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Background Originally, studies on exhaled droplets explored properties of airborne transmission of infectious diseases. More recently, the interest focuses on properties of exhaled droplets as biomarkers, enabled by the development of technical equipment and methods for chemical analysis. Because exhaled droplets contain nonvolatile substances, particles is the physical designation. This review aims to outline the development in the area of exhaled particles, particularly regarding biomarkers and the connection with small airways, i e airways with an internal diameter < 2 mm. Main body Generation mechanisms, sites of origin, number concentrations of exhaled particles and the content of nonvolatile substances are studied. Exhaled particles range in diameter from 0.01 and 1000 μm depending on generation mechanism and site of origin. Airway reopening is one scientifically substantiated particle generation mechanism. During deep expirations, small airways close and the reopening process produces minute particles. When exhaled, these particles have a diameter of < 4 μm. A size discriminating sampling of particles < 4 μm and determination of the size distribution, allows exhaled particle mass to be estimated. The median mass is represented by particles in the size range of 0.7 to 1.0 μm. Half an hour of repeated deep expirations result in samples in the order of nanogram to microgram. The source of these samples is the respiratory tract ling fluid of small airways and consists of lipids and proteins, similarly to surfactant. Early clinical studies of e g chronic obstructive pulmonary disease and asthma, reported altered particle formation and particle composition. Conclusion The physical properties and content of exhaled particles generated by the airway reopening mechanism offers an exciting noninvasive way to obtain samples from the respiratory tract lining fluid of small airways. The biomarker potential is only at the beginning to be explored.

[...]we emphasize that while exercise prescriptions and management plans (insulin and nutrition) can be based on known physiology and a limited number of clinical studies, they must often be individualized for young people in line with experience, goals, and safety in mind. [E] Children, adolescents, and relevant family members should be provided with a written or online copy of up-to-date and user-friendly evidence-based guidelines focusing on blood glucose management in exercise. [E] Where available, blood ketone measurement is recommended over urine ketone measurement—see ISPAD Clinical Practice Consensus Guidelines 2014 “Assessment and monitoring of glycemic control in children and adolescents with diabetes.” For Continuous Subcutaneous Insulin Infusion (CSII) users, the pump may be disconnected or suspended, or a temporary decrease in basal insulin infusion rate implemented at least 90 minutes before starting exercise to give a reduced basal effect during activity.

Myosin is a molecular motor indispensable for body movement and heart contractility. Apart from pure cardiomyopathy, mutations in MYH7 encoding slow/β-cardiac myosin heavy chain also cause skeletal muscle disease with or without cardiac involvement. Mutations within the α-helical rod domain of MYH7 are mainly associated with Laing distal myopathy. To investigate the mechanisms underlying the pathology of the recurrent causative MYH7 mutation (K1729del), we have developed a Drosophila melanogaster model of Laing distal myopathy by genomic engineering of the Drosophila Mhc locus. Homozygous MhcK1728del animals die during larval/pupal stages, and both homozygous and heterozygous larvae display reduced muscle function. Flies expressing only MhcK1728del in indirect flight and jump muscles, and heterozygous MhcK1728del animals, were flightless, with reduced movement and decreased lifespan. Sarcomeres of MhcK1728del mutant indirect flight muscles and larval body wall muscles were disrupted with clearly disorganized muscle filaments. Homozygous MhcK1728del larvae also demonstrated structural and functional impairments in heart muscle, which were not observed in heterozygous animals, indicating a dose-dependent effect of the mutated allele. The impaired jump and flight ability and the myopathy of indirect flight and leg muscles associated with MhcK1728del were fully suppressed by expression of Abba/Thin, an E3-ligase that is essential for maintaining sarcomere integrity. This model of Laing distal myopathy in Drosophila recapitulates certain morphological phenotypic features seen in Laing distal myopathy patients with the recurrent K1729del mutation. Our observations that Abba/Thin modulates these phenotypes suggest that manipulation of Abba/Thin activity levels may be beneficial in Laing distal myopathy.

An essential role for embryonic MyHC in foetal development has been found from its association with distal arthrogryposis syndromes, a heterogeneous group of disorders characterised by congenital contractions. The latter probably result from severe myopathy during foetal development. Lack of embryonic muscle biopsy material and suitable animal models has hindered study of the pathomechanisms linking mutations in MYH3 to prenatal myopathy. We determined the pathomechanisms of developmental myopathy caused by recurrent p.Thr178Ile MYH3 heterozygosity, using patient-derived skeletal muscle cells in culture as an experimental disease model to emulate early embryonic development. These cultured cells were processed for discrimination and quantitative analysis of mutant and wild-type MYH3 alleles and MyHC transcripts, real-time RT-qPCR, sequence analysis, immunofluorescence microscopy, immunoblot, and proteomic assessments. Involvement of the ubiquitin proteasome system was investigated in patients with p.Thr178Ile mutations in MYH3 and MYH2. We found equal overall expression of mutant and wild-type MyHC mRNAs and proteins. Compared to the controls, however, expression of embryonic MyHC transcripts and proteins was reduced whereas expression of myosin-specific E3 ubiquitin ligase (MuRF1) was increased. We also found delayed myofibrillogenesis and atrophic myotubes but structured sarcomeres. In conclusion, this study suggests that developmental p.Thr178Ile MYH3 myopathy is associated with a combined pathomechanism of insufficient dosage of functional embryonic MyHC and production of mutant protein.

The present study aimed to evaluate the effects of two types of 9-month adapted physical activity (APA) program, based on a muscle reinforcement training and a postural training, respectively, on muscle mass, muscle strength, and static balance in moderate sarcopenic older women. The diagnosis of sarcopenia was done in accordance with measurable variables and cut-off points suggested by the European Working Group on Sarcopenia in Older People (EWGSOP). Seventy-two participants were randomly assigned to two groups: the muscle reinforcement training group (RESISTANCE) (n=35; 69.9 ± 2.7 years) and the postural training group (POSTURAL) (n=37; 70.0±2.8 years). Body composition, muscle mass, skeletal muscle mass index (SMI), and handgrip strength (HGS) were evaluated for sarcopenia assessment, whereas Sway Path, Sway Area, Stay Time, and Spatial Distance were evaluated for static balance assessment. Sixty-six participants completed the study (RESISTANCE group: n=33; POSTURAL group: n=33). Significant increases of muscle mass, SMI, and handgrip strength values were found in the RESISTANCE group, after muscle reinforcement program. No significant differences appeared in the POSTURAL group, after postural training. Furthermore, RESISTANCE group showed significant improvements in static balance parameters, whereas no significant differences appeared in the POSTURAL group. On the whole, the results of this study suggest that the APA program based on muscle reinforcement applied on moderate sarcopenic older women was able to significantly improve muscle mass and muscle strength, and it was also more effective than the applied postural protocol in determining positive effects on static balance.

A rethinking of current heat-acclimation strategies is required as most research and advice for improving physiological strain in the heat includes maintaining hydration using long-term acclimation protocols (>10 days). Furthermore, these strategies have tended to use untrained and moderately trained participants. Therefore, the aims of this review were to (i) investigate the effectiveness of short-term heat acclimation (STHA) with moderately and highly trained athletes; (ii) determine the importance of fluid regulatory strain, which has a thermally independent role in heat adaptation; (iii) assess the impact of STHA on a marker of thermotolerance (inducible heat-shock protein 70 [HSP70]); and (iv) provide further information on the decay of acclimation to heat. The review suggests that 5-day STHA is effective, and adaptations may be more pronounced after fluid regulatory strain from a dehydration-acclimation regimen. Furthermore, highly trained athletes may have similar physiological gains to those who are less trained using STHA. However, research has tended to focus on untrained or moderately trained participants and more information is required for highly trained populations. HSP70 response is upregulated across STHA. This indicates increased thermotolerance and protective adaptive change that may indicate HSP70 response as a useful marker of heat acclimation. Physiological adaptations after heat acclimation are relatively short term and may vanish only a few days or weeks after removal from heat exposure. From a practical perspective 5-day STHA may be the preferred acclimation regimen for moderately and highly trained athletes as it has been shown to be effective, less expensive and less likely to disrupt the tapering for competition in elite performers. Furthermore, updated information on the time course of acclimation decay may allow a reliable estimate of how long individuals can be free from heat exposure before reacclimation is required. This is particularly pertinent in present times as many athletes, civilians andmilitary personnel increasingly have to relocate to different climates of the world, often within a short period of time.

Functional neuroimaging and electrophysiology studies are changing our understanding of patients with coma and related states. Some severely brain damaged patients may show residual cortical processing in the absence of behavioural signs of consciousness. Given these new findings, the diagnostic errors and their potential effects on treatment as well as concerns regarding the negative associations intrinsic to the term vegetative state, the European Task Force on Disorders of Consciousness has recently proposed the more neutral and descriptive term unresponsive wakefulness syndrome. When vegetative/unresponsive patients show minimal signs of consciousness but are unable to reliably communicate the term minimally responsive or minimally conscious state (MCS) is used. MCS was recently subcategorized based on the complexity of patients’ behaviours: MCS+ describes high-level behavioural responses (i.e., command following, intelligible verbalizations or non-functional communication) and MCS− describes low-level behavioural responses (i.e., visual pursuit, localization of noxious stimulation or contingent behaviour such as appropriate smiling or crying to emotional stimuli). Finally, patients who show non-behavioural evidence of consciousness or communication only measurable via para-clinical testing (i.e., functional MRI, positron emission tomography, EEG or evoked potentials) can be considered to be in a functional locked-in syndrome. An improved assessment of brain function in coma and related states is not only changing nosology and medical care but also offers a better-documented diagnosis and prognosis and helps to further identify the neural correlates of human consciousness.

Analysis of changes in functional groups of species and potential drivers of environmental change for protected areas across the world’s major tropical regions reveals large variation between reserves that have been effective and those experiencing an erosion of biodiversity, and shows that environmental changes immediately outside reserves are nearly as important as those inside in determining their ecological fate. How to protect protected areas Protected areas are a key component of tropical forest conservation strategy, but how well are they performing? These authors assemble a large data set from 60 protected areas across the globe, assessing 31 functional groups of species and 21 drivers of environmental change. They find that about half of the reserves are succeeding but half are experiencing substantial losses of biodiversity, driven as much by environmental change outside the reserves as by change within them. To protect what remains of these habitats, the authors suggest that it is vital to establish sizeable buffer zones around reserves, maintain substantial reserve connectivity to other forest areas and promote low-impact land uses near reserves. The rapid disruption of tropical forests probably imperils global biodiversity more than any other contemporary phenomenon 1 , 2 , 3 . With deforestation advancing quickly, protected areas are increasingly becoming final refuges for threatened species and natural ecosystem processes. However, many protected areas in the tropics are themselves vulnerable to human encroachment and other environmental stresses 4 , 5 , 6 , 7 , 8 , 9 . As pressures mount, it is vital to know whether existing reserves can sustain their biodiversity. A critical constraint in addressing this question has been that data describing a broad array of biodiversity groups have been unavailable for a sufficiently large and representative sample of reserves. Here we present a uniquely comprehensive data set on changes over the past 20 to 30 years in 31 functional groups of species and 21 potential drivers of environmental change, for 60 protected areas stratified across the world’s major tropical regions. Our analysis reveals great variation in reserve ‘health’: about half of all reserves have been effective or performed passably, but the rest are experiencing an erosion of biodiversity that is often alarmingly widespread taxonomically and functionally. Habitat disruption, hunting and forest-product exploitation were the strongest predictors of declining reserve health. Crucially, environmental changes immediately outside reserves seemed nearly as important as those inside in determining their ecological fate, with changes inside reserves strongly mirroring those occurring around them. These findings suggest that tropical protected areas are often intimately linked ecologically to their surrounding habitats, and that a failure to stem broad-scale loss and degradation of such habitats could sharply increase the likelihood of serious biodiversity declines.

The general consensus among sport and exercise genetics researchers is that genetic tests have no role to play in talent identification or the individualised prescription of training to maximise performance. Despite the lack of evidence, recent years have witnessed the rise of an emerging market of direct-to-consumer marketing (DTC) tests that claim to be able to identify children's athletic talents. Targeted consumers include mainly coaches and parents. There is concern among the scientific community that the current level of knowledge is being misrepresented for commercial purposes. There remains a lack of universally accepted guidelines and legislation for DTC testing in relation to all forms of genetic testing and not just for talent identification. There is concern over the lack of clarity of information over which specific genes or variants are being tested and the almost universal lack of appropriate genetic counselling for the interpretation of the genetic data to consumers. Furthermore independent studies have identified issues relating to quality control by DTC laboratories with different results being reported from samples from the same individual. Consequently, in the current state of knowledge, no child or young athlete should be exposed to DTC genetic testing to define or alter training or for talent identification aimed at selecting gifted children or adolescents. Large scale collaborative projects, may help to develop a stronger scientific foundation on these issues in the future.

A growing body of evidence suggests that the cerebellum is involved in both cognition and language. Abnormal cerebellar development may contribute to neurodevelopmental disorders such as attention deficit hyperactivity disorder (ADHD), autism, fetal alcohol syndrome, dyslexia, and specific language impairment. Performance in eyeblink conditioning, which depends on the cerebellum, can potentially be used to clarify the neural mechanisms underlying the cerebellar dysfunction in disorders like these. However, we must first understand how the performance develops in children who do not have a disorder. In this study we assessed the performance in eyeblink conditioning in 42 typically developing children between 6 and 11 years old as well as in 26 adults. Older children produced more conditioned eyeblink responses than younger children and adults produced more than children. In addition, females produced more conditioned eyeblink responses than males among both children and adults. These results highlight the importance of considering the influence of age and sex on the performance when studying eyeblink conditioning as a measure of cerebellar development.