cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.27205339.v1
title: Actionable insights for human factors and ergonomics to achieve the Sustainable Development Goals: mapping past advancements and proposing future strategic paths

description: Despite significant strides in linking Human Factors and Ergonomics (HFE) and sustainability, research lacks precision in debating HFE’s role, especially concerning the Sustainable Development Goals (SDGs). This paper maps concrete contributions of HFE to the SDGs, offering strategic actions for target achievement. The methodological approach involved the application of PRISMA to define a sample, SciMAT and VOSviewer for visual and temporal thematic mapping, deductive content analysis and categorical analysis. The results show that there is an already rich and unique set of contributions across a wide range of SDGs, not just the most common related to HFE, SDG8 (Decent work). The importance of HFE is highlighted in various aspects, such as the sustainable adoption of industry 4.0 technologies (SDG9) and the development of sustainable production (SDG12), energy (SDG7) and urban (SDG11) systems. Strategic actions specifying targets for each mapped SDG are offered for policymakers, industry professionals and researchers. This paper maps concrete contributions of HFE to the SDGs, including aspects such as sustainable adoption of industry 4.0 technologies and the development of sustainable production, energy and urban systems. Policymakers, industry professionals and researchers can benefit from the strategic pathways offered to further advance the SDGs.
DOI: 10.6084/m9.figshare.28593966
title: MSC-mediated mitochondrial transfer promotes metabolic reprograming in endothelial cells and vascular regeneration in ARDS

description: Mesenchymal stem cells (MSCs) are a potential therapy for acute respiratory distress syndrome (ARDS), but their mechanisms in repairing mitochondrial damage in ARDS endothelial cells remain unclear. We first examined MSCs’ mitochondrial transfer ability and mechanisms to mouse pulmonary microvascular endothelial cells (MPMECs) in ARDS. Then, we investigated how MSC-mediated mitochondrial transfer affects the repair of endothelial damage. Finally, we elucidated the mechanisms by which MSC-mediated mitochondrial transfer promotes vascular regeneration. Compared to mitochondrial-damaged MSCs, normal MSCs showed a significantly higher mitochondrial transfer rate to MPMECs, with increases of 41.68% in vitro (<i>P</i> &lt; 0.0001) and 10.50% in vivo (<i>P</i> = 0.0005). Furthermore, MSC-mediated mitochondrial transfer significantly reduced reactive oxygen species (<i>P</i> &lt; 0.05) and promoted proliferation (<i>P</i> &lt; 0.0001) in MPMECs. Finally, MSC-mediated mitochondrial transfer significantly increased the activity of the tricarboxylic acid (TCA) cycle (MD of CS mRNA: 23.76, <i>P</i> = 0.032), and further enhanced fatty acid synthesis (MD of FAS mRNA: 6.67, <i>P</i> = 0.0001), leading to a 6.7-fold increase in vascular endothelial growth factor release from MPMECs and promoted vascular regeneration in ARDS. MSC-mediated mitochondrial transfer to MPMECs activates the TCA cycle and fatty acid synthesis, promoting endothelial proliferation and pro-angiogenic factor release, thereby enhancing vascular regeneration in ARDS.
DOI: 10.6084/m9.figshare.28593966.v1
title: MSC-mediated mitochondrial transfer promotes metabolic reprograming in endothelial cells and vascular regeneration in ARDS

description: Mesenchymal stem cells (MSCs) are a potential therapy for acute respiratory distress syndrome (ARDS), but their mechanisms in repairing mitochondrial damage in ARDS endothelial cells remain unclear. We first examined MSCs’ mitochondrial transfer ability and mechanisms to mouse pulmonary microvascular endothelial cells (MPMECs) in ARDS. Then, we investigated how MSC-mediated mitochondrial transfer affects the repair of endothelial damage. Finally, we elucidated the mechanisms by which MSC-mediated mitochondrial transfer promotes vascular regeneration. Compared to mitochondrial-damaged MSCs, normal MSCs showed a significantly higher mitochondrial transfer rate to MPMECs, with increases of 41.68% in vitro (<i>P</i> &lt; 0.0001) and 10.50% in vivo (<i>P</i> = 0.0005). Furthermore, MSC-mediated mitochondrial transfer significantly reduced reactive oxygen species (<i>P</i> &lt; 0.05) and promoted proliferation (<i>P</i> &lt; 0.0001) in MPMECs. Finally, MSC-mediated mitochondrial transfer significantly increased the activity of the tricarboxylic acid (TCA) cycle (MD of CS mRNA: 23.76, <i>P</i> = 0.032), and further enhanced fatty acid synthesis (MD of FAS mRNA: 6.67, <i>P</i> = 0.0001), leading to a 6.7-fold increase in vascular endothelial growth factor release from MPMECs and promoted vascular regeneration in ARDS. MSC-mediated mitochondrial transfer to MPMECs activates the TCA cycle and fatty acid synthesis, promoting endothelial proliferation and pro-angiogenic factor release, thereby enhancing vascular regeneration in ARDS.
DOI: 10.6084/m9.figshare.28114132
title: METTL14 Mediates <i>Glut3</i> m6A methylation to improve osteogenesis under oxidative stress condition

description: Bone remodeling imbalance contributes to osteoporosis. Though current medications enhance osteoblast involvement in bone formation, the underlying pathways remain unclear. This study was aimed to explore the pathways involved in bone formation by osteoblasts, we investigate the protective role of glycolysis and N6-methyladenosine methylation (m6A) against oxidative stress-induced impairment of osteogenesis in MC3T3-E1 cells. We utilized a concentration of 200 μM hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) to establish an oxidative damage model of MC3T3-E1 cells. Subsequently, we examined the alterations in the m6A methyltransferases (METTL3, METTL14), glucose transporter proteins (GLUT1, GLUT3) and validated m6A methyltransferase overexpression in vitro and in an osteoporosis model. The osteoblast differentiation and osteogenesis-related molecules and serum bone resorption markers were measured by biochemical analysis, Alizarin Red S staining, Western blot and ELISA. H<sub>2</sub>O<sub>2</sub> treatment inhibited glycolysis and osteoblast differentiation in MC3T3-E1 cells. However, when METTL14 was overexpressed, these changes induced by H<sub>2</sub>O<sub>2</sub> could be mitigated. Our findings indicate that METTL14 promotes GLUT3 expression via YTHDF1, leading to the modulation of various parameters in the H<sub>2</sub>O<sub>2</sub>-induced model. Similar positive effects of METTL14 on osteogenesis were observed in an ovariectomized mouse osteoporosis model. METTL14 could serve as a potential therapeutic approach for enhancing osteoporosis treatment.
DOI: 10.6084/m9.figshare.28114132.v1
title: METTL14 Mediates <i>Glut3</i> m6A methylation to improve osteogenesis under oxidative stress condition

description: Bone remodeling imbalance contributes to osteoporosis. Though current medications enhance osteoblast involvement in bone formation, the underlying pathways remain unclear. This study was aimed to explore the pathways involved in bone formation by osteoblasts, we investigate the protective role of glycolysis and N6-methyladenosine methylation (m6A) against oxidative stress-induced impairment of osteogenesis in MC3T3-E1 cells. We utilized a concentration of 200 μM hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) to establish an oxidative damage model of MC3T3-E1 cells. Subsequently, we examined the alterations in the m6A methyltransferases (METTL3, METTL14), glucose transporter proteins (GLUT1, GLUT3) and validated m6A methyltransferase overexpression in vitro and in an osteoporosis model. The osteoblast differentiation and osteogenesis-related molecules and serum bone resorption markers were measured by biochemical analysis, Alizarin Red S staining, Western blot and ELISA. H<sub>2</sub>O<sub>2</sub> treatment inhibited glycolysis and osteoblast differentiation in MC3T3-E1 cells. However, when METTL14 was overexpressed, these changes induced by H<sub>2</sub>O<sub>2</sub> could be mitigated. Our findings indicate that METTL14 promotes GLUT3 expression via YTHDF1, leading to the modulation of various parameters in the H<sub>2</sub>O<sub>2</sub>-induced model. Similar positive effects of METTL14 on osteogenesis were observed in an ovariectomized mouse osteoporosis model. METTL14 could serve as a potential therapeutic approach for enhancing osteoporosis treatment.
DOI: 10.6084/m9.figshare.27931242
title: Observational methods for the analysis of biomechanical exposure in the workplace: a systematic review

description: Understanding the characteristics and measurement properties of the observational methods for biomechanical exposure analysis contributes to choosing and planning workplace ergonomic interventions. This systematic review search was performed in the four databases. In 99 studies, 75 observational methods were identified. Posture/movement, force and repetitiveness were the most evaluated risk factors for the upper limbs, trunk and head. EAWS, OCRA, the expanded PATH and QEC evaluate more biomechanical risk factors. EAWS, PATH, QEC, CADEP, ROSA, REBA, modified REBA, RULA, all body segments. Criterion validity, reliability and agreement are REBA and ROSA’s most tested measurement properties. The quality of evidence ranged from moderate to high for 23 methods. ALLA, HAL, OFFERA, simplified PATH and the expanded PATH stand out with high-quality evidence. The expanded PATH and QEC are the most complete in evaluating several occupational tasks, respectively, with high- and moderate-quality evidence. Workers’ exposure analysis is the first step to defining better ergonomics intervention strategies to reduce risk factors at the workplace. This study updates the observational methods existing to evaluate biomechanical exposure workers.
DOI: 10.6084/m9.figshare.27931242.v1
title: Observational methods for the analysis of biomechanical exposure in the workplace: a systematic review

description: Understanding the characteristics and measurement properties of the observational methods for biomechanical exposure analysis contributes to choosing and planning workplace ergonomic interventions. This systematic review search was performed in the four databases. In 99 studies, 75 observational methods were identified. Posture/movement, force and repetitiveness were the most evaluated risk factors for the upper limbs, trunk and head. EAWS, OCRA, the expanded PATH and QEC evaluate more biomechanical risk factors. EAWS, PATH, QEC, CADEP, ROSA, REBA, modified REBA, RULA, all body segments. Criterion validity, reliability and agreement are REBA and ROSA’s most tested measurement properties. The quality of evidence ranged from moderate to high for 23 methods. ALLA, HAL, OFFERA, simplified PATH and the expanded PATH stand out with high-quality evidence. The expanded PATH and QEC are the most complete in evaluating several occupational tasks, respectively, with high- and moderate-quality evidence. Workers’ exposure analysis is the first step to defining better ergonomics intervention strategies to reduce risk factors at the workplace. This study updates the observational methods existing to evaluate biomechanical exposure workers.
DOI: 10.6084/m9.figshare.28262754
title: CEACAM5 exacerbates asthma by inducing ferroptosis and autophagy in airway epithelial cells through the JAK/STAT6-dependent pathway

description: Asthma, a prevalent chronic disease, poses significant health threats and burdens healthcare systems. This study focused on the role of bronchial epithelial cells in asthma pathophysiology. Bioinformatics was used to identify key asthmarelated genes. An ovalbumin-sensitized mouse model and an IL-13-stimulated Beas-2B cell model were established for further investigation. Carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5) was identified as a crucial gene in asthma. CEACAM5 expression was elevated in asthmatic mouse lung tissues and IL-13-stimulated Beas-2B cells, primarily in bronchial epithelial cells. CEACAM5 induced reactive oxygen species (ROS), lipid peroxidation, and ferroptosis. Interfering with CEACAM5 reduced ROS, malondialdehyde levels, and enhanced antioxidant capacity, while inhibiting iron accumulation and autophagy. Overexpression of CEACAM5 in IL-13-stimulated cells activated the JAK/STAT6 pathway, which was necessary for CEACAM5-induced autophagy, ROS accumulation, lipid peroxidation, and ferroptosis. CEACAM5 promotes ferroptosis and autophagy in airway epithelial cells via the JAK/STAT6 pathway, exacerbating asthma symptoms. It represents a potential target for clinical treatment.
DOI: 10.6084/m9.figshare.28262754.v1
title: CEACAM5 exacerbates asthma by inducing ferroptosis and autophagy in airway epithelial cells through the JAK/STAT6-dependent pathway

description: Asthma, a prevalent chronic disease, poses significant health threats and burdens healthcare systems. This study focused on the role of bronchial epithelial cells in asthma pathophysiology. Bioinformatics was used to identify key asthmarelated genes. An ovalbumin-sensitized mouse model and an IL-13-stimulated Beas-2B cell model were established for further investigation. Carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5) was identified as a crucial gene in asthma. CEACAM5 expression was elevated in asthmatic mouse lung tissues and IL-13-stimulated Beas-2B cells, primarily in bronchial epithelial cells. CEACAM5 induced reactive oxygen species (ROS), lipid peroxidation, and ferroptosis. Interfering with CEACAM5 reduced ROS, malondialdehyde levels, and enhanced antioxidant capacity, while inhibiting iron accumulation and autophagy. Overexpression of CEACAM5 in IL-13-stimulated cells activated the JAK/STAT6 pathway, which was necessary for CEACAM5-induced autophagy, ROS accumulation, lipid peroxidation, and ferroptosis. CEACAM5 promotes ferroptosis and autophagy in airway epithelial cells via the JAK/STAT6 pathway, exacerbating asthma symptoms. It represents a potential target for clinical treatment.
DOI: 10.15468/dl.2wc79r
title: Occurrence Download

description: A dataset containing 5869 species occurrences available in GBIF matching the query:
{
 "and" : [
 "TaxonKey is Neogobius fluviatilis",
 "HasCoordinate is true",
 "HasGeospatialIssue is false"
 ]
}

 The dataset includes 5869 records from 76 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0002483-260120142942310/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.6084/m9.figshare.29042171
title: Assessment of the cytostasis and chromosomal instability potential of myricetin and its chemopreventive effect against bleomycin-induced cyto-genotoxicity

description: Myricetin (ME) is a major constituent of various foods and beverages consumed by humans, including vegetables, teas and fruits, and is primarily recognized for its iron-chelating, antioxidant, anti-inflammatory and anti-cancer properties. This study evaluated the cytostatic, genotoxic, and chemopreventive effects of ME in CHO-K1 cells using the Cytokinesis-Block Micronucleus (CBMN) assay and explored molecular interactions through <i>in silico</i> systems biology analysis. CHO-K1 cells were exposed to ME (2.5–40 µM). Cytostasis was assessed by the Cytokinesis-Block Proliferation Index (CBPI), and chromosomal instability was measured by the frequency of micronuclei (MNi), nucleoplasmic bridges (NPBs), and nuclear buds (NBUDs). ME at 40 µM significantly reduced CBPI, while concentrations of 20 and 40 µM increased chromosomal instability (<i>p</i> &lt; 0.05). For chemoprevention, ME (2.5–10 µM) was administered in pre-, co-, and post-treatment with bleomycin (BLM). ME significantly reduced BLM-induced MNi and NPBs in all protocols (<i>p</i> &lt; 0.05). <i>In silico</i> analysis revealed strong interactions between ME and key proteins related to DNA damage response, apoptosis, and bleomycin detoxification. Notably, the <i>in silico</i> analysis revealed a strong association between ME and bleomycin hydrolase (BLMH) and the interaction of ME with proteins related to DNA damage response and apoptosis regulation. Overall, ME exhibited genotoxicity at high concentrations but demonstrated a significant chemopreventive effect at lower, nontoxic doses. These findings provide insights into the dual biological activity of ME and support its potential use as a protective agent against genotoxic damage.
DOI: 10.6084/m9.figshare.29042171.v1
title: Assessment of the cytostasis and chromosomal instability potential of myricetin and its chemopreventive effect against bleomycin-induced cyto-genotoxicity

description: Myricetin (ME) is a major constituent of various foods and beverages consumed by humans, including vegetables, teas and fruits, and is primarily recognized for its iron-chelating, antioxidant, anti-inflammatory and anti-cancer properties. This study evaluated the cytostatic, genotoxic, and chemopreventive effects of ME in CHO-K1 cells using the Cytokinesis-Block Micronucleus (CBMN) assay and explored molecular interactions through <i>in silico</i> systems biology analysis. CHO-K1 cells were exposed to ME (2.5–40 µM). Cytostasis was assessed by the Cytokinesis-Block Proliferation Index (CBPI), and chromosomal instability was measured by the frequency of micronuclei (MNi), nucleoplasmic bridges (NPBs), and nuclear buds (NBUDs). ME at 40 µM significantly reduced CBPI, while concentrations of 20 and 40 µM increased chromosomal instability (<i>p</i> &lt; 0.05). For chemoprevention, ME (2.5–10 µM) was administered in pre-, co-, and post-treatment with bleomycin (BLM). ME significantly reduced BLM-induced MNi and NPBs in all protocols (<i>p</i> &lt; 0.05). <i>In silico</i> analysis revealed strong interactions between ME and key proteins related to DNA damage response, apoptosis, and bleomycin detoxification. Notably, the <i>in silico</i> analysis revealed a strong association between ME and bleomycin hydrolase (BLMH) and the interaction of ME with proteins related to DNA damage response and apoptosis regulation. Overall, ME exhibited genotoxicity at high concentrations but demonstrated a significant chemopreventive effect at lower, nontoxic doses. These findings provide insights into the dual biological activity of ME and support its potential use as a protective agent against genotoxic damage.
DOI: 10.11588/duerer.online.6970cc591e4d4
title: Eine Truhe, https://d-nb.info/gnd/1196241287
DOI: 10.6084/m9.figshare.28756084
title: Optimizing deoxidizer in maraging steel for additive manufacturing: Impact on oxide refinement and impact toughness

description: The high oxygen content in additive manufacturing powders (up to 100 ppm) significantly increases oxide inclusions and reduces toughness. This study explored various deoxidizers to control oxides in laser powder bed fusion-processed (L-PBFed) maraging steels. A strong deoxidizer (0.11 wt.% Al) forms 65 nm Al<sub>2</sub>O<sub>3</sub> due to its high oxide formation temperature. A weak deoxidizer (0.24 wt.% Si, 0.21 wt.% Mn) produces low-melting-point SiO<sub>2</sub>-Cr<sub>2</sub>MnO<sub>4</sub>, which grows fivefold (135 nm) after heat treatment. Trace deoxidizer (Si/Mn/Al/Ti &lt;0.01 wt.%) forms 45 nm TiO<sub>2</sub>-Cr<sub>2</sub>O<sub>3</sub>-SiO<sub>2</sub> and achieves the highest cryogenic toughness (84 J). Controlling deoxidizer content is essential for optimizing L-PBFed maraging steels. This study innovatively suggests limiting residual deoxidizers content to address increased oxide inclusions and reduced toughness caused by high oxygen (up to 100 ppm) in additive manufacturing-processed maraging steel.
DOI: 10.6084/m9.figshare.28756084.v1
title: Optimizing deoxidizer in maraging steel for additive manufacturing: Impact on oxide refinement and impact toughness

description: The high oxygen content in additive manufacturing powders (up to 100 ppm) significantly increases oxide inclusions and reduces toughness. This study explored various deoxidizers to control oxides in laser powder bed fusion-processed (L-PBFed) maraging steels. A strong deoxidizer (0.11 wt.% Al) forms 65 nm Al<sub>2</sub>O<sub>3</sub> due to its high oxide formation temperature. A weak deoxidizer (0.24 wt.% Si, 0.21 wt.% Mn) produces low-melting-point SiO<sub>2</sub>-Cr<sub>2</sub>MnO<sub>4</sub>, which grows fivefold (135 nm) after heat treatment. Trace deoxidizer (Si/Mn/Al/Ti &lt;0.01 wt.%) forms 45 nm TiO<sub>2</sub>-Cr<sub>2</sub>O<sub>3</sub>-SiO<sub>2</sub> and achieves the highest cryogenic toughness (84 J). Controlling deoxidizer content is essential for optimizing L-PBFed maraging steels. This study innovatively suggests limiting residual deoxidizers content to address increased oxide inclusions and reduced toughness caused by high oxygen (up to 100 ppm) in additive manufacturing-processed maraging steel.
DOI: 10.6084/m9.figshare.28675966
title: Ultra-high strength and ductility of low-Mn lightweight steel achieved through a four-phase lamellar structure design

description: Low-Mn lightweight steels typically face challenges in achieving high strength and ductility due to the presence of δ-ferrite, which also severely limits transverse elongation when present as long-strip formations. This study successfully overcame these limitations by constructing a four-phase lamellar structure, resulting in an optimal strength-ductility balance (∼1.0 GPa YS, ∼1.45 GPa UTS, and 14.0% UE) and a notable improvement in transverse elongation. The introduction of a soft phase and a strain transition zone near δ-ferrite and martensite enhanced strain distribution uniformity, while retained austenite, precipitation strengthening, and heterogeneous strengthening further contributed to the superior mechanical properties.
DOI: 10.6084/m9.figshare.28675966.v1
title: Ultra-high strength and ductility of low-Mn lightweight steel achieved through a four-phase lamellar structure design

description: Low-Mn lightweight steels typically face challenges in achieving high strength and ductility due to the presence of δ-ferrite, which also severely limits transverse elongation when present as long-strip formations. This study successfully overcame these limitations by constructing a four-phase lamellar structure, resulting in an optimal strength-ductility balance (∼1.0 GPa YS, ∼1.45 GPa UTS, and 14.0% UE) and a notable improvement in transverse elongation. The introduction of a soft phase and a strain transition zone near δ-ferrite and martensite enhanced strain distribution uniformity, while retained austenite, precipitation strengthening, and heterogeneous strengthening further contributed to the superior mechanical properties.