Ergonomic Assessment of Physical Load in Slovak Industry Using Wearable Technologies

The physical tasks of workers are demanding, particularly when performed long-term in unsuitable working position, with high frequency, heavy load, after injury, with developing damage of health or reduced performance due to advanced age. Work-related musculoskeletal disorders (WMSDs) result from overuse or develop over time. Work activities, which are frequent and repetitive, or activities with awkward postures, cause disorders that may be painful during work or at rest. There is a new technology in the market, occupational exoskeletons, which have the prerequisites for minimizing the negative consequences of workload on WMSDs. We provided pilot quantitative measurements of the ergonomic risk at one selected workplace in a Slovak automotive company with four different workers to prove our methodology using wearable wireless multi-sensor systems Captiv and Actigraph. At first, the test was performed in standard conditions without an exoskeleton. The unacceptable physical load was identified in considerable evaluated body areas—neck, hip, and shoulder. Next, the passive chair exoskeleton Chairless Chair 2.0 was used in trials as an ergonomic measure. Our intention was to determine whether an exoskeleton would be an effective tool for optimizing the workload in selected workplaces and whether the proposed unique quantitative measurement system would give reliable and quick results

Aurora kinase A is essential for meiosis in mouse oocytes.

The Aurora protein kinases are well-established regulators of spindle building and chromosome segregation in mitotic and meiotic cells. In mouse oocytes, there is significant Aurora kinase A (AURKA) compensatory abilities when the other Aurora kinase homologs are deleted. Whether the other homologs, AURKB or AURKC can compensate for loss of AURKA is not known. Using a conditional mouse oocyte knockout model, we demonstrate that this compensation is not reciprocal because female oocyte-specific knockout mice are sterile, and their oocytes fail to complete meiosis I. In determining AURKA-specific functions, we demonstrate that its first meiotic requirement is to activate Polo-like kinase 1 at acentriolar microtubule organizing centers (aMTOCs; meiotic spindle poles). This activation induces fragmentation of the aMTOCs, a step essential for building a bipolar spindle. We also show that AURKA is required for regulating localization of TACC3, another protein required for spindle building. We conclude that AURKA has multiple functions essential to completing MI that are distinct from AURKB and AURKC

Age-Related Oxidative Changes in Primary Porcine Fibroblasts Expressing Mutated Huntingtin

Background: Huntington’s disease (HD) is a devastating neurodegenerative disorder caused by CAG triplet expansions in the huntingtin gene. Oxidative stress is linked to HD pathology, although it is not clear whether this is an effect or a mediator of disease. The transgenic (TgHD) minipig expresses the N-terminal part of human-mutated huntingtin and represents a unique model to investigate therapeutic strategies towards HD. A more detailed characterization of this model is needed to fully utilize its potential. Methods: In this study, we focused on the molecular and cellular features of fibroblasts isolated from TgHD minipigs and the wild-type (WT) siblings at different ages, pre-symptomatic at the age of 24–36 months and with the onset of behavioural symptoms at the age of 48 months. We measured oxidative stress, the expression of oxidative stress-related genes, proliferation capacity along with the expression of cyclin B1 and D1 proteins, cellular permeability, and the integrity of the nuclear DNA (nDNA) and mitochondrial DNA in these cells. Results: TgHD fibroblasts isolated from 48-month-old animals showed increased oxidative stress, which correlated with the overexpression of SOD2 encoding mitochondrial superoxide dismutase 2, and the NEIL3 gene encoding DNA glycosylase involved in replication-associated repair of oxidized DNA. TgHD cells displayed an abnormal proliferation capacity and permeability. We further demonstrated increased nDNA damage in pre-symptomatic TgHD fibroblasts (isolated from animals aged 24–36 months). Conclusions: Our results unravel phenotypic alterations in primary fibroblasts isolated from the TgHD minipig model at the age of 48 months. Importantly, nDNA damage appears to precede these phenotypic alterations. Our results highlight the impact of fibroblasts from TgHD minipigs in studying the molecular mechanisms of HD pathophysiology that gradually occur with age