Respiratory difficulties caused by exercise-induced laryngeal obstructions (EILOs) are reported with increasing frequency. The aim of this study was to assess the prevalence and symptoms of EILOs and their relation to airway hyperresponsiveness (AHR). In total, 556 randomly selected youths in Copenhagen aged 14-24 years were invited over a 2-year period. The study included a mailed questionnaire and two visits: day 1 (an interview-based questionnaire, methacholine bronchial provocation test and physical exertion test); and day 2 [an exercise test with continuous laryngoscopic recordings (CLE test)]. The diagnosis of EILOs was based on the CLE test. In total, 237 answered the mailed questionnaire and 150 participated on day 1 whereof 98 participated on day 2 also. AHR was verified in 23 (4.1% of invitees) and EILOs in 42 (7.5% of invitees). Co-morbidity was verified in 6 cases (26.1% of verified AHR cases). No symptoms were found specific for either AHR or EILOs. The minimum prevalence of EILOs in this cohort was 7.5%. EILOs were verified in 26.1% of participants with AHR. Questionnaires could not differentiate between AHR and EILOs.

Individuals reporting episodes of breathing problems caused by re-occurring variable airflow obstructions in the larynx have been described in an increasing number of publications, with more than 40 different terms being used without consensus on definitions. This lack of an international consensus on nomenclature is a serious obstacle for the development of the area, as knowledge from different centres cannot be matched, pooled or readily utilised by others. Thus, an international Task Force has been created, led by the European Respiratory Society/European Laryngological Society/American College of Chest Physicians. This review describes the methods used to reach an international consensus on the subject and the resulting nomenclature, the 2013 international consensus conference nomenclature.

Apolipoprotein M (ApoM) transports sphingosine-1-phosphate (S1P) in plasma, and ApoM-deficient mice (Apom 2/2 ) have ∼50% reduced plasma S1P levels. There are 5 known S1P receptors, and S1P induces adherens junction formation between endothelial cells through the S1P 1 receptor, which in turn suppresses vascular leak. Increased vascular permeability is a hallmark of inflammation. The purpose of this study was to explore the relationships between vascular leakage in ApoM deficiency and S1P 1 function in normal physiology and in inflammation. Vascular permeability in the lungs was assessed by accumulation of dextran molecules (70 kDa) and was increased ∼40% in Apom 2/2 mice compared to WT (C57Bl6/j) mice. Reconstitution of plasma ApoM/S1P or treatment with an S1P 1 receptor agonist (SEW2871) rapidly reversed the vascular leakage to a level similar to that in WT mice, suggesting that it is caused by decreased plasma levels of S1P and reduced S1P 1 stimulation. In a carrageenan-induced model of inflammation, Apom 2/2 mice had increased vascular leakage compared with that in WT mice. Adenoviral overexpression of ApoM in Apom 2/2 mice decreased the vascular leakage compared to adenoviral overexpression of green fluorescent protein. The study suggests that vascular leakage of albumin-sized particles in ApoM deficiency is S1P-and S1P 1

The effect of a whey protein- and carbohydrate (CHO)-enriched diet on the rate of muscle glycogen resynthesis after a soccer match was examined. Sixteen elite soccer players were randomly assigned to a group ingesting a diet rich in carbohydrates and whey protein [CHO, protein, and fat content was 71, 21, and 8E%, respectively; high content of carbohydrates and whey protein (HCP), n = 9] or a group ingesting a normal diet (55, 18, and 26E%; control [CON], n = 7) during a 48-h recovery period after a soccer match. CON and three additional players carried out a 90- and 60-min simulated match without body contacts (SIM90 and SIM60). Muscle glycogen was lowered (P < 0.05) by 54, 48, 53, and 38% after the matches in CON, HCP, SIM90, and SIM60, respectively. Glycogen resynthesis during the first 48 h after the match was not different between CON and HCP, whereas glycogen resynthesis was slower (P < 0.05) during the first 24 h after SIM60 than SIM90 (2.88 ± 0.84 vs 4.32 ± 0.54 mmol/kg dw/h). In HCP, glycogen content in type II muscle fibers was still lowered 48 h after the match. In conclusion, glycogen resynthesis 48 h after a soccer match is not elevated by ingestion of a HCP diet. Furthermore, glycogen resynthesis does not appear to be impaired by body contacts during a match.

Purpose-How companies can become better at knowing what they know, and share what they know have in recent years become dominant fields of research within knowledge management. The literature focuses on why people share knowledge, or why they fail to share knowledge, whilst the discussion of what they actually share has been pinned down to the concept of best practices. In this paper it is argued that there is more to knowledge sharing than the sharing of best practices. Knowledge sharing is more than the closing of performance gaps and the sharing of stocks of knowledge-knowledge sharing is also about bridging situations of organizational interdependencies and thereby supporting ongoing organizational activities. Design/methodology/approach-The paper is both theoretical and empirical. Theoretically, the concept of organizational interdependence is applied to create a conceptual framework encompassing four types of knowledge to be shared. The theoretical framework is applied on a case company to empirically illustrate how knowledge sharing encompasses different types of knowledge. Findings-The paper identifies four types of knowledge that are pivotal to share: professional knowledge, coordinating knowledge, object-based knowledge, and know-who. Hence, the paper expands the common belief that knowledge sharing is solely about sharing best practices. Practical implications-Since knowledge sharing encompasses at least four types of knowledge, the practice of facilitating knowledge sharing must necessarily focus on different channels enabling the sharing of knowledge. The practical implications of the paper, hence, direct attention to not solely sharing best practices but also knowledge bridging organizational interdependencies. Originality/value-The paper argues that best practices have dominated the discourse on what knowledge is to be shared but, to become better at understanding and practising knowledge sharing, states that one must expand one's view on what knowledge is being shared.

We describe a diagnostic software measuring tool (EILOMEA) to objectively describe images obtained by the continuous laryngoscopic exercise (CLE) test, and assess the reproducibility and clinical applications of this tool for the diagnosis of exercise-induced laryngomalacia (EIL) and exercise-induced vocal cord dysfunction (EI-VCD). A total of 97 subjects, 14-24 years of age, were tested with a CLE test. For each laryngoscopic recording, the severity of EIL and/or EI-VCD was assessed by an expert and compared with data obtained using EILOMEA. For both EIL and EI-VCD, a separate objective factor was found describing the degree of laryngeal obstruction by measuring cross-sectional areas of the inspiratory laryngeal images. A threshold value was set giving the diagnosis of EI-VCD, with a sensitivity of 0.65, a specificity of 0.96, a positive-predictive value of 0.79, and a negative-predictive value of 0.93. The threshold set for diagnosing EIL gave sensitivity, specificity, positive and negative-predictive value of 1.00. EIL and EI-VCD show different objective findings confirming that they are two separate conditions both causing laryngeal obstruction. The use of the CLE test is mandatory, because this is the only way to differ between the two conditions and EILOMEA gives the diagnosis and the degree of obstruction objectively.

Apolipoprotein M (apoM) is the carrier of sphingosine-1-phosphate (S1P) in plasma high-density lipoproteins. S1P is a bioactive lipid interacting with five receptors (S1P). We show that lack of apoM in mice increases the amount of brown adipose tissue (BAT), accelerates the clearance of postprandial triglycerides, and protects against diet-induced obesity (i.e., a phenotype similar to that induced by cold exposure or β-adrenergic stimulation). Moreover, the data suggest that the phenotype of apoM-deficient mice is S1P dependent and reflects diminished S1P stimulation. The results reveal a link between the apoM/S1P axis and energy metabolism.

This article is available online at http://www.jlr.org Supplementary key words lipoprotein • low-density lipoprotein metabolism • apolipoprotein • familial hypercholesterolemia HDL-associated apoM was recently shown to be a physiological carrier of sphingosine-1-phosphate (S1P) ( 1 ). S1P affects vascular integrity, and the S1P-dependent effects of HDL are dependent on apoM. Moreover, several studies have suggested that apoM can accelerate effl ux of cholesterol from foam cells, delay oxidation of LDL, and increase production of pre-␤ -HDL, suggesting that apoM affects antiatherogenic functions of HDL ( 2-4 ). However, little is known about the plasma metabolism of apoM. ApoM is anchored in HDL via a retained hydrophobic signal peptide ( 5 ). Loss of the signal peptide abolishes apoM's binding to HDL, causing rapid clearance of the truncated apoM in the kidney. Even though >90% of plasma apoM resides in HDL plasma, apoM concentration has consistently been shown to be positively correlated with plasma LDL cholesterol in humans ( 6-8 ). Moreover, HDL-associated plasma apoM is increased 2-fold in Ldlr Ϫ / Ϫ mice lacking functional LDL receptors ( 9 ). These observations might refl ect that plasma apoM is controlled by the rate of LDL receptor-mediated clearance of apoBcontaining particles. LDL receptor binding and internalization of LDL represent a major pathway controlling plasma LDL levels ( 10, 11 ), and the ligand binding domain of the LDL receptor, as well as the LDL receptor binding domain in apoB, have been extensively characterized ( 12, 13 ). The clinical diagnosis of familial hypercholesterolemia (FH) and impaired clearance of LDL can be caused by mutations in the LDLR and APOB genes ( 14 ). Genetic studies Abstract ApoM is mainly associated with HDL. Nevertheless, we have consistently observed positive correlations of apoM with plasma LDL cholesterol in humans. Moreover, LDL receptor defi ciency is associated with increased plasma apoM in mice. Here, we tested the idea that plasma apoM concentrations are affected by the rate of LDL receptormediated clearance of apoB-containing particles. We measured apoM in humans each carrying one of three different LDL receptor mutations (n = 9) or the apoB3500 mutation (n = 12). These carriers had increased plasma apoM (1.34 ± 0.13 µM, P = 0.003, and 1.23 ± 0.10 µM, P = 0.02, respectively) as compared with noncarriers (0.93 ± 0.04 µM). When we injected human apoM-containing HDL into Wt (n = 6) or LDL receptor-defi cient mice (n = 6), the removal of HDLassociated human apoM was delayed in the LDL receptordefi cient mice. After 2 h, 54 ± 5% versus 90 ± 8% ( P < 0.005) of the initial amounts of human apoM remained in the plasma of Wt and LDL receptor-defi cient mice, respectively. Finally, we compared the turnover of radio-iodinated LDL and plasma apoM concentrations in 45 normocholesterolemic humans. There was a negative correlation between plasma apoM and the fractional catabolic rate of LDL ( r = ؊ 0.38, P = 0.009). These data suggest that the plasma clearance of apoM...