Словник української мови: додатковий том. Історія укладання та підсумки роботи

У статті висвітлено історію укладання Додаткового тому Словника української мови, описано принципи формування його реєстру та розроблення нових статей, а також статей з новими значеннями, відтінками значень і стійкими сполученнями слів, наведено приклади таких статей.The article highlights the history of making the Additional Ukrainian dictionary volume, describes principles of the words listing and the development of new articles and articles with new meanings and theirs shades and the stable words combinations. There are given the examples of such articles

New Insights into the Structural Roles of Nebulin in Skeletal Muscle

One important feature of muscle structure and function that has remained relatively obscure is the mechanism that regulates thin filament length. Filament length is an important aspect of muscle function as force production is proportional to the amount of overlap between thick and thin filaments. Recent advances, due in part to the generation of nebulin KO models, reveal that nebulin plays an important role in the regulation of thin filament length. Another structural feature of skeletal muscle that is not well understood is the mechanism involved in maintaining the regular lateral alignment of adjacent sarcomeres, that is, myofibrillar connectivity. Recent studies indicate that nebulin is part of a protein complex that mechanically links adjacent myofibrils. Thus, novel structural roles of nebulin in skeletal muscle involve the regulation of thin filament length and maintaining myofibrillar connectivity. When these functions of nebulin are absent, muscle weakness ensues, as is the case in patients with nemaline myopathy with mutations in nebulin. Here we review these new insights in the role of nebulin in skeletal muscle structure

Ultrasound imaging to tailor treatment of shoulder pain in general practice

The prognosis for patients with shoulder pain is poor. Unfortunately, general practitioners are not able to determine the underlying cause of shoulder pain during a consultation. Treatment therefore focuses on the symptoms and not the underlying cause. This dissertation shows that general practitioners find diagnosing shoulder pain complex, and that ultrasound is suitable for making a diagnosis and is also frequently used to do so. However, treatment based on ultrasound diagnosis in patients with a history of less than three months’ pain does not result in a better prognosis after one year. It is therefore recommended that general practitioners do not refer patients with shoulder pain for ultrasound

Trendrapport mbo. Technologieën van de toekomst

Ottenheijm, S., Rubens, W., & Vorstenbosch, P. (2011). Trendrapport mbo. Technologieën van de toekomst. Zoetermeer: Stichting Kennisnet en saMBO-ICT.Dit rapport beschrijft maatschappelijke ontwikkelingen (netwerksamenleving, 'persoonlijk en op maat', 'nieuwe organisatie- en verdienmodellen', en de 'technologisering van het leven'), uitdagingen voor het MBO ('het organiseerbaarheid van het mbo', 'optimalisering van de samenwerking', 'student als volwassen internetconsument' en 'meer met minder'), en de belangrijkste technologische ontwikkelingen ('cloud computing', 'social media', 'verrijkte content', 'augmented reality', 'semantisch web' en 'learning analytics').Stichting Kennisnet en saMBO-IC

Does the outcome of diagnostic ultrasound influence the treatment modalities and recovery in patients with shoulder pain in physiotherapy practice? Results from a prospective cohort study

© 2019 Elsevier Ltd Study design: Prospective cohort study including patients with shoulder pain in primary care physiotherapy. Background: There is an increased tendency to use diagnostic ultrasound to aid the diagnostic strategy and target treatment. It is a relatively cheap and accessible imaging technique but the implications for practice and patients are unknown. Objectives: To study the influence of diagnostic ultrasound (DUS) on diagnostic work-up, treatment modalities and recovery. Methods: Participants (n = 389) with a new episode of shoulder pain were assessed at baseline and followed for 6, 12 and 26 weeks. Diagnostic work-up, including the use of DUS, and treatment strategies were reported by the therapists at 3, 6 and 12 weeks. Results: Most patients (41%) were diagnosed with subacromial impingement/pain syndrome after physical examination or DUS. DUS was used in 31% of the participants. Tendinopathy was the most found abnormality in this sub-population. Patients who underwent DUS were more frequently treated using exercise therapy. Patients that not had DUS were more likely to receive massage therapy, trigger point therapy or mobilisation techniques. Logistic regression analyses did not show a significant association between DUS and recovery after 26 weeks (0.88, 95%CI:0.50–1.57). Correcting for the therapist as a confounder using a multilevel binary logistic regression did not show a significant cluster effect. Conclusion: Diagnostic US as a work-up component does not seem to influence diagnosis or recovery but does influence the choice of treatment modality. Conclusions are limited to observational data. High quality randomized trials should study the effect of DUS on recovery

Deleting titin's C-terminal PEVK exons increases passive stiffness, alters splicing, and induces cross-sectional and longitudinal hypertrophy in skeletal muscle

The Proline, Glutamate, Valine and Lysine-rich (PEVK) region of titin constitutes an entropic spring that provides passive tension to striated muscle. To study the functional and structural repercussions of a small reduction in the size of the PEVK region, we investigated skeletal muscles of a mouse with the constitutively expressed C-terminal PEVK exons 219–225 deleted, the Ttn(Δ219–225) model (MGI: Ttn(TM 2.1Mgot)). Based on this deletion, passive tension in skeletal muscle was predicted to be increased by ∼17% (sarcomere length 3.0 μm). In contrast, measured passive tension (sarcomere length 3.0 μm) in both soleus and EDL muscles was increased 53 ± 11% and 62 ± 4%, respectively. This unexpected increase was due to changes in titin, not to alterations in the extracellular matrix, and is likely caused by co-expression of two titin isoforms in Ttn(Δ219–225) muscles: a larger isoform that represents the Ttn(Δ219–225) N2A titin and a smaller isoform, referred to as N2A2. N2A2 represents a splicing adaption with reduced expression of spring element exons, as determined by titin exon microarray analysis. Maximal tetanic tension was increased in Ttn(Δ219–225) soleus muscle (WT 240 ± 9; Ttn(Δ219–225) 276 ± 17 mN/mm2), but was reduced in EDL muscle (WT 315 ± 9; Ttn(Δ219–225) 280 ± 14 mN/mm2). The changes in active tension coincided with a switch toward slow fiber types and, unexpectedly, faster kinetics of tension generation and relaxation. Functional overload (FO; ablation) and hindlimb suspension (HS; unloading) experiments were also conducted. Ttn(Δ219–225) mice showed increases in both longitudinal hypertrophy (increased number of sarcomeres in series) and cross-sectional hypertrophy (increased number of sarcomeres in parallel) in response to FO and attenuated cross-sectional atrophy in response to HS. In summary, slow- and fast-twitch muscles in a mouse model devoid of titin's PEVK exons 219–225 have high passive tension, due in part to alterations elsewhere in splicing of titin’s spring region, increased kinetics of tension generation and relaxation, and altered trophic responses to both functional overload and unloading. This implicates titin’s C-terminal PEVK region in regulating passive and active muscle mechanics and muscle plasticity

Muscle weakness in TPM3-myopathy is due to reduced Ca2+-sensitivity and impaired acto-myosin cross-bridge cycling in slow fibres.

Dominant mutations in TPM3, encoding α-tropomyosin(slow), cause a congenital myopathy characterized by generalized muscle weakness. Here, we used a multidisciplinary approach to investigate the mechanism of muscle dysfunction in 12 TPM3-myopathy patients. We confirm that slow myofibre hypotrophy is a diagnostic hallmark of TPM3-myopathy, and is commonly accompanied by skewing of fibre-type ratios (either slow or fast fibre predominance). Patient muscle contained normal ratios of the three tropomyosin isoforms and normal fibre-type expression of myosins and troponins. Using 2D-PAGE, we demonstrate that mutant α-tropomyosin(slow) was expressed, suggesting muscle dysfunction is due to a dominant-negative effect of mutant protein on muscle contraction. Molecular modelling suggested mutant α-tropomyosin(slow) likely impacts actin–tropomyosin interactions and, indeed, co-sedimentation assays showed reduced binding of mutant α-tropomyosin(slow) (R168C) to filamentous actin. Single fibre contractility studies of patient myofibres revealed marked slow myofibre specific abnormalities. At saturating [Ca(2+)] (pCa 4.5), patient slow fibres produced only 63% of the contractile force produced in control slow fibres and had reduced acto-myosin cross-bridge cycling kinetics. Importantly, due to reduced Ca(2+)-sensitivity, at sub-saturating [Ca(2+)] (pCa 6, levels typically released during in vivo contraction) patient slow fibres produced only 26% of the force generated by control slow fibres. Thus, weakness in TPM3-myopathy patients can be directly attributed to reduced slow fibre force at physiological [Ca(2+)], and impaired acto-myosin cross-bridge cycling kinetics. Fast myofibres are spared; however, they appear to be unable to compensate for slow fibre dysfunction. Abnormal Ca(2+)-sensitivity in TPM3-myopathy patients suggests Ca(2+)-sensitizing drugs may represent a useful treatment for this condition