Основні віхи розвитку української гірничої термінології

Ідеться про розвиток термінології й номенклатури гірничої справи, зокрема частково шахтобудування, яка активно розвивалася впродовж 20–З0-х рр. ХХ ст. Наголошено на спірних моментах в історії становлення цієї лексичної групи. Зроблено висновок про те, що нині гірнича термінологія української мови практично повністю унормована завдяки ретельній праці лексикографів та фахівців-гірників.The paper examines the ways mining terminology and nomenclature was developed. Special attention is drawn to the period of the 20th – 30th of the 20th century, when the term system was formed. The research focuses on disputable moments in the history of lexical group development; it concludes that mining terminology is normalized in the present-day Ukrainian language thanks to the careful work of lexicographers and mining specialist

Molecular characterization of MRSA collected during national surveillance between 2008 and 2019 in the Netherlands

Background.Although the Netherlands is a country with a low endemic level, methicillin-resistant Staphylococcus aureus (MRSA) poses a significant health care problem. Therefore, high coverage national MRSA surveillance has been in place since 1989. To monitor possible changes in the type-distribution and emergence of resistance and virulence, MRSA isolates are molecularly characterized.Methods.All 43,321 isolates from 36,520 persons, collected 2008–2019, were typed by multiple-locus variable number tandem repeats analysis (MLVA) with simultaneous PCR detection of the mecA, mecC and lukF-PV genes, indicative for PVL. Next-generation sequencing data of 4991 isolates from 4798 persons were used for whole genome multi-locus sequence typing (wgMLST) and identification of resistance and virulence genes.Results.We show temporal change in the molecular characteristics of the MRSA population with the proportion of PVL-positive isolates increasing from 15% in 2008–2010 to 25% in 2017–2019. In livestock-associated MRSA obtained from humans, PVL-positivity increases to 6% in 2017–2019 with isolates predominantly from regions with few pig farms. wgMLST reveals the presence of 35 genogroups with distinct resistance, virulence gene profiles and specimen origin. Typing shows prolonged persistent MRSA carriage with a mean carriage period of 407 days. There is a clear spatial and a weak temporal relationship between isolates that clustered in wgMLST, indicative for regional spread of MRSA strains.Conclusions.Using molecular characterization, this exceptionally large study shows genomic changes in the MRSA population at the national level. It reveals waxing and waning of types and genogroups and an increasing proportion of PVL-positive MRSA

Causes of Mortality in ICU-Acquired Weakness

Intensive care unit-acquired weakness (ICU-AW) is a common complication of critical illness and is associated with increased mortality, longer mechanical ventilation and longer hospital stay. Little is known about the causes of mortality in patients with ICU-AW. In this study, we aimed to give an overview of the causes of death in a population diagnosed with ICU-AW during hospital admission. Data from a prospective cohort study in the mixed medical-surgical ICU of the Academic Medical Center in Amsterdam were used. Patients were included when mechanically ventilated for more than 48 hours. Intensive care unit-acquired weakness was defined as a mean medical research council score <4. Baseline data and data on the time of death were collected. Fifty-three patients were included. Irreversible shock with multiple organ failure (MOF) was the most common cause of death (28/53 of patients; 26 patients with septic shock and 2 patients with hypovolemic shock). Most common site of sepsis was abdominal (38.5%) and pulmonary (19.2%). On admission to the ICU, 53% had a do-not-resuscitate code. In 74% of the patients, further treatment limitations were implemented during their ICU stay. In this cohort of patients with ICU-AW, most patients died of irreversible shock with MOF, caused by sepsi

<FamilyName>Vasankari</FamilyName> quired weakness: an observational pilot study

Early diagnosis of intensive care unit - acquired weakness (ICU-AW) using the current reference standard, that is, assessment of muscle strength, is often hampered due to impaired consciousness. Biological markers could solve this problem but have been scarcely investigated. We hypothesized that plasma levels of neurofilaments are elevated in ICU-AW and can diagnose ICU-AW before muscle strength assessment is possible. For this prospective observational cohort study, neurofilament levels were measured using ELISA (NfHSMI35 antibody) in daily plasma samples (index test). When patients were awake and attentive, ICU-AW was diagnosed using the Medical Research Council scale (reference standard). Differences and discriminative power (using the area under the receiver operating characteristic curve; AUC) of highest and cumulative (calculated using the area under the neurofilament curve) neurofilament levels were investigated in relation to the moment of muscle strength assessment for each patient. Both the index test and reference standard were available for 77 ICU patients. A total of 18 patients (23%) fulfilled the clinical criteria for ICU-AW. Peak neurofilament levels were higher in patients with ICU-AW and had good discriminative power (AUC: 0.85; 95% CI: 0.72 to 0.97). However, neurofilament levels did not peak before muscle strength assessment was possible. Highest or cumulative neurofilament levels measured before muscle strength assessment could not diagnose ICU-AW (AUC 0.59; 95% CI 0.37 to 0.80 and AUC 0.57; 95% CI 0.32 to 0.81, respectively). Plasma neurofilament levels are raised in ICU-AW and may serve as a biological marker for ICU-AW. However, our study suggests that an early diagnosis of ICU-AW, before muscle strength assessment, is not possible using neurofilament levels in plasm

Muscle weakness in a S. pneumoniae sepsis mouse model

Background: The pathophysiology of intensive care unit-acquired weakness (ICU-AW), which affects peripheral nerves, limb muscles and respiratory muscles, is complex and incompletely understood. This illustrates the need for an ICU-AW animal model. However, a translatable and easily applicable ICU-AW animal model does not exist. The objective of this study was to investigate whether induction of a S. pneumoniae sepsis could serve as a model for ICU-AW. Methods: A total of 24 C57BL/6J mice were infected intranasally with viable S. pneumoniae. Control mice (n=8) received intranasal saline and mice of the blank group (n=4) were not inoculated. Ceftriaxone was administered at 24 h (n=8) or at 48h after inoculation (n=8), or as soon as mice lost 10% of their body weight (n=8). The primary endpoint, in vivo grip strength, was measured daily. At the end of the experiment, at 120 h after inoculation, electrophysiological recordings were performed and diaphragm muscle was excised to determine ex vivo muscle fiber strength and myosin/action ratio. Results: Grip strength over time was similar between experimental and control groups and electrophysiological recordings did not show signs of ICU-AW. Diaphragm fiber contractility measurements showed reduced strength in the group that received ceftriaxone at 48 h after S. pneumoniae inoculation. Conclusions: Ex vivo diaphragm weakness, but no in vivo limb weakness was found in the S. pneumoniae mouse model in which severe illness was induced. This does not reflect the full clinical picture of ICU-AW as seen in humans and as such this model did not fulfill our predefined requirements. However, this model may be used to study inflammation induced diaphragmatic weakness

Assessment of intensive care unit-acquired weakness in young and old mice: An E. coli septic peritonitis model

There are few reports of in vivo muscle strength measurements in animal models of ICU-acquired weakness (ICU-AW). In this study we investigated whether the Escherichia coli (E. coli) septic peritonitis mouse model may serve as an ICU-AW model using in vivo strength measurements and myosin/actin assays, and whether development of ICU-AW is age-dependent in this model. Young and old mice were injected intraperitoneally with E. coli and treated with ceftriaxone. Forelimb grip strength was measured at multiple time points, and the myosin/actin ratio in muscle was determined. E. coli administration was not associated with grip strength decrease, neither in young nor in old mice. In old mice, the myosin/actin ratio was lower in E. coli mice at t = 48 h and higher at t = 72 h compared with controls. This E. coli septic peritonitis mouse model did not induce decreased grip strength. In its current form, it seems unsuitable as a model for ICU-A

No association between systemic complement activation and intensive care unit-acquired weakness

Background: The main risk factors for intensive care unit-acquired weakness (ICU-AW) are sepsis, the systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction. These risk factors are associated with systemic complement activation. We hypothesized that critically ill patients who develop ICU-AW have increased systemic complement activation compared to critically ill patients who do not develop ICU-AW. Methods: Complement activation products C3b/c, C4b/c and C5a were measured in plasma of ICU patients with mechanical ventilation for ≥48 hours. Samples were collected at admission to the ICU and for 6 consecutive days. ICU-AW was defined by a mean Medical Research Council (MRC) score <4. We compared the level of complement activation products between patients who did and who did not develop ICU-AW. Results: Muscle strength measurements and complement assays were available in 27 ICU patients, of whom 13 patients developed ICU-AW. Increased levels of C4b/c were seen in all patients. Neither admission levels, nor maximum, minimum and mean levels of complement activation products were different between patients who did and did not develop ICU-AW. Conclusions: Complement activation is seen in critically ill patients, but is not different between patients who did and who did not develop ICU-AW