0.01), while no differences were seen in actigraphic or subjective sleep quality. During the whole sleep, no differences were found in heart rate (HR) variability, whereas HR was higher after the exercise day than the control day (54 ± 7 versus 51 ± 7, P < 0.01), and especially during the first three sleeping hours. The results indicate that vigorous late-night exercise does not disturb sleep quality. However, it may have effects on cardiac autonomic control of heart during the first sleeping hours.k e y w o r d s actigraphy, heart rate variability, polysomnography, recovery, subjective sleep quality

The pls gene, coding for a large surface protein of methicillin-resistant Staphylococcus aureus, was cloned from a strain which adheres poorly to several mammalian proteins. The structure of pls revealed three distinct repeat regions, one of which was a serine-aspartate repeat characteristic of the Clf-Sdr family of surface proteins in staphylococci. The lengths of the repeat regions varied in different clinical strains and could be used as epidemiological markers. pls was found to be closely associated with the mecA gene by pulsed-field gel electrophoresis analysis of SmaI-digested DNA. A pls mutant constructed by allele replacement adhered well to immobilized fibronectin and immunoglobulin G, in contrast to the parental strain, suggesting that Pls could have a role in preventing adhesion at some stages during an infection.Bacterial adhesion to host cells or extracellular matrices in damaged tissues is a prerequisite for colonization of the host by infecting bacteria. Implanted biomaterial also becomes coated with host proteins, enabling a pathogen to adhere and initiate a device-related infection. Staphylococcus aureus expresses a number of surface proteins that promote binding to the host extracellular matrix or plasma proteins. Several have been characterized at the molecular level, namely, protein A (SpA), binding the Fc part of immunoglobulins and von Willebrand factor (12,16,43,46); the fibronectin-binding proteins FnBPA and FnBPB (11,14,24,42); the fibrinogen-binding proteins ClfA, ClfB, and Efb (previously Fib) (7,32,33); the collagenbinding protein Cna (44); the elastin-binding protein EbpS (37); and the bone sialoprotein-binding protein Bbp (45). S. aureus can bind a number of other host proteins, such as vitronectin, laminin, mucin, and thrombospondin, but the molecular bases of these interactions are still poorly understood.Some methicillin-resistant S. aureus (MRSA) strains show poor in vitro adherence to surfaces coated with several host plasma or extracellular matrix proteins. They were originally identified as strains giving a negative result in rapid S. aureus identification assays using particles coated with immunoglobulin G (IgG) and/or fibrinogen (27). These strains express a novel surface protein called Pls. The protein was originally purified from lysostaphin digests of a clinical MRSA strain, 1061, by affinity chromatography on immobilized wheat germ agglutinin (WGA) (17). Pls is sensitive to proteolysis by plasmin and trypsin. Similarly, the activation of receptor-bound plasminogen to plasmin on the S. aureus surface (28) leads to cleavage of the apparently 230-kDa Pls protein into 175-and 68-kDa segments-hence the name Pls for plasmin sensitive. Also, without prior proteolytic treatments, part of Pls exists as 175-and 68-kDa fragments in lysostaphin digests of Pls-expressing strains (17).Methicillin resistance is caused by the mecA gene, coding for a low-affinity penicillin-binding protein, PBP2a. mecA is part of a large mec DNA region which lacks a homolog in methicillinsensitive stra...

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Maternal depressive symptoms during pregnancy have been associated with child behavioural symptoms of attention-deficit/hyperactivity disorder (ADHD) in early childhood. However, it remains unclear if depressive symptoms throughout pregnancy are more harmful to the child than depressive symptoms only during certain times, and if maternal depressive symptoms after pregnancy add to or mediate any prenatal effects. 1,779 mother-child dyads participated in the Prediction and Prevention of Pre-eclampsia and Intrauterine Growth Restriction (PREDO) study. Mothers filled in the Center of Epidemiological Studies Depression Scale biweekly from 12+0–13+6 to 38+0–39+6 weeks+days of gestation or delivery, and the Beck Depression Inventory-II and the Conners’ Hyperactivity Index at the child’s age of 3 to 6 years (mean 3.8 years, standard deviation [SD] 0.5). Maternal depressive symptoms were highly stable throughout pregnancy, and children of mothers with consistently high depressive symptoms showed higher average levels (mean difference = 0.46 SD units, 95% Confidence Interval [CI] 0.36, 0.56, p < 0.001 compared to the low group), and proportion (32.1% vs. 14.7%) and odds (odds ratio = 2.80, 95% CI 2.20, 3.57, p < 0.001) of clinically significant ADHD symptoms. These associations were not explained by the effects of maternal depressive symptoms after pregnancy, which both added to and partially mediated the prenatal effects. Maternal depressive symptoms throughout pregnancy are associated with increased ADHD symptomatology in young children. Maternal depressive symptoms after pregnancy add to, but only partially mediate, the prenatal effects. Preventive interventions suited for the pregnancy period may benefit both maternal and offspring mental health.