Biology subjects

Barcia, C.

Publications and source records attributed to Barcia, C..

3 recordsLinked to original sources

bioRxiv2025

Press Releases Shape Online Attention for Neuroscience Articles

Alternative indexes (altmetrics), such as the number of social media posts or news mentions, assess the relevance of a publication beyond academia. At the same time, composite metrics, like Altmetric Attention Score (AAS), gather these indicators to provide an overall measure of the online attention of an article. Communication departments at research institutions aim to help publications reach the general public and, therefore, play a key role in improving the altmetrics performance of scientific articles. However, the most effective strategies to achieve this remain unclear. No standardized protocols exist to guide communication professionals in maximizing the impact of their outreach efforts. Thus, in the present research, carried out by the communication department of a neuroscience research center, we conducted three complementary analyses to help to fill this gap. First, a study involving more than 3,000 neuroscience publications from 8 similar research centers revealed correlations between altmetrics and citations. Second, a retrospective analysis of 201 in-house articles found that active communication campaigns were associated with better altmetric performance, with notable differences between publications that included a press release (PR) and those that did not. Finally, a prospective experiment involving 25 articles examined changes in altmetrics before and after the dissemination of a PR or posting on X. Results showed that PRs significantly increased the number of news mentions and X posts, leading to an average rise of approximately 70 points in the AAS. These findings highlight the importance of PRs in maximizing the societal visibility and impact of scientific publications.

scientific communication and education↗

bioRxiv2024

Microglial low-affinity FcγR mediates the phagocytic elimination of dopaminergic neurons in Parkinsons disease degeneration

Microglia-mediated neuroinflammation contributes to dopaminergic (DA) neurodegeneration in Parkinsons disease (PD). It is thought that microglial cells interact with DA neurons of the substantia nigra pars compacta (SNpc), the most vulnerable region in parkinsonian neuropathology, playing a critical role through the process of neuronal loss. However, the specific mechanisms by which microglial reactivity is triggered and exerts such a deleterious effect remains unclear. Experimental models of PD in mice have shown that phagocytosis plays an essential role in the elimination of degenerating neurons, suggesting that blocking this microglial function could be beneficial to preserve remaining DA neurons. In the present work, we pinpoint the role of the Fc{gamma} receptor (Fc{gamma}R) as a potential trigger of microglial phagocytosis in PD. We found that the Fc{gamma}R is overexpressed in the degenerating SNpc in postmortem samples of PD patients, alongside histological indications of phagocytic microglia. Likewise, experimental models of PD also show increased Fc{gamma}R expression, together with evidence of similar phagocytosis events. Most importantly, blocking Fc{gamma}R in vitro, by using neutralizing antibodies, reduced the microglial-mediated elimination of DA cells. High resolution imaging revealed that the Fc{gamma}R is involved in phagocytic synapse formation, and appeared polarized, and segregated to actin-rich protruding cups, when interacting one-on-one towards single target DA cells. Additionally, by inhibiting Fc{gamma}R downstream actin-polymerizing signaling Cdc42, microglia were unable to eliminate DA cells. Finally, experiments in vivo, using an experimental model of PD in mouse, revealed that passive immunotherapy with Fc{gamma}R neutralizing monoclonal antibodies, as well as inhibiting its downstream signaling Cdc42, protect DA neurons from elimination. These results indicate that the Fc{gamma}R may be a critical factor inducing DA neuron phagocytosis in PD and suggest a novel immunotherapeutic strategy targeting microglia to preserve neuronal loss.

neuroscience↗

bioRxiv2020

Ursolic acid inhibits cell migration and promotes JNK-dependent lysosomal associated cell death in Glioblastoma multiforme cells

Ursolic acid (UA) is a bioactive compound which has demonstrated therapeutic efficacy in a variety of cancer cell lines. UA activates various signalling pathways in Glioblastoma multiforme (GBM), however, the relationship between cell death and migration has yet to be elucidated. UA induces a dose dependent cytotoxic response demonstrated by flow cytometry and biochemical cytotoxicity assays. Inhibitor and fluorescent probe studies demonstrated that UA induces a caspase independent, JNK dependent, mechanism of cell death. Migration studies established that UA inhibits GBM cell migration in a time dependent manner that is independent of the JNK signalling pathway. The cytotoxic insult induced by UA resulted in the formation of acidic vesicle organelles (AVOs), speculating activation of autophagy. However, inhibitor and spectrophotometric analysis demonstrated that autophagy was not responsible for the formation of the AVOs and confocal microscopy identified the AVOs as lysosomes. Further investigation using isosurface visualisation of confocal imaging determined co-localisation of lysosomes with the previously identified acidic vesicles, thus providing evidence that lysosomes are likely to be playing a role in UA induced cell death. Collectively, our data identifies that UA rapidly induces a lysosomal associated mechanism of cell death in addition to UA acting as an inhibitor of GBM cell migration. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=128 SRC="FIGDIR/small/987578v1_ufig1.gif" ALT="Figure 1"> View larger version (27K): org.highwire.dtl.DTLVardef@1b00447org.highwire.dtl.DTLVardef@e8e39eorg.highwire.dtl.DTLVardef@1b7d816org.highwire.dtl.DTLVardef@cb8d3b_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗