Nickel tolerance and phytoremediation potential of the aquatic plant Lemna minuta and the cyanobacterium Trichormus variabilis in monoculture and consortium

One of the main threats to aquatic conservation is heavy metal pollution, with nickel (Ni) among the most significant contaminants. The Ni tolerance and remediation potential of Lemna minuta (vascular plant) and Trichormus variabilis (cyanobacterium) in contaminated water were investigated. The phytotoxic effects of nickel sulfate (NiSO4·7 H2O; 6.47 mg/L) on these two species, were assessed after 7- and 14-days exposure by measuring morphological changes, growth (fresh weight) and key physiological parameters (chlorophyll, malondialdehyde, protein content and catalase activity). The ability of L. minuta and T. variabilis to remove Ni was compared in both monoculture (single species) and consortium (mixed species) by measuring the reduction in Ni concentration in the culture medium. Nickel exposure induced phytotoxic effects in both species, as shown by decreases in fresh weight, chlorophyll and protein content, and increases in malondialdehyde content and catalase activity. These effects were more pronounced in monocultures, particularly in T. variabilis, compared to consortia. Lemna minuta exhibited good Ni tolerance and remediation capacity, removing 75 % and 86 % of the metal from the solution after 7 and 14 days, respectively. Trichormus variabilis removed 36 % and 27 % of the Ni after the same exposure time. Consortia exhibited high Ni removal, reaching 80 % and 90 % after 7 and 14 days, but this was not statistically different to L. minuta monocultures. These results demonstrate the potential of L. minuta in the remediation of Ni-contaminated waters and suggest that consortia might enhance the tolerance and viability of both species under Ni-stress

De la parole au corps du monde. Lorand Gaspar à la croisée des langues, des cultures et des disciplines

La ville de Târgu-Mureş (Roumanie) a légué à la postérité un des écrivains les plus personnels et originaux de la deuxième moitié du XXe siècle. Lauréat des prix Guillaume Apollinaire (1967) et Goncourt de la poésie (1998), Lorand Gaspar, poète, traducteur, historien, photographe mais aussi remarquable médecin chirurgien, y voit le jour le 28 février 1925. Sa naissance dans une famille hongroise d’origine arménienne et le contact direct avec le milieu roumain lui ont façonné un triple enracinement culturel de départ. Cette sensibilité à la diversité culturelle a depuis toujours sillonné son parcours personnel, professionnel et créatif. Située au confluent des cultures et des disciplines, l’œuvre de cet écrivain francophone aux origines transylvaines a déjà suscité l’intérêt de nombreux chercheurs et plusieurs travaux universitaires lui ont été consacrés, dont une partie importante s’est constituée par le biais des nombreuses traductions réalisées à partir de et par Gaspar lui-même. Par ailleurs, le parcours littéraire de l’écrivain ne saurait se détacher de son activité professionnelle: en tant que médecin chirurgien, il est témoin de la souffrance de ses patients, qu’il tentera de combattre par son engagement quotidien et par le travail d’écriture, véritable moyen d’expression de sa connaissance du monde et de l’homme. Observateur attentif des lieux qu’il a connus, Gaspar se sert également du dispositif photographique pour dire en images tout son émerveillement au regard du monde. De ce fait, chez Gaspar cohabitent trois vocations apparemment distantes qui partagent néanmoins son désir de scruter ce corps du monde qui prend la forme de la chair, du sol rugueux, de la lumière, de la parole. Sous ce triple éclairage sont ici réunies les contributions issues du colloque international De la parole au corps du monde. Lorand Gaspar à la croisée des langues, des cultures et des disciplines qui a eu lieu à Târgu Mureş les 27 et 28 février 2025 à l’occasion du centenaire de la naissance du poète

Air pollution-related neurodegeneration: effects of magnetite nanoparticles on cultured human astrocytes and neurons

Air pollution is a critical global public health problem deeply entangled with social, economic and legislative factors worldwide and it is exacerbated by the rapid rate of urbanisation and industrialisation (Olloquequi J et al., 2024). A major contributor to global air pollution are the traffic-related air pollutants (TRAPs), including magnetite nanoparticles (MNPs). Air pollution is estimated to have caused 4.2 million premature deaths worldwide in 2019, 89% of which occurred in low- and middle-income countries. It is thus imperative to investigate whether the exposure to airborne PM-derived MNPs may pose a risk to human health. The causes reported for these premature deaths are mostly cardiovascular diseases, ischaemia and cancers (WHO, air quality guidelines, 2021). Nevertheless, to date, a bunch of clinical and epidemiological studies are increasingly demonstrating also the adverse association between TRAPs and neurological diseases (Gómez-Budia M et al., 2020). Indeed, recent studies have shown that in highly trafficked and industrialised urban areas (e.g. Mexico City, Manchester) dementia cases at a younger age increased (Maher BA et al., 2019). Airborne particulate matter (PM) pollution is considered as an important environmental risk factor for neurotoxicity and may potentiate the risk of developing neurodegenerative diseases such as Alzheimer's disease (AD). Neurodegenerative diseases are constantly increasing as the world’s population ages. In the early stages, these diseases can be triggered by different types of stimuli, all leading to chronic oxidative stress. Among TRAPs, PM2.5, which include MNPs, can be inhaled and directly reach the brain promoting the formation of reactive oxygen species (ROS) and inducing oxidative stress, one of the hallmarks of AD (Jankowska-Kieltyka M et al., 2021). In this work we focussed our attention on the biological impact of magnetite nanoparticles pollution on the promotion and development of neurodegenerative diseases, while also exploring the potential role of astrocytes in this context. In light of these considerations, the effects of MNPs and Amyloid-β (Aβ1-42) were evaluated on human astroglial and neuronal cell models. Firstly, we demonstrated that MNPs do not directly affect neuronal viability, whereas astrocyte viability is impaired. Otherwise, amyloid impairs the viability of both astrocytes and neurons. The interaction between magnetite nanoparticles and amyloid has a dual impact on astrocytes: in addition to reducing the viability of these cells, MNPs and amyloid also exert a synergistic effect when used in combination. In the brain, astrocytes can efficiently counteract oxidative stress through the activation of an antioxidant response (Baxter PS et al., 2016) and are crucial for neuronal function. Indeed, they provide structural and metabolic support to neurons, maintaining homeostasis of the extracellular space of the brain parenchyma (Durkee CA et al., 2019). Moreover, glial cells play a pivotal role in iron homeostasis in the central nervous system through the action of ferroportin (Fpn), the only known mammalian iron exporter, and ceruloplasmin (Cp), an enzyme with ferroxidase activity (Hohnholt MC and Dringen R, 2013). Cp is required for Fpn function; indeed, it is thought that this protein may play a protective role in neurodegenerative diseases. In this study we demonstrated that astrocytes activate a response that culminates in the up-regulation of System Xc- and ceruloplasmin, while the iron exporter ferroportin is not up-regulated. These modifications may precipitate an elevation in extracellular glutamate release, impaired iron efflux, thereby leading to an augmented intracellular labile iron pool and diminished cellular viability. Taken together these data suggest a potential correlation between iron homeostasis, oxidative stress and cytotoxicity in this context. Given the numerous essential functions that astrocytes fulfil, any dysfunction in these cells has the potential to contribute to the development of several neurological disorders, including neurodegenerative diseases such as AD (Sofroniew MV et al., 2010). Therefore, following an evaluation of the impact of magnetite nanoparticles and amyloid on astrocyte behaviour, it was essential to ascertain whether the observed alterations in astrocytes could potentially influence neurons, as part of this research project. The results show that astrocyte supernatant has a harmful impact on neuronal viability that lasts over time. The synergistic effect of MNPs and amyloid on neuronal death may be due to the release of soluble factors by astrocytes that accumulate over time, highlighting the exacerbating effect that MNPs may have in chronic conditions. Nevertheless, it is important to acknowledge that under identical experimental conditions, the viability of astrocytes is also adversely affected. Consequently, the reduction in neuronal viability may likewise be attributable to the diminished trophic support rendered by astrocytes. Our findings collectively suggest that while exposure of neurons to MNPs does not directly affect their viability, it can potentially induce neurotoxicity through the action of astrocytes. The role of astrocytes may be attributed to their capacity to produce and release soluble factors that affect neuronal function. In conclusion, these findings suggest that airborne pollution-derived magnetite nanoparticles may contribute to the increased prevalence of neurodegenerative diseases observed in highly trafficked and industrialised urban areas

On the Impact of Microbeamformers in 3-D High Frame Rate Ultrasound Imaging: A Simulation Study

Background and objective: three-dimensional ultrasound imaging is based on two-dimensional (2-D) arrays controlled by application-specific integrated circuits, which implement the so-called microbeamformer (μB) to reduce the channel count. μBs are designed for line-by-line scan sequences based on focused beams (FBs), providing low frame rates. On the other hand, high frame rate (HFR) imaging techniques using defocused beams are increasingly attractive for reconstructing detailed tissue and blood motion information. Although an increasing number of researchers works with μBs integrated into 2-D probes, there is limited literature on the influence of the μB on image quality in HFR imaging applications. Methods: This simulation work evaluates the μB impact on multi-plane HFR transthoracic echocardiography by considering a μB connected to sub-arrays of different sizes (from 2×2 to 8×8 elements). Scan sequences based on the transmission of FBs, focused wide beams (FWB), and planar diverging waves (PDW) were tested. B-mode images were reconstructed and compared to the ideal case (no μB) to assess the image resolution and contrast loss due to the μB. Results: Compared to the ideal case, the μB presence can yield resolution and contrast deterioration up to 17.5% and -26 dB, respectively. Such a deterioration corresponds to the transmission of widest PDW, and can be partially recovered through the synthetic transmit beams technique. Conclusion and significance: A μB designed for FB applications can be used for HFR imaging, although with impaired imaging quality. Guidelines are provided to achieve a suitable trade-off among image quality, μB size, channel number and frame rate